Deja Review USMLE Step 2 CK Second Edition

MEDICAL SURGICAL OVERVIEW OF THE STRUCTURES & FUNCTIONS OF THE NERVOUS SYSTEM 3 PARTS OF THE NERVOUS SYSTEM 1. Central NS Brain & Spinal cord

2. Peripheral NS 31 Spinal & Cranial

3. Autonomic NS Sympathetic NS & Parasympathetic NS

Somatic NS

C-8 T - 12 L- 5 S–5 C-1

I. Autonomic Nervous System A. Sympathetic NS (SNS) 1. Fight or Aggression Response 2. Release of Norepinephrine (adrenaline – cathecolamine) = Adrenal Medulla (potent vasoconstrictor) 3. All body activities increased except GIT (GIT decreased motility) Bodily Effects of SNS a. Mydriasis = Dilated pupil , to be aware of surroundings b. Dry mouth VS = Increase c. BP & HR c. RR d. Constipation e. Urinary Retention f. Increased BF to heart, brain, skeletal muscles 4.

Adrenergic or Parasympatholitic Response Adrenergic Agents

a. Epinephrine (Adrenaline) S/E : SNS Effects b. Anti-Psychotics ex. Haldol (Haloperidol) S/E : SNS Effects

B. Parasympathetic NS 1. Flight or Withdrawal Response 2. Release of Acetylcholine (ACTH) 3. All bodily activities decreased except GIT Bodily Effects of PNS

a. Meiosis = constriction of pupils b. Increased salivation c. BP & HR d. RR =bronchoconstriction e. Diarrhea =Increased Motility f. Urinary Frequency

VS:decreased

4.

Cholinergic or Vagal or Sympatholitic Response

a. Beta-Adrenergic Blocking Agents (Beta-Blockers) (all end in –‘lol’) Ex. Propanolol, Metopanolol Blocks release of norepinephrine, Decrease body activities except GIT (diarrhea) S/E: B – broncho spasm (bronchoconstriction) E – elicits a decrease in myocardial contraction T – treats HPN A – AV conduction slows down Given To/As: a. Angina Pectoris b. MI – beta-blockers to rest heart c. Anti HPN agents: -Beta blockers (-lol) - Ace inhibitors (-pril) ex ENALAPRIL, CAPTOPRIL - Calcium antagonist ex. CALCIBLOC or NEFEDIPINE Created by Niňa E. Tubio

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b. Cholinergic agents

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d. Anti-arrhythmic agents (arrhythmia= irregular contraction of the heart) Ex. Mestinon (prostigmine) given to MG to increase ACTH S/E = PNS *Antidote – anti cholinergic agents Atropine Sulfate – S/E – SNS

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II. CNS (Brain & Spinal Cord) Part 1 : Parts: A. Cells – neurons = Basic living units Properties and Characteristics a. Excitability – ability of neuron to be affected by changes in the external environment b. Conductivity – ability of neuron to transmit a wave of excitation from one cell to another c. Permanent cells – once destroyed, can not regenerate (ex. heart, retina, brain, osteocytes) 3 Types of Cells According To Its Regenerative Capacity: 1. Labile – once destroyed, can regenerate: Epidermal, GIT, lung cells, GUT cells 2. Stable – capable of regeneration BUT limited survival time: salivary gland, pancreas, liver, kidney cells 3. Permanent – cannot regenerate: retina, brain, heart, osteocytes & myocardial cells B. Neuroglia : can cause brain tumors Functions & its 4 Types: 1. Astrocyte = maintain integrity of blood brain barrier (semi-permeable/selective) 2. Microglia = stationary cells 3. Ependymal Cells 4. Oligodendrocytes 1. Astrocytes: • # 1 type of brain tumor= Astrocytoma ( 90 – 95%) • Toxic substance that destroys astrocyte & passes the Blood Brain Barrier a. Ammonia = a cerebral toxin , product of protein catabolism Hepatic encephalopathy (liver cirrhosis) = death of liver d/t necrosis Primary Cause : Malnutrition Major Cause : Alcoholism Early Sign : Asterixis (Flapping hand tremors) Late Sign : Headache, Restlessness, Fetor Hepaticus (ammonia-like breath) Hepatic Coma -----N.P. Airway b. Bilirubin = yellow pigment -------- jaundice (Icteric Sclerae) others: Bilivedrin = green pigment Hemosiderin = golden-brown pigment Hemoglobin = red cell pigment

Hepatitis * Carotenemia = yellowish discoloration of the skin *Sign of Tumor in the Pituitary Gland

* Kernicterus (Hyperbilirubinemia) - Increased bilirubin in the brain, irreversible brain damage

b. Carbon Monoxide :Tx for Carbon monoxide poisoning = Hyperbaric Oxygenation (100%) Parkinson’s Disease Early Sign: Pill-Rolling Tremors d. Lead

Seizure = Antidote for lead poisoning ------ Calcium EDTA

e. Ketones - acids, CNS depressant Ketones in Blood DKA ---- Type 1 DM d/t increase fat catabolism free fatty acids Cholesterol Leads to: Atherosclerosis Created by Niňa E. Tubio

Ketones ----- DKA : Early Signs = Weakness/ Weight Loss Late Signs = Acetone Breath & Kussmaul’s Breathing 3

Leads to Coma HPN ==MI or Stroke --Death 2. Microglia = Stationary Cells ------- Phagocytosis • • • • •

Organ Brain Blood Kidney/Liver Lungs SC Tissues

Macrophage ---------- Microglia ---------- Monocytes ---------- Kupffer Cells ---------- Alveolar Macrophages ---------- Histiocytes

3. Ependymal Cells = acts as a defense in the CNS along with microglia secretes a glue ------ Chemoattractants 4. Oligodendrocytes = produces myelin sheath: acts as a cover for neurons acts as an insulator w/c facilitates rapid nerve impulse transmission No myelin sheath – degenerates neuron Damage to myelin sheath causes demyelinating disorders

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DEMYELINATING DISEASE 1. ALZHEIMER’S DISEASE – atrophy of brain tissue due to a deficiency of acetylcholine - Degenerative disorder - A type of Dementia Predisposing Factors: 1. Aging 2. Aluminum Accumulation S&Sx: A – amnesia – loss of memory

*Short-Term -- Anterograde Amnesia *Long-Term Retrograde Amnesia A – apraxia – unable to determine purpose of object thru movement A – agnosia – unable to recognize familiar object A – aphasia – 2 types: 1. Expressive – Brocca’s aphasia – inability to speak ex. (+) nodding TX: use of picture-boards - damage to frontal lobe - Brocca’s ---- motor speech center in the frontal lobe 2. Receptive – Wernicke’s aphasia – unable to understand spoken words ex. (+) illogical thoughts - damage to Temporal lobe - Wernicke’s Area --- general interpretative area - Common to Alzheimer – Receptive Aphasia - Drug of choice – ARICEPT or COGNEX ----- best given : at bedtime 2. MULTIPLE SCLEROSIS (MS) -Chronic intermittent disorder of CNS  Characterized by white patches of demyelenation in brain & spinal cord.  Remission & exacerbation  Common – women, 15 – 35 y/o Predisposing factor: 1. Idiopathic 2. Slow growing virus 3. Autoimmune – (supportive & palliative treatment only) self-killing immunity Normal Resident Antibodies: 5 types IgG – can pass placenta – passive immunity, temporary IgA – body secretions – saliva, tears, colostrum IgM – acute inflammation IgE – allergic reactions IgD – chronic inflammation S & Sx of MS: 1. Visual disturbances :

a. *Blurring of vision = Initial sign b. Diplopia/ double vision c. Scotomas (blind spots) 2. Impaired sensation to touch, pain, pressure, heat, cold: a. Numbness b. Tingling c. Paresthesia 3. Mood swings – common : EUPHORIA (sense of elation ) 4. Impaired motor function: a. Weakness b. Spasticity –“ tigas” c. Paralysis 5. Impaired cerebellar function Triad Sx of MS (INA) I – intentional tremors N – nystagmus A – Ataxia - unsteady gait

CHARCOT’S TRIAD (INA)

6. Scanning of Speech 7. Urinary retention or incontinence 8. Constipation Created by Niňa E. Tubio

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9. Decrease sexual ability Dx: 1. CSF analysis thru lumbar puncture : bet. L3 & L4 : Reveals CHON & IgG 2. MRI – reveals site & extent of demyelination 3. Lhermitte’s Sign : confirmatory Dx of MS - continuous contraction & pain of the SC following laminectomy ( removal portion of lamina) Nsg Mgt: -

Supportive mgt 1.) Administer Meds as ordered a. ACTH ( adrenocorticotropic hormone) : Acute exacerbation – to reduce edema at the site of demyelination to prevent paralysis - compression of spinal nerves b. Baclopen (Lioresol) or Dantrolene Na (Dantrene) : To c. Interferons – to alter immune response d. Immunosuppressant e. Diuretics f. Bethanecol Chloride ( Urecholine) : N.M.   

muscle spasticity

Administer only SC Monitor S/E : wheezing, bronchospasm Monitor breath sounds 1 hr. after SC admin.

h. Anti-spasmodic (Prophanthelene Bromide) Pro-banthene & anti-cholinergic 2. Maintain side rails 3. Assist passive ROM exercises – promote proper body alignment 4. Prevent complications of immobility (q 2 hr. elderly q 1 hr.) 5. Encourage fluid intake & increase fiber diet – to prevent constipation 6. Provide catheterization d/t urinary retention 7. Avoid heat application 8.. Give diuretics 9. Increase fiber & provide acid-ash diet – to acidify urine & prevent bacteria multiplication Ex. Grape, Plums, Cranberry, Orange juice, Prune juice, pineapple juice,Vit C *3 Causes of UTI In Women   

Shorter Urethra F= 1-2.5 inches (3-5 cm.) Poor Perineal Care Moist Vaginal Area

M= 5-6-8 inches (16-20 cm)

PART II: Compositions of Cord & Spinal cord 80% - brain mass 10% - CSF 10% - blood 1st: Brain mass A. CEREBRUM– Largest Part Function:

Connects Right & Left cerebral hemisphere - Corpus collusum 1. Sensory 2. Motor 3. Integrative

Compose of 6 Lobes: 1.) Frontal (garbled speech) a. Controls motor activity b. Controls personality development c. Where primitive reflexes are inhibited d. Site of development of sense of Humor Created by Niňa E. Tubio

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e. Control higher cortical thinking f. Brocca’s area – speech center Damage - expressive aphasia 2.) Temporal – a. Hearing b. Short term memory c. Wernicke's area – gen. interpretative Damage – receptive aphasia 3.) Parietal lobe – appreciation & discrimination of sensory impulses - Pain, touch, pressure, heat & cold 4.) Occipital – vision 5.) Insula/island of reil/ Central lobe- controls visceral fx Function: - activities of internal organ 6.) Rhinencephalon/ Limbic - Smell, libido, long-term memory

*Anosmia- absence of smell

Basal Ganglia – areas of gray matter located deep within a cerebral hemisphere  Extra pyramidal tract  Releases dopamine- a neurotransmitter  Controls gross voluntary unit Dopamine :Parkinson’s or Huntington’s Acetylcholine :Myasthenia Gravis & Alzheimer’s

Dopamine : Schizophrenia Acetylcholine : Bipolar Disorder

B. MID BRAIN/ MESENCEPHALON  relay station for sight & hearing  Controls size & reaction of pupil ( Normal: 2 – 3 mm)  Controls hearing acuity ( Normal Hearing Acuity : 30-40 decibels) *PERRLA= Pupil dilated round & reactive to light & accommodation :Normal * Isocoria – normal size (equal) *Anisocoria – uneven size – damage to mid brain C. DIENCEPHALON -------between brain 2 Parts: 1.Thalamus – acts as a relay station for sensation 2. Hypothalamus – Thermo-regulating center of temp, sleep & wakefulness, thirst, appetite/ satiety center Controls some emotional responses like fear, anxiety Controls pituitary function. D. BRAIN STEM a. PONS – Pneumotaxic center – controls rate & depth of respiration Cranial 5 – 8 CNS b. MEDULLA OBLONGATA- lowest portion of the brain -controls heart rate, respiratory rate, swallowing, vomiting, hiccups/ singutus -Vasomotor center - Site of Spinal Decuissation Termination, CN 9, 10, 11, 12 E. CEREBELLUM – smallest part of the brain - Controls posture, gait, balance, equilibrium Cerebellar Tests: a.) R – Romberg’s test- needs 2 RNs to assist - Pt. in Normal anatomical position 5 – 10 min (+) Romberg’s test is (+) ataxia or unsteady gait/drunken movement w/ loss of balance --seen in MS. b.) Finger to nose test – (+) To FTNT – seen in Dymetria – inability to stop a movement at a desired point c.) Alternate pronation & supination Palm up & down . (+) To alternate pronation & supination or damage to cerebellum Created by Niňa E. Tubio

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– seen in Dymetria 2nd: CerebroSpinal Fluid (CSF) 10% Blood 10% Compose of lipids  Normal amount produced: 125-250 ml /day  Produced at the Choroid Plexus  Composition: Clear, colorless, odorless: (+) glucose, protein,WBC but not RBC  Fx: cushions the brain  Alters if there is obstruction in the flow of CSF = Increase ICP Enlargement of the skull posteriorly d/t early closure of the posterior fontanel----Hydrocephalus 3rd: Blood Stroke: partial/total obstruction in brain blood supply :

2 Commonly Affected artery: 1. ICA or Internal Carotid Artery 2. MCA or Middle Cerebral Artery

*Composition of brain - based on Monroe Kellie Hypothesis o Skull is a closed container. Any alteration in 1 of 3 intracranial components = increase in ICP *Normal ICP – 0 – 15 mmHg Foramen Magnum = the hole in the skull where spinal cord enters C1 – atlas : carrying the entire skull C2 – axis ------------After C1 is the location of the medulla oblongata Brain Herniation = when the medulla forced thru in the foramen : Observe for signs of ICP (+) Projectile vomiting , irregular respiration & HR Observe for 24 hrs. before MRI DISORDER:

1. INCREASED ICP – increase IC bulk is due to increase in 1 of the IC components A. Predisposing factors:

1.) Head injury 2.) Tumor 3.) Localized abscess 4.) Hemorrhage (stroke) 5.) Cerebral edema 6.) Hydrocephalus 7.) Inflammatory conditions - Meningitis, encephalitis

B. S&Sx Earliest Sx: a.) Change or decrease LOC – Restlessness to confusion (conscious, lethargy, stupor, coma) - Disorientation to lethargy *conscious = awake - Stupor to coma Late Sx: a. Change in V/S : always a late sx 1. BP (systolic increase, diastole- same) Normal adult BP 120/80 : 40 (normal PP) 2. Widening pulse pressure Ex. Increase ICP = BP 140/80 = 140 – 80= 60 PP (wide) 3. RR : Cheyne-Stokes =rapid respiration w/ periods of apnea 4. Temperature increase DIFFERENCE BET.

SHOCK : & INCREASE ICP: Decrease BP Increase BP Increase HR Decrease HR CUSHING’S EFFECT Increase RR Decrease RR Decrease Temp Increase temp Narrowing PP Widening PP b.) Headache c.) Projectile vomiting d.) Papilledima (edema of optic disk – outer surface of retina) e.) Abnormal Posturing 1. Decorticate = abnormal flexion of arms = damage to cortico spinal tract 2. Decerebrate = abnormal extension of arms = damage to upper brainstem, cerebrum, midbrain & pons Except: Flaccid = loss of muscle tone, damage to the lower brain, medulla

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f. Uncal herniation – unilateral dilation of pupil g. Possible seizure Nursing Management: 1.) Maintain patent a/w & adequate ventilation a. Prevention of hypoxia =decrease tissue oxygenation & hypercarbia =increase in CO2 retention Hypoxia – cerebral edema - increase ICP Early Sx:

R – restlessness A- agitation T- tachycardia

Late Sx: B – bradycardia “RAT”

* Powerful respiratory stimulant : CO2 ---an

E – extreme restlessness D – dyspnea C – cyanosis =late

“BEDC”

CO2 retention/ hypercarbia ---stimulate medulla O.

stimulate lungs to Hyperventilate 2. Before & after suctioning, hyperventilate 100% - decrease CO2 – excrete CO2 Suctioning – 10-15 seconds, max 15 seconds Ambu bag – pump upon inspiration 3. Assist in mechanical ventilation 4. Monitor VS & I&O, neuro check 5. Positioning -- Elevate head of bed 30- 45 degrees angle neck in neutral position unless C/I to promote venous drainage 4. Limit fluid intake 1,200 – 1,500 ml/day (FORCE FLUID means: Increase fluid intake/day – 2,000 – 3,000 ml/day)- not for inc ICP. 5. Prevent complications of immobility 6. Prevent increase ICP by: a. Maintain quiet & comfy environment b. Avoid use of restraints – lead to fractures c. Maintain side rails up d. Instruct patient to avoid activities leading to:Valsalva maneuver or bearing down -Avoid straining of stool(give laxatives/ stool softener Dulcolax/ Duphalac) - Excessive cough – antitussive (Dextrometorpham) -Excessive vomiting – anti emetic (plasil) - Avoid Lifting of heavy objects, Bending & stooping - Avoid clustering of nursing activities 7. Administer meds as ordered: 1.) Osmotic diuretic – Mannitol/Osmitrol: promotes cerebral diuresis by decompressing brain tissue Nursing considerations: Mannitol 1. Monitor BP – S/E: hypotension 2. Monitor I&O every hr. report if < 30cc out put 3. Administer via side drip 4. Regulate fast drip – to prevent formation of crystals/precipitate 5. Inform client, will feel flushing sensation as drug is introduced 2.) Loop diuretic - Lasix (Furosemide) in ampule Nursing Mgt: Lasix Same as Mannitol except - Lasix is given via IV push (expect urine after 10-15mins) should be in the morning. If given at 7am. Pt will urinate at 7:15 Action of Lasix within 15 minutes. Max effect – 6 hrs due (7am – 1pm) S/E of LASIX 1. Hypokalemia (Normal K-3.5 – 5.5 meg/L) S&Sx : Compared to Hyperkalemia: 1. Weakness & fatigue 1. Irritability & Agitation 2. Constipation 2. Diarrhea, abdominal cramps 3. (+) “U” wave in ECG tracing 3. Peaked T-wave both will lead to arrhythmia Nursing Mgt: 1. Administer K supplements – ex. Kalium Durule, Oral Kcl Potassium Rich food: ABC’s of K Vegetables Fruits A - asparagus A – apple B – broccoli (highest) B – banana – green (highest) Created by Niňa E. Tubio

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C – carrots

C – cantaloupe/ melon O – orange (increase) Vit A – squash, carrots yellow vegetables & fruits, spinach, chesa Iron – raisins, *Food appropriate for toddler – spaghetti! Not milk – increase bronchial secretions, no grapes – may choke S/E of Lasix: 2. Hypocalcemia or Tetany: life-threatening (Normal level Ca = 8.5 – 11mg/100ml) S&Sx : Weakness Paresthesia (+) Trousseau sign or carpo-pedal spasm – pathognomonic (+) Chvostek’s sign Complications: Arrhythmia Laryngospasm N. M. - Administer – Ca gluconate – IV slowly Ca gluconate toxicity: Sx : seizure – administer Mg SO4 Mg SO4 toxicity– administer Ca gluconate : “BURP”

B – BP decrease U – urine output decrease R – RR decrease P – patellar reflexes absent

3. Hyponatremia S/Sx:

(Normal Na level = 135 – 145 meg/L) Hypotension Signs of Dehydration Early signs – thirst and agitation for adults --------------children: tachycardia, dry mucous m. Mgt: force fluid 2-3 L/day Administer isotonic fluid sol 4. Hyperglycemia – Increase blood sugar level P – polyuria P – polyphagia 3 P’s of Hyperglycemia P – polydipsia Nsg Mgt: a. Monitor FBS (Normal =80 – 120 mg/dl) *Lasix can be given to DM but strict FBS monitoring 5. Hyperurecemia – increase serum uric acid = by product of purine metabolism Gouty arthritis

kidney stones- renal colic (pain) Cool moist skin Sx joint pain & swelling ----great toe affected ----gouty arthritis Nsg Mgt of Gouty Arthritis a.) Cheese (not sardines, anchovies, organ meat) (Not good if pt taking MAO) b.) Force fluid c.) Administer meds – Allopurinol/ Zyloprim – inhibits synthesis of uric acid – drug of choice for gout: Colchicene – acute gout drug of choice ---promotes excretion of uric acid Kidney stones – renal colic (pain). Cool moist skin Mgt: 1.) Force fluid 2.) Meds – narcotic analgesic Morphine SO4 3.) Strain all urine using gauze pads S/E of Morphine SO4 toxicity Respiratory depression (check RR 1st) Antidote for morphine SO4 toxicity –Narcan (NALOXONE) Naloxone toxicity – tremors

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Cont. Increase ICP meds 3.) Corticosteroids - Dexamethsone – decrease cerebral edema (Decadrone) *Steroids best given: 2/3 dose am & 1/3 dose pm - to mimic normal diurnal rhythm 4.) Mild analgesic – codeine SO 5.) Anti consultants – Dilantin (Phenytoin) Increase ICP what is the immediate nsg action? Administer Mannitol as ordered Elevate head 30 – 75 degrees Restrict fluid Avoid use of restraints *Nsg Priority – ABC & safety Pt. suffering from epiglotitis. What is nsg priority? a. Administer steroids – least priority b. Assist in ET – temp, a/w c. Assist in tracheotomy – permanent (Answer) d. Apply warm moist pack? Least priority Rationale: Wont need to pass larynx due to larynx is inflamed. ET can’t pass. Need tracheostomy onlyMagic 2’s of Drug Monitoring Toxicity Level: “DLADA” Drug

Normal Range

Toxicity

Classification

D – digoxin L - lithium A – aminophylline D – Dilantin A – acetaminophen

.5 – 1.5 meq/L .6 – 1.2 meq/L 10 – 19 mg/100ml 10 -19 mg/100 ml 20 10 – 30 mg/100ml

2 2 20

D- Digitalis (Digoxin)

– increase cardiac contraction = increase CO

200

Cardiac glycosides Antimanic Bronchodilator Anticonvulsant Narcotic analgesic

Indication CHF Bipolar Disorder COPD Seizures Osteoarthritis

Cardiac Glycosides

Nursing Mgt: 1. Check PR, HR (if HR below 60bpm, don’t giveDigoxin) Increase force of cardiac contraction Digitalis toxicity – antidote - Digibind a. Anorexia increase cardiac output b. n/v GIT c. Diarrhea d. Confusion e. Photophobia f. Changes in color perception – yellow spots-----Xantopsia L – lithium (lithane) decrease levels of norepinephrine, serotonin, and acetylcholine Anti-manic agent Lithium toxicity S/Sx a. Anorexia *N.M. 1. Force Fluid b. n/s 2. Increase intake in diet 4-10g/d c. Diarrhea d. Dehydration – force fluid, maintain Na intake 4 – 10g daily e. Hypothyroidism f. Fine Tremors CRETINISM– the only endocrine disorder that can lead to mental retardation A – aminophyline (Theophylline) ---dilates the bronchial tree *Seizure= 1st attack *Febrile seizure= normal 5 y/o S/Sx : Aminophylline toxicity: * Epilepsy = succeeding attacks 1. Tachycardia Created by Niňa E. Tubio

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2. Hyperactivity – restlessness, agitation, tremors (CNS excitability) N.M. ---Avoid giving food with Aminophylline a.Cheese/butter– food rich in tyramine, avoided only if pt is given MAOI b. Beer/ wine – c. Hot chocolate & tea – caffeine – CNS stimulant tachycardia d. Organ meat/ box cereals – anti parkinsonian MAOI – antidepressant m AR plan n AR dilcan lead to CVA or hypertension crisis p AR nate 3 – 4 weeks - before will take effect Anti Parkinsonian agents – Vit B6 Pyridoxine reverses effect of Levodopa D – dilatin (Phenytoin) – anti convulsant/seizure Nursing Mgt: 1. Mixed with plain NSS or .9 NaCl to prevent formation of crystals or precipitate o Do sandwich method o Give NSS then Dilantin, then NSS! 2. Instruct the pt to avoid alcohol – bec. alcohol + dilantin can lead to severe CNS depression Dilantin toxicity: “GHAN” *Osteoarthritis: Sign –Heberdens nodes S/Sx: G – gingival hyperplasia – swollen gums i. Oral hygiene – soft toothbrush ii. Massage gums H – hairy tongue A - ataxia N – nystagmus – abnormal movement of eyeballs A – acetaminophen/ Tylenol – non-opoid analgesic & antipyretic – febrile pts a. Acetaminophen toxicity : 1. Hepato toxicity : Monitor liver enzyme SGPT (ALT) – Serum Glutamic Pyruvate Transaminase SGOT- Serum Glutamic Oxaloacetic Transaminase 2. Monitor BUN (10 – 20) *Creatinine (.8-1)most reliable, indicative for kidney clearance b. Acetaminophen toxicity can lead to hypoglycemia:”TIRED” T – tremors / Tachycardia I – irritability R – restlessness E – extreme fatigue D – depression Diaphoresis/Nightmares *Antidote for acetaminophen toxicity – Acetylcesteine ---- Prepare suctioning apparatus Exercise:

The following are symptoms of hypoglycemia except: a. Nightmares b. Extreme thirst – hyperglycemia symptoms

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c. Weakness

d. Diaphoresis

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PARKINSONS DISEASE (Parkinsonism)

-

Chronic, progressive disease of CNS characterized by degeneration of dopamine producing cells in substancia nigra at mid brain & basal ganglia (produces dopamine)

Mngt: Palliative & Supportive Only Predisposing Factors: 1. Poisoning (lead & carbon monoxide) 2. Hypoxia 3. Arteriosclerosis 4. Encephalitis 5. Drug Overdose High doses of the ff: a. Reserpine (serpasil)-----than only anti-HPN with S/E of depression -----suicidal ----- only HPN known to be link to breast cancer ----- promote safety b. Methyldopa (aldomet)---Anti-HPN c. Haloperidol (Haldol) - anti psychotic d. Phenothiazine - anti psychotic S/E of anti-psychotic drugs – Extra Pyramidal Symptom Over medication of anti psychotic drugs – neuroleptic malignant syndrome characterized by tremors (severe) S/Sx: Parkinsonism: 1. Pill-rolling tremors of extremities – 1st Sign 2. Bradykinesia – slow movement-----2nd Sign 3. Over fatigue 4. Rigidity (cogwheel type) ------- a. Stooped posture b. *Shuffling c.Propulsive gait 5. Mask like facial expression with decrease blinking of the eyelids 6. Monotone speech 7. Difficulty rising from sitting position 8. Mood labilety – Depression– suicide Nsg priority: Promote safety 9. Increase salivation – drooling type 10. Autonomic signs:  Increase sweating  Increase lacrimation  Seborrhea (increase sebaceous gland)  Constipation  Decrease sexual activity Nsg. Mgt. 1.) Administer Meds:Anti-parkinsonian agents Levodopa (L-Dopa)-------short-acting Carbidopa (Sinemet), Amantadine Hcl (Symmetrel)----long-acting Mechanism of action: Increase levels of dopa – relieving tremors & bradykinesia S/E of anti-parkinsonian  Anorexia  n/v  Confusion  *Orthostatic hypotension  Hallucination  Arrhythmia, GIT irritation ( administer with meals) Contraindication: 1. Pt. with glaucoma----because L-dopa intra-ocular pressure (N: 12-21 mmHg) 2. Pt. taking MAOI (Parnate, Marplan, Nardil) MAOI = Monoamine Oxydase Inhibitor ( anti-depressant) Created by Niňa E. Tubio

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= Takes effect : 2-6 wks. =If on MAOI avoid: Tyramine, tryptophan rich foods ex. aged cheese, liver, beer, alcohol----leads to hypertensive crisis—stroke Nsg. Mgt. when giving anti-parkinsonian a. Take with meals – to decrease GIT irritation b. Inform pt – urine/ stool may be darkened c. *Instruct pt. not to take food Vit B6 (Pyridoxine) cereals, organ meats, green leafy veg   

Because Vit. B6 reverses therapeutic effects of levodopa Only increase intake of Vit. B6 in taking INH (isoniazid, anti-TB) Isonicotinic Acid Hydrazide-----effect-----peripheral neuritis

2.) Anti- cholinergic agents – relieves tremors *Artane mechanism – inhibits acetylcholine *Cogentin action ---S/E - SNS 3.) Antihistamine – Diphenhydramine Hcl (Benadryl) – take at bedtime---relieves tremors S/E: adult– drowsiness – avoid driving & operating heavy equipment. Child – Hyperactivity (CNS excitability) 4.) Dopamine agonist: Bromocriptine Hcl (Parlodel)---relieves rigidity, bradykinesia S/E: CNS depression, Check RR Nsg. Mgt. 1.) 2.)

3.)

Maintain siderails to prevent falls Prevent complications of immobility - Turn pt every 2h - Turn pt every 1 h – elderly -Turn affected extremity every 30 minutes Assist in passive ROM exercises to prevent contractures

4.)

Maintain good nutrition: Protein CHON – in am CHON – in pm – to induce sleep – d/t Tryptopan ex. milk

5.)

Increase fluid in take, high fiber diet to prevent constipation

6.)

Assist in surgery – Stereotaxic Thalamotomy Common complications: a. Subarachnoid hemorrhage b. Encephalitis c. Aneurysm Assist in ambulation

7.)

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MYASTHENIA GRAVIS (MG) –A neuromuscular disorder characterized by a disturbance in transmission of impulses from nerve to muscle cell at neuro muscular junction leading to descending muscle weakness. Predisposing Factors:  Common in Women, 20 – 40 y/o, Unknown cause or idiopathic  Autoimmune – release of cholenesterase (enzyme that destroys acetylcholine) Pathophysiology: Cholinesterase destroys ACTH ACTH

Descending muscle weakness

M.G.

S/ Sx: 1.) Ptosis – drooping of upper lid ( initial sign) Palpebral fissure – normal opening of upper & lower lids 2.) Diplopia (double vision) 3.) Mask-like facial expression 4.) Dysphagia 5.) Weakening of laryngeal muscles – hoarseness of voice 6.) *Respiratory muscle weakness – lead respiratory arrest. Prepare at bedside tracheostomy set 7.) Extreme muscle weakness during activity especially in the morning. Priority: to watch out for: a. A/W b. Aspiration c. Physical immobility Dx. Test: 1. Tensilon test (Edrophonium Hcl) – an anti-cholinesterase/cholinergic agent----short-acting only) Administer to pt. for temporary relief for 5 – 10 mins. (+) for M.G. 2. CSF analysis- reveals cholinesterase Nsg Mgt. 1. Maintain patent a/w & adequate ventilator by: a.) Assist in mechanical ventilator – attach to ventilator b.) Monitor pulmonary function test using spirometer 2. Monitor VS, I&O neuro check, muscle strength or motor grading scale (4/5, O/S, etc) 3. Siderails up 4. Prevent complications of immobility 5. NGT feeding to prevent complications 6. Administer medication as ordered a. Cholinergics or anticholinesterase agents Mestinon (Pyridostinine) Action: Increases ACTH Neostignine (prostigmin) S/E : PNS b. Steroids, Corticosteroids – to suppress immune response Decadron (dexamethasone) Monitor for 2 types of Crisis: Myastinic crisis Cholinergic crisis 1. Under medication Cause: Over medication 2. Stress 3. Infection S/Sx - PNS S&Sx: 1. Unable to see – Ptosis & diplopia Mgt. 2. Dysphagia Administer anti-cholinergic 3. Unable to breath 1. Atropine SO4 Mgt.: Administer cholinergic agents: Mestinon S/E: SNS – dry mouth 7. Assist in surgical procedure – Thymectomy (removal of thymus) 8. Assist in plasmapheresis – filtering of blood 9. Prevent complication – Respiratory arrest----prepare tracheostomy set at bedside Cause:

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GBS – GUILLIAN BARRER SYNDROME

  

A disorder of the CNS characterized by bilateral symmetrical polyneuritis leading to ascending paralysis Polyneuritis ----- inflammation of the peripheral nerves Can leadto slow but complete recovery

Predisposing Factors: 1. Cause – unknown, idiopathic 2. Auto immune 3. *R/t antecedent viral infection (from LRTI) 4. Immunizations S&Sx 1. 2. 3.

