IM-STEP-2-notes

Internal Medicine study notes Neuro/brain/psych  Elevated intracranial pressure/ intracranial HTN o ICP>20 mm Hg o Causes: trauma, space-occupying lesions, hydrocephalus, impaired CNS venous outflow o Dx: diffuse headaches (worse in morning), N/V early in the day, vision changes, papilledema, CN deficit, somnolence, confusion, unsteadiness, cushings reflex (HTN and bradycardia) o Dx: CT or MRI  Cavernous sinus thrombosis o Secondary to infection of the medial aspect of the face around the eyes and nose (can also be ethmoid or sphenoid sinus infections) o Sx: headache, low grade fever, periorbital edema, cranial nerve palsies  CN 3,4,5 (V1,V2, V3) all pass through the cavernous sinus and can be affected  Headache d/t neuropathic pain d/t irritation of V1 and V2  Dx: MRI or CT w/ contrast of the orbits  Tx: IV broad=spectrum antibiotic; anticoagulation, glucocorticoid, or surgery may be indicated  Acoustic neuroma/ vestibular schwannoma o Typically unilateral o Sx: sensorineural hearing loss  Craniopharyngioma o Tumor of the sella and suprasellar space o Sx: headache, focal neurologic changes, visual problems; can cause central diabetes insipidus (decreased ADH)  Headaches o Dx: CT or MRI to exclude an intracranial mass lesion if the dx is unclear or the syndrome has recently started o Tension headache  Most common type  Dx of exclusion  Tx: NSAIDs or other analgesics o Migraine headache  Precipitants: emotions, food (chocolate, red wine, cheese), menses  Sx: visual disturbance (flashes, sparks, stars, luminous hallucinations), photophobia, aura, N/V, headaches lasting 4-72 hrs (usually unilateral, pulsating quality)  Other possible sx: aphasia, numbness, dysarthria, weakness  Tx: IV antiemetics (chlorpromazine, Prochlorperazine, or metoclopramide) +/- NSAIDS or triptans for acute migraine headaches; triptans or ergotamine  Triptans must be started early in the course of the migraine before sx become severe in order to be of benefit  Prophylactic (preventative) tx: propanolol (#1), calcium channel blockers, tricyclic antidepressants (amitriptyline), SSRIs, botulinum toxin injections o for pts with >3 migraine headaches/month o cluster headaches  M>F  Sx: frequent short duration high intensity headaches  Other possible sx: red tearing eye with rhinorrhea, horner syndrome  Tx: triptans, ergotamine, 100% oxygen, prednisone, or lithium o giant cell (temporal) arteritis  sx: visual sx (irreversible blindness), jaw claudication, scalp tenderness, headache; sx in other arteries (decreases arm pulses, bruits near clavicles, aortic regurgitation); systemic sx (muscle pain, fatigue, weakness)  dx: elevated ESR and CRP; biopsy of artery (most accurate)  tx: high dose prednisone (started before biopsy) o pseudotumor cerebri (benign/idiopathic intracranial HTN)  communicating hydrocephalus; diagnosis of exclusion  a/w obesity, venous sinus thrombosis, vitamin A toxicity, medications (corticosteroids, OCPs), trauma  sx: headache (pulsatile, wake pt from sleep, a/w pulsatile tinnitus; worse lying flat/ better standing up); mimics a brain tumor d/t elevated ICP (N/V, transient visual obscurations, blurry vision), papilledema w/ diplopia from 6th cranial nerve (abducens) palsy  vision loss, sluggish pupillary reflexes to light, papilledema,  dx: CT or MRI to exclude an intracranial mass lesion (empty sella d/t downward herniation of archnocele d/t high CSF pressure, slit like ventricles), lumbar puncture showing increased pressure (w/o CSF disturbances)  note: papilledema is not a contraindication to an LP unless the pt has evidence of obstructive to noncommunicating hydrocephalus and/or space-occupying lesion +/- mass effect or midline shift  tx: weight loss, acetazolamide (decreased CSF production), steroids, repeated lumbar puncture (rapidly lower ICP); ventriculoperitoneal shunt if medical therapy not sufficient  Transient ischemic attack (TIA)/ stroke o #3 cause of death o Causes: carotid stenosis, cardioembolism, lipohyalinosis, small-vessel disease, atheroembolism from carotid artery  Ischemia (85%), bleeding (15%)  Embolic sources: carotid stenosis, heart (atrial fibrillation, valvular heart disease, DVT through patent foramen ovale) o Risk factors: HTN, diabetes, hyperlipidemia, smoking  Hypertensive stroke is most common in the putamen and adjacent internal capsule hemiparesis, semi-sensory loss, homonymous hemianopsia o Sx: acute focal neuro deficits, amaurosis fugax  Amaurosis fugax: transient monocular blindness; “gray shade being pulled down over the eye” d/t ischemia to the retinal artery  TIA: transient neuro deficit secondary to ischemia in a defined vascular territory that lasts arm Posterior cerebral artery (PCA) stroke  Sx: ipsilateral sensory loss of face & CN 9/10, contralateral sensory loss of limbs, limb ataxia  Cerebellar hemorrhage: ataxia, vomiting, occipital headache, gaze palsy (towards the lesion), facial weakness (opposite lesion)  Lacunar stroke  Occurs d/t microatheroma and lipohyalinosis (small vessel hyalinosis); type of ischemic stroke o RF: HTN, diabetes o Most common in the posterior internal capsule pure motor stroke  Putamen hemorrhage: most common site of HTN hemorrhage; internal capsule lies adjacent to the putamen and is almost always involved hemiparesis; hemisensory loss, homonymous hemianopsia, stupor, coma; eye are deviated away form the paralytic side o Dx: CT w/o contrast (best initial; differentiate ischemic from hemorrhagic stroke), MRI (most accurate)  Determine etiology  carotid duplex U/S or MRA to evaluate for carotid artery stenosis o tx: >70% stenosis + symptomatic cerebrovascular disease carotid endarterectomy > angioplasty w/ stenting  >80% stenosis, asymptomatic, good surgical candidates carotid endarterectomy o consider carotid surgery for 50-60% stenosis o medical management with aspirin and statins phenytoin phenobarbital neuromuscular blocking agent (succinylcholine, vecuronium, or pancuronium) + intubation+ general anesthesia (midazolam or propafol)  Phenytoin SE: hypotension & AV block (b/c also a class Ib antiarrhythmic) o Treatment  Treatment is not always necessary following a single seizures  Treatment indications: status epilepticus, abnormal EEG, family hx of seizures  1st choice= phenytoin, valproic acid, or carbamazepine; alternatives= gabapentin, topiramate, lamotrigine, oxcarbazepine, levetiracetam  if single agent not effective, try an alternative drug; if still not effective 2 drugs; if still not effective surgical correction of a seizure focus  treat until pt is seizure-free for 2 yrs, then test if discontinuation can be done via a sleep deprivation EEG  driving restrictions: recommend that the patient find an alternate means of transportation Tremors o Physiologic  Causes: fear, anxiety, fatigue, metabolic (hypoglycemia, hyperthyroid, pheochromocytoma), toxic (alcohol withdrawal, valproic acid, lithium, methylxanthines=caffeine or theophylline) o Essential tremor  Autosomal dominant (~1/3 of cases)  Tremor occurs at rest and with intention  Exacerbated by intentional activity and caffeine, decreased by alcohol use  Tx: propanolol o Neurologic diseases: Parkinson’s, cerebellar disease, Wilson’s disease Meningitis o Causes: infectious, medications, SLE, sarcoidosis, carcinomatosis o Sx: headache, fever, N/V, stiff painful neck, malaise, photophobia, altered mental status (confusion, lethargy, coma), myalgias, seizures  Increased ICP, kerning’s sign (unable to extend knees with hips flexed), brudzinski’s sign (passive flexion of neck causes thigh/leg flexion)  N. meningitidis: Maculopapular rash w/ petechiae or purpura  Varicella or HSV: vesicular lesions  Complications: seizures, coma, brain abscess, subdural empyema, DIC, respiratory arrest; deafness, brain damage, hydrocephalus o Acute: onset w/in hrs-days  Bacterial  Neonates ( E.coli >listeria monocytogenes; klebsiella spp.  Kids (3mo-18yrs): Neisseria meningitidis > strep pneumoniae >H. influenzae  Adults (18-50): Strep pneumo > N. meningitidis > H. influenzae  Elderly (>50 yo): Strep pneumo > N. meningitidis > listeria monocytogenes  Immunocompromised: L. monocytogenes > gram (-) bacilli > strep pneumo  Aseptic meningitis  Enterovirus, HSV, certain bacteria, parasites, fungi o chronic: onset w/in wks-months  mycobacteria, fungi, lyme dz, parasites o differential diagnosis: meningitis, brain or epidural abscess, subarachnoid hemorrhage  bugs that cause meningitis: strep pneumo (#1), N. meningitidis (#2), GBS/strep agalactiae, listeria monocytogenes, H. influenzae; staph aureus or staph epidermidis following neuro procedures; enteroviruses, HSV 1 or 2, cryptococcus (HIV pts), TB, rocky mountain spotted fever o dx: CSF exam (lumbar puncture), blood cultures  CT scan before lumbar puncture if focal neurologic signs or abnormal level of consciousness, papilledema  Normal LP: WBC 50-60 yo)  d/t dopamine depletion in the substantia nigra (basal ganglia) and in the nigrostriatal pathway to the caudate & putamen increased inhibition of the thalamus & reduced excitatory input to the motor cortex o Secondary parkinsonism: antipsychotics (metoclopramide, prochlorperazine, reserpine, thorazine) & antiemetics are most common causes; repeated head trauma, encephalitis o Sx: tremor (“pill rolling”, at rest & decreased with purposeful action, 5-7 Hz frequency, may be a sensation of internal tremulousness), bradykinesia, rigidity (asymmetric, increased resistance to passive movement; cogwheel rigidity d/t tremor superimposed on increased tone), postural instability (orthostatic hypotension d/t inability of pulse and BP to reset appropriately with movement), micrographia (small writing), limited facial expression (hypomimia)  Shy-Drager syndrome (multiple system atrophy): parkinsonism predominantly with orthostasis o