4. 5. 6.

Clumsiness -------- Initial sign of GBS Ascending muscle weakness – lead to paralysis Dysphagia Decrease or diminished DTR (deep tendon reflexes) -----Paralysis *Alternate HPN to hypotension – complication: Can lead to arrhythmia Autonomic changes: a. Increase sweating b. Increase lacrimation c. Increase salivation d. Constipation

Dx: Most important: CSF analysis thru lumbar puncture reveals increase in : IgG & CHON---same with MS Nsg Mgt. 1. Maintain patent a/w & adequate vent a. Assist in mechanical vent b. Monitor pulmonary function test 2. Monitor vs., I&O neuro check, ECG tracing due to arrhythmia 3. Siderails 4. Prevent complicarions – immobility 5. Assist in passive ROM exercises 6. Institute NGT feeding 7. Administer medications as ordered: 1. Anti-cholinergic – Atropine SO4 2. Corticosteroids – to suppress immune response 3. Anti arrhythmic agents: a.) Lidocaine /Xylocaine—S/E: confusion & agitation b.) Bretyllium------blocks release of norepinephrine c.) Quinidines/Quinitine – anti malarial agent & anti-arrythmic > Toxic effect – Cinchonism Quinidine toxicity: S/E – anorexia, n/v, headache, vertigo, visual disturbances 8.

9.

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*Malaria ---king of tropical disease----antidote----Queen (Quinidine) Assist in plasmapheresis Prevent complications – a. Arrhythmias b. Respiratory arrest

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INFLAMMATORY CONDITIONS OF THE BRAIN Anatomy: Meninges –a 3-fold membrane that covers the brain & spinal cord Fx: 1. Protection & support 2. Nourishment 3. Blood supply 3 layers: 1. Duramater (outermost 2. Arachmoid matter (middle) 3. Pia matter (outermost)

in bet. is sub dural space sub arachnoid space

where CSF flows L3 & L4

1. MENINGITIS – An inflammation of the meninges of the brain & spinal cord Etiology:

a. b. c. d.

Meningococcus---most dangerous type Pneumococcus Hemophilous influenza – common to children Streptococcus –a type of adult meningitis

MOT:

Direct transmission via droplet nuclei (airborne)

S&Sx

        



Stiff neck or Nuchal Rigidity ------Initial Sign of meningeal irritation Headache Projectile vomiting Photophobia Fever chills, anorexia General body malaise Weight loss Decorticate/decerebration – abnormal posture Possible seizure Opisthotonus (arching of the back)-----2nd intital sign

*Pathognomonic Sign:

(+) Kernig’s & Brudzinski sign Leg pain

Neck pain

Dx: 1.

Lumbar Puncture: lumbar/ spinal tap – use of hallow spinal needle Aspiration in the sub arachnoid space between L3 & L4 or L4 & L5.

Nsg Mgt . For Lumbar Puncture------- invasive 1.

2. 3. Created by Niňa E. Tubio

Consent / explain procedure to pt  RN – will explain if laboratory exams  MD – will explain if operation procedure Empty bladder, bowel – promote comfort Arch back – to clearly visualize L3, L4 17

Nsg Mgt. Post Lumbar: 1. 2. 3. 4.

*Flat on bed – 12 – 24 h to prevent spinal headache & leak of CSF Force fluid Check punctured site for drainage, discoloration & leakage to tissue, discomfort Assess for movement & sensation of extremities

Result: 1. CSF analysis: Confirms Meningitis

a. Increase CHON & WBC b. Decrease glucose c. Increase CSF opening pressure d. (+) Culture microorganism

(Normal: 50 – 160 mmHg)

2. Complete blood count CBC – reveals increase WBC (Leukocytosis) Mgt: 1. Adm meds a.) Broad-spectrum antibiotic: Penicillin S/E : 1. GIT irritation – take with food 2. Hepatotoxicity, nephrotoxcicity 3. Allergic reaction 4.* Super infection – alteration in normal bacterial flora  

Normal flora: throat – streptococcus Normal flora : intestine –E. Coli

Sx: of superinfection of penicillin

Diarrhea

b.) Antipyretic c.) Mild analgesic for headache 2. Strict respiratory isolation 24 hrs. after start of antibiotic therapy 3. Comfy & dark room – due to photophobia & seizure 4. Prevent complications of immobility 5. Maintain F & E balance 6. Monitor VS, I&O , neuro check 7. Provide client health teaching & discharge plan a. Nutrition – Increase CHON & CHO but Small freq feeding b. *Prevent complication of Hydrocephalus & Nerve Deafness 8. Institute measures to prevent Increase ICP & seizures 9. Rehabilitation for residual deficit ( mental retardation & delayed psychomotor development) Exercise:

Where to bring 2 y/o post meningitis ?  Audiologist due to damage to post repair myelomeningocele  Urologist -Damage to sacral area – controls urination

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REVIEW: 3 Types of ISOLATION: 1. Strict Isolation 2. Reverse Isolation 3. Enteric Ex. Pt. with -Cushing’s syndrome – reverse isolation -Aplastic anemia – reverse isolation------ bone marrow depletion----pancytopenia -Cancer any type – reverse isolation -Post-Liver transplant – reverse isolation -Prolonged use steroids – reverse isolation -Meningitis – strict isolation -Asthma – not to be isolated - Hepatitis A - Enteric - Measles – Strict - Mumps – Strict - Pneumonia – Strict - PTB -Strict REVIEW: *Thrombosis & Stroke Initial sign: Late sign: * Anemia :

leads to atherosclerosis Headache Pruritus ------

Initial sign: Weakness & Fatifue

Blood: Leukopenia

WBC

Leukocytosis

Anemia

RBC

Polycythemia

Platelets

Thrombocytosis

Thrombocytopenia

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CEREBRO VASCULAR ACCIDENT : Or Stroke, Brain Attack or Cerebral Thrombosis, Apoplexy  



A partial or complete disruption in the brains blood supply 2 largest & common artery in stroke : a. Middle cerebral artery b. Internal carotid artery Common to male – 2 – 3x high risk, increases as you grow older

Predisposing factor: 1. 2.

3.

Thrombosis – clot (attached)-----------No. 1 cause of Stroke Hemorrhage Embolism – dislodged clot – pulmo embolism---2nd cause S/Sx: Pulmonary Embolism 1. Sudden sharp chest pain 2. Unexplained dyspnea, SOB 3. Tachycardia, palpitations, diaphoresis & mild restlessness S/Sx: Cerebral Embolism 1. Headache, disorientation, confusion & decrease in LOC----lead to coma

4. *Compartment Syndrome – compression of nerves/ arteries Test Analysis: *Femur Fracture Fx. Complications:> Fat embolism – most feared complication w/in 24hrs >Hemorrhage *Yellow bone marrow – produces fat cells at medullary cavity of long bone *Red bone marrow – provides WBC, platelets, RBC found at epiphysis Risk factors of CVA: a. b. c. d. e.

f. g.

HPN DM MI Artherosclerosis Valvular heart disease Post cardiac surgery-----*Mitral valve replacement Lifestyle: 1. Smoking – nicotine – potent vasoconstrictor 2. Sedentary lifestyle 3. Hyperlipidemia –genetic-genes that easily binds to cholesterol

h. Obesity ------20% of BW Overweight -----10% of BW i. Prolonged use of oral contraceptives 2 types:

- Macro pill – has large amount of estrogen - Mini pill – has large amount of progestin Mini-pill---- Promote lipolysis – artherosclerosis – HPN – stroke j. Type A personality Created by Niňa E. Tubio

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a. Deadline driven person b. 2 – 5 things at the same time c. Guilty when not dong anything k. Diet – increase saturated fats -----ex. whole milk l. Emotional & physical stress S & Sx: 1. Transient Ischemic Attack ( TIA)- 1st sign of Impending stroke attacks o o

o

Headache – initial sing of TIA Dizziness/ vertigo, numbness, tinnitus, visual & speech disturbances, paresis or phlegia (monoplegia – 1 extreme) (Paraplegia—lower extremeties) Increase ICP, *Temporary memory loss

2. Stroke in evolution – progression of S & Sx of stroke 3. Complete stroke – resolution of stroke a.) Headache b.) *Cheyne-Stokes Resp c.) Anorexia, n/v d.) Dysphagia e.) Increase BP f.) (+) Kernig’s & Brudzinski – Sx of Hemorrhage Stroke g.) Focal & neurological deficit 1. Phlegia 2. Dysarthria – inability to vocalize 3. Aphasia 4. Agraphia – difficulty in writing 5. Alexia – difficulty in reading 6. Homonymous Hemianopsia – loss of half of field of vision Left sided hemianopsia – approach Right side of pt – the unaffected side Nsng. Dx. = Unilateral Neglect Dx. 1. 2.

Computerized Tomography Scan – reveals brain lesion Cerebral Arteriography – rveals site & extent of mal-occlusion  Invasive procedure due to inject dye  Allergy test *All Dx ending in graphy/gram are invasive: injection of a dye, ask if allergic to seafoods Post-CT Scan 1.) Force fluid – to excrete dye because it is nephrotoxic---check BUN & Creatinine 2.) Check peripheral pulse 3.) Check Fluid imbalance----dye is an osmotic diuretic Nsg. Mgt. 1. Maintain patent a/w & adequate vent - Assist mechanical ventilation - Administer O2 inhalation 2. Restrict fluids – prevent cerebral edema 3. Instruct client to avoid valsalva maneuver 4. Monitor vs., I&O, neuro check 5. Prevent compl of immobility by: a. Turn client q2h Elderly q1h To prevent decubitus ulcer/ bed sores To prevent Hypostatic pneumonia –type of pneumonia r/t long immobility b. Egg crate mattress or H2O bed c. Sand bag or foot board- prevent foot drop Created by Niňa E. Tubio

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6. NGT feeding – if pt can’t swallow 7. *Passive ROM exercise q4h to prevent contractures & to promote proper body alignment 8. Alternative means of communication - Use Non-verbal cues - Magic slate - (+) To hemianopsia – approach on unaffected side 9. Position pt.: elevate heat 30 degrees angle/ semi-fowlers 10. Maintain siderails 11.Meds a. Osmotic diuretics – Mannitol ( Osmitrol) ---Side-drip—fast drip ----S/E: decrease BP b. Loop diuretics – Lasix/ Furosemide-----IV push 3. Corticosteroids – Dextamethazone (ends in one) 4. Mild analgesic------codeine Sulfate-------S/E: Respiratory Depression 5. Thrombolytic/ fibrolitic agents – tunaw clot Ex. Streptokinase-----S/E: Allergic Reaction Urokinase---------S/E: Hypertension Tissue Plasminogen Activating Factor ( TPAF)----S/E: Chest Pain *Monitor bleeding time 6. Anti-coagulants – Heparin & Coumadin----” sabay” Why : Coumadin will take effect after 3 days---long-acting Anti-Coagulants Heparin (Short-Acting) Monitor:

PTT (Partial Thromboplastin Time) If prolonged, indicates bleeding

Antidote:

Protamine Sulfate

Coumadin or Warfarin (Long-Acting) PT (Prothrombin Time) if prolonged, indicates bleeding Vitamin K (Aquamephyton)

7. Anti-platelet (PASA) – aspirin paraanemo aspirin -the only NSAID that has anti-platelet property - Do not give to pts. With Dengue, Ulcer & Headache - Aspirin----- No. 1 ulceronegenic agent S/E: Tinnitus, Anemia, Heartburn & Dyspepsia *EPISTAXIS/ nose bleeding--- parameter that indicates effectiveness of thrombolytic therapy Health Teachings: 1. Avoidance of modifiable lifestyle - Diet, smoking 2. Dietary modification - Avoid caffeine, decrease Na & decrease saturated fats 3. Prevent Complications: *Subarachnoid hemorrhage 4. Rehab for focal neurological deficit 1. Mental retardation 2. Delay in psychomotor development

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CONVULSIVE Disorder (CONVULSIONS)

o A disorder of the CNS characterized by paroxysmal seizures with or w/o loss of consciousness, abnormal motor activity, alteration in sensation & perception & changes in behavior. Exercise: Can you outgrow febrile seizure? Febrile seizure Normal if < 5 y/o Pathologic if > 5 y/o Predisposing Factor: a. Head injury d/t birth trauma------ No .1 cause of convulsions b. Toxicity of carbon monoxide c. Brain tumor d. Genetics e. Nutritional & metabolic deficit f. Physical stress g. Sudden withdrawal to anticonvulsants-----No .1 of status epilepticus Status epilepticus – Drug of Choice: Diazepam & glucos S & Sx. Of Epilepsy dependent upon stages: I. Generalized Seizure – 1.) Grand mal / tonic clonic seizures-----most common type of seizure - With or w/o Aura – warning symptoms of impending seizure attack Epigastric pain ---1st sign of aura

  



This is associated with olfactory, tactile, visual, auditory sensory experience Epileptic cry – fall *Loss of consciousness 3 – 5 minutes Tonic-clonic contractions Tonic - Direct symmetrical extension of extremities Clonic - contractions Post ictal (state of lethargy or drowsiness) sleep- unresponding sleep after tonic clonic

2.) Petit mal seizure – (same as daydreaming!) - Blank stare - Decrease blinking eye - Twitching of mouth - *Loss of consciousness – 5 – 10 seconds (quick & short) - *Common to children II. Localized/partial seizure 1. Jacksonian seizure or Focal seizure – tingling/jerky movement of index finger/thumb & spreads to shoulder & 1 side of the body with janksonian march 2. Psychomotor/ Focal-motorseizure -*Automatism – stereotype repetitive & non-purposive behavior - Clouding of consciousness – not in contact with environment - Mild hallucinatory sensory experience Created by Niňa E. Tubio

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3 Types of HALLUCINATION: 1. 2. 3.

Auditory – schitzophrenia – paranoid type Visual – Korsakoffs psychosis – chronic alcoholism Tactile – addict – substance abuse

III. Status Epilecticus – Continuous, uninterrupted seizure activity leading to hyperpyrexia – coma – death Drug of Choice : Diazepam & Glucose Pathophysiology:

Status Epilepticus Increase electrical firing in the brain: if left untreated Increase Heat production -------hyperpyrexia Increase metabolism using glucose & O2 ------need for glucose therapy Coma------Death

Dx: For All Types: 1. 2. 3.

CT scan – revealsbrain lesion EEG electroencephalography --revealsHyperactivity brain waves ECT therapy

Nsg. Mgt. Priority – Airway & Safety 1.

*If with seizure: S/E is PNS

Maintain patent a/w & promote safety Before seizure: 1. Remove blunt/sharp objects 2. Loosen clothing of pt. 3. Avoid restraints----can lead to fracture 4. Maintain siderails 5. Turn head to side to prevent aspiration 6. Tongue guard or mouth piece to prevent biting of tongue (emergency—clean piece of cloth) 7. Avoid precipitating stimulus – bright glaring lights & noises, drafts 8. Administer meds a. Dilantin (Phenytoin) –( toxicity level – 20 ) S/E: Gingival hyperplasia H-hairy tongue A-ataxia N-nystagmus b. Acetaminophen- febrile pt Mix only with NSS, sandwich method - Don’t give alcohol – lead to CNS depression c. (Tegretol) Carbamazepine d. Phenobarbital (Luminal) -------common S/E: hallucination & mild arrythmia e. Diazepam

2. Institute seizure & safety precaution By Post seizure: Administer O2 inhalation. Suction apparatus ready at bedside 3. Monitor onset & duration of - Type of seizure Created by Niňa E. Tubio

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- Duration of post ictal sleep----the longer the duration, the danger of status epilepticus 4. Assist in surgical procedure - Cortical resection Exercise: 1 y/o grand mal – immediate nursing action = a/w & safety a. Mouthpiece – 1 yr old – little teeth only b. Adm o2 inhalation – post! c. Give pillow – safety d. Prepare suction Neurological Assessment: 4 Objectives of Neurological Assessment: 1. To know the exact neurological deficit 2. To localized lesion 3. For rehabilitation 4. Guidance in nursing care 2 Types of N.A.

1. Glasgow Coma Scale (GCS)– objective measurement of LOC or quick neuro check 3 components of ECS (“MVE”) M – motor 6 V – verbal response 5 E – eye opening 4 15---- highest score Scaling: 15 – 14 – Conscious 13 – 11 – Lethargy 10 – 8 – Stupor 7 – Coma 3 – Deep coma – lowest score ( no 0 score on any response, lowest is only 1) 2.

Comprehensive Neuro Exam A. Survey of Mental status & speech (Comprehensice Neuro Exam) 1.) LOC & Test of memory 2.) Levels of orientation 3.) Cranial Nerve assessment 4.) Motor assessment 5.) Sensory assessment 6.) Cerebral test – Romhberg, finger to nose 7.) DTR 8.) Autonomics 1. a. Levels of consciousness (LOC) 1. Conscious (conscious) – awake – levels of wakefulness 2. Lethargy (lethargic) – drowsy, sleepy, obtunded 3. Stupor (stuporous) – awakened by vigorous stimulation Pt. has general body weakness, decrease bodily reflex 4. Coma (Comatose) Light – (+) all forms of painful stimulations Deep – (-) to painful stimulation *Watch out for the rise & fall of the chest b. Different types of pain stimulation o Don’t prick 1. Deep sternal pressure/stimulation: 3x– fist knuckle With response – light coma Without response – deep coma 2. Pressure on great toe – 3x 3. Orbital pressure – pressure on orbits only – below eye 4. Corneal reflex/ blinking reflex *Wisp of cotton – used to illicit blinking reflex among conscious patients *Instill 1-drop saline solution – unconscious pt if (-) response pt is in deep coma

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c. Test of memory – consider educational background a. Short term memory –  What did you eat for breakfast? Damage to temporal lobe – (+) antero grade amnesia b. Long term memory (+) Retrograde amnesia – damage to limbic system (rhinencephalon) 2. Levels of orientation: 1st: Time 2nd:: Person 3rd: Place Exercise:

Describe a conscious pt ? a. Alert – not all pt are alert & oriented to time & place b. Coherent c. Awake d. Aware 3. Cranial Nerve Assessment: 12 pairs of cranial nerves

I– II – III – IV – V– VI – VII – VIII – IX – X– XI– XII –

Olfactory Optic Oculomotor Trocheal Trigeminal Abducens Facial Acoustic/auditory (V) Glossopharyngeal Vagus Spinal accessory Hypoglossal

Old Opie Occasionaly Tries Trigonometry And Feels Very Gloomy Vague And Hypoactive

s s m m b m b s b b m m

smallest CN largest CN

longest CN

Some Say Marry Money But My Brother Says Bad Business Marry Money

I. Olfactory – don’t use ammonia, alcohol, cologne irritating to mucosa – use coffee granules, vinegar * Hyposmia – decrease sensitivity to smell *Diposmia – distorted sense of smell *Anosmia – absence of sense of smell *Either of 3 might indicate head injury – damage to cribriform plate of ethmoid bone where olfactory cells are located or indicate inflammation condition – sinusitis II Optic (Sensory or Vision) 1. Test of visual acuity or central or distance vision (test of near vision) Use Snellens Chart: a. Snellen’s Alphabet -----used for literate client b. Snellen’s E chart --------used for illiterate c. Animal Chart -----used for children Normal: 20/20 vision 20 numerator is constant: 20 ft (6-7 m) distance from the chart 20 denomenator ---vision distance the person can see the letters OD – Rt eye 20/20 =20/200 – blindness – can’t read E – biggest OS – left eye 20/20 OU – both eye 20/20 2. Test of Peripheral Vision/ visual field: facing the client a. Superiorily b. Bitemporally Created by Niňa E. Tubio

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c. Inferiorly d. Nasally Common Disorders 1. Glaucoma – (Normal 12 – 21 mmHg intra-ocular pressure) - Increase IOP - Loss of peripheral vision – “tunnel vision” 2. Cataract – opacity of lens - Loss of central vision, “Blurring or hazy vision” 3. Retinal detachment – curtain veil – like vision & floaters 4. Macular degeneration – black spots III Oculomotor, IV (Throclear), VI (Abducens) – Tested simultaneously because it controls or innervates the movement of extrinsic ocular muscle *6 Cardinal Gaze Extrinsic Ocular Movement Rt eye IO

SO

LR

MR

N O S E

left eye

SR Throclear – controls superior oblique (1) Abducens - lateral rectus (1) 9. Oculomotor- controls the size & response of pupil (Pupil size 2 -3 cm or 1.5 – 2 mm) - controls opening of the eyelids - controls the 4 gaze V – Trigeminal – Largest nerve – consists of - ophthalmic, maxillary & mandibular branch 1. Sensory – controls sensation of the face, mucus membrane; teeth & corneal reflex Unconscious – instill drop of saline solution 2. Motor – controls muscles of chewing/ muscles of mastication *Trigeminal neuralgia – difficulty in chewing & swallowing - damage to the trigeminal nerve - Drug of Choice: Tegritol -Extreme food temperatire is not recommended -Avoid hot or cold preparation Exercise:

Trigeminal neuralgia, RN should give a. Hot milk, butter, raisins b. Cereals c. Gelatin, toast, potato – all correct but d. Potato, salad, gelatin – salad easier to chew

VI Facial: a. Sensory – controls taste – anterior 2/3 of tongue: Test cotton applicator with sugar. -Put applicator with sugar to tip to tongue. -Start of taste insensitivity: Age group – 40 yrs old b. Motor- controls muscles of facial expression, smile frown, raise eyebrow if Damage causes --------Bells palsy or facial paralysis Cause of Bells palsy in children---No 1 cause : R/T forcep delivery Temporary only, resolve w/in 4-6 months *Most evident clinical sign of facial symmetry: Nasolabial folds VIII Acoustic/ Vestibulocochlear a. Cochlear ----controls hearing Created by Niňa E. Tubio

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b. Vestibule-----controls balance (kinesthesia /position sense) -----Movement & orientation of body in space ------located in the inner ear—if it moves—the head moves too--kinesthesia

*Meniere’s Disease----only disease of the inner ear----loss of balance---Nsg. Priority: Safety Parts of Ears: Outer – tympanic membrane, pinna, oricle (impacted cerumen), cerumen Middle – hammer, anvil, stirrup or melleus, incus, staples. Mid otitis media • Eustachean ear Inner ear- meniere ear, sensory hearing loss Remove vestibule – meniere’s dse – disease inner ear *Archimedes law --Bouyancy *Daltons law – Partial pressure of gases (Diffusion) *Inertia – law of motion (dizziness, vertigo) Exercise: 1.) Pt. with multiple stab wound in the chest - Movement of air in & out of lungs is carried by what principle? - Diffusion – Dalton’s law 2.) Pregnant – check up – ultrasound reveals fetus is carried by amniotic fluid - Archimedes 3.) Severe vertigo d/t Inertia Test for acoustic nerve: ---------Repeat words uttered IX – Glossopharyngeal X – Vagus

– controls taste – the posterior portion 1/3 of the tongue – controls gag reflex

Test 9 – 10 Pt say ah – check uvula (in the middle tonsils) – should be midline If there is deviation from L to R ----Damage to cerebral hemisphere Gag reflex – place tongue depression post part of tongue  Don’t touch uvula  Gag reflex----vagal stimulation -----PNS Effect XI – Spinal Accessory

- controls sternocleidomastoid (neck) & trapezius • Shrug shoulders, put pressure. Pt should resist pressure. Paresis or phlegia

XII – Hypoglossal - movement of tongue – say “ah” If L or R deviation-----damage to the cerebral hemisphere - Push tongue against cheek. Normal= tongue in midline, if (-) disorder called ------- Short frenulum lingue –or tongue tied – “bulol”

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EYES A. External Parts: 1. Orbital cavity – made up of connective tissue, protects eye from trauma. 2. EOM (Extrinsic Ocular Muscles ) – involuntary muscles of eye, needed for gazing movement. 3. Eyelashes/ eyebrows – aesthetic purposes 4. Eyelids – palpebral fissure – opening upper & lower lid. Protects eye from direct sunlight

5. 6.

Meibomean gland – secrets a lubricating fluid inside eyelid a.) Stye/ sty or Hordeolum- inflamed Meibomean gland Conjunctiva Lacrimal apparatus – tears

B. Intrinsic Coat I. Sclerotic coat – outer most a.) Sclera – white. Occupies ¾ posterior of eye. Refracts light rays b.) Canal of sclera – site of aqueous humor drainage c.) Cornea – transparent structure of eye II. Uveal Tract – provides nutritive care Uveitis – inflammation of the uveal tract Consist of: a.) Iris – colored muscular ring of the eye 2 Muscles of Iris: 1. Circular smooth muscle fiber 2.radial smooth muscle fiber

- Constricts the pupil - Dilates the pupil

2 Chambers of the Eye: 1. Anterior a.) Vitereous Humor – maintains spherical shape of the eye b.) Aqueous Humor – maintains intrinsic ocular pressure (Normal IOP= 12-21 mmHg) II. Retina (innermost layer) a. Optic discs or blind spot – nerve fibers only No auto receptors Cones (daylight/ colored vision) Phototopic vision

Rods – night, twilight vision “Scotopic vision” = Vit. A deficiency – rods insufficient

b. Maculla lutea – yellow spot center of retina c. Fovea centralis – area with highest visual acuity oracute vision Physiology of Vision: 4 Physiological Processes for Vision to occur: 1. Refraction of light rays – bending of light rays 2. Accommodation of lens 3. Constriction & dilation of pupils Created by Niňa E. Tubio

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4. Convergence of eyes *Unit of measurements of refraction – Diopters *Normal eye refraction – Emmetropia *PERRLA ---Normal Reaction ERROR of Refraction: 1. 2. 3. 4.

Myopia - near sightedness – Tx: biconcave lens Hyperopia - farsightedness – Tx: biconvex lens Astigmatisim -distorted vision – Tx: cylindrical Presbyopia - “old slight” – inelasticity of lens d/t aging – Tx: bifocal lens or double vista

*Accommodation of lenses – based on Thelmholtz Theory of accommodation Near vision: -Ciliary muscle contracts -Lens bulges

Far vision: - Ciliary muscle dilates / relaxes -Lens is flat

Convergence of the Eye: Error: 1.

2. 3. 4.

Exotropia – 1 eye normal Esophoria – Strabismus- squint eye Amblyopia – prolong squinting

corrected by corrective eye surgery

1. GLAUCOMA –An increase Intra Ocular Pressure – if untreated, atrophy of optic nerve disc – blindness - Preventable but not curable Predisposing Factors: 1. 2. 3. 4. 5. Type: 1. 2. 3.

High risk group – 40 y/o & above HPN Hereditary Obesity Recent eye surgery, trauma, inflammation

Chronic -------- (open angle G.) – *most common type Obstruct in flow of aqueous humor at trabecular meshwork of canal of schlema Acute --------- (close angle G.) – *Most dangerous type Forward displacement of iris to cornea leading to blindness. Chronic--------- (closed – angle) - Precipitated by acute attack

S/Sx: 1. *Loss of Peripheral Vision – a Tunnel-like vision 2. *Halos/Rainbows around lights 3. Headache & Dizziness 4. n/v 5. Steamy cornea 6. Eye discomfort 7. *Ocular Pain 7. If untreated – gradual loss of central vision – blindness Diagnosis: 1. *Tonometry –reveals increase IOP >12- 21 mmHg 2. Perimetry – reveals decrease peripheral visual field 3. *Gonioscopy – reveals abstruction in anterior chamber Nursing mgt: 1. Enforce CBR 2. Maintain siderails 3. Administer meds a.) *Miotics – lifetime ------ contracts ciliary muscles & constricts pupil. Created by Niňa E. Tubio

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Ex. Pilocarpine Na (Carbachol) b.) Epinephrine eye drops ------decrease formation & production of aqaueous humor c.) Carbonic anhydrase inhibitors. ----- Promotes increase out flow of aquaeous humor(drainage) Ex. Acetazolamide (Diamox) 2.

d.) Timoptics (Timolol maleate)- Increase outflow of aquaous humor (drainage) Surgery: Invasive: a.) Trabeculectomy --- eye-trephining – removal of trabelar meshwork of canal or schlera to drain aqueous humor b.) *Peripheral Iridectomy – portion of iris is excised to drain aqueous humor Non-invasive: a. Trabeculotomy (eye laser surgery)

Nursing Mgt.: Pre –operative for all types of surgery: 1. Apply eye patch on unaffected eye to force weaker eye to become stronger. Nursing Mgt. Post-operative – all types of surgery 1. Position unaffected/ unoperated side - to prevent tension on suture line. 2. Avoid valsalva maneuver 3. Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 2. Eye patch – for both eyes – post-operatively

2. CATARACT –A partial/ complete opacity of lens, can lead to blindness Predisposing Factor: 1. 2. 3. 4.

Aging : 90-95% (degenerative/ senile cataract)---60 y/o & above Congenital (very rare) Prolonged exposure to UV rays DM

S/Sx:

1. *Loss of Central Vision - “Hazy or blurring of vision” 2. 3.

4.

Painless Milky white appearance at center of pupil *Decrease perception of colors *Elderly can only see Red & Green

Dx: 1. Opthalmoscopic exam – reveals (+) opacity of lens Nsg Mgt: 1. Reorient pt. to environment – due opacity 2. Siderails 3. Medications a.) *Mydriatics – dilate pupil – not lifetime Ex. Mydriacyl b. ) Cycloplegics – paralyzes ciliary muscle. Ex. Cyclogyl c.) Atrophine 4. Surgery a.

b.

E – extra C - capsular C – cataract L - lens E – extraction

Partial removal of lens

I - intra C - capsular C – cataract L - lens E – extraction

Total removal of lens & surrounding capsules

Complications of Lens Extraction: Hemorrhage Created by Niňa E. Tubio

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Retinal Detachment Endopthalmitis Nursing Mgt: 1.Position unaffected/ unoperated side - to prevent tension on suture line. 2.Avoid valsalva maneuver 3.Monitor symptoms of IOP a.) Headache b.) n/v c.) Eye discomfort d.) Tachycardia 4.Eye patch – both eyes - post op

3. RETINAL DETACHMENT - The separation of 2 layers of retina, can lead to blindness Predisposing factors: 1. 2. 3. 4. 5.

*Severe myopia – near sightedness Diabetic Retinopathy Trauma *Following lens extraction HPN

S/Sx: 1. 2. 3. 4.

*“Curtain –veil” like vision Flashes of lights *Floaters d/t seepage of blood (Photopsia) Gradual decrease in central vision

Dx: Opthaloscopic exam Drug of Choice: Cycloplegics Nursing Mgt: 1. 2.

Siderails (all visual disease) Surgery: a.) Cryosurgery (cold application) b.) *Scleral buckling c.) Diathermy ------heat application

4. MACULAR DEGENERATION -----the appearance of black spots in the eyes

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Addison’s Disease

PATHOGNOMONIC SIGNS Bronze-Like Skin

Angina Pectoris

Levine’s Sign

Appendicitis

Rebound Tenderness

Asthma

Wheezing On Expiration

Bulimia Nervosa

Chipmunk Face

Cataract (loss of central vision)

Hazy Vision

Cholecyctitis

(+) Murphy’s Sign

Cholera

Rice-Watery Stool

Cushing’s Disease

Moon Face Appearance

Dengue

Petechiae

Diptheria

Pseudomembrane

Down Syndrome

Protrusion Of Tongue

Down Syndrome

Simean Creases on Palms

Emphysema

Barrel Chest

Glaucoma (peripheral vision)

Tunnel-like Vision

Grave’s Disease (Hyperthyroidism)

Exopthalmus

Hepatitis

Jaundice

Hyperpituitarism ( Acromegaly)

Carotenemia ( yellowish skin)

Kawasaki Disease

Strawberry Tongue

Leprosy

Leioning Face

Liver Cirrhosis

Spider Angioma

Malaria

Chills

Measles

Koplik’s spot

Meningitis

(+) Kernig’s & Brudzinski’s Sign

Myasthenia Gravis

Ptosis

Pancreatitis( Ectopic Pregnancy) Parkinson’s Disease Patent ductus Arteriosus

(+) Cullen’s Sign (ecchymosis of umbilicus) (+) Grey-Turner’s (ecchymosis of flank) Pill-Rolling Tremors Machine-like Murmur

Pernicious Anemia

Beefy Red Tongue

Pneumonia PTB Pyloric Stenosis

Rusty Sputum Low-Grade Fever Olive Shape Mass

Retinal Detachment Systemic Lupus Erythematosus Tetanus Tetany Tetralogy Of Fallot Thombophlebitis

Curtain Veil-Like Vision Butterfly rash Risus Sardonicus (+) Trousseau & (+) Chvostek Sign Clubbing of Fingers (+) Homan’s Sign

Typhoid Fever

Rose Spots in Abdomen

Created by Niňa E. Tubio

34

RELATED DISORDERS: 1. COPD = # 1 cause: Smoking ----- 4 Types: ---- all needs bronchodilators BRONCHITIS Blue bloaters Dyspnea on Exertion Lead to cor pulmonale

Created by Niňa E. Tubio

ASTHMA Wheezing on Expiration Cause by allergens Hereditary Reversible

BRONCHOIECTASIS Hemoptysis Undergo Pneumonectomy Bronchoscopy

EMPHYSEMA Barrel Chest Pink Puffers Dyspnea at Rest Lead to Cor Pulmonale Cause by Allergens Hereditary CO2 narcosis Purse Lip Breathing Irreversible Terminal Stage

35

To Prevent STD Local – practice monogamous relationship CGFNS/NCLEX – condom

ENDOCRINE SYSTEM The endocrine system integrates body functions by the synthesis & release of hormones. Hypothalamus: link between the nervous system & the endocrine system.