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Sx: parkinsonism, autonomic dysfunction (postural hypotension, abnormal sweating, dry mouth, dry skin, disturbance of bowel/bladder control, abnormal salivation or lacrimation, impotence, gastroparesis), widespread neuro signs (cerebella, pyramidal, or lower motor neuron) Tx: intravascular volume expansion (fludrocortisone, salt supplementation, alpha-adrenergic agonists, application of constrictive garments to the lower body); note that anti-parkinson drugs are generally ineffective

Motor sx  Craniofacial: hypomimia (masked facial expression), decreased spontaneous eye blink rate, speech impairment (hypokinetic dysarthria, hypophonia, palilalia= involuntary repetition of syllables/words/phrases), dysphagia, sialorrhea= drooling  Visual: blurred vision, impaired contrast sensitivity, hypometric saccades, impaired vestibuloocular reflex, impaired upward gaze & convergence, eyelid opening apraxia  Musculoskeletal: micrographia (small handwriting), dystonia, myoclonus, stooped posture, camptocormia (severe anterior flexion of the thoracolumbar spine), kyphosis, scoliosis, difficulty turning in bed  Gait: shuffling, short stepped gait, freezing, festination (involuntary quickening of the gait)  Nonmotor sx  Cognitive dysfunction and dementia, psychosis and hallucinations (paranoid psychosis; visual hallucinations most common), mood disorders (depression, anxiety, apathy/abulia), sleep disturbances (insomnia sleep initiation problems, frequent awakening, and early morning awakening), fatigue, autonomic dysfunction, olfactory dysfunction, pain and sensory disturbances, dermatologic findings (seborrheic dermatitis) o Ambulia= loss of impulse/will/motivation to think, speak, and act  Dementia: subcortical; psychomotor retardation, memory difficulty, altered personality, problems with executive function (decision making or multi-tasking), memory retrieval, visuospatial misperception o Cortical neuronal Lewy inclusion bodies filled with alpha synuclein+ amyloid plaques & neurofibrillary tangles (more common to Alzheimer’s disease) Dx: Based on clinical impression  Brain MRI to r/o structural lesions  Striatal dopamine transporter imaging (DaTscan) may be useful for pts where clinical diagnosis is unclear Treatment 