ENDOCRINE GLANDS: Secrete their products directly into the bloodstream Different from exocrine glands Exocrine glands: secrete through ducts unto epithelial surfaces or into the GIT Parts: Pituitary Gland Adrenal Glands Pancreas Thyroid Glands Created by Niňa E. Tubio

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Parathyroid Glands Gonads

HORMONES: - Are chemical substances that are secreted by the endocrine glands. - Can travel moderate to long distances or very short distances. - Acts only on cells or tissues that have receptors for the specific hormone. - Target Organ: The cell or tissue that responds to a particular hormone - Regulation of Hormones: Negative Feedback Mechanism When the hormone concentration rises, further production of that hormone is inhibited. When the hormone concentration falls, the rate of production of that hormone increases.

2 BASIC PATHOPHYSIOLOGICAL DISORDER OF THE ENDOCRINE

A. Hyposecretion/ Hypoactivity

B. Hypersecretion / Hyperactivity

D/T 1. Congenital absence of glands Ex. No pancreas

D/T 1. Tumor w/n or outside the gland Ex. Tumor in adrenal gland

2. Surgical removal of glands Ex. Total Thyroidectomy Primary” Disease  Problem in target gland; autonomous

“Secondary” disease  problem outside the target gland; Most often d/t a problem in pituitary gland

Parts: I. PINEAL GLAND Function:

Secretes Melatonin – Inhibits leutenizing hormone (LH) secretion – Regulates body clock, sleeping pattern or circadian rhythm

II. PITUITARY GLAND (Hypophysis Cerebri) The main gland located at base of the brain at Sella Turcica Fx: Master gland of body/ Master clock of body---it controls all the metabolic activity of the body 2 Divisions: Anterior Pituitary Gland – Adenohypophysis

Posterior Pituitary Gland – Neurohypophysis

A. ANTERIOR PITUITARY GLAND Function: 1. Responsible for Growth Hormone (GH) (Somatotropic Hormone) Function: For elongation of long bones *Puberty age: 9 y/o – 21 y/o & the Epiphysial plate closes at 21 y/o DISORDER:

Hypopituitarism *Dwarfism -- Children

1. Frohlick’s Syndrome Created by Niňa E. Tubio

GH

hH

Hyperpituitarism Acromegaly -- Adult 1. Gigantism 37

-Dwarf w/ obesity - Mentally retarded - Loss of reproductive ability d/t genital atrophy 2. Simmond’s Disorder/ Pituitary Cachexia - Appearance of a “wizened old man” - Premature senility, Skin dry & wrinkled - Mental retardation - Male: Absence of spermatogenesis - Female: Amenorrhea

- If s/s appear before closure of epiphyseal plate - rapid growth of long bones 2. Acromegaly - If s/s appear after closure of epiphyseal plate - Hyperthrophy of soft tissue & bone thickness - Disproportional growth Enlargement of cartilage ( nose & ears) Enlargement of larynx (deep voice) Progmatism: Protrusion of jaw Square face & jaw Macroglossia  Obstructive Sleep Apnea

Dx: - X-ray, MRI or CT scan: pituitary tumor - Plasma hormone levels: decreased Tx:

Drug of Choice in acromegaly: Octreotide (Sandostatin) --S/E: Seizure & GIT irritation Somatostatin Hormone - antagonizes the release of GH 2. Melanocytes Stimulating Hormone (MSH) Function: For skin pigmentation DISORDER: *Albinism ---hyposecretion of MSH ----prone to develop skin cancer & blindness

*Vitiligo -----hypersecretion of MSH

3. Prolactin/ Lactogenic Hormone  Initiates milk let-down reflex with help of oxytocin  Promotes development of mammary gland/breast tissue Disorder: Prolactin Deficiency : Failure to lactate 4. Adrenocorticotropic Hormone – ACTH  Development & maturation of adrenal cortex S & Sx in Deficiency: - Results in diminished cortisol secretion. - Weakness, fatigue, weight loss, and hypotension. 5. LH -----Progesterone 6. FSH----Estrogen B. POSTERIOR PITUITARY GLAND: secretes---1.) Oxytocin a. Promotes uterine contractions-----preventing bleeding/ hemorrhage. - Best time to administer Oxytocin: after placental delivery to prevent uterine atony. b. Initiates the Milk let-down reflex with help of prolactin. 2.) Anti-Diuretic Hormones (ADH) /ADH-replacement ---Vasopressin or Pitressin Function: Prevents urination – conserve H2O Regulates water metabolism Released during stress or in response to an increase in plasma osmolality to stimulate reabsorption of water & decreased urine output DISORDERS OF THE POSTERIOR PITUARY GLAND 1. DIABETIS INSIPIDUS (DI) – The hyposecretion of ADH Disorder w/ massive polyuria d/t either lack of ADH or kidney’s insensitivity to it Cause: Idiopathic/ unknown Predisposing factor: “PITT” 1. Pituitary surgery Created by Niňa E. Tubio

38

2. Inflammation 3. Trauma 4. Tumor Pathophysiology :

Diabetes Insipidus Disorder of

H20 metabolism

ADH

* Alcohol inhibits release of ADH

Prevents renal tubules from reabsorbing H20 POLYURIA

S &Sx:

Polydipsia Dehydration

F & E imbalance

(excessive urine output 5-29 L/24 hrs.)

Diluted Urine

Urine Specific gravity

Other S & Sx: 2. Sx of Dehydration: Excessive thirst, Agitation, Poor skin turgor, Dry mucus membrane 3. Weakness & Fatigue 4. Hypotension – if left untreated 5. Hypovolemic shock *Anuria – Late sign hypovolemic shock 6. Weight loss Dx:

1.Decrease urine specific gravity- concentrated urine 2.Serum Na = Increase d/t compensation to attract more H2o

(N = 1.015 – 1.035) (N =135 -145 meq/L)

Mgt: 1. Force fluid 2,000 – 3,000ml/day 2.Administer IV fluid replacement as ordered ( Isotonic fluid solution) 3. Monitor VS, I&O 4.Administer meds as ordered (Commercially-Prepared ADH) a. Pitressin Tannate Oily preparation: Give deep I.M. b. Vasopressin Tannate May cause lipodystrophy , rotate site of administration Will cause vasoconstriction--Monitor BP before & after c. Desmopressin Acetate Given by Nasal Spray d. Lypressin 5. Prevent complications: Most feared complication – Hypovolemic shock 2. SYNDROME OF INAPPROPRIATE ANTI-DIURETIC HORMONE (SIADH) - An increase production of ADH or Hypersecretion of ADH - Idiopathic/ unknown Predisposing Factor: 1.

2.

Head injury R/T Bronchogenic cancer or lung cancerEarly Sign of Lung Ca : Cough – productive, non productive

3. Hyperplasia of Pituitary gland 4. Increase size of organ d/t increase # of cells S&Sx 1. 2. 3. 4.

5. Created by Niňa E. Tubio

Fluid Retention Increase BP – HPN Edema Wt gain Danger of Water Intoxication

(The only Endocrine Gland with Water Intoxication) 39

Cerebral Edema

Increase ICP Complications of SIADH Seizure Activity

Dx : 1. Urine specific gravity increase: Reveals a diluted urine 2. Serum Na ----Decrease 3. Low serum osmolality 4. High urine osmolality (urine osmolality >100 mosmol/kg) 5. Normal renal function (low BUN Stress > Infection All can cause an increase in

a. Place far from sea – no iodine seafood’s rich in iodine

2. Mountainous area results to an increase intake of goitrogenic foods Ex. Baguio/Cordilllera Ex. Turnips (singkamas) radish, peas, strawberries, sweet potato, beans, kamote, cassava (root crops), nuts, broccoli

3. Goitrogenic Drugs that contains progoitrin--- an anti-thyroid agent that has no iodine Ex.

Anti thyroid agents (PTU) prephyl thiupil Lithium carbonate, Aspirin PASA, Cobalt, Phenyl butasone “Sporadic Goiter –“ if caused by goitrogenic drugs or from an increase intake of goitrogenic foods S & Sx : 1. Enlarged TG 2. Mild restlessness 3. Mild dysphagia Created by Niňa E. Tubio

46

Dx.

1. Thyroid Scanning – Reveals enlarged TG 2. 3.

Done to evaluate the amount of Iodine 131 accumulated by the thyroid gland *Serum Thyroid Stimulating Hormone (TSH) Result: Increase (Confirmatory Dx of Goiter) T3, T4 Determination More reliable test, more potent & rapid effect on metabolism Result : Serum T3, T4 will Normal or below N

Nsg Mgt: 1. Administer meds as ordered: a. Iodine solution – Logol’s solution or Saturated Solution of K iodide (SSKI) - Violet/Purple Color Nsg Mgt For Lugol’s Solution

1. Use straw to prevent staining of teeth 2. Prophylaxis 2 -3 drops , Treatment – 5 to 6 drops b. Thyroid Hormone / Agents 1. Levothyroxine (Synthroid) 2. Liothyronine (cytomel) 3. Thyroid extract

Drugs Given Using Straw To Prevent Staining 1. Tetracycline 2. Iron preparation 3. Nitrofurantoin (Macrodantin)

Nsg Mgt for Thyroid Hormones/agents

1. Monitor VS – HR d/t tachycardia & palpation 2. Take it early AM – S/E : Insomnia 3. Monitor S/E: Tachycardia, palpations Insomnia Restlessness agitation Heat intolerance HPN

Signs of Hyperthyroidism

4.

Encourage increase intake iodine 1. Seaweeds – highest source 99% 2. Seafood: Highest iodine content: 1st: Oysters 2nd: Crabs 3rd: Lobster 3. Iodized salt –easily destroyed by heat, take it raw not cooked 5. Assist surgery: Sub-Total Thyroidectomy 2. HYPOTHROIDISM

Least iodine: Shrimps

– The Hyposecretion of T3, T4 leading to MI, Atherosclerosis, HPN & stroke. Classified According To Onset of S & Sx: 1. CRETINISM – appear during childhood / only endocrine d/o that leads to mental retardation 2. MYXEDEMA – appear in adulthood (both pitting & non-pitting edema) Classified According To Cause: 1. PRIMARY – failure of thyroid to secrete T3 T4 2. SECONDARY – failure of APG to secrete TSH 3. TERTIARY - failure of Hypothalamus to secrete TRH (Thyroid Releasing Hormone) Predisposing Factors:

1. Iatrogenic causes – disease caused by medical intervention or surgery 2.Atrophy of TG d/t: a. b.

c. Created by Niňa E. Tubio

Irradiation Trauma Tumor & Inflammation 47

3.Iodine deficiency 4.Autoimmune – “ Hashimoto disease” Pathophysiology: Hypothalamus

APG secretes-----TSH---stimulate----Thyroid Gland---secrete--- T3 T4 Any disorder of T.G. will decrease T3 T4 Leading to Tertiary causes or Hypothyroidism Altered Metabolism Hypometabolic Hypoactive

Memory Impairment Decrease O2 in metabolism Weight Gain Decrease VS Unable to tolerate Cold weather

S&Sx: Everything decreased except weight gain & menstruation w/c are both increase Early Sx :

Weakness & Fatigue Loss of appetite Weight gain Cold Intolerance – Myxedema - Coma Constipation Dry skin

Late Sx :

Brittle hair/ nails Non pitting edema d/t increase accumulation of mucopolysacharide in SQ tissue Hoarseness of voice – only endocrine d/o that can be Dx thru telephone conversation Decrease libido Decrease VS – Hypotension, Bradycardia, Bradypnea & Hypothermia Lethargy Memory Impairment leading to Psychosis Menorrhagia (high)

Dx:

1. T3 T4 Determination: Serum T3 T4 Decrease 2. Serum Cholesterol: Increase – can lead to MI 3. Radio Iodine Uptake (RAIU): Decrease - Use to evaluate the amount of radiation RAI 131 accumulated by the T.G. & excreted by the kidneys - Most reliable Diagnostic Test Normal Uptake : 15 - 40 % Urine : 40 – 80%

of the administered dose Result: Directly proportional to Uptake, inversely proportional to urine

Nsg Mgt In RAIU: 1. No iodine in diet prior to test 2. Taken P.O. RAI 131 cocktail (liquid)

2 Endocrine D/O that leads to Cardiac Complications 1. DM 2. Hypothyroidism

Nsg Mgt:

1. Monitor strictly V/S. I&O – to determine presence of Myxedema Coma A severe form of hypothyroidism Characterized by: Created by Niňa E. Tubio

48

Hypotension Hypoventilation Bradycardia Bradypnea, Hyponatremia & Hypoglycemia That can lead to progressive stupor & coma Important Mgt For Myxedema Coma:

1. Assist in mechanical ventilator 2. Administer thyroid hormone 3. Administer IVF replacement 2.

Monitor VS, I&O

3. Provide dietary intake : Low in calories d/t weight gain 4. Skin care d/t dry skin 5. Comfortable & warm environment d/ to cold intolerance that can lead to Coma 6. 7.

8.

Administer IVF replacements Force fluid Administer meds as ordered – Take AM Supplement Thyroid Hormones/Extract Synthetic:

Levothyroxine S/E: Constipation

Thyroid Extracts: Proloid ( Thyroglobulin) Cytomel Synthroid Euthroid Thyrolar Eltroxime 9.

Health teaching & discharge plan a. Avoidance precipitating factors leading to myxedema coma: 1. Exposure to cold environment 2. Stress 3. Infection 4. Use of sedative, narcotics, anesthetics not allowed – CNS depressants V/S already down

b. Prevent Complications: Hypovolemic shock, Myxedema coma, HPN, LHF, MI, Stroke c. Hormonal replacement therapy - lifetime d. Importance of follow up care 3. HYPERTHYROIDISM “GRAVE’S DISEASE” or “THYROTOXICOSIS” “TOXIC GOITER/ BASEDOU/ PARRY’S DISEASE” -

The hypersecretion of T3 & T4

Predisposing Factors:

1. Autoimmune Disease – Release of LATS 2.

3.

Exopthalmos Enopthalmos – severe dehydration depressed eye Excessive iodine intake Hyperplasia of TG d/t increase # of cells

Pathophysiology:

1. Theory Of LATS: (Long Acting Thyroid Stimulator) In blood, there is gamma globulin

that causes

Iodine Accumulation Thyroid Hyperplasia

W/c will manifest the TRIAD SYMPTOMS: Created by Niňa E. Tubio

49

1. GOITER d/t iodine accumulation 2. EXOPTHALMOS (eye signs seen in EPS) 3. HYPERTHYROIDISM (seen in EPS) 2. EPS ( Exopthalmus Producing Substance) APG -----releases EPS----responsible for the Triad S & Sx Proptosis (downward displacement of eyeball) Lid lag (sleepy eyes) Infrequent blinking Fixed stare DALYRIMPLE SIGN Peri-orbital Edema Von Graefe ------------ failure of eyelids to follow movement of eyes when looking down 3. Hyperthyroidism ---------- Hyperactive, Voracious but losing weight, hypermetabolic T3 T4 ------the cause is over-excitability of SNS Tremors

Hallucinations

Diaphoresis

Palpitation

Nervousness

Irritability

Insomnia

S & Sx:

1. Increase appetite : Hyperphagia but weight loss d/t increase metabolism 2. 3. 4.

5. 6. 7. 8. 9.

Skin is moist Heat intolerance Diarrhea – most common gastric complications of Grave’s Disease All VS increase = HPN, Tachycardia, Tachypnea, Hyperthermia CNS changes Goiter Exopthalmos Constipation – common in advanced Amenorrhea graves disease d/t constant increase in T3

Dx:

1. Serum T3 & T4 - Increased 2. RAIU : Increase 3. Thyroid Scanning: Reveals an enlarged TG Nsg Mgt: 1. Monitor VS & I & O – To determine presence of thyroid storm or most feared complication: Thyrotoxicosis 2. Administer meds as ordered

a. Antithyroid Agents 1. Prophylthiouracil (PTU) 2. 3.

Methimazole (Tapazole) Neomercazole ( Carbimazole) Most Toxic S/E for prolonged Used: Agranulocytosis Common S/S: Complications R/T infections - Fever, Sore throat, Mild Leukocytosis Dx Test To Check For Toxicity: Differential Platelet Count If not available, Monitor CBC Throat Swab & Culture Most feared complication : Thrombosis ----Stroke CVS

b. Adrenergic Blocking Created by Niňa E. Tubio

50

To control the symptoms brought about by the over-excitability of SNS - Propanolol, Inderal, Betaloc, Neobloc, Metoprolol, Nadol, Visken, Aptin, Sotalex, Corgard 3. Diet – Increase caloric intake to correct weight loss 4. Skin care 5. Comfy & cool environment 6. Maintain siderails d/t restlessness 7. Provide bilateral eye patch (dry material) – to prevent drying of eyes 8. Hormonal Replacement Therapy 10. Importance of follow-up care 11. Assist in surgery – Subtotal Thyroidectomy Tx: 1. RAI 131 To reduce size of T.G. Isotope: Risk of genetic abnormalities or genetic mutation 2. Surgery :

Subtotal Thyroidectomy Nsg Mgt: Peri-Operative 1. Administer Lugol’s solution (SSKI) K iodide Function: To decrease vascularity of TG To prevent bleeding & hemorrhage during & after surgery To increase firmness Promote T3 T4 storage 2. Diet : a. High in calories Increase CHO Increase CHON Increase in polyunsaturated fats To satisfy increase in appetite & restore loss of glycogen reserve b. Avoid stimulant in diet (No colas, caffeine) c. Increase fluid intake d. Monitor body weight e. Provide physical & mental rest to reduce metabolism f. Provide quiet & calm environment to decrease irritability 3. If (+) for exopthalmus -----dryness of the cornea ----corneal ulceration---blindness

Nsg Mgt: 1. Cover eyes w/ bilateral eye patch 2. Instill saline to moisten eyes ( Drug: Methylcellulose OD) 3. Elevate head on pillow to promote drainage & reduce peri-orbital edema 4. Give psychological preparation by telling pt. that eye signs will remain even after surgery Nsg Mgt: Post-Operative Thyroidectomy Complication:

1. Watch out for signs of Thyroid Storm or Thyrotoxicosis - If no emotional preparation pre-operative: Stress - Post-opt wound infection Pathphysiology: Pre-opt (euthyroid state----post-opt----thyroid compensates for T3 T4 production (Hyperthyroid d/t stress, infection) Increase PR, Increase BP Triad Signs of Thyroid Storm: “HAT” a. Hyperthermia b. Agitation c. Tachycardia ----------Early Sign: Fever w/ Tachycardia Nsg Mgt Thyroid Storm: 1.

Created by Niňa E. Tubio

Monitor VS & neuro check 51

Agitated might decrease LOC 2. Antipyretic – fever/ TSB Tachycardia - β blockers (-lol) 3. Siderails – agitated Complication

2. Watch for inadvertent (accidental) removal of parathyroid gland Secretes Parathormone (Calcium Reabsorption) TETANY : Hypocalcemia If 1 removed If 2 removed If 3 or more removed

– No sign of tetany – Mild signs of tetany - Classic Sx of Tetany: (+) Trousseau sign & (+) Chvosteck’s sign (Twitching of fingers) (Facial paralysis)

Nsg Mgt: 1. Administer calcium gluconate Slowly – to prevent arrhythmia Ca gluconate toxicity – antidote – MsSO4 Complication

3. Watch out for accidental Laryngeal nerve damage Sx:

Hoarseness of Voice Aphonia (no voice)

2 recurrent laryngeal nerves that control vocal cords (bilateral laryngeal) Responsible for voice production

If 1 removed – whispery, hoarseness If Trauma only – Whispery, Hoarseness Edema on glottis – Whispery, Hoarseness If 2 removed – Aphonia -----start speech therapy Nsg Mgt: 1. Encourage pt to talk or speak postoperatively 2. Notify physician immediately 4. Watch out for Signs of Laryngeal Spasm--------- Inflammation of Larynx Sx: DOB SOB

Narrow opening ---- O2 cannot enter

Laryngeal Spasm Nsg Mgt: 1. Prepare at bedside tracheostomy 5. Watch Out for Signs of bleeding Post-Subtotal Thyroidectomy D/T : Failure to administer Logul’s Solution (SSKI) pre-opt Failure to tie/ ligate blood vessels --------bring back to OR for emergency operation Sx: “Feeling of fullness” at incision site “ Feeling of Choking sensation” BP -------- Rapid, feeble, thready pulse Rapid but shallow respiration Cold, Clammy diaphoretic skin Nsg Mgt: 1. Check soiled dressing at nape area (Slip hand under neck to check for dampness) 2. Evaluate VS 3. Notify Physician immediately Bleeding can lead to-------------- 1. Respiratory Obstruction D/T blood occlusion & Hematoma Accumulation of Tracheobronchial secretions Created by Niňa E. Tubio

52

Can also lead to Laryngospsam/Laryngoedema Prepare for Emergency Tracheostomy OTH ER DIAGNOSTIC TEST FOR THYROID DISORDERS: 1. Protein Bound Iodine (PBI) - Done to evaluate amount of iodine attached to protein molecule of the blood Normal: 4-8 ug % Nsg. Care: 1. 2-3 days prior to test, no taking of foods & drugs containing iodine Ex. Seafoods, iodized salt, No cough syrup, ASA Estrogenic Preparations: Pills, Dyes, X-ray 2. Basal Metabolic Rate (BMR) - Done to evaluate O2 consumption when client is at rest Nsg Mgt: 1. At night, NPO for 12 hrs. 2. Ensure client had a good night sleep to decrease anxiety level Procedure: 1. When client no activity yet, no food yet 2. Clamp nose, breathe through tube connected to a tank w/ machine evaluating O2 consumption 3. TBMR (Theoretical) - Compute pulse pressure + PR/ minute – 111 - Not conclusive, but if s/s submit to other test

( Normal: 20-30)

Summary: HYPOTHYROIDISM Lethargy Memory Impairment Diarrhea Decrease VS ALL DECREASE Except: Wt: Weight Gain Menstruation: Menorrhagia

T3 T4

HYPERTHYROIDISM Agitation & Restlessness Hallucination Constipation Increase VS ALL INCREASE Except: Weight Loss Amenorrhea

V. PARATHYROID GLAND

– – Anatomy:

A pair of small nodules located behind the Thyroid Gland There are 4 Parathyroid glands PTH------secretes---- PARATHORMONE Function: Essential to the absorption of Calcium & secretion of Phosphorus by renal tubules Promotes reabsorption of Calcium Regulates cardiac rythmicity Essential for blood coagulation *Thyrocalcitonin – Antagonizes secretion of parathyroid hormone

CODE: CALCIUM DISORDERS OF THE PARATHYROID GLAND

Created by Niňa E. Tubio

53

1. HYPOPARATHYROIDISM – Hypoactive PTH or a decreased secretion of parathormones HYPOCALCEMIA (TETANY)

HYPERPHOSPHOTEMIA [If Ca decreases, phosphate increases]

Uncontrolled spasm/Hyperactivity Predisposing Factors: 1. Following subtotal thyroidectomy d/t accidental removal of PTH 2. Atrophy of parathyroid gland due to a. Inflammation b. Tumor S&Sx:

1. Acute Tetany a. b. c. d. e. f. g.

Tingling sensation Paresthesia Dysphagia Laryngospasm Bronchospasm Seizure Most feared complications Arrhythmia

Pathognomonic Sign of Tetany:

a. (+) Chvosteck’s Sign : Tap facial nerve, if facial spasm of facial muscle (+) b. (+) Trousseau’s /Carpopedial spasm: Occlude blood flow to vascular extremity (legs) Use tourniquet Test for 1-2 min. & observe for carpopedial spasm 2.

Chronic tetany a. Loss of tooth enamel b. Photophobia & cataract formation c. GIT changes : Anorexia, N/V & generalized body malaise d. CNS changes : Memory impairment, Irritability

Dx:

1. 2. 3. 4. Nsg Mgt: 1.

Serum Calcium Serum Phosphate X - ray of long bone CT Scan

– – – –

Decrease (N 8.5 – 11 mg/100ml or 4.5 -5.5 mEq/L) Increase (N 2.5 – 4.5 mg/100ml) Increase bone density Reveals degeneration of basal ganglia

Administration of meds: a. Acute Tetany: Administer Ca gluconate – IV, slowly to prevent cardiac arrest b.

Chronic tetany 1. Give Oral Ca supplements Ex.

Ca gluconate - Calci-aid Ca carbonate - Calsan Ca lactate Ca chloride 10% - Caltrate

2. Give Vit. D for calcium to be readily absorb Created by Niňa E. Tubio

54

Vitamin D (Cholecalceferol) Drug

Diet

Cholecalceferol

Sunlight

Calcidiol

Calcitriol

7am – 9am

Commercially-Prepared: *Calciferol Hytakerol Calcidiol *Rocatriol Dihydrotachysterol 3. Give Phosphate binder for excretion of phosphate Ex. Aluminum OH gel (ampho gel) S/E: Constipation Antacid AAC Aluminum Containing Acids

MAD Magnesium Containing Antacids

Aluminum OH gel

Milk or Magnesia

Constipation

Diarrhea

*Maalox: Magnesium & Aluminum – With Lesser S/E 2. Avoid precipitating stimulus such as bright lights & noise to prevent seizure 3. Diet : Increase Ca & decrease phosphorus - Don’t give milk – due to increase phosphorus Diet : Also For Osteoporosis a. Baked Salmon b. Dilis/Anchovies c. Green Turnips (Singkamas) 4. Bedside: Tracheostomy set d/t laryngospasm 5. Encourage to breath with paper bag in order to produce mild respiratory acidosis – To promote increase ionized Ca levels 6. Most feared complication : Seizure & arrhythmia 7. Hormonal Replacement Therapy: Lifetime 8. Institute Seizure & safety precautions 9. Important follow up care 2. HYPERPARATHYROIDISM / “Von Reclinghausen” - Increase secretion of parathormones - HYPERCALCEMIA -------w/c can lead to Hypophosphotemia Pathophysiology: PTH

Increase bone resorption Normal: Ca – 99% bones 1% blood

Hypercalcemia Hypophospotemia

Calcium loss from bones Reverse effect: Ca in bone goes to blood

Bone Demineralization bones are brittle Leads to bone fracture

Created by Niňa E. Tubio

Hypercalciuria Formation of Calcium crystals in Urine Nidus/ Nucleus 55

Forms Kidney Stones Predisposing Factors: 1. Hyperplasia of the parathyroid gland 2. Over compensation of PTG d/t Vit D deficiency Children – Rickets Adults – Osteomalacia Vitamin D deficiency *Sippy’s diet – Vit D diet – not good for pt with ulcer: 2 -4 cups of milk & butter *Karrel’s diet – Vit D diet – not good for pt with ulcer: 6 cups of milk & whole cream *Food rich in CHON – eggnog – combination of egg & milk S/Sx: 1. Bone fracture a. Bone pain (especially at back) 2. Kidney Stones a. Renal colic b. Cool moist skin & body malaise 3. GIT changes: Anorexia, N/V, Ulcerations ----- only endocrine D/O that causes ulceration 4. CNS involvement: Irritability, Memory impairment Dx :

1. Serum Ca: Increase 2. Serum phosphorus: Decreases 3. X-ray of long bones : Reveals bone demineralization Tx:

Hypo : Replacement w/ commercial preparation Hyper: Removal or Destruction of

1. Removal of the gland - Parathyroidectomy 2. Destruction of the gland – Cobalt Therapy 3. Drug of Choice: Calcitonin ---- inhibits resorption

ACID-ASH DIET

Nsg Mgt: Kidney Stone

3 C’s

1. Force fluids : 2,000 – 3,000/day or 2-3L/day 2. 3. 4.

Isotonic solution Warm sitz bath – for comfort Strain all urine with gauze pad 5. Acid Ash diet to acidify urine 6. Adm meds as ordered a. Narcotic analgesic – Morphine SO4, Demerol S/E – Respiratory Depression Antidote - Narcan/ Naloxone Naloxone toxicity – Tremors 7. Siderails 8. Assist in ambulation 9. Diet – low in Ca, increase phosphorus lean meat 10. Prevent complication of Parathyroidectomy : Most Feared – Renal Failure 11. Hormonal Replacement Therapy: Lifetime 12. Importance of follow up care VI. PANCREAS

1G

Cranberry Calamansi Vit. C Grapefruit

- Located behind the stomach , a mixed gland Pancreas: Consists of

Acinar Cells (Exocrine gland)

Islets of Langerhans (Endocrine Gland: Ductless)

Secrete Pancreatic juices

Secretes 3 Types of Cells

Flows in the pancreatic duct α Cells Created by Niňa E. Tubio

β Cells

Delta Cells 56

Aids in digestion (in stomach)

Secretes Glucagon Fx: Hyperglycemia

Secretes Insulin Fx: Hypoglycemia

Secretes Somatostatin Fx: Antagonizes Growth Hormones

DISORDER OF THE PANCREAS 1. PANCREATITIS – Acute inflammation of the pancreas leading to Pancreatic Edema, Hemorrhage & Necrosis d/t

Autodigestion (Self-digestion )

Cause: Unknown/idiopathic Alcoholism Obstruction in the pancreatic duct ---- backflow of pancreatic juice to the pancreas Will cause autodigestion Pathognomonic Sign: (+) Cullen’s Sign (+) Grey Turner’s Spots

- Ecchymosis of umbilicus (bluish color) - Ecchymosis of flank area

Both Signs Means Hemorrhage

2. CHRONIC HEMORRHAGIC PANCREATITIS “Bangugot” Predisposing Factors: Unknown Risk factor: 1. 2.

History of hepatobiliary disorder Alcohol 3. Drugs: Thiazide diuretics Oral contraceptives Aspirin Penthan 4. Obesity 5. Hyperlipidemia 6. Hyperthyroidism 7. High intake of fatty food – Saturated fats 3. DIABETES MELLITUS - A metabolic disorder characterized by non-utilization of CHO, CHON,& fat metabolism d/t 1. Absolute Insulin Deficiency - Cause is unknown but the islets of langerhans do not produce insulin - Congenital - Beta-Cell damage by VIRUS ----- Human Leukoantigin----Human Leuko Antibodies (Chicken Pox) Autoimmune: Destroys B-cells 2. Relative Insulin Deficiency - Capable of producing insulin but not used efficiently d/t Blocked by chemical antagonist at site of production Created by Niňa E. Tubio

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Epinephrine

Thyroxin

Glucogen

Glucagon

All causes Glucogenolysis

Physiology: Pancreas → glucose → ATP (Main fuel of cell) (reserve glucose – glycogen) Glucogenesis ( synthesis of glucagons) Glycogenolysis ( breakdown of glucagons) Liver will undergo Gluconeogenesis (formation of glucose from CHO sources – CHON & fats)

Pathphysiology: DIABETES MELLITUS Little or No Supply of Insulin

CHO Metabolism

CHON metabolism

CHO utilization of glucose

breakdown of stored glucose

Cell Starvation

Cell weakness d/t cellular starvation

Hyperglycemia

Lipolysis

Cell to Tissue Starvation

Oxidation of fatty acid

Stimulate Satiety Center (Hypothalamus)

Glucose go to blood

Hyperlipidemia

Ketone Production

POLYPHAGIA (excessive hunger)

Weight loss

DKA (Diabetic

Blood Osmolarity Ketoacidosis)

(result from increase breakdown of fats) kidney Kidney’s tubular secretion Coma

POLYURIA

Death

Diabetic

Stimulate thirst center

(needs O2) Glucose in blood Act as osmotic diuretic (Increase)

ECF dehydration POLYDIPSIA (excessive thirst)

Renal tubules fail to reabsorb glucose HONKC GLYCOSURIA Irritate perineal area Fungi in the area (-) Nitrogen Balance Pruritus A. CLASSIFICATION: 1.

TYPE 1 IDDM “ Brittle Disease” Juvenile Onset Common among children Non- obese Weight loss Symptomatic Absolute Deficiency Created by Niňa E. Tubio

DKA Early Sx: Weight loss Weakness Late Sx: Acetone-breath odor Kausmaul’s Respiration

Tissue Wasting (Cachexia) 2.

TYPE II NIDDM

Adult/ Maturity onset 40 y/o & Above Obese Weight gain Asymptomatic Relative Deficiency 58

Tx: Insulin Administration Diet Exercise

Tx: OHA (Oral Hypoglycemic Agents) Diet Regimen Exercise Complication: H – hyper O – osmolar N – non K – ketotic C – coma

Complications: Diabetic Ketoacidosis (DKA) Metabolic Acidosis Tx: Sodium Bicarbonate Incidence Rate:

Incidence Rate:

- 10% of population with DM have Type I

- 90% of population w/ DM have Type II Mid 1980’s increase in type II d/t fast food chains

Predisposing Factor:

Predisposing Factors:

1. 90% hereditary – total destruction of pancreatic dells 2. Virus 3. Toxicity to carbon tetrachloride (CC14) 4. Drugs – Steroids Lasix - Loop diuretics DIABETES S/Sx: MELLITUS 1. 3 P’S + G 2. Weight loss 3. Anorexia 4. N/V 5. Blurring of Vision 6. Increase susceptibility to infection 7. Delayed/ poor wound healing

P

ia

1. Obesity – lack insulin receptors binding site - # 1 cause of Type 2 DM 2. Hereditary

Polyuria Polydips

S/Sx: 1. 3 P’s + G 2. Asymptomatic

Polyphagia

3. GESTATIONAL DM – Occurs during pregnancy & terminates upon delivery of child Predisposing Factors: 1. Unknown/ idiopathic 2. Influence of maternal hormones S/Sx : Same as type II – 1. Asymptomatic 2. 3 P’s & 1G Mgt: 1. Type of delivery: CS d/t macrosomia (large baby) Sx of Hypoglycemia on Newborn: 1. High pitched shrill cry 2. Poor sucking reflex B. COMPLICATIONS OF DIABETES MELLITUS 1. HYPERLIPIDEMIA Formation of atheromatous plaques (atherosclerosis) in the arteries Narrowed arterial lumen

(

blood flow) -----result to thickening of BV--- inelastic blood vessels

Formation of vascular lesion ( micro/macro-angiopathy) Created by Niňa E. Tubio

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Vascular Degeneration Cerebral blood flow vessels

Coronary arteries

Brain

Heart

CVA

Myocardial Ischemia

Retinal Blood Vessels

Eyes

In 30 minutes

Renal blood vessels

Kidney

Lower extremities

Retinopathy Nephropathy (Kimmiel-Stiel Wilson Syndrome) Cataract

Irreversible M.I.

Tissue Ischemia Peripheral Neuritis

RENAL FAILURE Retinal Hemorrhage Exudation

Aggregation of CHON In Retinal Molecules Opacified 3 Pathies of DM Nephropathy Retinopathy

Peripheral blood

Diabetic Cataract

Tissue Necrosis

Diabetic Gangrene Hardening of renal tubules Ischemia KSW Sx: Proteinuria Edema Puffiness of eyelids

1st d/t Ischemia PERIPHERAL NEURITIS Sx: Numbness of exremity Coldness of extremity Tingling sensation of

Sx of Nephropathy is a progressive destruction of glomeruli --RF 2. DIABETIC KETOACIDOSIS (DKA) - Acute complication of Type I DM due to severe hyperglycemia leading to CNS depression & Diabetic Coma. Predisposing Factors: 1. Stress ------ # 1 cause of DKA Nsg Mgt: 2. Hyperglycemia 3. Infection 1. Can lead to coma: assist in mechanical ventilation 4. Missed dose/Omitting dose of insulin 2. Administer .9NaCl – isotonic solution Sx: 3 P’s & 1 G Followed by .45 NaCl hypotonic solution Early Sx: To counteract dehydration. Weight loss 3. Monitor VS, I&O, blood sugar levels Weakness 4. Administer meds as ordered: Late Sx: a. Insulin therapy – IV push Anorexia, N/V, Dim Vision Regular Acting Insulin : Clear Acetone-breath odor (2-4hrs, peak action) Kausmaul’s Respiration b. To counteract acidosis – Na HCO3 (rapid, shallow breathing) CNS depression, Coma 5. Antibiotic to prevent infection “Cherry Red Lips” Dx : 1. FBS: Increase 2. Hct: Increase (compensate d/t dehydration) C. DIAGNOSTIC PROCEDURES FOR DIABETES MELLITUS:

1. FBS/ FPG (Fasting Plasma Glucose) -

NPO 6-8 hrs. or NPO 12 hrs. with sips of water

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2. RBS (Random Blood Sugar) -

No NPO, anytime

3. PPBS ( Post Prandial Blood Sugar) Determination -

Test 1-5 Use to Diagnosed Glycemia

NPO 2 hrs. after diet of 100 gm CHO

4. Hgt (Hemaglukotest) -

Finger prick or Capillary Blood Glucose Determination (CBg)

5. OGTT ( Oral Glucose Tolerance Test) - NPO 6-8 hrs. then collect fasting specimen (am) Administer p.o. 100 gms: Urine Glucose + fruit juice

Blood

After 1 hr. -----extract venous blood ---- Rise glucose Increase BS (Normal) 2 hrs. --- next extraction ---- start to normalized Decreased BS Final 3 hrs. --- next extraction ---- w/in normal BS (+) Diabetic if: Rise glucose till the 3rd extraction still not normal & there is sugar in urine

6. BT, CT (Benedict’s Test) (Clini Test)

Test For Glycosuria

- Double voided or 2nd voided specimen = accurately test presence of glucose in urine - Discard 1st void, offer 1-2 glass of H20 after 1 hr. or 30 minutes collect urine 7. Acetest

-

To test for presence of ketone bodies in urine (Ketonuria) (Result from incomplete breakdown of fats) How? Get acutest tablet (creamy/white/ off-white in color) ---drop in urine If there is no change (-), if color changes to purple (+) for ketonuria

8. Glycosylated HgB

(HgBAC)

- To evaluate the amount of glucose attached to the hemoglobin of the blood for the previous 120 days---lifespan of HgB

D. MANAGEMENT OF DIABETES MELLITUS: Supportive & Palliative 1. TYPE 1 DM INSULIN THERAPY A. Sources:

1. Animal source – beef/ pork : rarely given because it causes allergic reaction Created by Niňa E. Tubio

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2. 3.

Human – has less antigenetic property Ex. Humulin – most commonly used If kid is allergic to chicken – don’t give measles vaccine, it comes from chicken embryo. Artificially compound

B. Types of Insulin Types of Insulin

1. Rapid Acting Insulin - Regular Acting - Humulin R - Semi-Lente - Crystallized Zinc - Velosulin - Novolin R - MC Actrapid

Onset

Peak

Given

Color & Consistenc y

Durati on

30 minutes after administrati on

2-4 hrs.

3x/day

Clear

6-8 hrs.

1-2 hrs

8-16 hrs.

OD

Cloudy

24 hrs.

3-4 hrs.

16-24 hrs.

Cloudy, Mixed

36 hrs.

2. Intermediate Insulin - NPH (Non-protamine Hagedorn 1) - Humulin N - Monotard - Lente - Globin - Novolin L 3. Long Acting Insulin - Ultra Lente - PZI (Protamine Zinc Insulin) - Humulin U

5 R’s Of Insulin Administration 1. Right Patient: Give insulin only if there are signs of glycosuria & hypergylcemia 2. Right Drug : Administer right type of Insulin 3. Right Route: Not given P.O., insulin destroyed in the GIT by proteinase Given: SQ, IM, I.V. Humulin R Crystalline Zinc Regular Insulin 4.

Incorporated w/ water, given by drip (IVF)

Right Time: Best time given – 60-90 minutes before meal or an hour before meal Physiologic effect of insulin will parallel the absorption of glucose

5.

Right Dose: Know stock dose of insulin 10 ml vial 40 units/ml or 80 units/ml or 100 units/ml Nsg Mgt For Insulin Therapy: 1.

Administer insulin at room temperature. Do not expose to sunlight • Refrigerate insulin once opened only • Before administration, gently roll vial between palms. Avoid shaking to prevent formation of bubbles

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2. Use gauge 25 – 26 needle : Tuberculin syringe 3. Administer insulin at either 45 or 90° depending on the client tissue deposit. 5. Don’t aspirate after injection • Rotate injection site to prevent lipodystrophy (atrophy/ hypertrophy of SQ tissue) Deltoid Rectus Femoris R & L Vastus Lateralis Gluteus Maximus

IM

Upper Arm R & L Below breast Lower Central Abdominal Wall Lateral thigh R & L Below scapula R & L Buttocks R & L

SQ

6. Most accessible site – abdomen 7. When mixing 2 types of insulin, aspirate 1st regular/ clear – before cloudy to prevent contaminating clear insulin & to promote accurate calibration. 8. In giving insulin: Before meals but if pt. eating already: Give insulin If pt. already eaten 2 hrs. : Do not give, repeat CBC> MD will adjust the dose 9. 1ml or cc of tuberculin = 100 units of insulin - - 1 cc = 10 units = 100 units - - .5cc = 5 units = 50 units - - .1 cc = 1 unit = 10 units 6 units RA 10. Monitor for signs of complications: a. Allergic reactions b. Lipodystrophy c. Somogyi’s Phenomenon – Rebound Effect of Insulin characterized by hypoglycemia followed by periods of hyperglycemia (Insulin Shock, Hyperinsulinism, Insulin Overdose, Hyperglycemia) d/t • • • Sx:

Occurs w/ insulin overdose Prolonged NPO, vomiting Long interval of insulin from the serving of food * If allowed to eat, give anything to eat an hour after administration of insulin

Hunger Pangs Double Vision Pallor, cold clammy skin Tremors

Mgt: 1. Give 20-30 gm of carbo 2. Drugs

4-8 ounces of softdrinks 4-8 ounces of fruitjuice 1 tbs. of sugar ---best alternative, put in oral cavity 5 ml of honey 5 ml of karo syrup 2-4 pcs. Of candies 2 slices of graham crackers

Epinephrine 1.1000 SQ Glucagon 1-2 mg IM *IV glucose H20 ---- D50% by IV push ---- D5W by venoclysis 2. TYPE 2 DIABETES MELLITUS Most Feared Complication of Type II DM Hyper Osmolar Created by Niňa E. Tubio

↑ osmolarity = severe dehydration 63

Non Ketotic Coma –

- absence of lipolysis - no ketosis S/Sx: headache, restlessness, seizure, decrease LOC

Dx :

1. FBS: N 80 – 120 mg/dl 2. 3. 4.

Increase , 3 consecutive times 3 P’s & 1G = confirmed DM Oral Glucose Tolerance (OGTT) Most sensitive test Random Blood Sugar : Increased Alpha Glucosylated Hgb : Elevated (Normal: 94 ----- Macrocytic Cell (abnormal size)

- To evaluate the presence of immune bodies that adheres to RBC causing hemolysis/agglutinization of RBC (Rh Incompatibility, ABO Incompatibility)

Normal Hgb content of RBC: 22-28 micromicrogram < 22 5. SCHILLING TEST - To evaluate rate of absorption of Vit. B12 (Cyanocobalamine) - Use to diagnosed Pernicious Anemia Procedure: Administer P.O. radioactive Vit. B12 ------24 hr. urine Check (+) (-) of Vit. B12 ------ if (-) Pernicious Anemia (do not give P.O. give parenterally) ------ if (+) in urine ---normal Common in Pts. Who undergone gastrectomy/ cancer----they do not have intrinsic factor

6. BONE MARROW ASPIRATION/PUNCTURE/TAP POIKILOCYTOSIS = abnormality in shape of RBC METARUBRICYTE = abnormal RBC w/

- To evaluate size, shape, character of RBC cells - Invasive (consent) - Local anesthesia (lidocaine 1-2%) - Sites: Sternum ------ Position: Supine A & P Iliac Crest ------ Position: Supine (A) & Prone/Lateral (P) - Pediatric pts. --- use the long bones (femur, humerus)-----as we grow older the # of marrows in long bones decreases - Apply pressure dressing over site to prevent bleeding

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7. LYMPH NODE BIOPSY - Site : Cervical LN, Axilla LN, Inguinal LN

IV. BLOOD TRANSFUSION: Objectives: 1. 2. 3. 4.

To replace circulating blood volume To increase O2 carrying capacity of blood To combat infection if there’s decrease WBC To prevent bleeding if there’s platelet deficiency

Packed RBC = 250 ml Refrigerated = 3-5 days

Nsg Mgt & Principles in Blood Transfusion 1.

2.

3.

Proper refrigeration Proper typing & cross matching Type O – universal donor AB – universal recipient 85% of people are RH (+) Aseptically assemble all materials needed: a.) Filter set b.) Isotonic or PNSS or .9NaClfor flushing to prevent Hemolysis Hypotonic solution – Cell swells or burst Hypertonic solution – Cell will shrink or crenate c.) Needle gauge 18 - 19 or large bore needle to prevent hemolysis. d.) Instruct another RN to recheck the following . Pts name, blood typing & cross typing expiration date, serial number – Most important e.) Check blood unit for bubbles, cloudiness, dark in color & sediments – indicates bacterial contamination. Return to blood bank, do not dispose f.) Never warm blood products – may destroy vital factors in blood. - Warming is done if with warming device – only in EMERGENCY! - Within 30 mins room temp only! g.) Blood transfusion should be completed < 4hrs because blood that is exposed at room temp for > 2h causes blood deterioration------can lead to bacterial contamination h.) Avoid mixing or administering drug at BT line – leads to hemolysis i.) Regulate BT 10 – 12 gtts/min KVO or 100cc/hr to prevent circulatory overload j.) Monitor VS before, during & after BT especially q15 mins for 1st hour - Majority of BT reaction occurs within 1h.

BLOOD TRANSFUSION REACTIONS: BT REACTIONS: 1. HEMOLYTIC REACTION Sx: Headache Dizziness Dyspnea Palpitation Lumbar/Sternal flank pain Hypotension, Flushed Skin---red port wine urine

H A P C A T C H expired

Hemolytic Reaction Allergic Reaction Pyrogenic Reaction Circulatory Reaction Air Embolism Thrombocytopenia Citrate Intoxication Hyperkalemia d/t blood

Nsg Mgt: Created by Niňa E. Tubio

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1. Stop BT 2. Notify Doc 3. Flush with plain NSS 4. Administer isotonic fluid sol – to prevent acute tubular necrosis & counteract shock 5. Send blood unit to blood bank for reexamination 6. Obtain urine & blood samples of pt & send to lab for reexamination 7. Monitor VS & Allergic Rxn 2. ALLERGIC REACTION S/Sx: 1. 2. 3. 4. 5.

Fever/ chills Urticaria/ pruritus Dyspnea Laryngospasm/ bronchospasm Bronchial wheezing

Nsg Mgt: 1. 2. 3. 4.

Stop BT Notify Doc Flush with PNSS Administer antihistamine – diphenhydramine Hcl (Benadryl) If (+) Hypotension – anaphylactic shock administer – epinephrine 5. Send blood unit to blood bank 6. Obtain urine & blood samples – send to lab 7. Monitor VS & IO 8. Adm. Antihistamine as ordered for Allergic Rxn, if (+) to hypotension – indicates anaphylactic shock Shock -----administer epinephrine 9. Administer antipyretic & antibiotic for pyrogenic Rxn & TSB

3. PYROGENIC REACTION: S/Sx:

a.) Fever/ chills b.) Headache c.) Dyspnea

d.) Tachycardia e.) Palpitations f.) Diaphoresis (Pyrogens -----fever-producing agents)

Nsg Mgt: 1. 2. 3. 4. 5. 6. 7. 8.

Stop BT Notify Doc Flush with PNSS Administer antipyretics, antibiotics Send blood unit to blood bank Obtain urine & blood samples – send to lab Monitor VS & IO Tepid sponge bath – offer hypothermic blanket

4. CIRCULATORY OVERLOAD Sx: -

Dyspnea

Created by Niňa E. Tubio

PRIORITY CASES Hemolytic Reaction = 1st d/t Hypotension---attend to destruction of Hgb ------ O2----- Brain Damage Circulatory Reaction = 2nd Allergic Reaction = 3rd Pyrogenic Reaction = 4th But: Anaphylactic = 1st priority Hemolytic = 2nd

79

-

Orthopnea Rales or crackles Exertional discomfort

Nsg Mgt: 1. 2. 3.

Stop BT Notify Doc Administer diuretics

ONCOLOGIC NURSING Oncology – study of neoplasia –new growth Benign (tumor)

Malignancy (cancer)

Well differentiated Encapulation – (+) Metastasis – (-) Prognosis – good Surgery

Poorly or undifferentiated (-) (+) Poor prognosis 1. Chemotherapy Many S/E 2. Radiation 3. Surgery most preferred treatment 4. Bone marrow transplant - Leukemia only

Predisposing Factors: (Carcinogenesis) G – genetic factors I – immunologic factors V – viral factors a. Human Papiloma Virus – causing warts b. Epstein Barr Virus E – environmental Factors 90% a. Physical – irradiation, UV rays, nuclear explosion, chronic irritation, direct trauma b. Chemical factors – - Food additives (nitrates - Hydrocarbon vesicants, alkalies Warning / Danger Sx of CANCER - Drugs (stillbestrol) - Urethane C – change in bowel /bladder habits - Hormones A – a sore that doesn’t heal - Smoking U – unusual bleeding/ Discharge Male: st T – thickening of lump – breast or 1 Lung Cancer – Bronchogenic d/t smoking nd elsewhere 2 Liver Cancer – Hepatic d/t alcohol rd I – indigestion/Dysphagia 3 Prostate cancer – 40 y/o & above (middle age & above) th O – obvious change in wart/ mole 4 Testicular Cancer – 30 y/o N – nagging cough/ hoarseness BPH – 50 & above U – unexplained anemia A - anemia Female: S – sudden wt loss 1st Breast Cancer – 40 yrs old & up – Mammography 15 – 20 mins (SBE – 7 days after mens) 2nd Cervical Cancer – 90% Multi-sexual partners 5% Early Pregnancy 3 L’S TRIAD 3rd Ovarian Cancer – common to squamous cell type Sx 4th Uterine Cancer

CLASSES OF CANCER:

Large Lump Loaded

Tissue Typing: Created by Niňa E. Tubio

80

1.

Carcinoma – arises from surface epithelium & glandular tissues

2.

Sarcoma- from connective tissue or bones

3.

Multiple myeloma – from bone marrow Pathological fracture of ribs & back pain

4. Lymphoma – from lymph glands 5. Leukemia – from blood 1. LEUKEMIA -

Cancer of the WBC

Pathology:

Uncontrolled abnormal proliferation ---------------immature WBC known as Blast Cells activity of cell Proliferation of BLAST CELLS

cellular metabolism prone to infection

Invade/Infiltrate vital organs Spleen Spleenomegaly

Liver Hepatomegaly

Temperature

Crowd/ Congest/Accumulate

Kidney

Brain

RF

ICP

Joint Pain, Swell Hinder/Prevent Production of Cells RBC

Platelets

CLASSIFICATION:

1. ACUTE LEUKEMIA

ONSET

DURATION

CELLS

Sudden

Short < 6 months

Immature blast cells

2. CHRONIC LEUKEMIA Gradual long duration - Characterized by periods of remission (absence) & exacerbation (recurrence)

Mature WBC

PREDOMINANT CELLS PRESENT IN BLOOD: 1. Acute/Chronic Lymphocytic Leukemia = 2. Acute/ Chronic Myelocytic Leukemia =

Lymphocytes &

monocytes ---- ALL (common to children)

myeloblasts ----- CML (common to Adult)

Cells Derived 1. Bone Marrow Granulocyte Created by Niňa E. Tubio

Agranulocyte

2. Lymphoid Tissue Agranulocyte 81

Immature

immature

immature

Myeloblast

Monoblast

mature

Myelocyctes

Monocyte

Lymphocyte

2. BREAST CANCER Predisposing Factors: 1. Family Hx (mother/sister) 2. Obesity 3. Unmarried at age 40 y/o 4. Married w/o children 5. Married w/ children but did not breastfeed 6. Women w/ prolonged menstruation 7. Early menarche at 11 y/o 8. Late menopause at 52 y/o 9. 1st pregnancy at age 35 y/o Prevention:

SBE

Early Sign of Breast Ca: Non-tender Non-mobile Painless breast mass/lump

= 7-10 days after menstruation = after menopause----- 1x/month Late Sign of Breast Ca:

Sx: 1. Dimpling of skin 2. Orange skin 3. Asymmetry of breast 4. Discharges of nipple Dx: 1. Mammography 2. Breast Biopsy = Best confirmatory Dx Tx:

MASTOIDYNA = breast pain

Common Site Of Breast Ca UPPER OUTER QUADRANT LEFT

1. Surgery: Lumpectomy Modified Mastectomy – mass, tissue, pectoralis major or minor at axillary Radical Mastectomy - leave either pectoralis major or minor muscle

3. ONCOLOGIC EMERGENCIES Obstructive or Compressive Disorders Superior vena cava syndrome Pericardial effusion/cardiac tamponade Leukostasis Spinal Cord Compression Metabolic Disorders Hypercalcemia Symptoms of SIADH Tumor lysis syndrome

PROGNOSIS Lung = 6 yrs Breast = 2-6 yrs. Colon = 2-6 yrs. Pancreatic = 3-6 months Liver = 3 mnths

3. Disruptions of hematologic/im-munologic function Created by Niňa E. Tubio

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DIC Septic shock

3. BRAIN TUMOR Location: 1. Supratentorial – Cerebrum, anterior 2/3 of the brain 2. Infratentorial – Cerebellum, brainstem, posterior 1/3 of the brain *Both will manifest Increased ICP

Early Sign of Brain Tumor: PAPILLEDEMA (tumor compress on optic chiasm)

Both will undergo Brain Surgery: a. CRANIOTOMY/CRANIECTOMY - Use general endotracheal anesthesia (For all brain surgery) If surgery lasts for more than 2 hrs, assured of patent airway - Type of incision: Coronal or Butterfly - Skin Preparation: Shaving of head done at stage 3 of anesthesia Nursing Management: DONT’S POST-OPERATIVE: 1. Do not put client on Trendelenberg position---- it will increase ICP & abdominal content will compress stomach 2. If pt. in shock: Supine w/ pillow, head turned to one side 3. If pt. not in shock: Supratentorial---- elevate head 45 degrees (SF) ---- to promote venous return to heart Infratentorial ---- elevate head 10-15 degrees ------ to prevent compression of brain stem --- turn head to one side, unoperated side especially if bone flap not returned --- allowed on affected side but not more than 20 minutes to prevent ischemia 4. Do not give narcotic agent/analgesic No Demerol------ respiratory depressant 5. No suctioning---- mere suction will trigger coughing----- Increased ICP --- If needed: Oropharyngeal suctioning only --- Nasal suctioning will damaged nasal mucosa---leakage of CSF 6. Do not restrain client -- Makes client agitated --- Increased ICP 7. No rectal tube, rectal movement or manual extraction of feces. -- Vagal stimulation------Bradycardia Treatment Modality: 1. Radiotherapy

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Therapeutic Modality: 1. CHEMOTHERAPY – Use various chemotherapeutic agents that kills cancer cells & kills normal rapidly producing cells – GIT, bone marrow, and hair follicle. Classification of Cytotoxic Agents: Cell-Cycle Non-specific 1. Alkylating Agents

Classification of Cytotoxic Agents: Cell-Cycle Specific 1. Antimetabolite (S phase)

Action: Binds w/ DNA & prevents cell replication Nitrogen Mustard Cyclophosphamide (Cytoxan) Chlorambucil (Leukeran) Nitrosureas Carmustine Lomustine Alkylating-like agents Busulfan (Myeleran) Carboplatin Cisplatin (Platinol)* common Thiotepa Ifex (Ifosfamide) 2. Antitumor/Anti-Neoplastics Antibiotics Action: Inhibits cell division by interfering w/ synthesis of nucleic acid Bleomycin Doxorubicin Dactinomycin Mitomycin Idarubicin Adriamycine (Doxorubicin) Mithramycin Plimcamycin Actinomycin

Action: Foster cell death by interfering w/ the cellular metabolic process Cytarabine (Cytosar/Ara C) 5-fluorouracil (5-FU) Hydroxyurea 6-mercaptopurine (Purinethol) Methotrexate (Mexate)

2. Vinca/Plant Alkaloids (M phase) Action: Mitotic Inhibitors Docetaxel Etoposide (Toposar) Vinblastine (Velban,Velbie) Vincristine (Oncovin)

Classification of Cytotoxic Agents 1. Hormones & Steroids Action: Reduces cellular metabolism by providing a non-favorable environment for growth of Ca cells Estrogens DES (Post-menopausal) (Diethylstibestrol) Ethinyl estridiol Antiestrogens Tamoxifen Raloxifene Others Aminogluthetimide Asparaginase Leuprolide Mitotane Androgens (Pre-menopausal) Fluoxymesterone Testosterone Propionate Halotestin Antiandrogens Bicalutamide Flutamide Progestins Medroxyprogesterone Megestrol acetate

Side-Effects:

PROTOCOL IN THERAPY

1. GIT - -Nausea & Vomiting

6 cycle of Chemotherapy Interval of 28 days

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1.

Administer anti-emetic (Plasil) 4 – 6h before start of chemotherapy Ex. Ondansetrone – Zofran Alprazolan - Zanax 2. Withhold food/ fluid before start of chemo 3. Provide bland diet post chemotherapy: Avoid spic foods---irritants Ex. Non irritating / non spicy 4. Avoid bulky course diet 5. Advise Neutropenic Diet : Avoid raw foods, raw vegetable - Diarrhea 1. Administer anti diarrhea 4 – 6h before start of chemo 2. Monitor urine, I&O qh - Stomatitis/ Mouth Sores

Doxorubicin -Toxic to myocardium - Do not give if client is not hooked up to a cardiac monitor

1. Oral care – offer ice chips/ popsickles Use alkalanizer for mouth sores 2. Inform patient that 10-15 days after chemotherapy there will be hair loss – Temporary Alopecia - Loss from other hair of the body - Hair will grow back after 4 – 6 months post chemo. -Bone Marrow Depression --------Leukopenia/Anemia 1. Enforce CBR 2. O2 inhalation 3. Reverse isolation 4. Monitor signs of bleeding 5. Inform pt. it will last only for 21 days 2. Reproductive Organ – Sterility 1.

Do sperm banking before start of chemo

3. Renal System – Increase uric acid 1.

Administer allopurinol/ xyloprin (gout) Fx: Inhibits uric acid Acute gout – colchicines Increase secretion of uric acid

3. Neurological Changes – peristalsis – paralytic ileus Most feared complication following any abdominal surgery Vincristine – plant alkaloid causes peripheral neuropathy Mngt: 1. Cancer drugs can be very potent------- it can destroy normal cells 2. Protect yourself from Ca drugs that can destroy the skin: cover everything 3. Increase fluid intake post-chemo d/t drugs are hepato-toxic 4. Avoid exposure of Ca drugs to light----reduces the potency of the drug---cover w/ carbon paper, dim lights REVERSE ISOLATION TECHNIQUE 1. Private room, laminar air flow (positive pressure room) 2. Sterile linen, sterile hygiene equipment 3. Dedicated equipment 4. Put on shoe covers, mask & cap, sterile gown & gloves. 5. Low bacteria diet: no fresh fruits & vegetables; avoid drinking water allowed to stand for more than 15 min. 6. No fresh flowers or potted plants 7. Institute prophylactic oral hygiene regimen before, within 30 minutes after each meal & q2H–q4H during waking hours 8. May use ¼ tsp salt, pinch of baking soda & 8 oz. of H2O or saline 9. Avoid alcohol- or glycerine-based mouthwash Created by Niňa E. Tubio

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10. Use soft–bristled toothbrush 11. Use foam stick moistened with mouthwash to remove debris from mucosa 12. May apply topical anesthetic, as prescribed 13. Encourage fluid intake of 2000 ml/day 14. Encourage bland diet high in CHON to promote healing. Avoid hard or spicy food Avoid citrus juices 15. If patient has difficulty in eating & maintaining fluid intake, parenteral nutrition may be necessary 16. Assess the need for use of antifungal or antibacterial agents 2. RADIATION THERAPY – Involves use of ionizing radiation that kills cancer cells & inhibit their growth & kill rapidly producing cells. Types of Energy Emitted:

1. Alpha rays 2. Beta rays 3. Gamma ray

– rarely used – doesn’t penetrate skin tissues – internal radiation – more penetration – external radiation – penetrates deeper underlying tissues

2 Methods of Delivery:

1. External Radiation

- Involves electro magnetic waves Ex. Cobalt Therapy, Teletherapy, External Beam Radiation

Nursing Responsibility: a.

Explain that it is a painless procedure

b. During procedure: “Pencil Markings “ on skin indicating area to be radiated c. d. e. f. g. h.

Tell pt. not to erase markings & cleanse area only w/ H2O. No soap. Pat dry. Avoid sunlight over site Avoid pressure over the site Avoid hot/cold application over site Avoid use of oil cream solution/lotion to prevent skin reaction Observed for S/S of RADIATION SICKNESS

Locally Manifested - Erythema - Dryness of skin - Loss of skin hair - Blister formation - Skin desquamation

2. Internal Radiation

Systematically - Leukopenia—bone marrow - Sterility---- Gonads—both sensitive to radiation

– Injection/ implantation of radioisotopes proximal to CA site for a specific period of time. - Form of wire, seed, needle - Isotope inside client’s body

Administering ISOTOPE: a. Implant or “Intracavitary Implantation - Insert isotope into body cavity - Radium seed/Radom seed (sealed) b. Brachytherapy - Intralesion/ intratumor - Cesium 135 (sealed) c. P.O. - RAI 135, RAI 131 (unsealed liquid) d. Intra-arterial Perfusion Created by Niňa E. Tubio

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- RA Gold 198 (liver cancer) - RA Phosphorus (bone cancer) 2 Types: a. Sealed Implant

– Radioisotope with a container & doesn’t contaminate body fluid. Ex. Radium Seed, Radom Seed, Cesium 135

b. Unsealed Implant

– Radioisotope without a container & contaminates body fluid. - Liquid given either P.O. or Intra-arterial Ex. Phosphorus 32, RAI, RA

Nursing Responsibility: 1. Isolate patient. 2. Offer diversional therapy 3. Post at door radiation sign 4. Separate set of utensils 5. articles not needed in room should be removed 6. In Unsealed: All excreta, vomitus are considered contaminated. Throw directly to toilet bowl 7. Observe for Time: Longer exposure means more radiation Not more than 5 minutes/exposure, 30 minutes/shift Distance: 3-8 ft. from site Shielding: Stay at the farthest part/ use lead apron 8. Prevent accidental dislodgement of the radium: Place on CBR NO bed pan, insert indwelling catheter Give diet constipation: Decreased fiber & roughage Once dislodge, pick-up w/ long forcep, put in lead container 9. Use scanner, Geiger counter to detect remaining traces of radiation 10. Tell partner to resume sex, once edema has subsided 11. Tell pt. if dysuria & burning in urination: SUSPECT URETHRAL ATHROPHY Meatus, Urinary bladder---- CYSTITIS, HEMATURIA 3 Factors Affecting Exposure: a. Half life b. Distance c. Time d. Shielding

–Time period required for half of radioisotopes to decay. - At end of half life – less exposure – The farther the distance – lesser exposure – The shorter the time, the lesser exposure – Rays can be shielded or blocked by using rubber gloves – α & β gamma – use thick lead on concrete.