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     Multiple sclerosis

Dopamine agonists (pramipexole, ropinirole): best initial tx for severe parkinsonism  Pergolide and cabergoline should NOT be used d/t risk of valvular heart disease  Bromocriptine is also not frequently used d/t SE Levodopa + peripheral decarboxylase inhibitor (carbidopa) is most effective for symptomatic treatment  Carbidopa inhibits aromatic AA decarboxylation; inhibits metabolism of levodopa in the peripheral circulation  SE: “on/off” phenomena (episodes of too much dopamine and insufficient dopamine) COMT inhibitor (Entacapone, tolcapone): extend the duration of levodopa/carbidopa by blocking the metabolism of dopamine MAO B inhibitors (Selegiline, rasagiline): block metabolism of dopamine; only MAO-B inhibitors are a/w the possibility of retarding the progression of parkinsonism  mild symptomatic benefit; only used for early disease  Avoid tyramine-containing foods (wine, cheese); they precipitate HTN Anticholinergic drugs (benztropine, trihexyphenidyl): used for young pts when tremor or rigidity is the predominant sx (mild disease)  SE: dry mouth, worsening prostatic hypertrophy, constipation Amantadine: used for early or mild PD or for problematic dyskinesia  Increases release of dopamine & NE from nerve endings; weak NMDA receptor antagonist; anticholinergic Psychosis: quetiapine or clozapine (atypical neuroleptics); stop or reduce drugs causing psychosis in reverse order of potency (anticholinergic, amantadine, COMT inhibitors, and lastly dopamine agonists)  Choose antipsychotics with the least extrapyramidal sx (antidopaminergic)  Note: clozapine requires weekly or bi-weekly blood counts d/t risk of granulocytopenia (risk exponentially decreased with time; almost nothing >6mo) Daytime sleepiness: sleep hygiene, modafinil, methylphenidate, or judicious use of coffee during the day Fatigue: amantadine, stimulants (methylphenidate, pemoline) Depression: SSRI (SE possibly aggravates motor sx, adverse interaction with selegiline causing serotonin syndrome) Deep brain stimulation (electrical stimulation) Dopamine agonist for pt 65

Multiple neurologic deficits of the CNS; presents in 20-40s; insidious onset of intermittent neurologic deficits Sx: scattered motor & sensory deficits (paresthesias and numbness, weakness, gait disturbance, visual disturbances); optic neuritis blurry vision or visual disturbances (most common), painless loss of vision; diplopia, internuclear ophthalmoplegia; b/l trigeminal neuralgia; cognitive defects, mental status changes, emotional lability, dementia; spasticity (painful contracted muscles), hyperreflexia, fatigue, cerebellar deficits; scanning speech  Internuclear ophthalmoplegia: inability to adduct 1 eye with nystagmus in the other eye o Dx: MRI ( demyelination plaques= white matter lesions surrounding the ventricles, corpus callosum, basal ganglia); lumbar puncture of CSF (elevated protein, 100 lymphocytes Normal Normal/slightly increased Normal/ slightly increased Pseudotumor cerebri Normal Normal Normal >200 Guillain-barre syndrome 0-100 lymphocytes Normal >100 Normal Cerebral hemorrhage Blood (RBC) Normal >45 >200 Multiple sclerosis Normal/ slightly increased lymphocytes Normal Normal/slightly increased normal  Sleep disorders o Circadian rhythm disorders  Delayed sleep phase syndrome: inability to fall asleep at “normal” bedtimes such as 10pm-midnight; pt cannot fall asleep until 4-5am but have normal sleep if they are allowed to sleep until late morning; pt c/o insomnia and excessive daytime sleepiness  Dx: sleep hx and sleep diary  Advanced sleep phase disorder: inability to stay awake in the evening (usually after 7pm) making social functioning difficult; c/o early morning insomnia d/t early bedtime Head and neck  Meniere’s disease o

Distention of the endolymphatic compartment of the inner ear  Triggers: alcohol, caffeine, nicotine, food high in salt o Sx: sense of ear fullness, vertigo (20 min-24 hr), low-frequency sensorineural hearing loss, tinnitus; vertigo can cause N/V and postural instability; symptoms wax & wane; nystagmus during an acute attack o Tx: salt restricted diet (2-3g /day); if persistant diuretics, antihistamines, anticholinergics Otosclerosis/otospongiosis o Abnormal remodeling of the otic capsule (bony overgrowth of the stapes) stapes footplate becomes fixed to the oval window causing loss of piston action  Age 20-30, F>M, possible autoimmune o Sx: Conductive hearing loss o Dx: PE, CT (may show lucent or sclerotic focus in the temporal bone near the oval window)  Rinne test (bone conduction> air conduction), Weber test (sound lateralizes to the affected ear; sound is perceived as louder b/c ambient noise of the room is perceived less on that side, so bone conduction seems louder) o Tx: hearing amplification or surgical stapedectomy Presbycusis o Elderly pts (>50yo) o Sx: sensorineural hearing loss (starts as symmetric high-frequency hearing loss)  Difficulty hearing in corwsed or noisy environments; trouble hearing high-pitched noises or voices Medication induced ototoxicity o Sx: bilateral sensorineural hearing loss (reversible or permanent), and/or tinnitus o Drugs: aminoglycosides, loop diuretics (furosemide), chemotherapeutic agents, aspirin Serous otitis media (non-infectious effusion) o Most common middle ear pathology in pts with HIV o Auditory tube disfunction d/t HIV lymphadenopathy or obstructing lymphomas o Sx: middle ear effusion w/o signs of inflammation dull tympanic membrane that is hypomobile, conductive hearing loss o Dx: pneumatic otoscopy Ramsay Hunt syndrome o Herpes zoster infection in the ear o Sx: facial nerve palsy (bell’s palsy), vesicles in the auditory canal and auricle Malignant otitis externa o Elderly pts w/poorly controlled diabetes; pseudomonas aeruginosa infection o Sx: ear pain & drainage, granulation tissue seen w/in the ear canal  Complications: osteomyelitis of the skull base, destruction of the facial nerve o Dx: CT or MRI o Tx: ciprofloxacin presbyopia o normal aging (starts age 40, peaks age 60) o loss of elasticity in the lens lack of accommodation of the lens difficulty focusing in near objects Optic neuritis o Age 20-45 yo; F>M; a/w multiple sclerosis o Sx: rapid impairment of vision in 1 eye (rarely b/l) and pain on eye movement (retrobulbar pain); marked changes in color perception; afferent pupillary defect and filed loss (usually with central scotoma) Papilledema o d/t increased ICP o Sx: transient loss of vision that lasts a few seconds with changes in head position, morning headaches Central retinal vein occlusion o RFs: coagulopathy, hyperviscosity, chronic glaucoma, atherosclerotic RFs (age, HTN, diabetes) o Sx: sudden painless unilateral loss of vision o Dx: disk swelling, venous dilation and tortuosity, retinal hemorrhages, cotton wool spots Central retinal artery occlusions o d/t embolism ischemia of the inner retina  RFs: carotid artery disease, endocarditis, cardiac valvular disease, long bone fracture, hypercoagulable conditions, vasculitis, atrial myxoma  Recall ophthalmic artery is the first intracranial branch of the internal carotid artery; supplies blood to eye via central retinal artery (supplies inner retina) and ciliary branches (supplies choroids and anterior portion of globe) o Sx: sudden painless loss of vision in 1 eye; commonly a/w amaurosis fugax before the occlusion o Dx: ophthalmoscopy (pallor of the optic disc, cherry red fovea, boxcar segmentation of blood in the retinal veins; diffuse ischemia retinal whitening and cherry red spots) o Tx: ocular massage and high flow oxygen Amaurosis fugax o Retinal emboli  a/w atherosclerosis, CV disease, HTN o Sx: monocular transient visual loss; “like a curtain falling down” o Dx: ophthalmoscopy (zones of whitened edematous retina following the distribution of the retinal arterioles) Choroidal rupture o d/t blunt ocular trauma o dx: ophthalmoscopy (central scotoma, retinal edema, hemorrhagic detachment of the macula, subretinal hemorrhage, crescent-shaped streak concentric to the optic nerve) Vitreous hemorrhage` o Causes: diabetic retinopathy (#1) o Sx: sudden loss of vision and onset of floaters o Dx: fundus is hard to visualize o Tx: conservative (upright position during sleep which enhances settling of hemorrhage) Retinal detachment o Most common age 40-70 yo; usually the inciting event is months before retinal detachment (myopia or trauma retinal breaks fluid seeps in an separates the retinal layers) o Separation of the inner layers of the retina o