S/E & Mgt: a.) Skin errythema, redness, sloughing

1. Assist in bathing pt 2. 3. 4.

Force fluid – 2,000 – 3,000 ml/day Avoid lotion or talcum powder – skin irritation Apply cornstarch or olive oil

b.) GIT –Nausea / Vomiting /

Stomatitis

1. Administer antiemetic 4 – 6h before start of chemo - Plasil 2 Withhold food/ fluid before start of chemo 3. Provide bland diet post chemo Non irritating / non spicy Dysglusia – decrease taste sensitivity -When atrophy papilla (taste buds) – 40 y/o Created by Niňa E. Tubio

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c.) Bone Marrow Depression 1. 2. 3. 4.

Enforce CBR O2 inhalation Reverse isolation Monitor signs of bleeding

CARDIOVASCULAR SYSTEM OVERVIEW: HEART: -

-

-

Muscular, pumping organ of the body Occupies most of the Left mediastinum Weigh 300 – 400 grams Microscopic Resembles a closed fist Covered by a serous membrane – Pericardium 2 Parts

Parietal layer

Pericardial Space Fluid – prevent Friction rub

Cardio Physiology: The main functions of this system are: To transport oxygen, hormones & nutrients to the tissues To transport waste products to the

Visceral layer

CONSISTS OF 3 LAYERS:

1. Epicardium 2. Myocardium 3. Endocardium

– Outermost - ( Essential, coronary arteries arelocated here) --------- M.I. & AP – Inner – Responsible for pumping action/ Most dangerous layer -- Cardiogenic shock & RHD –Innermost layer – Connected to Tunica Intica ------------------------ Endocarditis

2 CHAMBERS:

1. Upper – Collecting/ Receiving chamber - Atria 2. Lower – Pumping/ Contracting chamber – Ventricles

VALVES & HEART SOUNDS:

1. Atrioventricular Valves - Tricuspid & Mitral Valve Closure of AV valves – gives rise to 1st heart sound or S1 or “lub”

2. Semi-lunar Valve – Pulmonic & Aortic Closure of semilunar valve – gives rise to 2nd heart sound or

S2 or “dub”

Extra heart Sound:

S3 – d/t Increased Ventricular Filling -Ventricular Gallop

– Left CHF, Left ventricular hypertrophy

S4 – d/t Forceful Atrial Contraction - Atrial Gallop

– MI, HPN, Pulmonic Stenosis, Aging

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CORONARY ARTERIES: The Blood supply of the heart comes from the Coronary arteries a. Right coronary artery b. Left coronary artery Both supply the myocardium with blood 1.Arises from the base of the aorta : RMCA & LMCA CONDUCTION SYSTEM OF THE HEART: 1.

Sino atrial node (SA node) (or Keith-Flock node) Location: Junction of SVC & Right Atrium Function: Primary pace maker of heart Initiates electric impulse of 60 – 100 bpm

2. Atrioventicular Node (AV node or Tawara node) Location: Inter atrial septum Delay of electric impulse to allow ventricular filling of 0.8 milliseconds Slowest conduction 3.

Bundle of His Location: Interventricular septum Branches out into: Rt main Bundle Branch & Lt main Bundle Branch

4.

Purkenjie Fiber Location: Walls of ventricles-- Ventricular contractions Fastest conduction

Physiology The intrinsic conduction system causes the heart muscle to depolarize in one direction The rate of depolarization is around 75 beats per minute (60-100/min) The SA node sets the pace of the conduction This electrical activity is recorded by the Electrocardiogram (ECG) Sympathetic system INCREASES HR Parasympathetic system (Vagus) DECREASES HR ANATOMY OF THE HEART

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SA node

AV

Septum Purkenjie Fibers

Bundle of His

BLOOD SUPPLY: Amount of blood the heart pumps out in each beat Stroke Vol.

X HR/min

Cardiac Output

X

(Normal C.O: 4-6 L/min)

Total Peripheral Resistance

= Blood Pressure

Factors in Cardiac Output: 1. Systole 2. Diastole

- Contraction - Relaxation

The PRELOAD refers to the amount of blood contained in the ventricle at the end of a diastole. Degree of stretching of the heart muscle when it is filled-up with blood (reduced with hypovolemia) The AFTERLOAD force that LV has to exert in order to pump blood to the aorta. The resistance to which the heart must pump to eject the blood (increased with HPN) Control is neural (central & peripheral) & hormonal Baroreceptors in the carotid & aorta Hormones- ADH, Adrenergic hormones, Aldosterone & ANF ADH increases water retention Aldosterone increases sodium retention & water retention secondarily Epinephrine & NE increase HR & BP ANF= causes sodium excretion The vascular system consists of the arteries, veins & capillaries The arteries are vessels that carry blood away from the heart to the periphery The veins are the vessels that carry blood to the heart Created by Niňa E. Tubio

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The capillaries are lined with squamos cells, they connect the veins & arteries The lymphatic system also is part of the vascular system & the function of this system is to collect the extravagated fluid from the tissues & returns it to the blood IRREGULARITIES: 1. Complete Heart Block – Insertion of pacemaker at Bundle Branch Metal – Pace Maker – change q3 – 5 y/o 2. ECG Tracings Prolonged PR ST segment Depression ST elevated T wave inversion Widening QRS

– Atrial Fibrillation – Angina Pectoris – MI – MI – Arrhythmia

3. Coronary Artery Disease Atherosclerosis Angina Pectoris MI

– Myocardial Injury – Myocardial Ischemia - Myocardial Necrosis

DISORDERS OF THE HEART I. CORONARY ARTERY DISEASE/ ISCHEMIC HEART DISEASE Results from the focal narrowing of the large & medium-sized coronary arteries d/t deposition of atheromatous plaque in the vessel wall If 50% of the left coronary arterial lumen is reduced or 75% of the other coronary artery, becomes significant Pathophysiology: Fatty streak formation in the vascular intima T-cells & monocytes ingest lipids in the area of deposition Potential For: Thrombosis Embolism

Atherosclerosis Narrowed arterial lumen Reduced coronary blood flow

With Coronary occlusion

Without Coronary Occlusion

Myocardial Ischemia ( 8-10 seconds : Anginal Pain) Chest Pain

Myocardial Necrosis Akinesia/Dyskinesia of the myocardium

“SAVERS”

*DECREASED CARDIAC OUTPUT

S – sudden onset (myocardial & anginal)

CARDIOGENIC SHOCK

A – anterior or substernal

Renal Damage (Acute Renal Failure)

V – vague Created by Niňa E. Tubio discomfort

E – exercise

PULMONARY EDEMA Right Ventricular Hypertrophy 91

Electrical Failure

Right Ventricular Hypertrophy

Rales Cough Hemoptysis Orthopnea Excertional dyspnea Easy fatigability

Dysrrythmia Ventricular Fibrillation Sudden Heart Arrest

Sx of Right CHF

Pitting Edema

Weight Gain

Ascites

Hepatomegaly

(+) Hepato-Jugular Reflux

Dyskinesia - difficult contraction of the myocardium Akinesia -temporary

1. ATHEROSCLEROSIS ATHEROSCLEROSIS - Narrowing of artery d/t fat/ lipid deposits at tunica intima.

Sx of Left CHF

ARTEROSCLEROSIS - Hardening of artery d/t calcium & CHON deposits at tunica media.

Predisposing Factor: 1. Sex – male 2. Black race 3. Hyperlipidemia - Genetic 4. Smoking 5. HPN 6. DM 7. Oral contraceptive/Steroids - prolonged use 8. Sedentary lifestyle 9. Obesity >20 % of Body weight 10. Hypothyroidism

LAYERS OF THE ARTERY TUNICA ADVENTITIA – outer TUNICA INTIMA innermost TUNICA MEDIA - middle

Sx: 1. 2. 3. 4. 5.

Chest pain Dyspnea Tachycardia Palpitations Diaphoresis

Tx: 1. PTCA 2. CABG (Refer to MI for management)

2. ANGINA PECTORIS Created by Niňa E. Tubio

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-

A clinical syndrome characterized by paroxysmal chest pain d/t temporary myocardial ischemia usually relieved by REST or NGT nitroglycerin Reversible, no dead cells yet Chest pain resulting from coronary atherosclerosis or myocardial ischemia (tissue ischemia)

3 COMMON TYPES OF ANGINA 1. Stable Angina - The typical angina that occurs during exertion - Relieved by rest and drugs & the severity does not change - < 15 minutes 2. Unstable Angina

Variant Angina smoking Angina Decubitus when lying-down

– From – pain

-Occurs unpredictably during exertion & emotion - Severity increases with time & pain may not be relieved by rest & drug - Mimics M.I. 3. Variant angina - Prinzmetal angina, results from coronary artery VASOSPASMS - May occur at rest Pathophysiology: STERLING LAW = the greater the myocardium fiber stretch = the greater the pressure on contraction For Myocardium to survive: Supply = Demand If < then it will suffer ISCHEMIA If blood supply decreased or 8-10 seconds (partially occluded) Suffer Ischemia CHEST PAIN (Anginal Pain) If more than 30 minutes, the heart cannot withstand Myocardial Infarction/Necrosis CHEST PAIN Angina Pectoris: Predisposing Factor:

1. 2. 3. 4. 5. 6.

7. 8. 9. 10.

Sex – male Black raise Hyperlipidemia Smoking HPN DM Oral contraceptive prolonged Sedentary lifestyle Obesity Hypothyroidism

Created by Niňa E. Tubio

Precipitating Factors:

4 E’s

1. Excessive physical exertion 2. Exposure to cold environment (vasoconstriction) 3. Extreme emotional response Angina 4. Sx: Excessive intake of foods high in S – sudden onset 1st: Levine’s Sx: hand clutching chest A – anterior or substernal pain Type: sharp, stabbing, excruciating pain Radiates to back, shoulders, axilla, arms & jaw muscles V – vague discomfort E – exercise will intensify the pain R – rest Relieved by rest or NGT

93

Sx: Others: 1. Dyspnea 2. Tachycardia 3. Palpitation 6. Diaphoresis Dx: 1.History taking & PE 2. ECG – ST segment depression 3. Stress test – treadmill = abnormal ECG 4. Serum cholesterol & uric acid - increase. 5. Cardiac Catherization

If chest pain does not radiate: Cause: Pulmonary

Nsg Mngt: To decrease Myocardial Demand 1. Administer prescribed medications Nitrates- to dilate the venous vessels decreasing venous return and to some extent dilate the coronary arteries NTG – small doses – Venodilator (sublingual) Large dose – vasodilator 1st dose NTG – give 3 – 5 min 2nd dose NTG – 3 – 5 min Given 3x at 3-5 minutes interval 3rd & last dose – 3 – 5 min Still painful after 3rd dose – notify doc. MI! Exercise: 55 yrs old with chest pain: 1st question to ask pt: what did you do before you had chest pain. 2nd question: does pain radiate? If radiate – heart in nature. If not radiate – pulmonary origin Venodilator – veins of lower ext – increase venous pooling lead to decrease venous return. Nsg Mgt For NGT: 1.

Keep in a dry place. Avoid moisture & heat, may inactivate the drug.

2.

Monitor S/E: Vasodilation Orthostatic hypotension Transient headache Dizziness

3.

Rise slowly from sitting position

4.

Assist in ambulation.

5.

If giving NTG via Patch:

a. Avoid placing it near hairy areas-will decrease drug absorption b. Avoid rotating transdermal patches- will decrease drug absorption c. Avoid placing near microwave oven or during defibrillation-will burn pt d/t aluminum foil in patch (color: blue & white) Aspirin- to prevent thrombus formation Beta-blockers- to reduce BP & HR (Propanolol) Calcium-channel blockers- to dilate coronary artery & reduce vasospasm ACE inhibitors – Captopril Ca antagonist – Nefedipine (anti-hypertensive) 2. Teach the patient management of anginal attacks Advise patient to stop all activities Created by Niňa E. Tubio

Nursing Diagnoses For Angina Pectoris: Decreased cardiac output Altered comfort Impaired gas exchange Activity intolerance Anxiety

94

3. Enforce CBR 4. Administer O2 inhalation 5. Semi-fowler 6. Diet- Decrease Na & saturated fats, low caffeine 7. Monitor VS, I&O, ECG 8. HT: Discharge Planning: a. b.

c. d.

Avoid precipitating factors – 4 E’s Prevent complications – MI Instruct client to take meds before physical exertion-to achieve maximum therapeutic effect of drug Importance of follow-up care.

3. MYOCARDIAL INFARCTION (MI)

– Anatomy:

A terminal stage of CAD characterized by necrosis & scarring leading to permanent mal-occlusion

Coronary Artery 1. 2.

Right CA ---supply blood------ RA, RV, Posterior Wall Left CA

i. j.

Anterior Descending LCA --- supply--- RV, LV, Septum, Anterior Wall Circumflex LCA -------------- supply --- LA, LV, Lateral Wall

2 Blood vessels supplying ventricles------ventricles receive higher blood than atria LV – needs more blood to pump to pulmonary circulation RV – pump blood to systemic Ex. If occlusion is in Circumflex LCA-------affected LA, LV so basis of nursing DX----- systemic Circumflex----

CO2

TYPES OF MI: 1. Clot RCA

Zone RA, RV Posterior Wall

ECG Inferior Wall MI Posterior Wall MI

2. Anterior Descending LCA

RV, LV

Anterior Wall MI

3. Circumflex LCA

Septum LA LV lateral wall

Antero-Septal MI Lateral Wall MI

TYPES OF MI BY LAYERS: 1. Sub-endocardial MI 2. Myocardial Infarction 3. Trasmural MI

– Mal-occlusion of either R & L coronary artery, Ischemia of the inner part – muscle layer affected: most common – Most dangerous MI – Mal-occlusion of both R&L coronary artery, Involves all layers

PATHOLOGY OF CHEST PAIN IN MI & Sx: Created by Niňa E. Tubio

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Myocardial Ischemia

Anaerobic Metabolism

reverse effect if occluded (KREB’s CYCLE)

causes Increased BP Vasodilation

Metabolite will release enzyme LACTIC ACID

Alters conduction of electrical impulses Dysrrythmia Weakness:

PR or

Irritate sensory nerve endings PR

CHEST PAIN

Ensuing inflammatory process Causes release of increased neutrophils (1st cells to migrate when inflammation occurs) LEUKOCYTOSIS LOW GRADE FEVER (38 degree C) lasts for 3-5 days---best indicator for monitoring of MI progression or healing If responding to treatment & N.I. Neutrophils will be replaced by fibroblastic cells----result to scarring/fibrolysis---- the healing process---- Normal Temperature MYOCARDIAL INFARCTION Predisposing Factors Sex – male Black raise Hyperlipidemia Smoking HPN DM Oral contraceptive Sedentary lifestyle Obesity Hypothyroidism

S/Sx

Dx Exam

1. CHEST PAIN

1. Cardiac Enzymes Go to blood following cardiac death

S – sudden onset of pain

a. CPK – MB – Creatinine Phosphokinase

A – anterior/substernal/precordial area Excruciating, vice like, visceral pain Radiates back, arm, shoulders, axilla, jaw

b. LDH – lactic acid dehydrogenase

via afferent nerve cells pain

w/ referred epigastric

V – vague discomfort Feeling of tightness or heavy chest E – exercise increases pain R – rest does not relieved the pain or by NGT 2. Dyspnea 3. Erthermia 4. Initial increase in BP 5. Mild restlessness & apprehensions 6. Cool, moist, ashen skin

c. SGPT – (ALT) Serum Glutamic Pyruvate Transaminase d. SGOT (AST) – Serum Glutamic Oxaloacetic 2. Troponin test – increase 3. ECG Tracing – ST segment elevation, Widening of QRS complexes – means arrhythmia in MI indicating PVC 4. Serum Cholesterol & Uric acid 5. CBC – increase WBC

Myocardial Infarction Nursing Diagnoses Pain (Altered comfort) Decreased cardiac output Impaired gas exchange Activity intolerance Altered tissue perfusion

7. Occasional findings Created by Niňa E. Tubio

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a. Split S1 & S2 b. Pericardial friction rub (inspiration) c. Rales /crackles d. S4 (atrial gallop)

*Most critical period after Dx of MI – 6-8 hrs. d/t arrhythmia, a type of PVC premature ventricular contraction. COMPLICATIONS: (Refer to Pathophysiology of Atherosclerosis)

1. Cardiogenic Shock – d/t poor contraction/akinesia . 2.

Renal Failure – decreased CO2----decreased renal failure---renal ischemia----cessation—RF

3. Ventricular Fibrillation--- heart beat very irregular, erratic & very rapid 180 bpm 4.

5. 6. 7. 8.

9. 10.

Pulmonary Edema Right Ventricular Hypertrophy Left-sided HF Late Sx of Cardiogenic Right-sided HF Shock In MI Thrombophlebitis – DVT Oliguria Arrhythmias – PVC Dressler’s Syndrome – post MI syndrome - Non-resistant to Pharmacological agents -Administer 150,000 – 450,000 units of streptokinase

Management of Myocardial Infarction: 1. Increase Myocardial O2 supply - Administer O2 inhalation (low-flow) - Also to prevent extension of necrosis - Monitor VS, I&O & ECG tracings 2. Relieve pt. of chest pain - Give drug of choice: Narcotic Analgesic Morphine SO4 ------ Action: Decreased preload & afterload through vasodilation Decrease level of anxiety Relieves severe intensity of pain Longer sustained effect If not available: Demerol but S/E: Hypotension Created by Niňa E. Tubio

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3. Relieve pt. of anginal pain - *Give NITRITES or NITRATES Action: Relax smooth muscles of the coronary artery/ also as vasodilators Ex.

a. Isosorbade (Isordil) b. Isosorbide Mononitirite (Indur) c. NGT (Nitroglycerine) 5 mg – SL Ex. Nitrostatic 10 mg - P.O. Patch, cream – Topical Ex> Nitral Patch, Transderm

Nsg. Mgnt For Nitroglycerine: 1. Explain that drug may cause S/E : Throbbing headache Flushing of skin Warm sensation & stringing, biting Burning sensation under tongue if taken SL

*continue taking the drug s/s will disappear w/ the continued medication

2. S/E : Postural hypotension d/t vasodilation Give drugs while on bed or in a sitting position 3. Keep drug in dark, opaque container because exposure to light/sun will reduce potency of nitrates 4. If topical administration: Cleanse area w/ H2O only, Avoid hairy areas, rotate administration Place on precardium: 5th ICS or site of pain 5. If SL : Advise pt. to place under tongue, allow to dissolve, swallow saliva NEVER follow it w/ H2O (interrupt sustained effect) 6. Keep away from your own skin, causes vasodilation & headache 4. R - rest - To decrease cardiac workload - To decrease work for breathing - To decrease myocardial O2 demand - To increase cardiac reserve - Enforce CBR without BRP - Provide Bedside commode - Abstain from sexual activity (4-6 wks. After MI attack) - Take nitrate prior to sex & if w/ insomnia, chest pain, SOB-----seek medical advice - Avoid valsalva maneuver - Semi fowler - Resume ADL – activity - Post-cardiac rehab: 1.)Sex as an appetizer rather then dessert Before meals not after, after meals increase metabolism – heart is pumping hard after meals. 2.) Assume a non-weight bearing position. *When to resume sex/ act: When pt can already use staircase, then he can resume sex. 5. D – diet - To decreased caloric intake in order to decrease cardiac load - General liquid to soft diet - Low in Na 2-4 grams/day to get rid of ECF fluid excess - Avoid food high in saturated fat & avoid gas-forming foods - Avoid drugs w/ high Na like laxative - Avoid cardiac stimulant (caffeine, colas) - Increase fiber intake to avoid constipation - Avoid too hot drinks ------abdominal distention----- SOB - Avoid too cold drinks------ vagal stimulation-------- Decreased PR (Bradycardia) - Take 20 – 30 ml/week – wine, brandy/whisky to induce vasodilation

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6. D- diuretic - To prevent reabsorption of H20 by the renal tubules-----absorption---Hypokalemia----Use K-sparing diuretics Ex. Aldactone Spironolactone Ex.

Furosemide (lasix) Frusema Diuret Edecrine Mercuhydrin

Sign that diuretic is effective? *Absence of rales indicates (+) effect of diuretics

7. D- digitalis - Drug categorized as “CARDIAC GLYCOSIDES Ex. Digitoxin, Digoxin, Lanoxin, Gdiranid

3-FOLD ACTION OF DIGITALIS 1. Strengthen myocardial contraction-----------(+) Inotropic Effect Any drug that influences myocardial contraction has an inotropic effect 2. Increase cardiac output -------- Increase renal blood flow/renal perfusion Increase urinary output (secondary effect: Diuretic) 3. Decrease Cardiac Rate --------- (-) Chronotropic Effect Any drug that influences cardiac rate has a chronotropic effect (- or +) Nursing Management in Giving Digitalis:

1. Check CR, if below 60 do not give drug 2. 3.

Monitor serum potassium d/t its secondary effect as a diuretic Check for DIGITALIS Toxicity: Anorexia-----------------most common complaint Headache w/ N/V------ Early Sx of toxicity Diarrhea Photophobia Dysrrythmia Yellow spots in eyes Gynecomastia ----- Late Sx of Toxicity Antidote: DIGIBIND or DIGOXIN IMMUNE Fab ---------bind w/ lanoxin to decrease toxicity of lanoxin

8. If patient undergoes CARDIOGENIC SHOCK: a. Prepare for vasopressor------

BP

Ex.

Dopamine Intropine Aramine --- Metaraminol Bitartrate Levophed – Levartenenol Adrenalin /Epinephrine

b. Increase rate of impulse formation in SA node Ex. Lidocaine 1-2% Pronestyl --------Procainamide HCI Quinidine SO4 -- Quinidex Brethylium ------blocks release of norepenephrine Created by Niňa E. Tubio

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c. Dysrrythmia ----------- Give anti-arrhythmic drugs Ex. 1. Lydocaine blocks release of norepenephrine 2. Brithylium S/E: Confusion & Agitation If not corrected by medications: - Install artificial pacemaker or when SA node is damaged - Equipped with wire electrode & pulse generator PACEMAKER Type

Insertion

1. Temporary

Antecubital basilic vein

Wire/Electrode

Pulse Generator

Tip rest on RA or RV

Outside

2. Permanent: Epicardial-------- thru Thoracotomy RV Endocardial-----Thoracotomy RV (5-6 yrs. ) Permanent SA so attach to chamber w/ thicker myocardium

Implanted in abdominal wall Implanted subcutaneously below the device (subclavicular)

Nursing Management: 1.

Temporary:

2. Permanent: Both:

Avoid toying w/ the pulse generator Wrapped w/ rubber gloves Avoid vigorous arm & shoulder movements Avoid lifting heavy objects Do not come closer to a microwave oven, cell site, electrical power Or any apparatus emitting power voltage Do not go through X-rays, scanner Teach pt. how to monitor PR for 1 whole minute S/S of malfunctioning pacemaker: HICCUP Bradycardia Palpitation Syncope

9. Prevent other complications. Give medications a. Beta-blockers – “lol” 1. Propanolol (inderal) b. ACE inhibitors - pril 1. Captopril – (enalapril) c. Ca – antagonist 1. Nifedipine d. Anti platelet PASA (aspirin) e. Thrombolitics or fibrinolytics– to dissolve clots/ thrombus S/E allergic reactions/ uticaria Ex. Created by Niňa E. Tubio

1. Streptokinase--------most common 100

2. Urokinase ----------- S/E: Hypotension 3. Tissue Plasminogen Activating Factor (TPAF) ------- S/E: Chest Pain Monitor for bleeding: Anticoagulants 1. Heparin

2. Coumadin – delayed reaction 2 – 3 days

PTT

PT

If prolonged bleeding

Prolonged bleeding

Antidote : Protamine Sulfate

Antidote Vit K

10. For patient w/ VENTRICULAR FIBRILLATION a. Administer: DEFIBRILLATION – To terminate a life-threatening dysrrythmia thru unsynchoronous application (anytime) at any rate (200-360 joules) CARDIOVERSION - To correct dangerous dysrrythmia (sinus tachycardia) thru a synchronous application during R wave w/ 50-200 joules 11. Relieve patient of Sx of PULMONARY EDEMA: a.

Rotating Tourniquet/ Dry, bloodless Phlebotomy - To reduce right atrial flow

Indicative of too tight Tourniquet: Absence of Peripheral

Nursing Management:

1. Only 3 extremities should be pressed at the same time 2. Tourniquet should not be applied too tight 3. Rotate tourniquet every 15 minutes 4. Rotate clockwise ---use BP cuff if not available (at Pulse pressure) 5. Remove at interval of 15 minutes 6. No single extremity should be compressed for more than 45 minutes Cause VENOUS STASIS ----- stagnation of blood in 3 extremities Decrease blood to enter RA----

pulmonary system---- blood will

edema

12. Treatment for patient with CORONARY ARTERY DISEASE: 1. Prepare for Revascularization Surgery to restore myocardial blood flow

a. PTCA –Done to pt with single occluded vessel/simple vessel - Done under direct fluoroscopic guidance - Indicated for Angina less than 1 year & coronary artery not calcified Objective of PTCA: Created by Niňa E. Tubio

PTCA P– percutaneou s T– transluminar 101

1. To revascularize the myocardium 2. To prevent angina 3. Increase survival rate 4. To compress plaque against vessel wall increasing arterial lumen Procedure: Balloon-tipped catheter to/from femoral to CA to dilate CA or dislodge an atheroma/plaque b. CABG - For Multiple occluded vessels: - Done to improve blood flow to myocardial tissue - Uses saphinous vein/mammary artery - Done on an “open heart technique” & jump-graft from lower extremities Nsg Mgt Before CABG: 1. Deep breathing cough exercises 2. Use of incentive spirometer 3. Leg exercises 4. Cut at sigmoid process to umbilicus

CABAG C – coronary A – arterial B – bypass G – graft surgery

Feared Complications 2 P’s Pneumonia Pulmonary

- Once thoracic is opened, change in normal pressure (-) intrapleural pressure lungs will collapse Prepare for 1 way or 3 way Chest drainage

13.

CHEST DRAINAGE -Done to restore (-) intrapleural pressure of lungs to prevent collapse a. One-way H20 Sealed Chest Drainage System - Maintain an air-tight water-sealed system To patient

Glass rod 2-3 cm. Tip below H2O level Created by Niňa E. Tubio

Air vent, above H2O level (Emerson/Steidmann’s Pump)

H2O 102

b. 3-Way Chest Drainage To suction provides (-) pressure

To patient

H2O

Output Bottle

H2O

H2O

H2O Sealed Bottle

Vacuum

Controlled Nursing Management For Chest Drainage: 1. The 3 bottles should be below chest level (18 inches) to prevent backflow 2. Bottles should be taped to the floor to prevent accidental leakage 3. Observe for OSCILLATION fluctuation, Tidalling---- rise & fall of H2O Important that there is constant communication bet. thoracic cavity & output bottle a. Observe for OSCILLATION - Favorable ---- indicates that the lungs has re-expanded Non-Favorable ---- Absence may mean: Turn client side to side, if still (-) (To dislodge adhesion to wall) Tell client to do deep breathing exercise, if still (-) Stripping/Milking of the tube----an occlusion/clot will come out b. Observe for BUBBLING - Normal in vacuum bottle connected to suction machine - If present in H2O sealed bottle----- indicates PLEURAL LEAKAGE/DAMAGE - Measure output correctly. Put tape on bottle - Change bottle when empty - Do not clamp when changing bottle---- Tension Pneumothorax - For accidental breakage: Immediately get a bottle w/ sterile H2O & immersed tube If none available----clamp - In any set-up: 1st bottle is always the output bottle - Observe aseptic technique - Removal: Do not remove test tube during inhalation. Inhale deeply then pull during expiratory phase to prevent entry of air & suction residual fluid Apply petrolatum gauze dressing (non-porous dressing0 After removal, continue observing for S/S of hypoxia 4. CONGESTIVE HEART FAILURE - Inability of the heart to pump blood towards systemic circulation d/t obstruction. - Backflow - A syndrome of congestion of both pulmonary & systemic circulation caused by inadequate cardiac function & inadequate cardiac output to meet the metabolic demands of tissues - Inability of the heart to pump sufficiently - The heart is unable to maintain adequate circulation to meet the metabolic needs of the body This can happen acutely or chronically Acute as in Myocardial infarction Chronic as in cardiomyopathies Created by Niňa E. Tubio

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Classified according to the major ventricular dysfunction1.Left Ventricular failure 2. Right ventricular failure Etiology of CHF 1. CAD 2. Valvular heart diseases 3. Hypertension 4. MI 5. Cardiomyopathy 6. Lung diseases 7. Post-partum 8. Pericarditis & cardiac tamponade Systemic Circulation *Inferior Vena Cava

&

Superior Vena cava

UnO2

RSHF Blood goes back to TV-circulation

Aorta

Right Atrium

Left Ventricles

Tricuspid Valve

Mitral Valve

Right Ventricles

Left Atrium

Pulmonary Artery

Lungs (For Oxygenation)

A. RIGHT-SIDED HF -#1 Cause: Tricuspid Valve Stenosis S/S: Jugular Vein Distention Pitting Edema---IVC from toes Ascites Weight Gain Hepatospleenomegaly Jaundice Pruritus---Urticaria Esophageal Varices Anorexia

LSHF blood goes back to PV

Pulmonary Veins

B. LEFT-SIDED HF -#1 Cause: Mitral Valve Stenosis S/S: Pulmonary Edema/ congestion Dyspnea Paroxysmal Nocturnal Dyspnea –2 pillows/High-fowlers Orthopnea Productive Cough (blood-tinged sputum) Frothy Salivation Rales/Crackles Bronchial Wheezing Pulsus Alterans (weak-strong pulse) Anorexia & generalized body malaise S3 (Ventricular Gallop) Cyanosis PMI is displaced laterally : 4th -5th ICSMCL -----if below 5th ---cardiomegaly

1. LEFT-SIDED HEART FAILURE: Predisposing Factors: 1. 90% Mitral Valve Stenosis – d/t RHD, Aging RHD affects mitral valve – streptococcal infection Dx: 1. ASO Titer (Anti-Streptolysine O) > 300 total units - Steroids - Penicillin - Aspirin Complication: Created by Niňa E. Tubio

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RS-CHF Aging – degeneration / calcification of mitral valve Ischemic heart disease HPN, MI, Aortic stenosis Dx:

1. CXR – Reveals Cardiomegaly 2. 3.

PAP – Pulmonary Arterial Pressure PCWP – Pulmonary Capillary Wedge Pressure PAP PCWP

– Measures pressure of R ventricle. Indicates cardiac status. – Measures end systolic/ diastolic pressure

PAP & PCWP: Swan – Ganz Catheterization – cardiac catheterization is done at bedside at ICU (Tracheostomy – bedside) - Done 5 – 20 mins – scalpel & tracheostomy set CVP – Indicates fluid or hydration status Increase CVP – decrease flow rate of IV Decrease CVP – increase flow rate of IV 4.

Echocardiography – Reveals enlarged heart chamber or cardiomayopathy

5.

ABG – PCO2 increase, PO2 decrease = = hypoxemia = respiratory acidosis

Tx: M

- Morphine SO4 (to induce vasodilation)

A

- Aminophylline

D

- Digoxin

D

- Diuretics

O

- O2

G

- Monitor Blood Gases ----------- PO2 Respiratory Acidosis Hypoxemia Cyanosis

2. RIGHT-SIDED HEART FAILURE Predisposing Factor:

1. 90% - Tricuspid Stenosis 2. 3. 4. 5.

COPD Pulmonary embolism Pulmonic stenosis Left sided heart failure

S/Sx: Venous Congestion - Neck or jugular vein distension Created by Niňa E. Tubio

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-

-

-

Pitting edema Ascites Wt gain Hepatomegaly/ Splenomegaly Jaundice Pruritus Esophageal Varices----- Dilation of the veins of the esophagus Anorexia, General body malaise, Nausea Pulsus alternans Nocturia = urination at night at frequent intervals as the blood moves from interstitial space to the intravascular space & is excreted

Dx:

-

CXR – Reveals Cardiomegaly CVP – Measures the pressure at R atrium Normal: 4 to 10 cm of water Increase CVP > 10 – hypervolemia Decrease CVP < 4 – hypovolemia Flat on bed – post of pt when giving CVP Position during CVP insertion – Trendelenburg to prevent pulmonary embolism & promote ventricular filling.

3. Echocardiography – enlarged heart chamber / cardiomyopathy 4.Liver enzyme SGPT ( ALT) SGOT AST Nsg mgt: Increase force of myocardial contraction = increase CO 3 – 6L of CO 1. Administer meds: M – morphine SO4 to induce vasodilatation A – aminophylline & decrease anxiety D – digitalis (digoxin) D - diuretics O - oxygen G - gases a.) Cardiac Glycosides Increase myocardial = increase CO Digoxin (Lanoxin) Antidote: digivine Digitoxin: metabolizes in liver not in kidneys not given if with kidney failure. b.) Loop diuretics: Lasix – effect with in 10-15 min. Max = 6 hrs c.) Bronchodilators: Aminophylline (Theophyllin). Avoid giving caffeine d.) Narcotic analgesic: Morphine SO4 - induce vasodilator & decrease anxiety e.) Vasodilators – NTG f.) Anti-arrhythmic – Lidocaine 2. Administer O2 inhalation – high! @ 3 -4L/min via nasal cannula 3. High –Fowlers (2-3 pillows) 4. Restrict Na 5. Provide meticulous skin care 6. Weigh pt daily. Assess for pitting edema. Measure abdominal girth daily & notify MD 7. Monitor V/S, I&O, breath sounds 8. Institute bloodless phlebotomy. Rotating tourniquet or BP cuff rotated clockwise q 15 mins = to promote decrease venous return 9. Diet – decrease salt, fats & caffeine 10. HT: a) Prevent Complications : Shock Created by Niňa E. Tubio

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Arrhythmia Thrombophlebitis MI Cor Pulmonale – RT ventricular hypertrophy b.) Dietary modifications c.) Adherence to meds

CLASSIFICATION BASED ON New York Heart Association Class 1 Ordinary physical activity does NOT cause chest pain & fatigue No pulmonary congestion Asymptomatic NO limitation of ADLs Class 2 SLIGHT limitation of ADLs NO symptom at rest Symptoms with INCREASED activity Basilar crackles and S3 Class 3 Markedly limitation on ADLs Comfortable at rest BUT symptoms present in LESS than ordinary activity Class 4 SYMPTOMS are present at rest

OTHER PROBLEMS ASSOCIATED WITH THE CARDIOVASCULAR SYSTEM 1. CARDIAC TAMPONADE - A condition where the heart is unable to pump blood d/T accumulation of fluid in the pericardial sac (pericardial effusion) - This condition restricts ventricular filling resulting to decreased cardiac output - Acute tamponade happens when there is a sudden accumulation of more than 50 ml fluid in the pericardial sac Causative Factors: 1. Cardiac trauma 2. Complication of Myocardial infarction 3. Pericarditis 4. Cancer metastasis ASSESSMENT FINDINGS 1. BECK’s Triad- Jugular vein distention, hypotension & distant/muffled heart sound Created by Niňa E. Tubio

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2. Pulsus paradoxus 3. Increased CVP 4. Decreased cardiac output 5. Syncope 6. Anxiety 7. Dyspnea 8. Percussion- Flatness across the anterior chest

Laboratory FINDINGS 1. Echocardiogram= shows accumulate fluid in the pericardial sac 2. Chest X-ray NURSING INTERVENTIONS 1. Assist in PERICARDIOCENTESIS 2. Administer IVF 3. Monitor ECG, urine output & BP 4. Monitor for recurrence of tamponade Pericardiocentesis Patient is monitored by ECG Maintain emergency equipments Elevate head of bed 45-60 degrees Monitor for complications- coronary artery rupture, dysrhythmias, pleural laceration & myocardial trauma

2. CARDIOGENIC SHOCK - Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion - This shock occurs when the heart’s ability to contract & to pump blood is impaired & the supply of oxygen is inadequate for the heart & tissues Risk factors: Coronary factor- Myocardial infarction Risks factors: NON coronary: Cardiomyopathies Valvular damage Cardiac tamponade Dysrhythmias Severe CHF

Pathophysiology: Precipitating factors will cause decreased cardiac contractility Decreased stroke volume & cardiac output leading to 3 things: Damming up of blood in the pulmonary vein will cause pulmonary congestion Decreased blood pressure will cause decreased systemic perfusion Created by Niňa E. Tubio

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Decreased pressure causes decreased perfusion of the coronary arteries leading to weaker contractility of the heart ASSESSMENT FINDINGS 1. HYPOTENSION 2. Oliguria (less than 30 ml/hour) 3. Tachycardia 4. Narrow pulse pressure 5. Weak peripheral pulses 6. Cold clammy skin 7. Changes in sensorium/LOC 8. Pulmonary congestion LABORATORY FINDINGS 1. Increased CVP due to pooling of blood in the venous system Normal is 4-10 cmH2O 2. Metabolic acidosis

NURSING INTERVENTIONS 1. Place patient in a modified Trendelenburg (shock ) position 2. Administer IVF, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE These drugs will increase cardiac contractility 3. Administer O2 4. Morphine is administered to decreased pulmonary congestion & to relieve pain, relieve anxiety 5. Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz catherization & IABP 6. Monitor urinary output, BP & pulses 7. Cautiously administer diuretics & nitrates

DIAGNOSTIC PROCEDURES FOR CARDIOVASCULAR DISORDERS 1.

ECG/EKG -Done To measure the electrical impulses of the heart to Dx heart rate & rhythm Pathology: SA node------starts myocardial contractions Initiates electrical (+) impulses (emikts 60-100 bpm) Goes into Intra-atrial Track-------- A-V Node (located at right side of intra-atrial septum) Bundle of His (L & R) Purkinje Fibers Ventricular Contraction

• • • Created by Niňa E. Tubio

If below 60---- Sinus Bradycardia If above 100--- Sinus Tachycardia If 60-100 ------ Normal Sinus Rhythm

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•

•

DEPOLARIZATION – is the myocardial contraction REPOLARIZATION – Refractory Period/relaxation –regaining its (-) charge Normal Refractory Period 0.15-0.30 seconds

SA NODE ----- located at posterior wall of RA close to the entrance to Vena Cava • •

• •

During depolarization ---- permeable to entry of Na & Cal----- influencing myocardial contraction During repolarization----- permeable to entry of K & Cl P Wave – Atrial depolarization or contraction PR interval – travel time of impulse from atria to ventricle ( Normal: 0.12-0.20 seconds) Any delay in flow of impulse ------heart block

•

QRS Complex – Ventricular Repolarization (From ventricular contraction A---V to time it will be (+) charged After a brief period of resting----- (-) charge refractory period

• • •

ST Segment - completion of depolarization & beginning if repolarization T Wave – ventricular repolarization QT Interval – entire duration of depolarization & repolarization ( lasts for 0.42-0.43 seconds) (From QRS to T)

5 IMPORTANT ECG TRACINGS 1. MYOCARDIAL INFARCTION - Inverted T wave - Elevated ST -Pathological prominent T wave

area of ischemia ---- reversible with time area of infarction ----- irreversible, will always appear for life

2. HYPERKALEMIA - Peaked T wave - Prolonged PR Interval - Widened QRS complex 3. HYPOKALEMIA - Flat T wave - Depressed ST - Prominent U wave ----- Pathological--- influences myocardial repolarization Decreased K ---- weakened contraction or repolarization Prolonged T wave Forming an abnormal U wave Created by Niňa E. Tubio

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4. HYPERCALCEMIA - Shortened QT interval 5. HYPOCALCEMIA - Prologed QT interval 2. 24 HOUR HOLTER MONITORING/DYNAMIC ECG - Done to monitor 24 hrs. cardiac activity - Given pen & paper to record 24 hrs. - Non-invasive 3. STRESS TEST/ THREADMILL TEST/BICYCLE/ERGOMETRIC TEST - Done to evaluate amount of activities that the heart can tolerate Nsg Responsibility: - Avoid smoking the night before the threadmill - Wear comfortable light material - Wear rubber-soled shoes - Avoid heavy meal prior to test - Allowed light snack 2 hrs. before test - Avoid hot shower 2 hrs. after test to prevent syncope - Rest after the exercise 4. PHONO-ECHOCARDIOGRAPHY - Non-invasive - Use to detect any abnormal anatomical structure & abnormal heart sounds 5. ECHOCARDIOGRAPHY - Use to evaluate changes in the cardiac dimension during the cardiac cycle 6. ELECTROLYTE STUDIES - No NPO - Na & Ca ------- Depolarization - K & Cl ------- Repolarization 7. BLOOD TEST - Use to evaluate atheromatous changes Serum Cholesterol ------ NPO 6-8 hrs. Serum Triglyceride ----- NPO 12 hrs Serum Lipids -------- NPO 12 hrs. Nsg. Responsibility: - No lipid forming drugs Ex. Salicylates Estrogen Steroids No alcohol----- influence 8. ENZYMATIC TEST - No NPO------ it is normally released by the myocardium---- if elevated enzymes----problem to the myocardium Created by Niňa E. Tubio

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a. SGOT

(Serum Glutamic Oxaloacitic Aminotransferase) or AST (Serum Aspartate Aminotransferase)

b. SGPT (Serum Glutamic Pyruvic Transaminase) or ALT ( Serum Alanine Amintransfirase)

SGOT/AST : 5-40 u/L

SGPT/ALT : 4-36 u/L

c. CPK mb ( Creatinine Phosphokinase ) 3 Isoenzymes MB Increases myocardial insult/damage

BB Increased brain, bladder, bowel

MM Increased skeletal muscle

d. SLDH (Serum Lactic Dehydrogenase)

1&2 Myocardial insult *BEST CONFIRM MI

3 lung parenchymal damage

4&5 liver damage

-------- SGOT

* BEST DIAGNOSED MI -------- CPKmb *Nsg Intervention prior to blood extraction ----- No IM injection------- Increased CPK when skeletal muscle injury CARDIOVASCULAR ASSESSMENT Assessment: I. During Interview: 1. (+) Family History 2. Smoking Pathology: a.)

Nicotine -----stimulates release of Catecholamines--------------------------Epinephrine Platelet Aggregation

Increased Myocardial O2 demand

Vasoconstrictor

Increased cardiac workload

HPN

Risk for thrombus formation Increased cardiac workload b.) Carbon Monoxide ------ + Hgb (blood) ------interfere w/ O2 transport (carboxyhgb) Tissue hypoxia/hypoxemia 3. Stress 4. DM------can lead to MI 5. Atherosclerosis Created by Niňa E. Tubio

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6. HPN 7. Age ------- above 40 y/o 8. Sex ------- M: high risk F: high risk after menopause 9. Personality ---- high among Type A individual 10. Assess for history of easy fatigability----- 1st sign of poor cardiac reserve Ability of the heart to adjust to cardiac demand 11. History of Palpitations 2 Types: a. Physiologic ------ diet (coffee), strenuous activity, strong emotion, after eating b. Pathologic ------- clients w/ hyperthyroidism clients w/ cardiomegaly ( enlarged heart) contractions----hit cardiac wall----- palpitations Palpitations---pounding, jumping sensations for every myocardial contractions 12. Listen for normal & abnormal sounds S1 – lubb ----systole S2 – dub ----- diastole Abnormal:

Best heard at PMI ( Point of Maximum Impulse) on the 4th-5th ICSMCLL

S3 sound -----heard on early part of diastole------ Sign of Ventricular Dysfunction Sign of Left Ventricular Hypertension S4 sound ----- heard on late part of diastole------- Seen in MI, HPN, Pulmonic Stenosis *S3 sound-----normal to children

Assess for audible sound: Murmur ------ audible vibration Thrill --------- palpable vibration Heave --------- visible vibration

Stenotic Valvular Opening/narrowing Increased velocity of bloodflow Abnormal vibrations

13. Lifestyle----- Diet ----- High in calories, saturated fats, Na & heart stimulant like caffeine, alcohol ---- Exercise—Sedentary lifestyle----venous stasis---- Risk for thrombus formation 14. Assess for history of chest pain 15. Assess for Dyspnea & its cause --- Positioning: Orthopnea Time : Night (Paroxysmal Nocturnal Dyspnea) 16. Check for history of CYANOSIS 2 Types: a. Central Cyanosis----- circum-oral (lips, oral mucus membrane) Sign of decreased arterial O2 saturation

(Normal: 95-100%)

b. Peripheral Cyanosis---- cyanosis of nail beds, earlobes Sign of decreased cardiac output 17. Assess for pitting edema:

a. Elevate 1st the legs w/ edema, if still (+) b.

Press skin, if indentation is present = (+) Pitting Edema

18. Assess for HPN: Created by Niňa E. Tubio

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Systole---- Atrio-ventricular contraction & closure of the A-V valves—-----TV & BV Strength of Myocardial contractions Diastole – Atrio-ventricular relaxation & closure of Semi-lunar valves---- PV & AV More dangerous because it is systematic

Degree of systolic arterial resistance

TYPES OF HPN: 1. Systolic HPN & Diastolic HPN 2. Primary/Essential/Idiopathic - Unknown cause 2 Theory: a. R-A-A Pathology:

Juxtaglomerular Cells (kidney) Renin releases Angiotensin I (activated by enzymes that converts it to) Angiotensin II ------- stimulates adrenal cortex to release aldosterone

Potent vasoconstrictor

Fx: Fluid & Na retention & K excretion

HPN

Increased IV volume Hypovolemic Shock

3. Secondary HPN - Due to pregnancy related to toxemia - Children w/ coarctation of the aorta - Pheochromocytoma ( 5 H) 4. Accelerated HPN ----- persistent high BP with signs of retinal hemorrhages + epistaxis 5. Malignant HPN ----- persistent high BP with signs of papilledema (Increased ICP)

FLUIDS & ELECTROLYTES 1. WATER Adult: Child:

50-60% TBS 70-80% TBS

*Volume of Distribution Depends On: 1. Age - H2O decreases with age 2. Sex – Male with more muscles so increase H2O 3. Adipose Tissues – More Obese so more H2O *Fluid Intake:

2 – 2.5 L/day 24 hrs.

Fluid: Food

1 -1.5 L/24 hrs. 1 L/24 hrs.

By-product of oxidation-nitrogen process = 100 ml/24 hrs. Created by Niňa E. Tubio

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*Avenues Of Losses/Routes: 1. Kidney 2. Skin 3. Lungs 4. GIT

= 1-1.5 L/24 hrs = 600-700 ml/24 hrs = 400-500 ml/24 hrs = 100 ml/24 hrs

CELLS Intracellular Extravascular

BLOOD ICF ECF

= 2/3 of BF 70 % = 1/3 of BF 30 %

Intravascular (blood, lymph vessels) Intercellular ( interstitial space)

2. ELECTROLYTES

1. CATION (+) =

Sodium Potassium Calcium Magnesium

Na K Cal Mg

2. ANION (-)

=

Chloride Phosphorus Sulfate Bicarbonate

Cl PO4 SO4 HCO3

3.

= =

K & PO4 Na & Cl

ICF ECF

Homeostasis--- continuous shifting of fluids in Intravascular compartment

FLUID SHIFTING 1. IV-ITS-IV

(Normally exercised by circulatory blood)

Arteriolar End

COP = 22 mmHg

Venular End

HP = 40 mmHg

HP = 12 mmHg

Start: Fluid pushed into ITS COP> HP Fluid drawn back into capillaries ITS •

HP greater than COP so that fluid movement occurs 2 Governing forces for IV-ITS Shifting

1. COLLOID OSMOTIC PRESSURE - Pressure exerted by plasma protein/albumin on semi-permeable membrane 2. HYDROSTATIC PRESSURE - Pressure exerted by fluid against wall of BV Created by Niňa E. Tubio

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Example: 1. MALNUTRITION

(Protein)

Less COP----venous HPN congestion-----fluids remains in ITS---Edema, Anasarca, Ascites 2. ABNORMAL If HP less than COP---fluid stays in the VC------ Circulatory Overload------ Hypovolemia 3. BLOOD TRANSFUSION BT/Protein/Albumin----- High COP----fluid stays in capillary---- Circulatory Overload 4. FLUID SHIFTING IC ----TO----- EC *Movement of fluids governed by Osmosis & Diffusion Solvent (H2O)

Solute (Electrolyte)

* High H2O EC------ Low Na concentration-------- H2O will enter the cell If continues Cell will Swell/Burst H2O Intoxication/ Hypo-Osmolar Imbalance * Less H20 E ----- High Na-----leave the cell-----cell shrink-----Dehydration

3. BURNS – Direct tissue injury caused by thermal, electric, chemical & smoke inhalation (TECS) Nursing Priority – infection (all kinds of burns) Head burn-priority- a/w 2nd priority for 1st & 2nd ° - pain 2nd priority for 3rd ° - F&E CLASSIFICATION: 1. CAUSE a. Thermal b. Electric c. Chemical 4. Smoke

- direct contact – flames, hot grease, sunburn. -- wrapped – wires – direct contact – corrosive materials acids-------flush with saline solution – gas / fume inhalation

2. DEPTH OF TISSUE DAMAGE & AREA I. Partial Thickness Burn Created by Niňa E. Tubio

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1. 1st degree – Superficial Partial Thickness Burns - Affects epidermis - Cause: Thermal burn/sun burn - Painful -No edema - Redness (erythema) & (+) blanching upon pressure with no fluid filled vesicles - Healing Duration : 1-2 wks. w/ any residual evidence of tissue damage 2. 2nd degree – Deep Partial Thickness Burns - Affects epidermis & dermis - Cause –chem. Burns - With edema - (+) Very painful - (+) Erythema & fluid filled vesicles (blisters) - Mottled (bluish & reddish) - Healing duration: 2-3 wks. w/ signs of minimal scarring II . Full Thickness Burns 1. Third & 4th Degrees Burn - Affects all layers of skin, muscles, bones - Cause – electrical - Without pain or less painful - Blanched, pale, charred - Dry, thick, leathery wound surface – known as ESCHAR – devitalized or necrotic tissue. - Healing duration: No exact time-frame. Depends on the actual depth of tissue damage, infection

3. ACCORDING TO EXTENT OF BODY SURFACE BURNED Rule of 9 Head & Neck & Face Upper Anterior Trunk/Chest Upper Posterior Trunk/Chest @ Arm 9+9 Lower Anterior Extremity (leg) Upper Posterior Extremity (leg) Genitalia/ perineum Total

= 9% = 18% = 18% = 18% = 18% = 18 % = 1% 100%

4. CLASSIFICATION AS MINOR & MAJOR 1. Minor : 2nd Degree : 2nd Degree: 3rd Degree:

10-20% BSA (C) 15-25 % BSA (A) 2-10 % BSA

2. Major: 2nd Degree: 2nd Degree: 3rd Degree:

10-20 % (C) 15-25 % (A) 2-10 %

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3. Critical: 2nd Degree: 2nd Degree: 3rd Degree

> 21 % ( C) > 25 % (A) > 10 %

STAGES:

1. Emergent Phase – Removal of pt from cause of burn. Determine source or loc or burn 2. Shock Phase

– 24 - 48°. Characterized by shifting of fluids from intravascular to interstitial space = Hypovolemia

S/Sx:

-

-

BP Decrease Urine output HR Increase Hct Elevated Serum Na Decrease Serum K Increase Metabolic Acidosis

Priority To All Types of Burn: INFECTION

3. Diuretic/ Fluid Remobilization Phase - 3 to 5 days. Return of fluid from interstitial to intravascular space 4. Recovery/ Convalescent Phase – complete diuresis. Wound healing starts immediately after burn injury.

Pathophysiology Of THERMAL BURN: (2ND Stage in the 1st 24-48 hrs.) Intense heat ------------- activates a sympatho-adrenal medullary response Tissue Trauma Release of Histamine Vasodilation Increased Capillary Permeability Fluid shifts from IV to ITS (seepage of plasma fluid to ITS) 1

Edema formation HYPOVOLEMIA 3

Hyponatremia

2

Decreased Cardiac Output Created by Niňa E. Tubio

Sluggish BF 118

Thrombus Formation Hypovolemic Shock

Renal Perfusion

Hourly Urine Output

BUN

Tissue Ischemia Evaluate: 1. Decreased BP Creatinine Hematuria Hyperkalemia2. Increase Hct (Evaluate vol. % of RBC in plasma Ventricular Fibrillation hemoconcentration) 3. Decreased CVP Sudden Cardiac Arrest

Weight loss

Tissue Starvation

Anaerobic Metabolism

(-) Nitrogen balance

Lactic Acid Production

Weakness

METABOLIC ACIDOSIS (Common problem)

Legend: 1 - Stage of Neurogenic Shock 2 – Stage of Hypovolemic Shock/ Oligenic Shock 3 – Stage of Diuresis 4 – Stage of Repair COMPLICATIONS OF BURNS: 1. SODIUM (Na) (Normal: 135-145 mEq/L) a. Decrease Na system of burn victim d/t Hyponatremia Edema----- trapping of Na----------------- Na activated in 3 Ways/Causes Hyponatremia S/Sx:

- Decreased BP - Increased rapid, weak pulse - Diaphoresis - Poor memory - Hypoactive - (-) reflexes - Oliguria-Anuria

1. R-A—Aldosterone --- Na reabsorption & K excretion 2. Prostaglandin-Renin 3. Kallikreen---Kinin--- Increase urination, Na excretion Distal tubules of the kidneys

b. Hypernatremia S/Sx: - Thirst - Flushed Skin - Increase temperature - Dry tongue - Dry & sticky mucus membrane - Hyperactive reflexes

Normal CVP 6-12 mmHg

c. Hypovolemia - Assess for BP, Hct, CVP d. CVP - Pressure exerted by blood appropriately at the right atrium of the heart - Done to evaluate cardiac efficiency - Done to evaluate state of hydration - CVP: decrease in burn victims -If CVP, prepare for Cut-down or Venesection------prior insert 3-way polyethylene tubing e. Hypovolemic Shock (Oligenic) Created by Niňa E. Tubio

Normal Hourly Urine Output: 30 – 60 ml/hour

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- Evaluate BP, Hct, CVP - LOC decreased - PR increased - RR increased but shallow - Skin cold & clammy (Hypo, Tachy, Tachy) BUN Creatinine

2. POTASSIUM (K) b. c.

------ 10-20 mg% w/ NPO ------ 0.9 -1.5 mg % w/o NPO--- Reliable indicator of renal function Not influenced by protein content & diet Product of muscle metabolism

(Normal: 3-5 – 5.5 mEq/L)

causes R-A-A Insulin/Glucose/ Glucagon ----- Increase Uptake of K----- cell

Ex. In DM pt.--- insulin decrease or none--- potassium will leave the cell (EC to IV)--- K in blood (Hyperkalemia) a. Increased K in Burns S/Sx: - Decreased PR - Abdominal cramps - Diarrhea - Muscular weakness - ECG changes b. Decreased K in Diarrhea S/Sx: - Increased PR followed by decreased PR - Weakness - Weak respiratory muscle - Shallow respiration------- Paralytic Ileus Hypo-active bowel sound (K influences intestinal tone)

Abdominal distention

3. Evaluate METABOLIC ACIDOSIS: ABG Interpretation S/Sx: Acidosis = CNS depression + Increased K Alkalosis = CNS excitability + Decreased K MANAGEMENT OF BURN VICTIMS: 1. Extinguish the flame - Roll over the pt. - If burn w/in the eyes, irrigate the eyes. - Remove clothing that can impede circulation - Get piece of cloth & place on wound 2. Hospital: - Establish patent airway - Make initial assessment including body weight---needed for fluid replacement - If (+) for hypokalemia: hook patient to a cardiac monitor - Get an open IV line for cardiac replacement - If veins are collapsed, do a cut-down or venisection - Prepare for insertion of indwelling catheter to monitor urine output - Prepare for NGT ----- to evacuate/decompress gastric content to prevent aspiration 3. Administer isotonic fluid solution 4. Strict aseptic technique 5. Diet – increase CHO, increase CHON, increase Vit C, and increase K- orange 6. If (+) to burns on head, neck, face - Assist in intubation Created by Niňa E. Tubio

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7. Assist in surgical wound debridement. Administer analgesic 15 – 30 minutes before debridement 8. Prevent Complications: 1. Infection ------ Increase anerobic circulation, risk for anaerobic infection a. Prepare Tetanus Toxoid Injection------ .5 ml IM - Prevent Tetanus: Burn surface area is source of anaerobic growth – Clostridium tetany Tetanus Tetanolysin

Tetanospasmin

Hemolysis

Muscle Spasm b. Morphine SO4

2. Hypovolemic Shock - Replace fluid losses. Use solution a. EVAN’S FORMULA •

Colloid

• •

Non-Electrolyte Electrolyte

– 1 ml x kgBW x % BSA Ex. Isotonic solution---- NSS, LRS - 2,000 ml of glucose in H2O - 1 ml x Kg BW x % BSA

b. BROOKE’S FORMULA • •

Colloid Electrolyte

- 0.5 ml x Kg BW x % BSA - 1.5 ml x kg BW x % BSA

c. PARKLAND/BAXTER FORMULA •

Ex.

4 ml LRS x KgBW x % BSA

Colloid – Plasma Expanders ------ will increase IV volume Dextran Polyrpan Electrolyte

- Isotonic solution--- NSS, LRS------ will increase IV volume

Non- Electrolyte - Glucose in H2O - D5 in H2O INDICATIONS FOR FLUID RESUSCITATION/REPLACEMENT 1. Child below 2 y/o ----- resuscitate ---- Increase 10 % BSA 2. Adult 60 y/o ------ resuscitate ------- Increase 10 % BSA Ex. Face & Neck = 45 Abdomen =9 Posterior forearm = 2.25 Whole RLE = 18 Buttocks =6 Perineum =1 Total 40.75 = 41% Created by Niňa E. Tubio

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33 y/o with BW 60 Using Evan’s Formula:

Colloid = 1 x 60 x 41 = 2,460 ml/24 hrs. Electrolyte = 1 x 60 x 41 = 2,460 ml/24 hrs. Non-electrolyte = 2,000 ml/24 hrs. *Replace losses 1 hr. after incident to prevent hypovolemic shock Time 12-8pm 8-4 pm 4-12

% 1st 8 hrs. – 50% 2nd 8 hrs. – 25 % 3rd 8 hrs. – 25 %

Colloid 1,230 ml 615 615

Electrolyte 1,230 ml 615 615

Non-Electrolyte 1,000 ml 500 500

*If only 1 IV line (cut-down) ---- transfuse LRS, NSS---- piggyback glucose H2O *Maximum volume in 24 hrs. is only 10 liters (divided) * Should replaced only 50 % of body losses * No plasma in cut-down * WBC---- FWB given only to burn pt. 1 unit = 500 ml to run for 4 hrs. to prevent hemolysis 3. Paralytic ileus – d/t hypovolemia & hypokalemia 4. Curling’s ulcer – H2 receptor antagonist 5. Septicemia blood poisoning 6. Surgery: Skin grafting 9. Management to promote wound healing: a. Diet : Increase CHON replacements & K-orange for repair of tissue damage &o promote wound healing Vitamin C ----- for formation of collagen fibers Granulation of tissue Scarring/ fibrosis Healing Process b. Cleanse wound/ dress - Use aseptic technique, use betadine or NSS c. Apply ointment as anti-microbic agent Topical antibiotic : 1. Silver Sulfadiazine (silvadene) ----- anti-microbic---promote re-epithelization of wound tissue 2. Sulfamylon 3. Silver nitrate 4. Povidone iodine (betadine) d. Systemic Antibiotic Ex. 1. Ampicillin 2. Cephalosporin 3. Tetracycline e. Dressing 1. Open/Exposure Method 2. Closed/Occlusive *Reverse isolation if open wound/method (bed cradle) f. Do hydrotherapy/Tubbing ------ to loosen the eschar Created by Niňa E. Tubio

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- In Hubbard Tank Done only when VS are stable & level of electrolyte is normal 2 to 3x/day for 15-20 minutes Prior to tubbing, check temperature of solution Give analgesic 30 minutes before tubbing Take VS prior to tubbing While pt. in tub, encourage ROM exercises to prevent contracture deformity If wound is severely infected, mix betadine solution

4. RELATED TO F & E BALANCE 1. BLOOD GASES

R

pH pH

HCO3 PCO2

Respiratory Alkalosis

O

ph

PCO2

Respiratory Acidosis

M

ph

HCO3

Metabolic Alkalosis

E

ph

HCO3

Metabolic Acidosis

RESPIRATORY ALKALOSIS

RESPIRATORY ACIDOSIS Chronic Bronchitis

METABOLIC ALKALOSIS Vomiting

METABOLIC ACIDOSIS Ileostomy

Pyloric Stenosis

Intestinal Tubing DM Diarrhea

Cushing

VASCULAR DISEASES I. HYPERTENSION CLASSIFICATION OF HYPERTENSION by JNC-VII Pathophysiology: Multi-factorial etiology BP= CO (SV X HR) x TPR Any increase in the above parameters will increase BP 1. Increased sympathetic activity 2. Increased absorption of Sodium & water in the kidney Risk factors for Cardiovascular Problems in 3. Increased activity of the RAAS Hypertensive patients 4. Increased vasoconstriction of the peripheral vessels 5. Insulin resistance Major Risk factors ASSESSMENT FINDINGS Created by Niňa E. Tubio

1. Smoking 2. Hyperlipidemia 3. DM 4. Age older than 60 5. Gender- Male & post menopausal Women 6. Family History

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1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V DIAGNOSTIC STUDIES 1. Health history & PE 2. Routine laboratory - Urinalysis, ECG, lipid profile, BUN, serum creatinine , FBS 3. Other lab- CXR, creatinine clearance, 24-huour urine protein MEDICAL MANAGEMENT 1. Lifestyle modification 2. Drug therapy 3. Diet therapy 4. Drug therapy

NURSING INTERVENTIONS

Drug Therapy For HPN: Diuretics Beta blockers Calcium channel blockers ACE inhibitors

1. Provide health teaching to patient Teach about the disease process Elaborate on lifestyle changes Assist in meal planning to lose weight Provide list of LOW fat , LOW sodium diet of less than 2-3 grams of Na/day Limit alcohol intake to 30 ml/day Regular aerobic exercise Advise to completely Stop smoking 2. Provide information about anti-hypertensive drugs Instruct proper compliance and not abrupt cessation of drugs even if pt becomes asymptomatic/ improved condition Instruct to avoid over-the-counter drugs that may interfere with the current medication 3. Promote Home care management Instruct regular monitoring of BP Involve family members in care Instruct regular follow-up 4. Manage hypertensive emergency & urgency properly II. ANEURYSM - Dilation involving an artery formed at a weak point in the vessel wall Types: 1. Saccular= when one side of the vessel is affected 2. Fusiform= when the entire segment becomes dilated

RISK FACTORS 1. Atherosclerosis 2. Infection= syphilis 3. Connective tissue disorder 4. Genetic disorder= Marfan’s Syndrome PATHOPHYSIOLOGY Created by Niňa E. Tubio

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Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers ASSESSMENT 1. Asymptomatic 2. Pulsatile sensation on the abdomen 3. Palpable bruit LABORATORY: 1. CT scan 2. Ultrasound 3. X-ray 4. Aortography Medical Management: 1. Anti-hypertensives 2. Synthetic graft Nursing Management: 1. Administer medications 2. Emphasize the need to avoid increased abdominal pressure 3. No deep abdominal palpation 4. Remind patient the need for serial ultrasound to detect diameter changes

III. PERIPHERAL VALVULAR DISEASES A. PERIPHERAL ARTERIAL OCCLUSIVE DISEASE (PAOD) - Refers to arterial insufficiency of the extremities usually secondary to peripheral atherosclerosis. - Found in males age 50 & above - The legs are most often affected Risk factors for Peripheral Arterial occlusive disease Non-Modifiable 1. Age 2. gender 3. family predisposition Risk factors for Peripheral Arterial occlusive disease Modifiable 1. Smoking Created by Niňa E. Tubio

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2. HPN 3. Obesity 4. Sedentary lifestyle 5. DM 6. Stress ASSESSMENT FINDINGS: 1. INTERMITTENT CLAUDICATION- the hallmark of PAOD This is PAIN described as aching, cramping or fatiguing discomfort consistently reproduced with the same degree of exercise or activity This pain is RELIEVED by REST This commonly affects the muscle group below the arterial occlusion 2. Progressive pain on the extremity as the disease advances 3. Sensation of cold and numbness of the extremities 4. Skin is pale when elevated and cyanotic/ruddy when placed on a dependent position 5. Muscle atrophy, leg ulceration and gangrene Diagnostic Findings 1. Unequal pulses between the extremities 2. Duplex ultrasonography 3. Doppler flow studies Medical Management 1. Drug therapy Pentoxyfylline (Trental) reduces blood viscosity and improves supply of O2 blood to muscles Cilostazol (Pletaal) inhibits platelet aggregation and increases vasodilatation 2. Surgery- Bypass graft and anastomoses Nursing Interventions 1. Maintain Circulation to the extremity Evaluate regularly peripheral pulses, temperature, sensation, motor function and capillary refill time Administer post-operative care to patient who underwent surgery 2. Monitor and manage complications Note for bleeding, hematoma, decreased urine output Elevate the legs to diminish edema Encourage exercise of the extremity while on bed Teach patient to avoid leg-crossing 3. Promote Home management Encourage lifestyle changes Instruct to AVOID smoking Instruct to avoid leg crossing B. ARTERIAL ULCERS 1. BUERGER’S DISEASE / THROMBOANGIITIS OBLITERANS -Acute inflammatory disorder characterized by recurring inflammation of the medium sized small arteries & veins of the lower extremities - Occurs in MEN ages 30 y/o /FEET - SMOKING! Pathophysiology: Cause is UNKNOWN Probably an Autoimmune disease Inflammation of the arteries thrombus formation occlusion of the vessels Sx:

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1. INTERMITTENT CLAUDICATION Leg PAIN upon walking but relieved by rest Foot cramps in the arch (instep claudication) after exercise Aggravated by smoking, emotional disturbance & cold chilling 2. Digital rest pain not changed by activity or rest 3. Cold sensitivity & skin color changes Intense RUBOR (reddish-blue discoloration), progresses to CYANOSIS as disease advances FEET----becomes White Pallor d/t vasoconstriction

Bluish

Red (W-B-R)

Cyanosis d/t pooling of deoxygenated blood

Rubor – with dependency (+) especially post-smoking d/t exaggerated reflow/hyperemia

4. Paresthesia 5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 6. Tropic changes 7. Ulcerations 8. Gangrene formation Dx:

1. Oscillometry 2. Doppler UTZ 3.

– Reveals a decrease peripheral pulse volume. – (Duplex ultrasnography) Reveals a decrease blood flow to affected extremities. Angiography (Contrast angiography) – reveals site & extent of mal-occulsion.