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 May be a/w metabolic disorder (DM), trauma (including ocular surgery), vascular disease, myopia, or degeneration o Sx: loss of vision, photopsia (flashes of light) with showers of floaters (spots in the visual field); “a curtain coming down over my eyes” o Dx: fundoscopy (elevated retina with folds and/or a tear) o Tx: laser therapy and cryotherapy (create permanent adhesions between the neurosensory retina, retinal pigment epithelium, and choroid) Diabetic retinopathy o Diabetic retinopathy occurs before nephropathy o Background/simple retinopathy: microaneurysm, dot and blot hemorrhages, hard exudates, retinal edema o Per-proliferative retinopathy: cotton wool spots o Proliferative/malignant retinopathy: neovascularization o Eventual blindness o Tx: argon laser photocoagulation to prevent complications Hypertensive retinopathy o initally focal spasm of arterioles then progressive sclerosis and narrowing o Dx: fundoscopy (AV nicking, copper wiring or silver wiring, exudates and hemorrhages) Acute angle-closure glaucoma o Seen in elderly pts (age 55-70); usually occurs following pupillary dilation (ex. In a dark movie theatre, during times of stress, or due to drug intake) o Sx: acute onset of sever eye pain, visual loss, halos around lights, headache, N/V  Eye is red with a hazy/steamy cornea; fixed dilated pupil that is nonreactive to light; anterior chamber is shallow ith inflammatory changes; tonometry (increased intraocular pressure) o Dx: tonometry (elevated intraocular pressure) o Tx: medical emergency; narcotics for pain control, decrease intraocular pressure (mannitol, acetazolamide, timolol, or pilocarpine); laser peripheral iridotomy for permanent cure  Avoid atropine (dilates the pupil and worsen the glaucoma)  Timolol (topical beta blocker) and acetazolamide (carbonic anhydrase inhibitor) reduce the production of aqueous humor  Pilocarpine opens the canals os Schlemm to allow drainage of aqueous humor Open angle glaucoma o Sx: gradual loss of peripheral vision (over years) tunnel vision; central vision is spared o Dx: elevated intraocular pressure, cupping of the optic disk o Tx: beta-blocker (timolol eye drops), laser trabeculoplasty, surgical trabeculectomy Sympathetic ophthalmia/ “spared eye injury” o Immune mediated inflammation of ene eye (the sympathetic eye) after a penetrating injury to the other eye  d/t the uncovering of “hidden antigens” (some antigens are contained w/in the eye are protected from immunologic recognition by natural barrier; breaking the barrier results in release of these antigens autoantibodies and cell mediated immunity) o Sx: anterior uveitis, panuveitis, papillary edema, or blindness Cataracts o Progressive thickening of the lens  Caused by oxidative damage that occurs with aging o Sx: gradual blurred vision and glare o Tx: lens extraction (phacoemulsification, extracapsular or intracapsular cataract extraction) Uveitis o a/w HLA B27-related conditions o Sx: blurred vision, moderate pain, conjunctival injection, constricted pupils; hypopyon in severe anterior uveitis; keratic precipitates (“mutton fat”) and iris nodules may be present macular degeneration o RF: Pt >50 yo (age related), smoking o Degeneration and atrophy of the outer retina, retinal pigment epithelium, bruch’s membrane, and choriocapillaries o Sx: painless progressive and unilateral or bilateral loss of central vision (burring of central vision); intact peripheral fields and navigational vision; distortion of straight lines (lines appear wavy) o Dx: drusen deposits in the macula intraocular foreign body o RF: high-velocity injuries (drilling, grinding, etc) o Dx: pen light exam with topical anesthetic; if no gross abnormalities fluorescein application followed by a slit lamp> wood’s lamp exam; if no abrasion or foreign body seen with high suspicion CT or ultrasonography of orbit  MRI contraindicated! (can dislodge the foreign body d/t strong magnetic field) Allergic conjunctivitis o Acute HSR reaction d/t environmental exposure to allergens  a/w personal/family hx of asthmas, seasonal rhinitis, atopic ermatitis, food allergies, urticaria o Sx: intense itching, hyperemia, tearing, and conjunctival edema and eyelid edema; photophobia, burning sensation o Tx: self-limited w/in 24hrs, decrease exposure to allergens, avoid rubbing eyes, topical antihistamines, artificial tears, cool compresses Atopic keratoconjunctivitis o Severe form of ocular allergy o Sx: itching, tearing, thick mucus discharge, photophobia, blurred vision Toxic conjunctivitis o d/t direct damage to ocular tissues from drugs after prolonged use (aminoglycosides, glaucoma drops, artificial tears, contact lens solution) Herpes simplex keratitis o RF: excessive sun exposure, outdoor occupation, fever, immunodeficiency (HIV) o Sx: pain, photophobia, blurred vision, tearing, redness; can cause corneal blindness  Corneal vesicles and dendritic ulcers o Dx: clinical; epithelial scrapings (multi-nucleated giant cells) o T: oral or topical antiviral tx Bacterial keratitis o RF: contact lenses, corneal trauma, foreign body o Sx: cornea appears hazy with a central ulcer and adjacent stromal abscess; hypopyon may be present Herpes simplex retinitis o Occurs in HIV pts

Sx: rapidly progressing b/l necrotizing retinitis (acute retinal necrosis syndrome); starts as keratitis and conjunctivitis with eye pain rapidly progressive visual loss & blindness o Dx: fundoscopy (widespread pale peripheral lesions and central necrosis of the retina) CMV retinitis o Occurs in HIV pts o Sx: painless loss of vision o Dx: fundoscopy (fluffy or granular retinal lesions located near the retinal vessels and associated hemorrhages) Herpes zoster ophthalmicus o d/t varicella-zoster virus reactivation in the trigeminal ganglion travels to the ophthalmic branch to the forehead and eye  mostly in elderly or immunosuppressed o sx: fever, malaise, burning/itching sensation in the periorbital region; vesicular rash in the distribution of the cutaneous branch of the 1st division of the trigeminal nerve o dx: conjunctivity and dendriform corneal ulcers o tx: high dose acyclovir (started w/in 72hrs after eruption) to recues the development of complications Postoperative endophthalmitis o Occurs w/in 6 wks of surgery; infection within the vitreous of the eye o Sx: eye pain, decreased visual acuity; swollen eyelids and conjunctiva, hypopyon (pus in the eye), corneal edema and infection o Dx: sent vitreous for gram stain and culture o Tx: intravitreal antibiotics or vitrectomy Xanthelasma o a/w primary biliary cirrhosis o bilateral cholesterol-filled soft yellow plaques on the medial aspects of the eyelids; benign; lipid-filled macrophages in the dermis Hordeolum/stye o agent: staphlococci o purulent infection of one of the glands of the eyelids (abscess located over the upper or lower eyelid)  stye=small external hordeolum involving Zeis’s or Moll’s glands o tx: frequent hot compresses, incision and drainage if unresolved within 48 hrs after starting tx; antibiotics against staph chalazion o chronic sterile granulomatous inflammatory lesion of the meibomian glands  painful swelling that progresses to a nodular rubbery lesion (hard painless lid nodule)  persistent or recurrent chalazion can be d/t meibomian gland carcinoma (sebaceous carcinoma)  basal cell carcinoma=most common malignancy of the lid margin & may appear similar to chalazion o dx: histopathologic exam to r/o malignancy o tx: incision and drainage blepharitis o choric inflammatory condition involving b/l lid margins o sx:  anterior blepharitis: crusty discharge clinging to the lashes  posterior blepharitis: hyperemic lid margins with telangiectasias episcleritis o infection of the episcleral tissue between the conjunctiva and sclera o sx: acute onset mild-moderate discomfort, photophobia, watery discharge; diffuse or localized bulbar conjunctival injection dacrocystitis o usually pt >40 yo o infection of the lacrimal sac d/t obstruction of the nasolacrimal duct  agents: staph aureus, beta-hemolytic strep o sx: pain, swelling, tenderness, redness in the tear sac area (medial canthal region); mucous or pus can be expressed; may have fever or leukoctyosis Nasal polyp o a/w chronic rhinitis, post-nasal drainage, asthma, aspirin (or NSAID) exacerbated respiratory disease (bronchospasm) o sx: bilateral nasal obstruction & discharge, anosmia (decreased smell decreased taste); bilateral grey glistening mucoid masses in the nasal cavities Leukoplakia o Whitish patch or plaque that can not be scraped off; can’t be characterized as any other disease (dx of exclusion)  a/w chronic irritation to the oral mucosa d/t smoking, alcohol, or ill-fitting dentures  complications: squamous cell carcinoma Oral ulcers o Gingivostomatitis d/t HSV1  Multiple vesicular intraoral lesions that have a red border Oral candidiasis o Risk factors: diabetes o Whitish plaques that can be scraped off with a tongue depressor Temporomandibular joint (TMJ) dysfunction o Hx of nocturnal teeth grinding o Sx: “ear pain” (d/t proximity of joint; pain worse with chewing), audible clocks or crepitus with jaw movement o Tx: nighttime bit guard, surgery Thyroid cancer o Papillary thyroid cancer  Most common thyroid malignancy; epithelial origin  Slow infiltrative local spread to other parts of the thyroid and lymp nodes  Dx: histology (psammoma bodies; large cells with ground glass cytoplasm and pale nuclei with inclusion bodies and central grooving; hurthle cells may be present) o Follicular thyroid cancer  Epithelial origin  Encapsulated; invasion of tumor capsule and blood vessels distinguishes it from follicular adenoma  Early hematogenous spread to lung, brain, and bone  Dx: histology (hurthle cells may be present) o