Nsg Mgt: 1. Encourage a slow but progressive physical activity a.) Walk 3 -4 x / day b.) Out of bed 2 – 3 x a / day 2. Meds a.) Analgesic b.) Vasodilator c.) Anticoagulant 3. Foot care mgt like DM to prevent gangrene formation– a.) Avoid walking barefoot b.) Cut toe nails straight c.) Apply lanolin lotion – prevent skin breakdown d.) Avoid wearing constrictive garments 4. Avoid smoking & exposure to cold environment 5. Assist in the medical and surgical management Surgery: BKA (Below the knee amputation) Bypass graft/amputation Post-operative care: after amputation Elevate stump for the FIRST 24 HOURS to minimize edema & promote venous return Place patient on PRONE position after 24 hours Assess skin for bleeding and hematoma Wrap the extremity with elastic bandage 2. RAYNAUD’S DISEASE/

- A form of intermittent arteriolar VASOCONSTRICTION that results in coldness, pain & pallor of the fingertips or toes - Acute episodes of arterial spasm affecting digits of hands & fingers

Cause : UNKNOWN Predisposing Factors:

1. WOMEN 16- 40 yrs 2.

Smoking

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1. SLE – Pathognomonic sign – butterfly rash on face Chipmunk face – bulimia nervosa Cherry red skin – carbon monoxide poisoning Spider angioma – liver cirrhosis Caput medusae – leg & trunk umbilicus-127 Liver cirrhosis Lion face – leprosy

2. Rheumatoid Arthritis

- Direct hand trauma

3. Collagen Disease

Sx: 1. RAYNAUD’S PHENOMENON - A localized episode of vasoconstriction of the small arteries of the hands that causes color & temperature changes 2. Intermittent claudication - leg pain upon walking - Relieved by rest 3. Cold sensitivity (same with buerger’s) W-B-R 4. Paresthesia 5. Decrease or diminished peripheral pulses - Post tibial, Dorsalis pedis 6. Ulcerations 7. Gangrene formation 8. Tingling sensation 9. Burning pain on the hands and feet Nsg Mgt: a. Analgesics to relieve pain Vasodilators -----CALCIUM channel blockers To prevent vasospasms b. Encourage to wear gloves especially when opening a refrigerator. c. Avoid smoking & exposure to cold environment Instruct patient to avoid situations that may be stressful Instruct to avoid exposure to cold & remain indoors when the climate is cold g. Instruct to avoid all kinds of nicotine h. Instruct about safety. Careful handling of sharp objects

DIFFERENTIATION: PERIPHERAL VALVULAR DISEASE

Arterial Ulcers 1. Thromboangiitis Obliterans – male/ feet 2. Raynauds – female/ hands

Venous Ulcer 1. Varicose veins 2. Thrombophlebitis

C. VENOUS ULCERS 1. VARICOSE VEINS / Varicosities - Abnormal dilation of veins usually in the lower extremities & trunk Pathophysiology Factors  venous stasis increased hydrostatic pressure  edema

Veins in valve Fx: To increase venous return If incompetent

Due to: a.) Incompetent valves leading to

valve

b.) Increase venous pooling & stasis leading to

down

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Pump blood 128

Pooling of blood in veins heart

Cannot return to

c.) Decrease venous return Predisposing Factors: a. b. c. d. e. f.

g. h. i.

Hereditary Congenital weakness of veins Thrombophlebitis Cardiac diseases Pregnancy Obesity Prolonged immobility - Prolonged standing/sitting -------dorsiflex feet Constipation (for hemorrhoids) Incompetent venous valves

Sx: -

-

-

Pain especially after prolonged standing Dilated tortuous superficial skin veins on the legs Warm to touch Leg pain & Heaviness in legs Dependent edema

Dx: 1.

Venography

2. Trendelenberg’s Test – Reveals that veins distends quickly in < 35 secs. How: Elevate legs in 45 degrees angle. After 15-30 minutes, let pt. stand & see the varicosities Medical Management: 1. Pharmacological therapy 2. Leg vein stripping/ligation Sclerotherapy----------Spider Wed Varicosities (small-like) (Cold-solution injection) S/E: Thrombosis 3. Anti-embolic stockings Nsg Mgt: “Consistent to all venous ulcers” 1. 2.

Elevate legs above heart level – to promote venous return – 1 to 2 pillows Measure circumference of leg muscles to determine if swollen. 3. Wear anti embolic or knee high stockings. Women – full panty hose 4. Meds: Analgesics for pain 5. Caution patient to avoid prolonged standing or sitting 6. Provide high-fiber foods to prevent constipation 7. Teach simple exercise to promote venous return 8. Caution patient to avoid knee-length stockings & constrictive clothings 9. Avoid massage on the affected area 2. THROMBOPHLEBITIS / DVT- Deep Vein Thrombosis - Inflammation of the deep veins of the lower extremities & the pelvic veins - The inflammation results to formation of blood clots in the area

Predisposing Factors: 1. 2. 4. -

Smoking Obesity 2. Hyperlipedemia Prolonged use of oral contraceptives Chronic anemia DM

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-

-

-

MI CHF Post-surgical complications Post cannulation – insertion of various cardiac catheters Prolonged immobility Varicosities Traumatic procedures Diet high in saturated fats

Complication: •

Pulmonary Embolism: Sx: - Sudden sharp chest pain - Dyspnea - Tachycardia - Palpitation - Diaphoresis - Mild restlessness

Sx: 1. 2.

3. 4. 5. 6.

Pain at affected extremities Cyanosis (+) HOMAN’S SIGN - Pain at leg muscles upon dorsiflexion of foot ---- Pathognomonic sign Leg tenderness Leg pain & edema Dilated tortous vein

Dx: 1. 2. 3.

Angiography Doppler UTZ Duplex Scan

Medical Management: Antiplatelets Vein stripping & grafting Anti-embolic stockings Analgesics. Anticoagulant: Heparin Nsg Mgt: 1. Elevate legs above heart level. 2. Apply warm, moist packs to reduce lymphatic congestion. 3. Measure circumference of leg muscles to detect if swollen. 4. Use anti embolic stockings. 5. Provide measures to avoid prolonged immobility Repositioning Q2 Provide passive ROM Early ambulation 6. Provide skin care to prevent the complication of leg ulcers 7. Monitor for signs of pulmonary embolism (sudden respiratory distress)

GASTROINTESTINAL TRACT Overview: The GIT is composed of two general parts The main GIT starts from the mouthEsophagusStomachSILI I. Upper Alimentary Canal: Function for digestion

a. Mouth ------------------------ where digestion starts Contains the lips, cheeks, palate, tongue, teeth, salivary glands, masticatory/facial muscles & bones Anteriorly bounded by the lips Posteriorly bounded by the oropharynx Important for the mechanical digestion of food Created by Niňa E. Tubio

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The saliva contains SALIVARY AMYLASE or PTYALIN that starts the INITIAL digestion of CHO b. c.

Pharynx (throat) Esophagus A hollow collapsible tube Length- 10 inches Made up of stratified squamos epithelium The upper third contains skeletal muscles The middle third contains mixed skeletal and smooth muscles The lower third contains smooth muscles and the esophago-gastric/ cardiac sphincter is found here Functions to carry or propel foods from the oropharynx to the stomach

d. Stomach ---------------------- widest section of UAC: Digestion ends here e. 1st half of duodenum II. Middle Alimentary canal – Function: For Absorption

a. b. c.

d.

* Small Intestine – Absorption starts * Large Intestine - Complete absorption / 90% of water absorbed 2nd half of duodenum Jejunum Ileum 1st half of ascending colon

III. Lower Alimentary Canal – Function: Elimination

a. 2nd half of ascending colon b. c. d. e.

Transverse Descending colon Sigmoid Rectum

IV. Accessory Organ

a. Salivary Gland b. Verniform Appendix ---------------------- commonly inflammed c. Liver ---------------------- site of bile production d. e.

Pancreas – auto digestion Gallbladder – storage of bile

The GIT Physiology Absorbs water Eliminates wastes Bacteria in the colon synthesize Vitamin K Appendix participates in the immune system SYMPATHETIC Generally INHIBITORY! Decreased gastric secretions Decreased GIT motility But: Increased sphincteric tone and constriction of blood vessels PARASYMPATHETIC Generally EXCITATORY! Increased gastric secretions Created by Niňa E. Tubio

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Increased gastric motility But: Decreased sphincteric tone and dilation of blood vessels

Gastrointestinal Assessment : Physical Exam Sequence Inspection Auscultation Percussion Palpation

The ABDOMINAL examination The sequence to follow is: Inspection Auscultation Percussion Palpation

COMMON LABORATORY PROCEDURES 1. FECALYSIS Examination of stool consistency, color and the presence of occult blood. Special tests for fat, nitrogen, parasites, ova, pathogens and others FECALYSIS: Occult Blood Testing Instruct the patient to adhere to a 3-day meatless diet No intake of NSAIDS, aspirin and anti-coagulant Screening test for colonic cancer 2. Upper GIT study: barium swallow Examines the upper GI tract Barium sulfate is usually used as contrast Pre-test: NPO post-midnight Post-test: increase pt fluid intake, instruct that stools will turn white, monitor for obstruction, laxative is also ordered 3. Lower GIT study: barium enema Examines the lower GI tract Pre-test: Clear liquid diet and laxatives, NPO post-midnight, cleansing enema prior to the test Post-test: Laxative is ordered, increase patient fluid intake, instruct that stools will turn white, monitor for obstruction 4. Gastric analysis Aspiration of gastric juice to measure pH, appearance, volume and contents Pre-test: NPO 8 hours, avoidance of stimulants, drugs and smoking Post-test: resume normal activities 5. EGD (Esophagogastroduodenoscopy) Visualization of the upper GIT by endoscope Pre-test: ensure consent, NPO 8 hours, pre-medications like atropine and anxiolytics Created by Niňa E. Tubio

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Intra-test: position : LEFT lateral to facilitate salivary drainage and easy access Post-test: NPO until gag reflex returns, place patient in SIMS position until he awakens, monitor for complications, saline gargles for mild oral discomfort 6. Lower GI- scopy Use of endoscope to visualize the anus, rectum, sigmoid and colon Pre-test: consent, NPO 8 hours, cleansing enema until return is clear Intra-test: position is LEFT lateral, right leg is bent and placed anteriorly Post-test: bed rest, monitor for complications like bleeding and perforation 7. Cholecystography Examination of the gallbladder to detect stones, its ability to concentrate, store and release the bile Pre-test: ensure consent, ask allergies to iodine, seafood and dyes; contrast medium is administered the night prior, NPO after contrast administration Post-test: Advise that dysuria is common as the dye is excreted in the urine, resume normal activities 8. Paracentesis Removal of peritoneal fluid for analysis Pre-test: ensure consent, instruct to VOID and empty bladder, measure abdominal girth Intra-test: Upright on the edge of the bed, back supported and feet resting on a foot stool 9. Liver biopsy Pretest Consent NPO Check for the bleeding parameters Intratest Position: Semi fowler’s LEFT lateral to expose right side of abdomen Post-test: position on RIGHT lateral with pillow underneath, monitor VS and complications like bleeding, perforation. Instruct to avoid lifting objects for 1 week

I. ACCESSORY ORGANS DISORDER SALIVARY GLANDS Function: Produces saliva for mechanical digestion 1200 -1500 ml/day - saliva produced 3 Types of Saliva produced: Parotid – below & front of ear Sublingual Submaxillary

1. PAROTITIS - “ Endemic Mumps” - Inflammation of the parotid gland - Contagious Causative Agent: Paramyxo Virus --------- Target:

Parotid Glands, Respiratory Glands & Meninges Swollen Parotid Glands Ear Ache (Otalgia)

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Fever

Dysphagia

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S/Sx: 1. Fever, chills anorexia, gen body malaise 2. Swelling of parotid gland 3. Dysphagia 4. Ear ache – Otalgia MOT: Direct transmission & droplet nuclei Incubation Period: 14 – 21 days Period of Communicability – 1 week before swelling & immediately when swelling begins. Nsg Mgt: 1.

CBR

2. Strict isolation (Gentan Violet for aesthetic purposes only) 3. Meds: Analgesic 4.

5. 6.

Antipyretic Antibiotics – to prevent 2° complications Alternate warm & cold compress at affected part General liquid to soft diet Prevent Complications : 1.Women – Cervicitis, Vaginitis, Oophoritis 2.Both sexes – meningitis & encephalitis/ reason why antibiotics is needed 3. Men – Orchitis (inflammation of testes) might lead to sterility if it occur during / after puberty.

VERNIFORM APPENDIX Location: Right Iliac or Right Inguinal area Function : As a Lymphatic organ that produces WBC during fetal life - ceases to function upon birth of baby 1. APENDICITIS – Inflamation of verniform appendix Predisposing Factor:

1. 2. 3. 4.

Microbial infection cause by bacteria Fecalith – undigested food particles – Ex. Tomato seeds, guava seeds Intestinal obstruction, lymphoid hyperplasia, foreign body & helminthic obstruction Kinking & external occlusion by adhesions, fibrous conditions of abdomen

Pathophysiology: Obstruction of lumen increased pressure decreased blood supply bacterial proliferation and mucosal inflammation ischemia necrosis rupture Stages: 1. Congestive 2. Suppurative 3. Gangenous 4. Perforation S/Sx:

1. Pathognomonic sign: (+) REBOUND TENDERNESS 2.

Low grade fever, anorexia, n/v

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3. 4.

5. 6.

7.

Diarrhea / & or constipation Pain at Rt iliac region Late sign : Tachycardia D/T pain Abdominal pain: begins in the umbilicus then localizes in the RLQ (Mc Burney’s point) Abdominal rigidity (if perforated)

Dx:

1. CBC : Reveals mild leukocytosis – increase WBC---------- Confirmatory DX 2. PE : (+) Rebound Tenderness (flexion of Rightt leg, palpate Rt iliac area – rebound) 3. Urinalysis --- Reveals (+) to acetone 4. 5.

Ultrasound Abdominal X-ray

Treatment: 1. Surgical Intervention Appendectomy- Should be operated 24 – 48° to prevent rupture---- Peritonitis * MC BURNEY’S POINT – site of surgical incision for appendectomy Nsg Mgt: PRE- OPERATIVE 1. 2. 3.

Consent Notify MD----- local anesthesia Routinary nursing measures: a.) Skin preparation b.) NPO c.) Avoid enema – lead to rupture of appendix 4. Meds: Antipyretic Antibiotics to prevent secondary infection *Don’t give analgesic – will mask the pain - Presence of pain means appendix has not ruptured. 4. Avoid heat application, enemas & laxative – will rupture appendix. 5. Monitor VS, I&O bowel sound, fever & hydration status 6. Monitor for perforation and signs of shock 7. POSITION of Comfort: RIGHT SIDELYING in a low FOWLER’S

PAIN sensation an important parameter: (-) to pain : Ruptured appendix (+) to pain : Inflammation

Nursing Mgt: POST-OPERATIVE

1. If (+) to Pendrose Drain – indicates rupture of appendix Position- affected side to drain If no Penrose Drain, position based on pt. comfort 2. 3. 4.

Meds: analgesic due post op pain Antibiotics, Antipyretics PRN Monitor VS, I&O, bowel sound Maintain patent IV line

5. Complications: Peritonitis & Septicemia 6. Monitor VS and signs of surgical complications 7. Maintain NPO until bowel function returns 8. If rupture occurred, expect drains and IV antibiotics 9. POSITION post-op: RIGHT side-lying, SEMI- FOWLER’S to decrease tension on incision & legs flexed to promote drainage 10. Administer prescribed pain medications

COMMON GIT SYMPTOMS AND MANAGEMENT 1. CONSTIPATION - An abnormal infrequency and irregularity of defecation - Multiple causations Created by Niňa E. Tubio

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Pathophysiology Interference with three functions of the colon 1. Mucosal transport 2. Myoelectric activity 3. Process of defecation NURSING INTERVENTIONS 1. Assist physician in treating the underlying cause of constipation 2. Encourage to eat HIGH fiber diet to increase the bulk 3. Increase fluid intake 4. Administer prescribed laxatives, stool softeners 5. Assist in relieving stress 2. DIARRHEA -Abnormal fluidity of the stool Multiple causes Gastrointestinal Diseases Hyperthyroidism Food poisoning Nursing Interventions 1. Increase fluid intake- ORESOL is the most important treatment! 2. Determine and manage the cause 3. Anti-diarrheal drugs

LIVER

In locating organs of the abdomen: Use the 9 regions

The largest internal organ Located in the right upper quadrant/ Right Hypochondriac Region Contains two lobes- the right & the left Color: Scarlet Red Covered by a fibrous capsule--------- GLISSON’S CAPSULE The hepatic ducts join together with the cystic duct to become the common bile duct Functions to store excess glucose, fats and amino acids Also stores the fat soluble vitamins- A, D and the water soluble- Vitamin B12 Produces the BILE for normal fat digestion The Von Kupffer cells remove bacteria in the portal blood Detoxifies ammonia into urea Functional Unit – Liver Lobules

Function: 1.

Produces bile Bile: Function is to emulsifies fats Gives color to urine – Urobilin (light yellow) Stool – Stircobilin (brown)

2. Detoxifies toxic substances from drugs 3. Promotes synthesis of Vit A, D, E, K Created by Niňa E. Tubio

Precursor: Cholesterol water

Bile salt +

Vitamin A = Retinol Vitamin D = Cholecalciferol Vitamin E = Tococalciferol Vitamin K = Phetione Excess Vit. D & K = Hypervitaminosis Deficiency Vit. A = Night Blindness

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(Fat soluble vitamins) 4. It destroys excess estrogen hormone 5. For metabolism of: A. CHO 1. Glycogenesis – synthesis of glycogens 2. Glycogenolysis – breakdown of glycogen 3. Gluconeogenesis – formation of glucose from non- CHO sources B. CHON 1. Promotes synthesis of albumin & globulin Cirrhosis – decrease albumin Albumin – maintains osmotic pressure, prevents edema 2. Promotes synthesis of prothrombin & fibrinogen 3. Promotes conversion of ammonia to urea. Ammonia like breath – fetor hepaticus C. FATS 1. Promotes synthesis of cholesterol to neutral fats – called triglycerides

1. LIVER CIRRHOSIS / “Laennec’s Cirrhosis”

• • •

Lost of architectural design of liver leading to fat necrosis & scarring A chronic, progressive disease characterized by a diffuse damage to the hepatic cells The liver heals with scarring, fibrosis and nodular regeneration

Predisposing Factor: Laennac’s Cirrhosis – caused by alcoholism 1. Chronic alcoholism ------ Common Cause 2. Malnutrition – DecreaseVit B- Thiamine - main cause 3. Virus 4. Toxicity to Carbon Tetrachloride 5. Use of hepatotoxic agents 6. Post-infection 7. Cardiac diseases 8. Schistosomiasis 9. Biliary obstruction 10. Portal Hypertension Compression of the intra-liver vessels Decreased protein (colloid pressure) Increased hydrostatic pressure S/Sx: Early signs:

a.) Weakness & Fatigue b.) Anorexia, Early mornig Nausea & vomiting, Weight loss c.) Stomatitis d.) Urine – Tea color / Stool – Clay color e.) Amenorrhea Created by Niňa E. Tubio

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f.) Decrease sexual urge g.) Loss of pubic & axilla hair h.) Hepatomegaly i.) Jaundice j.) Pruritus or Urticaria k.) RUQ abdominal pain 2. Late signs a.) Hematological changes – all blood cells decrease---- Pancytopenia Leukopenia- decrease Thrombocytopenia- decrease Anemia- decrease b.) Endocrine changes Spider Angiomas (Teleangectasis---nose), Gynecomastia Caput medusae (Abdomen—loss of tortousity of the umbilicus) , Palmar errythema (redness) c.) GIT changes Ascitis, bleeding esophageal varices – due to portal HPN d.) Neurological Changes: Hepatic Encephalopathy Dx: Liver enzymes- increase SGPT (ALT) SGOT (AST) Serum cholesterol & ammonia = Iincrease Indirect Bilirubin or Unconjugated Bilirubin = Increase CBC = Pancytopenia PTT = Prolonged Hepatic Ultrasonogram = Reveals fat necrosis of liver lobules Pathophysiology: CIRRHOSIS * 1-3 : Complications No production of albumin Decreases Osmotic Pressure Edema to Liver ASCITES 2 ASCITES (Fluid Accumulation in the Peritoneal cavity) Nsg Mgt: 1. Medication: Loop Diuretics (10-15 minutes) K- sparing diuretics 2. Assist in abdominal Paracentesis (Aspiration of fluid in the peritoneum) *Void before paracentesis to prevent accidental puncture of bladder Created by Niňa E. Tubio as

No convertion of Ammonia to urea Ammonia reabsorb back to blood

No Prothrombin & Firinogen No clotting Factor

HEPATIC ENCEPHALOPATHY 1 HEPATIC ENCEPHALOPATHY (accumulation of ammonia-a cerebral toxin)

BLEEDING 3

1st Sign: Asterixis (Flapping Hand Tremors)

BLEEDING ESOPHAGEAL VARICES (d/t Portal HPN—dilation of esophageal veins) Sx: Vomiting---- accompanied by blood

Late Signs: Headache Fetor Hepaticus Restlessness Disorientation/ Confusion Decrease LOC—can lead to Hepatic Coma Nsg. Priortity: Assist In Mechanical Ventilation Nsg. Mgt: 1. Assist in mechanical ventilation d/t coma 2. Monitor VS, neuro check 3. Siderails – d/t restless 4. Meds:

Nsg Mgt: 1. Medication: Vit. K Pitressin or Vasopressin (IM) 2. NGT DecompressionLavage Give before lavage - ice or cold saline solution Monitor NGT output 3.Assist in Mechanical

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Liver cirrhosis – bedside scissor – if pt complaints of DOB Nsg Mgt: Cut cystachean tube to 1. CBR ---- Elevate the head of the bed to minimize dyspnea 2. Restrict Na before fluids 3. Monitor VS, I&O, weight, LOC & bleeding 4. With pt daily & assess pitting edema 5. Measure abdominal girth daily – notify MD 6. Meticulous skin care 7. Provide Moderate to LOW-protein (1 g/kg/day) & LOW-sodium diet DIET 8. Diet – Increase CHO, Vit. & minerals. Moderate fats. Well balanced diet Early Stage 9. Provide supplemental Vit. (especially K) & minerals 10. Administer prescribed: High in: CHO Diuretics= to reduce ascites & edema CHON Lactulose= to reduce NH4 in the bowel Vitamins Antacids= to prevent ulcer & bleeding Minerals Neomycin= to kill bacterial flora that cause NH production Low in : Fats 11. Avoid hepatotoxic drugs Paracetamol Late Stage: Anti-tubercular drugs High in: CHO 12. Reduce the risk of injury Vit. & Side rails reorientation Minerals Assistance in ambulation Low in : CHON Use of electric razor & soft-bristled toothbrush 13. Keep equipments ready including Sengstaken-Blakemore tube, IV fluids, Medications to treat hemorrhage PANCREAS - Mixed gland (Functions as an exocrine & endocrine gland) - A retroperitoneal gland The pancreatic duct (major) joins the common bile duct in the sphincter of Oddi The exocrine function of the pancreas is the secretion of digestive enzymes for carbohydrates, fats & proteins Pancreatic amylase carbohydrates Pancreatic lipase (steapsin) fats Trypsin, Chymotrypsin and Peptidases proteins Bicarbonate to neutralize the acidic chyme. Stimulated by SECRETIN! Pancreas----- with acinar cells----secretes pancreatic juice going to--- pancreatic duct--- to--stomach 1. PANCREATITIS

– –

An Inflammation of pancreas leading to pancreatic edema, hemorrhage & necrosis due to auto digestion Can be acute or chronic

Predisposing Factors: 1. 2. 3. 4. 5.

6. 7. 8.

Chronic alcoholism Hepatobilary disease Obesity Hyperlipidemia Hypoparathyroidism Drugs – Thiazide diuretics, pills, Pentamidine HCL (Pentam)---for AIDS Diet – increase saturated fats Hypercalcemia

Created by Niňa E. Tubio

Cullen’s Sign at the Umbilicus: Bleeding of

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9. 10. 11. 12. 13.

Trauma Biliary tract disease Bacterial disease PUD Mumps

- cholelithiasis

Pathophysiology of Acute Pancreatitis: Self-digestion of the pancreas by its own digestive enzymes principally TRYPSIN Spasm, edema or block in the Ampulla of Vater reflux of proteolytic enzymes Auto digestion of the Pancreatic Tissue INFLAMMATION Hemorrhage----- Necrosis KININ ACTIVATION will result to increased permeability Loss of Protein-rich fluid into the peritoneum HYPOVOLEMIA S/Sx:

1. Severe Left epigastric pain – radiates from back &flank area Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake 2. Aggravated by eating, with DOB---- rest the GIT 2. N/V, Jaundice, Anorexia 3. Tachycardia 4. Palpitation due to pain 5. Dyspepsia – indigestion 6. Decrease bowel sounds 7. (+) Cullen’s sign - ecchymosis of umbilicus Hemorrhage------ Chronic Hemorrhagic Pancreatitis 8. (+) Grey Turner’s spots – ecchymosis of flank area Confirmatory Dx 9. Hypocalcemia 10. Hypotension & Hypovolemia 11. Signs of Shock Dx: 1. Serum amylase & lipase – Increase---- Confirm the presence of pancreatitis 2. Urine lipase – Increase 3. Serum Ca – Decrease 4. Ultrasound 5. WBC 6. CT scan 7. Hemoglobin and hematocrit Nursing Mgt: 1. Meds: Assist in pain management. Usually, Demerol is given. Morphine is AVOIDED a.) Narcotic analgesic - Meperidine Hcl (Demerol) Don’t give Morphine SO4 –will cause spasm of sphincter. b.) Smooth muscle relaxant/ anti cholinergic Ex. Papavarine Hcl Prophantheline Bromide (Profanthene) c.) Vasodilator – NTG d.) Antacid – Maalox e.) H2 receptor antagonist - Ranitidine (Zantac) To decrease pancreatic stimulation *Ranitidine ---- more common & with less S/E f.) Ca – gluconate A Phosphate binder---- Antacid-----Constipation---- Amphogel Created by Niňa E. Tubio

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2. Withold food & fluid – aggravates pain 3. Assist in Total Parenteral Nutrition (TPN) or hyperalimentation Complications of TPN: 1. Infection 2. Air Embolism -----Tape all connections to the system 3. Hyperglycemia 4. Hyponatremia 4. Institute stress mgt tech a.) DBE b.) Biofeedback 5. Comfy position - Knee chest or fetal like position to decrease pain Position patient in SEMI-FOWLER’s to decrease pressure on the diaphragm 6. If pt can tolerate food, give increase CHO, decrease fats, and increase CHON 7. Assist in correction of Fluid and Blood loss 8. lace patient on NPO to inhibit pancreatic stimulation 9. NGT insertion to decompress distention and remove gastric secretions 10. Maintain on bed rest 11. Deep breathing and coughing exercises 12. Introduce oral feedings gradually- HIGH carbo, LOW FAT 13. Maintain skin integrity 14. Manage shock and other complications: Chronic hemorrhagic pancreatitis Shock Pulmonary Complications---- Pneumonia, Air embolism & Pleural effusion GALLBLADDER Located below the liver The cystic duct joins the hepatic duct to become the bile duct The common bile duct joins the pancreatic duct in the sphincter of Oddi in the first part of the duodenum Storage of bile (made of cholesterol) & concentrates bile Contracts during the digestion of fats to deliver the bile Cholecystokinin is released by the duodenal cells, causing the contraction of the gallbladder & relaxation of the sphincter of Oddi DISORDER OF THE GALLBLADDER 1. CHOLECYSTITIS – Inflammation of the gallbladder Can be acute or chronic: 1. Acute cholecystitis usually is due to gallbladder stones 2. Chronic cholecystitis is usually due to long standing gall bladder inflammation CHOLELITHIASIS - Inflammation of the gallbladder with Formation of GALLSTONES in the biliary apparatus Predisposing FACTORS: 1.

5 “F” Female Fat (Obesity) Forty (High Risk : 40 y/o) Fertile

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Fair 2. Post menopausal women – undergoing estrogen therapy 3. Sedentary lifestyle 4. Hyperlipidemia 5. Neoplasm Pathophysiology: Supersaturated bile, Biliary stasis Stone formation Blockage of Gallbladder Inflammation, Mucosal Damage and WBC infiltration S/Sx: 1.

Severe Right abdominal pain (after eating fatty food). Occurring especially at night Epigastric pain that radiates to the scapula or localized at the RUQ Mass at the RUQ 2. Fatty intolerance 3. Anorexia, n/v 4. Jaundice 5. Pruritus 6. Easy bruising 7. Tea colored urine / Dark-orange & foamy urine 8. Steatorrhea 9. Indigestion, belching and flatulence 10. Murphy’s sign Dx:

1. Oral cholecystogram (or gallbladder series)- Confirms presence of stones but cannot visualize the gallbladder 2. Ultrasonography- can detect the stones 3. Abdominal X-ray 4. Cholecystography WBC count increased ERCP: Revaels inflamed gallbladder with gallstone 5. Serum Lipase – Increase 6. Indirect Bilirubin - Increase Tx: Analgesic- Meperidine Chenodeoxycholic acid= to dissolve the gallstones Antacids Anti-emetics Nursing Mgt: 1.