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Medullary cancer of the thyroid  C-cell origin; Secretion of calcitonin o Lymphoma of the thyroid  Increased risk from hashimoto’s thyroiditis  Sx: rapid enlargement of the thyroid gland, compressive sx (dysphagia, voice change)  Dx: CT scan of neck (enlargement of the thyroid gland around the trachea; “doughnut sign”), thyroid U/S (pseudocystic pattern), reduced radioactive iodine uptake; core needle biopsy  Epiglottitis o d/t infection with Haemophilus influenzae or steptococcus pyogenes o sx: high grade fever, severe sore throat, odynophagia (painful swallowing), droolin, progressive airway obstruction  stridor o tx: prevention with Hib vaccine;  Peritonsillar abscess o Complication from tosillitis o Sx: fever, chills, sore throat; “hot potato voice”, deviation of the uvula; unilateral lymphadenopathy  Complications: airway obstruction, spear to the parapharyngeal space involvement of the carotid sheath o Tx: aspiration of the abscess, IV antibiotics  Retropharyngeal abscess o Sx: sore throat, fever, difficulty swallowing (dysphagia), pain with swallowing (odynophagia), pain with certain neck movements (extension), trismus (inability ot open the mouth normally) o Complication: spread of infection to mediastinum acute necrotizing mediastinitis  “danger space” of infection is between the alar and prevertebral fasciae o dx: CT or lateral x-ray of neck o tx; IV broad-spectrum antibiotics, urgent drainage of the abscess  infectious mononucleosis o sx: fever, pharyngitis, posterior cervical lymphadenopathy, malaise, splenomegaly; risk of splenic rupture (avoid contact sports until the physical exam is normal no splenomegaly) o dx: atypical lymphocytosis, positive heterophile antibody test  diphtheria o sx: pseudomembranous pharyngitis, low grade fever, unilateral nasal discharge, pharyngitis, cervical lymphadenopathy cardiovascular  ECG interpretation o Inferior surface: Leads II, III, aVF; supplied by right coronary artery o Anterior surface: leads V2-V4; supplied by left anterior descending coronary artery (LAD) o Lateral surface: leads I, aVL, V5 & V6; supplied by left circumflex artery o Posterior surface: R waves in leads V1 & V2 o Horizontally: 1 small box= 0.04 sec , each large box=0.2 sec (200 ms) if paper speed is 25 mm/sec o Vertically: 1 small box=10mm=1mV o Steps: rate, rhythm, axis, intervals, P wave, QRS complex, ST segment, T wave, overall interpretation o Heart rate  Counting boxes from R-R interval (300/ # big boxes): 300, 150, 100, 75, 60, 50  If irregular rhythm: count # QRS complexes x 6  Divide by 6 b/c standard ECG displays 10 sec of time to get 60 sec (bpm) o Rhythm:  Sinus rhythm:  P wave upright in leads I, II, aVF, and V4-V6; negative in aVR. Negative or biphasic in III and V1 o Most important: up in I & aVF, down in aVR  P waves before every QRS complex  If QRS 0.12 sec), then the rhythm is either supraventricular with aberrant conduction, pre-excitation, or ventricular pacing, or it is of ventricular origin o Axis: direction and magnitude of various complexes  Normal between -30 to 90 degrees (directed downward/ inferior and to the left)  Left axis deviation: between -30 to -90  Right axis deviation: between 90 and 180  Between -90 and -180 is either extreme L or R deviation  Determining axis  If the QRS complex is positive (upright) in both leads I and II, then the axis falls between -30 and 90o, and the axis is normal.  If the QRS complex is positive in lead I but negative in lead II, then the axis is leftward (-30 to -90o).
  If the complexes are negative in lead I and positive in aVF, then the axis is rightward (90 to 180o).
  If the complexes are negative in both I and II, then the axis is extreme (180 to -90o).  Another method of axis determination is to find the lead in which the complex is most isoelectric; the axis is directed perpendicular to this lead. As an example, if the QRS is isoelectric in lead 3 which is directed at 120o, then the electrical axis is either 30o or -150o.  A third method is to determine the frontal lead in which the QRS is of the greatest positive amplitude. The axis is parallel to this lead. o P wave: atrial depolarization  duration 25 mm, S V1 or V2 +  R V5 or V6 > 35 mm, R I + S III > 25 mm o Any precordial lead (V1-V6) >35 mm Dysrhythmias/ conduction disturbances o Premature atrial complexes (PACs)  Premature activation of the atria originating form a site other than the SA node  RFs: tobacco, alcohol, caffeine, stress  Dx: EKG (early P wave)  Treatment  Asymptomatic: avoid reversible risk factors  Symptomatic: beta-blocker o Premature ventricular contractions (PVCs)  Wide QRS (>120 ms), bizarre morphology, compensatory pause  More common in pt with cardiac pathology; increased frequency after MI  Tx: observation  not treated with antiarrhythmic agents unless they occur very frequently, are sustained, or induce hemodynamic compromise o beta blockers (#1) for symptomatic patients; amiodarone 2nd line  check magnesium and phosphate levels o Supraventricular tachycardia  Tx: direct current (DC) cardioversion if sx or hemodynamic instability; antiarrhythmics (adenosine, metoprolol, procainamide)  Ventricular tachycardia/fibrillation  Tx: immediate defibrillation; antiarrhythmics (lidocaine, procainamide, amiodarone); maintain K+>4 mEq/L and Mg >2 mEq/L o atrial fibrillation  abnormal irregular heart rhythm with chaotic generation of electrical signals in the atria of the heart; disordered atrial depolarization  rapid ventricular response w/ HR>110  paroxysmal is self-limiting; persistent >7 days, permanent >1 yr  impulses come from the pulmonary veins 