Medications: Administer prescribed medications to relieve pain. a.) Narcotic Analgesic - Usually Demerol (MEPERIDINE) NOT Codeine & Morphine may cause spasm of the Sphincter increased pain. Morphine cause MOREPAIN b.) Anti cholinergic - Atropine SO4 c.) Anti emetic – Metoclopramide (Plasil) Phenergan – Phenothiazide with anti emetic properties

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2. Diet – increase CHO, moderate CHON, decrease fats 3. Meticulous skin care d/t Urticaria 4. Maintain NPO in the active phase 5. Maintain NGT decompression 6. Instruct patient to AVOID HIGH- fat diet & GAS-forming foods 7. Surgical Procedures : Cholecystectomy---removal of gallbladder Choledochotomy Laparoscopy Post-operative Nursing Interventions Cholecystectomy: 1. Monitor for surgical complications 2. Post-operative position after recovery from anesthesia- LOW FOWLER’s 3. Encourage early ambulation 4. Administer medication before coughing and deep breathing exercises 5. Advise client to splint the abdomen to prevent discomfort during coughing 6. Administer analgesics, antiemetics, antacids 7. Care of the biliary drainage or T-tube drainage 8. Fat restriction is only limited to 4-6 weeks. Normal diet is resumed IMPORTANT: -Maintain patency of T-tube . Check if intact & drain to prevent infection Purpose: To prevent entry of bile into the peritoneal cavity

STOMACH

A J-shaped structure organ in the epigastrium - Capacity is 1,500 ml Contains 4 Parts: Fundus/ Anthrum Cardia Body Pylorus

•

Valves ------ prevents reflux or regurgitation of food 1. Cardiac Sphincter - prevents the reflux of the contents into the esophagus (bet. esophagus & stomach) 2. Pyloric Sphincter - regulates the rate of gastric emptying into the duodenum (bet. stomach & half of pylorus)

The glands & cells in the stomach secrete digestive enzymes: 1. Parietal / Oxyntic Cells Function: a. Produces intrinsic factor - promotes reabsorption of Vit. B12 – promotes maturation of RBC b.

HCl Acid - Aids in digestion

2. Chief Cells/ Zymogenic Cells : Secretes a. b. Created by Niňa E. Tubio

Ph of Hydrocholoric Acid: 1-2

Gastric amylase - digest CHO Gastric lipase – digest fats 143

c. d.

Pepsin – digests PROTEIN Rennin – digests milk products

3. Antral G-cells- gastrin 4. Argentaffin cells- serotonin 5. Mucus neck cells- mucus 6. Endocrine cells - Secrets gastrin – increase Hcl acid secretion Function of the Stomach: Generally to digest the food (proteins) & to propel the digested materials into the SI for final digestion 1.Mechanical 2.Chemical Digestion 3.Storage of food

CHO & CHON : Stored in the stomach for 1 -2 hrs. FATS

: Stored in stomach for 2 – 3 hrs

DISORDERS OF THE STOMACH 1. PEPTIC ULCER DISEASE (PUD)

–

An ulceration of the gastric & duodenal lining characterized by excoriation / erosion of submucosa & mucosal lining due to: a.) Hypercecretion of acid – pepsin b.) Decrease resistance of mucosal barrier to HCl acid secretion - May be referred as to location as Gastric ulcer in the stomach, or Duodenal ulcer in the duodenum - Most common Peptic ulceration: anterior part of the upper duodenum Incidence Rate:

1. Men : 40 – 55 yrs old 2.

Aggressive persons

PATHOPHYSIOLOGY of PUD: Disturbance in acid secretion & mucosal protection Increased acidity or decreased mucosal resistance erosion & ulceration Infection with H. pylori------ # 1 cause of ULCER Predisposing Factors: 1. Hereditary 2. Emotional Stress 3. Smoking – vasoconstriction – GIT ischemia---lead to resistance of HCl----- ulceration 4. Alcoholism – stimulates release of histamine = stimulates Parietal cell release Hcl acid = Hypersecretion ----Ulceration 5. Caffeine – tea, soda, chocolate 6. Irregular diet 7. Rapid eating 8. Ulcerogenic drugs – NSAIDS, aspirin, steroids, indomethacin, ibuprofen Indomethacin - S/E corneal cloudiness. Needs annual eye check up. 9. Gastrin producing tumor or Gastrinoma “ Zollinger Ellison’ Syndrome” 10. Microbial invasion R/T helicobacter pylori. Metromidazole (Flagyl) Created by Niňa E. Tubio

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TYPES OF ULCERS I. Ascending to severity: 1. Acute – affects submucosal lining 2. Chronic – affects underlying tissue – heals & forms a scar

Most feared complications of Bruns in GIT : Curling’s Ulcer

II. According to location:

1. Stress ulcer ---common among critically-ill patients 2.

3.

Gastric ulcer Duodenal ulcer – most common----- 90% of ulcers because it has less bicarbonate ions Buffers that neutralizes acidity

A. STRESS ULCER 2 Types Of Stress Ulcer 2. CUSHING’S ULCER:

1. CURLING’S ULCER : Cause: Trauma & Burns

Cause:

Bleeding

Stroke/ CVA / Head Injury Increase vagal stimulation

Hypovolemia

Hyperacidity

GIT schemia

Ulcerations

Decrease resistance of mucosal barriers to Hcl acid

B.

Ulcerations Drug Of Choice: Ranitidine (Zantax) GASTRIC ULCER DEFINITION

- Ulceration of the gastric mucosa, submucosa & rarely the muscularis d/t break in the mucosal barrier w/ reduced production 2nd to incompetent pylorus.

DUODENAL ULCER - Ulceration of duodenal mucosa & submucosa - Usually d/t increased gastric acidity

- Hypoperfusion-ischemia to gastric mucosa is also a factor. H.pylori in >90% cases RISK FACTORS (same) PATHOLOGY SITE Other Sx

EPIGASTRIC PAIN

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Stress Smoking Alcohol History of gastritis Decreased mucosal protection---------Infection with H. pylori-----Decreased blood supply to the stomach Antrum or lesser curvature 1. Nausea 2. Vomiting is more common 3. Hematemesis>melena 4. Weight loss -30 min – 1 hr AFTER EATING - epigastrium - Hot , gaseous & burning - not usually relieved by food & antacid - Gnawing, sharp pain in the midepigastrium - NOT RELIEVED by food intake,

Helicobacter pylori infection NSAIDS abuse Type A personality Increased gastric acidity------Infection with H pylori Duodenal bulb

-2-4 hrs after eating or during the night - mid epigastrium - Cramping & Burning PAIN - usually relieved by food intake & antacid - 12 MN – 3am pain 145

sometimes AGGRAVATING the pain!

GASTRIC SECRETION VOMITING HEMORRHAGE WT COMPLICATION S HIGH RISK

Normal gastric acid secretion

Increased gastric acid secretion

common

Not common

Hematemesis

Melena

Wt loss

Wt gain

a. Stomach Cancer b. Hemorrhage

a. Perforation

40 - 60 y/o Incidence is high in older adults, male>female,

20 y/o

1. EGD to visualize the ulceration 2. Urea breath test for H. pylori infection 3. Biopsy- to rule out gastric cancer d/t malignancy risk 4. Barium swallow 5. Gastric analysis = NORMAL

1. EGD & Biopsy 2. Endoscopic exam 3.Stool from occult blood 4.Gastric analysis = INCREASE 5. Upper GI series – confirms presence of ulceration

Dx

NURSING INTERVENTIONS: 1. Give BLAND diet, small frequent meals during the active phase of the disease a.

b.

Diet – bland, non irritating, non spicy Avoid caffeine & milk/ milk products, carbonated drinks Increase gastric acid secretion

2. Administer prescribed medications- H2 blockers, Protein pump inhibitor, mucosal barrier protectants & antacids a.) Antacids ACA Aluminum Containing Antacids Ex. Aluminum OH gel (Ampho-gel) S/E constipation

MA Magnesium Containing Antacids Ex. Milk Of Magnesia S/E diarrhea

Maalox (fewer S/E)

b.) H2 Receptor Antagonist Ex.

1. Ranitidine (Zantac) – lesser S/E---- Best given if OD = AM or BID = AM & Nightime to prevent nocturnal acid gastric secretion

2. Cimetidine (Tagamet) – more S/E Created by Niňa E. Tubio

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3. Famotidine (Pepcid) 3.

Avoid smoking – decrease effectiveness of drug

Nursing Mgt For Both: 1.

Administer antacid & H2 receptor antagonist – 1hr apart -Cimetidine decrease antacid absorption & vise versa - Instruct client to avoid smoking because it decreases effectiveness of the drug

c.) Cytoprotective Agents Ex. 1. Sucralfate (Carafate) - Provides a paste-like substance that coats mucosal lining of stomach 2. Cytotec - causes severe spasm ( abortive effect) d.) Sedatives/ Tranquilizers - Valium, lithium e.)Anticholinergics / Anti-spasmodic Agent 1. Atropine SO4 2. Prophantheline Bromide (Probanthine) (Pt has history of HPN crisis With peptic ulcer disease. Rn should not administer alka seltzer- has large amount of Na. 4. Provide teaching about stress reduction & relaxation techniques 5. Surgery: Subtotal Gastrectomy - Partial removal of stomach Billroth I (Gastroduodenostomy) -Removal of 1/3 of stomach & anastomoses of gastric stump to the duodenum.

Billroth II (Gastrojejunostomy) - Removal of 1/2 -3/4 of stomach & duodenal bulb & anastomostosis of gastric stump to jejunum.

Before surgery for BI or BII - Do vagotomy (severing of vagus nerve) & pyloroplasty (drainage) first. `

Nursing Mgt For B1 or B II: 1.

2.

3. 4.

5.

Monitor NGT output a.) Immediately post op should be bright red drainage b.) Within 6-8 hrs – output is greenish in color c.) After 24h – output is dark red d/t influence of HCI acid Administer meds: a.) Narcotic Analgesic b.) Antibiotic c.) Antiemetics Maintain patent IV line VS, I&O & bowel sounds Monitor for Complications:

SURGICAL PROCEDURES FOR PUD Total gastrectomy, vagotomy, gastric resection, Billroth I & II, pyloroplasty Post-operative Nursing management 1. Monitor VS 2. Post-op position: FOWLER’S 3. NPO until peristalsis returns 4. Monitor for bowel sounds 5. Monitor for complications of surgery 6. Monitor I & O- report U.O:/=60 y/o, female>male, history of trauma, increased intraabdominal pressure conditions Sx: 1. Heartburn (30-60min after meal) in sliding type, (-) in rolling type. 2. Regurgitation 3. Dysphagia, chestpain 4. 50%- without symptoms Pathophysiology: Weakness/ Enlarged Esophagial hiatus Increased intraabdominal pressure Protrusion of the stomach

sliding hernia

rolling hernia

LES exposed to low thoracic pressure

Obstruction Strangulation Volvulus

Reflux/regurgitation & motor dysfunction manifestations Dx: 1. Barium swallow & Fluoroscopy NURSING INTERVENTIONS 1. Provide small frequent feedings 2. AVOID supine position for 1 hour after eating 3. Elevate the head of the bed on 8-inch block 4. Provide pre-op and post-op care Surgical Management: -Nissen fundoplication (suturing the fundus around esophagus, most common procedure) - Angelchick prosthesis insertion Pre-op nursing: Health teaching, consent Post-op nursing: Monitor respi distress especially if chest tubes are in place. Instruct coughing and deep breathing exercises, ambulation Assess for bleeding, thrombosis and infection NGT maintained patent Diet transition, starts with fluids after 24hrs, then small frequent feeding, avoid carbonated beverages

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LOWER GIT The Small Intestine Grossly divided into the Duodenum, Jejunum & Ileum The duodenum contains the two openings for the bile & pancreatic ducts The ileum is the longest part (about 12 feet) The intestinal glands secrete digestive enzymes that finalize the digestion of all foodstuff Enzymes for carbohydrates disaccharidases Enzymes for proteins dipeptidases & aminopeptidases Enzyme for lipids intestinal lipase The Large intestine Approximately 5 feet long, with parts: 1. The cecum widest diameter, prone to rupture 2. The appendix 3. The ascending colon 4. The transverse colon 5. The descending colon 6. The sigmoid most mobile, prone to twisting 7. The rectum 1. CROHN’S DISEASE -Also called Regional Enteritis - An inflammatory disease of the GIT affecting usually the small intestine Inflammatory Bowel Disease ETIOLOGY: unknown, genetics,environmental, immune defect 1. CROHN’S DISEASE The terminal ileum thickens, with scarring, ulcerations, abscess formation and narrowing of the lumen Sx: 1. Fever 2. Abdominal distention 3. Diarrhea 4. Colicky abdominal pain 5. Anorexia/N/V 6. Weight loss 7. Anemia CONDITIONS OF THE LARGE INTESTINE 2. ULCERATIVE COLITIS - Ulcerative and inflammatory condition of the GIT usually affecting the large intestine - The colon becomes edematous and develops bleeding ulcerations - Scarring develops overtime with impaired water absorption and loss of elasticity Sx: 1. Anorexia 2. Weight loss 3. Fever 4. SEVERE diarrhea with Rectal bleeding 5. Anemia 6. Dehydration 7. Abdominal pain and cramping NURSING INTERVENTIONS for CD & UC 1. Maintain NPO during the active phase 2. Monitor for complications like severe bleeding, dehydration, electrolyte imbalance 3. Monitor bowel sounds, stool and blood studies 4. Restrict activities= rest and comfort 5. Administer IVF, electrolytes and TPN if prescribed Monitor complications of diarrhea 6. Instruct the patient to AVOID gas-forming foods, MILK products and foods such as whole grains, nuts, RAW fruits and Created by Niňa E. Tubio

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vegetables especially SPINACH, pepper, alcohol and caffeine 7. Diet progression- clear liquid LOW residue, high protein diet 8. Administer drugs- anti-inflammatory, antibiotics, steroids, bulk-forming agents and vitamin/iron supplements 3. HEMORRHOIDS - Abnormal dilation and weakness of the veins of the anal canal - Variously classified as Internal or External, Prolapsed, Thrombosed and Reducible PATHOPHYSIOLOGY -Increased pressure in the hemorrhoidal tissue due to straining, pregnancy, etc dilatation of veins Internal hemorrhoids These dilated veins lie above the internal anal sphincter Usually, the condition is PAINLESS External hemorrhoids These dilated veins lie below the internal anal sphincter Usually, the condition is PAINFUL Sx: 1. Internal hemorrhoids- cannot be seen on the peri-anal area 2. External hemorrhoids- can be seen 3. Bright red bleeding with each defecation 4. Rectal/ perianal pain 5. Rectal itching 6. Skin tags Dx: 1. Anoscopy 2. Digital rectal examination NURSING INTERVENTIONS 1. Advise patient to apply cold packs to the anal/rectal area followed by a SITZ bath 2. Apply astringent like witch hazel soaks 3. Encourage HIGH-fiber diet and fluids 4. Administer stool softener as prescribed Post-operative care for hemorrhoidectomy 1. Position: Prone or Side-lying 2. Maintain dressing over the surgical site 3. Monitor for bleeding 4. Administer analgesics and stool softeners 5. Advise the use of SITZ bath 3-4 times a day

BOWEL OBSTRUCTION Condition where the segment of the intestine is obstructed by: Tumors Paralysis Volvolus Signs and Symptoms Abdominal pain Abdominal rigidity Increased BOWEL sound in early stage and ABSENT BOWEL sound in late stage Abdominal distention Created by Niňa E. Tubio

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Vomiting and fluid imbalance DX: 1. Abdominal x-ray Management: Surgery Nursing care of abdominal surgery

Quick Summary Peptic Ulcer Ulceration of mucosa; In the stomach or duodenum Outstanding Symptom: PAIN Nursing Goal: Allow ulcer to heal, prevent complication Rest: physical and Mental Eliminate certain foods Medications: antacid, H2 blockers, Proton Pump inhibitors, antibiotics, mucosal protectants Surgery: Vagotomy, Billroth 1 and 2 Quick Summary Liver Cirrhosis Destruction of liver with replacement by scars Common causes: alcoholism, post-hepatitic Manifestations related to liver derangements Jaundice, Ascites, splenomegaly, bleeding, enceph Nursing goal: Control manifestations and maximize liver function

GENITO-URINARY TRACT Overview: Function: 1. 2.

Promote excretion of nitrogenous waste products Maintain F&E & acid base balance

I. KIDNEYS: – Pair of bean shaped organ - Located Retro peritonially (back of peritoneum) on either side of vertebral column. Encased in Bowmans’s Capsule. Parts: 1. Renal pelvis --------If there’s inflammation----Pyelonephritis 2. Cortex Created by Niňa E. Tubio

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3.

Medulla

* Nephrons = Basic living unit * Glomerulus = Filters blood going to kidneys Function of Kidneys: 1.

Urine formation Urine formation – 25% of total CO (Cardiac Output) is received by kidneys

1. Filtration -------------any disorder affecting filtration results to decreased renal output *Normal GFR/ min is 125 ml of blood /minute filtered by glomerulus 2.

Tubular Reabsorption Tubular reabsorption – 124ml of ultra infiltrates (Na,K,Mg,Cl, H2O) (H2O & electrolytes is for reabsorption)

3. Tubular Excretion Tubular Excretion – 1 ml is excreted in urine/minute 2. Regulation of BP: Predisposing Factor: Ex. CS – hypovolemia – decrease BP going to kidneys Activation of RAAS Release of Renin (hydrolytic enzyme) at juxtaglomerular apparatus Angiotensin I mild vasoconstrictor Angiotensin II Vasoconstrictor Adrenal cortex

increase CO

increase PR

Aldosterone Increase BP Increase Na & H2O reabsorption Hypervolemia

II. URETERS

– –

25 – 30 cm long, passageway of urine to bladder Capable of peristalis movement

III. BLADDER – Located behind the symphysis pubis. Consists of muscular & elastic tissue that is distensible Function: Reservoir of urine Maximum capacity: 1200 – 1800 ml – Normal adult can hold 250 – 500 ml – needed to initiate micturition reflex Created by Niňa E. Tubio

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NORMAL COMPOSITION OF URINE: Color = Odor = Consistency = Ph = Specific Gravity = WBC/ RBC = Albumin = E coli = Mucus thread = Amorphous urate = CHON =

Pale yellow toAmber Faint Aromatic Clear or slightly turbid 4–8 1.015 – 1.030 (-) (-) (-) few (-) None

Catheters: Pediatric Female Male

= = =

8-10 french 12-14 french 16-18 french

IV. URETHRA – Extends to external surface of body. Passage of urine, seminal & vaginal fluids. Female : Male:

3 – 5 cm or 1 to 1 ½ “ 20 cm or 8”

Urological Assessment I. Nursing History Reason for seeking care Current illness Previous illness Family History Social History Sexual history II. Key Signs & Symptoms of Urological Problems 1. EDEMA Associated with fluid retention Renal dysfunctions usually produce ANASARCA 2. PAIN Suprapubic pain= bladder Created by Niňa E. Tubio

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Colicky pain on the flank= kidney 3. HEMATURIA Painless hematuria may indicate URINARY CANCER! Initial/Early-stream hematuria= urethral lesion,prostatic,seminal vesicle Terminal/Late-stream hematuria= bladder lesion,post urethra Throughout: glomerulonephritis Pneumaturia: gas in urine;bladder-bowel fistula 4. DYSURIA Pain with urination= lower UTI Normal urine output: 1cc/kg/hr or 800-1800ml/24hr 5.POLYURIA More than 2 Liters urine per day 6. OLIGURIA 100- 400 mL per day 7. ANURIA Less than 100 mL per day 8.

Urinary Urgency: sudden controllable strong desire to void Urinary retention: sense of incomplete bladder emptying(100ml left) Urinary frequency: voiding more often than every 2hrs Urinary Hesitancy: at least 10 sec delay in initiation of urination Urinary incontinence: involuntary loss of urine Nocturia: excessive urination at night Implementation Steps for selected III. PHYSICAL EXAMINATION problems Inspection Auscultation Percussion Palpation IV. Laboratory examination Urinalysis BUN and Creatinine levels of the serum Serum electrolytes Radiographic IVP KUB x-ray KUB ultrasound CT and MRI Cystography DISORDERS OF THE GUT

1. Provide PAIN relief Assess the level of pain Administer medications usually narcotic ANALGESICS 2. Maintain Fluid and Electrolyte Balance Encourage to consume at least 2 liters of fluid per day In cases of ARF, limit fluid as directed Weigh client daily to detect fluid retention 3. Ensure Adequate urinary elimination Encourage to void at least every 2-3 hours Promote measures to relieve urinary retention: Alternating warm and cold compress Bedpan Open faucet

1. URINARY TRACK INFECTION (UTI) - Bacterial invasion of the kidneys or bladder (CYSTITIS) usually caused by Escherichia coli - Bacteria (+) 10 to the 5th in culture Predisposing Factors: Poor hygiene Irritation from bubble baths Urinary reflux Instrumentation Residual urine, urinary stasis Dehydration

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Pathophysiology: The invading organism ascends the urinary tract, irritating the mucosa & causing characteristic symptoms: Ureter= ureteritis Bladder= cystitis Urethra=Urethritis Pelvis= Pyelonephritis Sx: Low-grade fever Abdominal pain Enuresis Pain/burning on urination Urinary frequency Hematuria Upper UTI Fever and CHIILS Flank pain Costovertebral angle tenderness Laboratory Examination Urinalysis Urine Culture Nursing interventions: Administer antibiotics as ordered Provide warm baths and allow client to void in water to alleviate painful voiding. Force fluids. Nurses may give 3-4 liters of fluid per day if not contraindicated Encourage measures to acidify urine (cranberry juice, acid-ash diet). Provide client teaching and discharge planning concerning a. Avoidance of tub baths b. Avoidance of bubble baths that might irritate urethra c. Importance for girls to wipe perineum from front to back d. Increase in foods/fluids that acidify urine. Pharmacology for urine bacteria >100,000/ml 1. Sulfa drugs Highly concentrated in the urine Effective against E. coli! Can cause CRYSTALLURIA 2. Quinolones Not given to less than 18 because they can cause cartilage degradation 3. Pyridium= urinary antiseptic Can cause urine discoloration a. CYSTITIS – Inflammation of bladder Predisposing Factors: 1. 2. 3.

4. 5. 6.

Microbial invasion – E. coli High risk – women Obstruction Urinary retention/stagnation Increase estrogen levels Sexual intercourse

S/Sx:

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2. 3. 4. 5.

Urinary frequency & urgency Burning upon urination Dysuria & hematuria Fever, chills, anorexia, gen body malaise

Dx:

1. Urine culture & sensitivity = (+) to E. coli (80-90% cause) Nursing Mgt:

1. Force fluid = 2000 ml-3000 ml/day 2.

Warm sitz bath – to promote comfort

3. Monitor & assess for gross hematuria, assess odor of urine 4. Acid Ash Diet – cranberry, vit C -OJ to acidify urine & prevent bacterial multiplication 5.

Meds: a. Systemic antibiotics Ampicillin Cephalosporin b. Sulfonamides – cotrimaxazole (Bactrim) - Gantrism (ganthanol) c. Urinary Antiseptics – Nitrofurantoin (Macrodantin) S/E: Staining of Teeth Peripheral Nephropathy GIT irritants Hemolytic Anemia ----- 1st Sign: Fever d. Urinary analgesic- Pyridum

6. Health Teaching a.) Importance of Hydration b.) Void after sex c.) Female – avoids cleaning front to back Do not use Bubble bath, Tissue paper, Powder, perfume----alters the ph of vagina & irritants d.) Complications: Pyelonephritis *Ph = measures acidity of solution

b. PYELONEPHRITIS - Acute/Cchronic inflammation of 1 or 2 renal pelvis of kidneys leading to tubular destruction, interstitial abscess formation & can leadt to Renal Failure Predisposing Factor: 1. Microbial invasion a. E. Coli b. Streptococcus 2. Urinary retention /obstruction 3. Pregnancy 4. DM 5. Exposure to renal toxins S/Sx: Created by Niňa E. Tubio

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Acute Pyelonephritis:

a. Costovertibral angle pain & tenderness “FLANK PAIN” b. c. d. e.

Fever, anorexia, gen body malaise Urinary frequency, urgency Nocturia, dsyuria, hematuria Burning on urination

Chronic Pyelonephritis: a. b. c.

Fatigue, wt loss Polyuuria, polydypsia HPN

Dx:

1. Urine culture & sensitivity – (+) E. coli & streptococcus---- (+) Cultured Microorganisms 2.

3.

Urinalysis Increase WBC, CHON & pus cells Cystoscopic exam – Reveals urinary obstruction

Nursing Mgt:

1. Provide CBR – acute phase. Especially during acute attack 2. 3. 4.

Force fluid Acid ash diet Meds: a.) Urinary antiseptic – nitrofurantoin (macrodantin) SE: peripheral neuropathy GI irritation Hemolytic anemia Staining of teeth

b.) Urinary analgesic – Pyridium 2.

Complication- Renal Failure

2. NEPHROLITHIASIS/ UROLITHIASIS - Formation/ Presence of stones elsewhere in the urinary tract 3 Major Types of Stone 1. Calcium

2. Oxalate

3. Uric Acid

Milk

Cabbage Cranberries Nuts tea Chocolates

Anchovies Organ meat Nuts Sardines

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Predisposing Factors:

1. Diet – large amounts of Ca & oxalate 2. 3. 4. 5. 6.

7.

Hereditary – gout Obesity Sedentary lifestyle, immobility Hyperparathyroidism Increased uric acid levels(diet) Dehydration,urinary stasis

Pathophysiology: Supersaturation of crystals due to stasis Stone formation May pass through the urinary tract OBSTRUCTION, INFECTION & HYDRONEPHROSIS S/Sx:

1. Renal Colic radiating to the groin 2. Cool moist skin (shock) 3. Burning upon urination 4. Hematuria 5. Anorexia, n/v Abdominal or flank pain Dx:

1. 2. 3. 4.

IVP (Intravenous Pyelography) = Identifies site of obstruction and presence of non-radiopaque stones KUB Ultrasound & X-ray = Reveals location of stone, number & size Cytoscopic exam = Reveals urinary obstruction Stone analysis = Reveals composition & type of stone 5. Urinalysis = Indicates presence of bacteria, increased protein, increased WBC and RBC (hematuria) Medical Mgt: 1. Surgery a. Percutaneous Nephrostomy: tube is inserted through skin & underlying tissues into renal pelvis to remove calculi. b. Percutaneous Nephrostolithotomy: delivers ultrasound waves through a probe placed on the calculus. 2.

Extracorporeal shock-wave lithotripsy: delivers shock waves from outside the body to the stone, causing pulverization - Non-invasive - Dissolves stone through shock wave application Pain management : Morphine or Meperidine Diet modification

3. Nephrectomy – Removal of affected kidney 4. Litholapoxy – removal of 1/3 of stones- Stones will recur. Not advised for pt with big stones Nursing interventions 1. Strain all urine through gauze to detect stones and crush all clots. 2. Force fluids (3000—4000 cc/day). 3. Encourage ambulation to prevent stasis. 4. Relieve pain by administration of analgesics as ordered and application of moist heat to flank area. 5. Monitor I & O 6. Warm sitz bath – for comfort 7. Alternate warm compress at flank area 8. Medications: a.) Narcotic analgesic- Morphine SO4 Created by Niňa E. Tubio

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b.) Allopurinol (Zyloprim) to decrease uric acid production S/E : Allergic Reactions-----rashes, nasal congestion 9. Patent IV line 10. Provide modified diet, depending upon stone consistency: Calcium, Oxalate and Uric acid stones 1. Calcium Stones Limit milk/dairy products Acid-Ash Diet to acidify urine (cranberry or prune juice, meat, eggs, poultry, fish, grapes & whole grains) 2. Oxalate Stones Avoid excess intake of foods/ fluids high in oxalate (tea, chocolate, rhubarb, spinach) Alkaline-Ash Diet to alkalinize urine (Milk, milk products, vegetables; fruits except prunes, cranberries & plums) 3. Uric Acid Stones Reduce foods high in purine (liver, beans, kidneys, venison, shellfish, meat soups, gravies, legumes) Maintain alkaline urine 11. Provide client teaching and discharge planning concerning Prevention of Urinary stasis by maintaining increased fluid intake especially in hot weather & during illness; mobility; voiding whenever the urge is felt and at least twice during the night 12. Provide client teaching & discharge planning concerning: Adherence to prescribed diet Need for routine urinalysis (at least every 3—4 months) Need to recognize and report signs/ symptoms of recurrence (hematuria, flank pain).

3. ACUTE RENAL FAILURE (ARF) – Sudden inability of the kidneys to excrete nitrogenous waste products & maintain F&E balance d/t a decrease in GFR. Most important manifestation: OLIGURIA Pathophysiology: 3 Stages/Causes:

Created by Niňa E. Tubio

Normal GFR = 125 ml/min

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1. Pre-Renal Cause: Decrease in GFR Causes: 1. 2.

3. 4. 5. 6. 7. 8. 9.

Septic shock Hypovolemia Hypotension CHF Hemorrhage Chronic Diarrhea Burns Cardiogenic Shock Anaphylaxis

Decrease flow to kidneys

2. Intra-Renal Cause: Involves renal pathology – Kidney Problem Conditions that cause damage to the nephrons: Acute tubular necrosis (ATN Endocarditis DM Malignant HPN AGN Ttumors BT Reactions Hypercalcemia Nephrotoxins (certain antibiotics, x-ray dyes, pesticides, anesthetics) Pyelonephritis 3. Post-Renal Cause: Mechanical Obstruction anywhere from the tubules to the urethra Calculi BPH Tumors Strictures Blood clots Trauma Anatomic malformation Urolithiasis Laboratory Findings: 1. Urinalysis: Urine osmo and sodium 2. BUN & Creatinine levels increased 3. Hyperkalemia 4. Anemia 5. ABG: Metabolic Acidosis

3 Phases of Acute Renal Failure 1. Oliguric Phase Urine output less than 400 cc/24 hours Duration 1—2 weeks Manifested by a. Dilutional Hyponatremia Created by Niňa E. Tubio

4 Phases of Acute Renal Failure (Brunner & Suddarth) Initiation phase ( 0-2 days) Oliguric phase Diuretic phase Convalescence or recovery phase

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b. Hyperkalemia c. Hyperphosphatemia d. Hypocalcemia e. Hypermagnesemia f. Metabolic Acidosis Dx: BUN & creatinine elevated 2. Diuretic Phase Diuresis may occur (output 3—5 liters/day) d/t partially regenerated tubule’s inability to concentrate urine Duration: 2—3 week Manifested by: a. Hyponatremia b.Hyperkalemia c. Hypovolemia d. Metabolic Acidosis Dx: BUN & Creatinine slightly elevated 3. Convalescence or Recovery Phase Renal function stabilizes with gradual improvement over next 3—12 months. Complete Diuresis

Nursing Interventions: 1. Monitor & maintain fluid & electrolyte balance. Measure l & O every hour. note excessive losses in diuretic phase Administer IV F & E supplements as ordered. Weigh daily & report gains. Monitor lab values; assess/treat F & E & acid-base imbalances as needed 2. Monitor alteration in fluid volume. Monitor vital signs, PAP, PCWP, CVP as needed. Weigh client daily. Maintain strict I & O records. 3. Assess every hour for hypervolemia Maintain adequate ventilation. Restrict FLUID intake Administer diuretics & antihypertensives 4. Promote optimal nutritional status. Administer TPN as ordered. With enteral feedings, check for residual & notify physician if residual volume increases. Restrict protein intake to 1 g/kg/day Restrict POTASSIUM intake HIGH CARBOHYDRATE DIET, calcium supplements 5. Prevent complications from impaired mobility (pulmonary embolism, skin breakdown & atelectasis) 6. Prevent fever/infection. Assess for signs of infection. Use strict aseptic technique for wound & catheter care. 7. Support client/significant others & reduce/ relieve anxiety. Explain pathophysiology & relationship to symptoms. Explain all procedures and answer all questions in easy-to-understand terms Refer to counseling services as needed 8. Provide care for the client receiving dialysis 9. Provide client teaching & discharge planning concerning Adherence to prescribed dietary regimen Signs and symptoms of recurrent renal disease Importance of planned rest periods Use of prescribed drugs only: Sx of UTI or respiratory infection need to report to physician immediately 4. CHRONIC RENAL FAILURE (CRF) – Irreversible loss of kidney function - Gradual, Progressive irreversible destruction of the kidneys causing severe renal dysfunction. The result is azotemia to UREMIA Predisposing Factors:

1. DM – worldwide leading cause Created by Niňa E. Tubio

Hallmark of Renal Failure: AZOTEMIA & OLIGURIA

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2. HPN -2nd cause 3. Recurrent UTI/ Pyelonephritis 4. 5.

6.

Exposure to renal toxins Recurrent infections Urinary tract obstruction

Pathophysiology:

As renal functions decline Retention of end-products of metabolism

STAGE 1= Reduced renal reserve volume (Asymptomatic) 40-75% loss of nephron function Normal BUN & Creatinine GFR