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complications: myocardial ischemia, exacerbation of heart failure, thrombus formation in the noncontractile atria systemic embolization stroke  AF >48 hrs increases risk of intraatrial thrombus formation  causes: anything that causes atrial dilation or excessive sympathetic tone  Most common: HTN, coronary atherosclerosis  Inflammatory disease (pericarditis, myocarditis), surgery (post-bypass surgery, post-valvular surgery), drugs (theophylline, caffeine, digitalis, amphetamines), atherosclerotic coronary artery disease, rheumatic heart disease (esp w/ mitral stenosis), hyperthyroidism/thyrotoxicosis, congenital heart disease (ASD, Ebstein anomaly), HTN heart disease, alcohol consumption (holiday heart syndrome, alcoholic cardiomyopathy), pulmonary disease (esp pulmonary embolus), CHF, MI, infections (urosepsis), hypoxia, anxiety  CHAD 2 score: predictor for risk of stroke in pt with non-rheumatic atrial fibrillation  CHF (1 pt), HTN >140/90 or on meds (1 pt), age >75 yo (1pt), DM, (1pt), prior stroke/tia/thromboembolism (2 pts) o Stroke risk: 0=1.9%, 1=2.8%, 2= 4%, 3= 5.9%, 4=8.5%, 5=12.5%, 6=18.2%  CHA2DS2-VASc score: additional non-major stroke risk factors include age 65-74, female gender and vascular disease. In the CHA2DS2-VASc score score, 'age 75 and above' also has extra weight, with 2 points.  Anticoagulation: 0= non or aspirin daily, 1= aspirin daily or warfarin, >2= warfarin  dx: ECG (absence of discrete P waves, irregularly irregular ventricular response), CXR (dilated L. atrium), echo (increased left atrial size, thrombus, ejection fraction), CMP, cardiac markers, TSH level to r/o thyroid etiology  treatment  if hemodynamically unstable (hypotension, angina pectoris, pulmonary edema) DC cardioversion  hemodynamically stable ventricular rate control (IV beta-blocker, calcium channel blocker, or digoxin)  if >48 hr AF 3-4 wks of warfarin therapy o monitor warfarin with INR levels; goal 2-3  elevated INR but asymptomatic hold warfarin until INR reach acceptable range  Elevated INR & excessive bleeding vit K & fresh frozen plasma o low-dose aspirin is alternative for pt w/o any structural heart disease/HTN/or other factors for stroke (“lone atrial fibrillation”); doesn’t require anticoagulation meds  pharmacologic cardioverting agents: procainamide, sotalol, amiodarone o if a-fib present 48 hrs, first do TEE to check for presence of thrombus  If no thrombus cardioversion; if thrombus present anticoagulate for 3-4 wks then cardiovert o Atrial flutter  Macro re-entry narrow complex tachycardia; re-entry around tricuspid valve (250-300 bpm possible; 1:1 every circle around valve stimulates AV node conduction)  Dx: adenosine challenge (rhythm does not break with adenosine), Cardizem challenge (rhythm slows with Cardizem= diltiazem)  Tx: AV node blocking agents to decrease electrical conduction; ablation at isthmus to stop re-entrant circuit o Bradycardia/atrioventricular block  Sinus bradycardia is seen after inferior MI (b/c R. coronary artery also supplies the sinoatrial node)  Dx: ECG, echo  First-degree AV block: PR interval prolongation (>200 ms=1 large box); d/t conduction delay in AV node  Tx: pacing only if symptomatic (bradycardia, syncope, heart failure, asystole >3 sec)  Second degree heart block  Mobitz I second degree AV block (wenkebach): gradual prolongation of the PR interval before a nonconducted P wave/ “drop beat” (P wave w/o QRS); d/t abnormal AV node conduction (can be d/t inferior MI)  Mobitz II second degree AV block: nonconducted P waves not preceded by PR prolongation  Tx: atropine 0.5-1.0mg or isoproterenol used if block @ AV node w/ severe bradycardia o Stand-by pacemaker if risk of complete heart block, new L bundle branch block w/ primary atrioventricular block, new bifascicular block  Third-degree AV block: complete AV dissociated with no P-wave conduction; SA & AV node fire at independent waves; complete independence of P waves and QRS complexes  Tx: temporary transcutaneous or transvenous pacemaker & evaluate for permanent pacemaker o Ventricular fibrillation  Causes: MI, electrolyte imbalance, myocarditis, cardiomyopathy, drug side effect  Dx: EKG (fibrillary waves, absence of regular QRS complexes)  Tx: early defibrillation o Ventricular tachycardia  Regular wide complex tachycardia  Tx  If not hemodynamically compromised IV amiodarone>lidocaine  If hemodynamically compromised cardioversion o torsades de pointes  polymorphic ventricular tachycardia a/w prolonged QT interval  risk factors: familial long QT syndrome, malnourished pts (hypomagnesemia), drugs (TCAs, moxifloxacin, fluconazole)  tx: magnesium sulfate o wolff-parkinson-white syndrome  accessory pathway between atria and ventricles Preexcitation (early ventricular depolarization; delta wave= early up-slurring of the R wave; widens QRS complex >0.12 sec, shortens PR interval 45 M, >55 F), 1 st degree family hx of premature ( prasugrel or ticlopidine o clopidogrel or prasugrel used following angioplasty w/ stenting o side effects: clopidogrel (TPP), prasugrel (risk of hemorrhagic stroke don’t use in pt >75 yo), ticlopidine (neutropenia)  ranolazine for refractor/persistent angina  ACE inhibitors/ARBs: used for low EF/systolic dysfucntion or regurgitant valve disease o SE: cough (not ARB), hyperkalemia (d/t aldosterone inhibition)  If hyperkalemia switch to hydralazine (arterial vasodilator decreased afterload) + nitrate (coronary a. dilator)  Calcium channel blockers (verapamil, diltiazem) only used if: severe asthmas or cocaine-induced chest pain (can’t tolerate beta-blockers), Prinzmetal variant angina o SE: edema, constipation, heart block o Dihydropyridine CCBs (-dipine) are contraindicated d/t reflex tachycardia (increased oxygen consumption, increased mortality)  Lipid management o Statin (HMG-CoA reductase inhibitor) to keep LDL 70% stenosis), 2 vessel disease + DM, L. main coronary a. occlusion, persistent sx despite medical therapy  Internal mammary a. lasts ~10 yrs > saphenous vein last ~5 yrs o Percutaneous coronary intervention (PCI; angioplasty) is best for acute coronary syndromes (esp. ST segment elevation)  Medical tx (aspirin, beta blocker, ACEi/ARB, statin) is greater than or equal to PCI for stable CAD acute coronary syndrome: spectrum of acute cardiac ischemia ranging from unstable angina to acute MI o usually d/t thrombus formation in a coronary artery with an atherosclerotic plaque; other causes are embolic occlusion, coronary vasospasm, vasculitis, aortic root or coronary artery dissection, cocaine use (vasospasm & thrombosis) o risk factors: same as CAD o sx: crushing substernal chest pain (sore/dull, radiates to L. arm), anxiety, diaphoresis, nausea; s4 gallop (during atrial systole; d/t ischemia LV noncompliance) o complications of acute MI (hypotension a/w all)  bradycardia: sinus bradycardia (d/t vascular insufficiency of SA node) vs third degree (complete) AV block  third degree heart block: cannon a waves (atrial systole against a closed tricuspid valve b/c atria and ventricle are contracting out of coordination with each other; bounding jugulovenous wave bouncing up into the neck) o tx: atropine; if refractory pacemaker 

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tachycardia: R. ventricular infarct, tamponade/free wall rupture, V. tach or V. fibrillation, valve or septal rupture, extension of the infarction/reinfarction, aneurysm/mural thrombus  R. ventricular infarct a/w new inferior MI o R. coronary a. supplies the RV, AV node, and inferior wall of heart o Dx: flip EKG leads to right side (ST elevation in RV4 most specific)  Lungs clear to auscultation o Tx: high volume fluid replacement; avoid nitrates (worsen cardiac filling)  Tamponade/free wall rupture o Several days after infarct; sudden loss of pulse, jugulovenous distention o Dx: emergency echo  Lungs clear to auscultation o Tx: emergency pericardiocentesis on the way to OR for repair  Ventricular tachycardia or fibrillation can cause sudden death; loss of pulse o Dx: EKG o Tx: emergency electrical shock (cardioversion/defibrillation)  Valve or septal defect o Sx: new onset murmur, pulmonary congestion o Dx: echo; step-up in O2 sat from right atria to right ventricle indicates septal rupture  Extension of the infarction/reinfarction o Sx: recurrence of pain, new rales, new increase in CK-MBs, sudden onset pulmonary edema o Dx: EKG o Tx: same meds as acute MI: re-treat with angioplasty or thrombolytics  Aneurysm/mural thrombus o Dx: echo o Tx: heparin followed by warfarin for mural thrombi dx: ECG, cardiac enzymes  ECG changes: ST changes become Q waves over days-1wk  ST elevation in V2-V4= anterior wall LV MI; worst mortality of left untreated  ST elevation in II, III, aVF= inferior wall MI  ST depression in V1 & V2= posterior wall MI  Cardiac enzymes Enzyme Time to become abnormal Duration of abnormality Myoglobin 1-4 hrs 1-2 days CK-MB 4-6 hrs 1-2 days Troponin 4-6 hrs 10-14 days 

o

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angina

 CM-MB is best to detect a new ischemic event a few days after a previous one  Troponin can have false (+) results in renal insufficiency b/c it’s excreted through kidney Tx: aspirin (#1; decreases mortality), morphine, oxygen, nitroglycerin, thrombolytics or angioplasty (greatest decrease in mortality); transfer to ICU; beta-blocker (metoprolol), statin, ACE inhibitor/ARB  Stable angina: aspirin, beta-blocker, nitrates  Unstable angina/NON-STEMI: aspirin, beta blocker, nitrates, heparin, GPIIb/IIIa inhibitors  Non-STEMI refractory to med tx urgent angiography & possible PCI o Indications of medical failure: persistent pain, S3 or CHF developing, worse EKG changes, rising troponin levels  STEMI: aspirin, beta blocker, nitrates, heparin (only after thrombolytics); PCI> thrombolytics  Decrease mortality; not time dependent: beta-blocker (metoprolol), statin, ACE inhibitor/ARB  Prasugrel> clopidogrel if intolerance to aspirin or angioplasty w/ stenting in the past year  Monitor in ICU w/ continuous rhythm monitoring; #1 cause of death w/in days post-MI= ventricular arrhythmia (v. tach or V. Fib)  PCI> thrombolytics; done w/in 90 min of pt arriving to ED w/chest pain  Heparin is used at the time of the procedure  Complications of PCI: rupture of coronary a., restenosis of the vessel, hematoma at entry site (femoral area) o Drug eluting stent (paclitaxel, sirolimus) that inhibits local T cell response decreases risk of restenosis  Thrombolytics (tPA)  Absolute contraindications: major bleeding in GI (melena) or CNS, recent surgery (2 wks), severe HTN (>180/110), nonhemorrhagic stroke w/in last 6 mo  Should be started w/in 30 min of arriving to ED if pt unable to get PCI; can be given w/in 12 hrs of chest pain (best relative risk reduction w/in 2 hrs)  ACE inhibitor/ARB: benefit best in pt w/ ejection fraction unfractionated heparin  No benefit of thrombolytic tx if no ST elevation  Heparin prevent clot from forming/growing further  Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban, eptifibatide): inhibits aggregation of platelets  Decreases mortality in ST depression; used for pt going for angioplasty & stenting  Hospital discharge planning  Post-MI stress test to asses if angiography is needed--> assess if angioplasty or CABG needed o Do not do stress test is symptomatic o Do not do angiography if no signs of reversible myocardial ischemia  Home meds: aspirin, beta blocker, statin, ACE inhibitor o Clopidogrel if intolerant to aspirin or post-stent; ticlopidine if intolerant to both o ACE inhibitor is best for anterior wall infarcts; use ARB if cough  Post-MI sex: no wait time needed; erectile dysfunction may occur d/t anxiety or beta-blocker; do no combine nitrates with sildenafil (both vasodilators hypotension)  Re-start any exercise as tolerated

stable: flow-limiting stenosis by an atherosclerotic plaque; ischemia during exercise unstable: ischemic pain at rest or at lower threshold of exertion or new onset of chest pain  occurs if thrombotic occlusion is complete or undergoes spontaneous lysis  complete occlusion >30 min ischemia o variant angina (prinzmetal’s angina)  d/t temporary spasm of the coronary arteries  RF: smoking (#1)  Episodes often occur in the middle of the night; precipitated by exercise, hyperventilation, emotional stress, cold exposure, cocaine use  Dx: holter monitor (transient ST elevations with return of ST segments to baseline upon resolution of sx)  Tx: calcium channel blockers or nitrates tako-tsubo cardiomyopathy o acute myocardial damage following an emotionally stressful event (loss of loved one, natural disaster) or hypoglycemia o ballooning and L. ventricular dyskinesis chest pain; can cause sudden death o tx: beta blocker and ACE inhibitor acute myocardial infarction o risk factors: smoking, hypercholesterolemia  Non-ST segment elevation MI (NSTEMI): partial occlusion of vessel  STEMI: full vessel occlusion  TIMI risk score  1 pt each: >65 yo, >3 RF for CAD, prior coronary stenosis >50%, ST deviation >1mm (up or down), > anginal events in prior 24hrs, use of aspirin in prior 7 days, increased cardiac biomarkers o risk factors for CAD: Hypertension > 140/90 or on antihypertensives, Cigarette smoking, HDL < 40, Diabetes, Family history of premature CAD (CAD in male first-degree relative, or father less than 55, or female firstdegree relative or mother less than 65).  % risk at 14 days of: all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring urgent revascularization. o Score of 0-1 = 4.7% risk o Score of 2 = 8.3% risk o Score of 3 = 13.2% risk o Score of 4 = 19.9% risk o Score of 5 = 26.2% risk o Score of 6-7 = at least 40.9% risk  GRACE risk score  Variables: Age, HR, systolic BP, creatinine, Killip class, cardiac arrest at admission, elevated cardiac markers, ST segment deviation o sx: retrosternal or epigastric pressure sensation/pain (heavy, squeezing, crushing); tachycardia, HTN, and diaphoresis d/t sympathetic activation; N/V, sense of impending doom; S4 gallop may be seen d/t noncompliance of ischemic heart  pain may radiate to the arm, lower jaw, or neck; persists >30 min an is not relieved by rest  diabetic pts: sudden onset of dyspnea, pulmonary edema, or ventricular arrhythmias  complications:  myocardial pump failurecardiogenic shock or ventricular arrhythmias (V tach or V fib.);  papillary muscle dysfunction or papillary muscle rupture  ventricular septal rupture  rupture of ventricular free wall cardiac tamponade  ventricular aneurysm o occurs days-months after MI o complications: sx of CHF, ventricular arrhythmias, mitral regurg, and/or thrombus formation o dx: ST-segment elevations persists weeks after acute event; echo (kyskinetic wall motion of a portion of the L. ventricle)  Dressler syndrome: immune pericarditis, pleuritis, and fever o Occurs weeks after an MI o pericarditis: pain worse with deep inspiration, improved by leaning forward  EKG: diffuse ST elevation (reciprocal depression in aVR), elevated ESR o Tx: NSAIDs or prednisone  Avoid anticoagulation to prevent development of hemorrhagic pericardial effusion o dx: ECG, cardiac enzymes; submaximal exercise stress testing (stable pts before hospital discharge), LV systolic function via echo  initial ECG findings and cardiac enzymes may be normal, so serial studies are necessary  Creatine phosphokinase-myocardial band (CK-MB) rises within 4-8 hrs, returns to normal by 48-72 hrs  Better marker for reinfarction following a recent MI  Cardiac-specific troponin I (cTnI), cardiac-specific troponin T (CTnT): rise ~6 hrs after infact; cTNI remain elevated for 7-10 days, cTnT for 10-14 days  NSTEMI (subendocardial): ST segment depression  STEMI (transmural): ST segment elevation >0.1mV in 2+ contiguous leads and/or new L. bundle branch block  Tall, positive, hyperacute T waves in the ischemic vascular territory elevation of the ST segments T-wave inversion (hrs to days later) diminished R wave amplitude or Q waves (signified significant myocardial necrosis and replacement by scar tissue) o o

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tx: for any acute coronary event (oxygen, nitroglycerin, aspirin)  (beta-blocker, ACE inhibitors, nitroglycerin, aspirin, heparin, lipid lowering agent)  Ca2+ channel blockers if beta-blocker contraindicated  Morphine if nitroglycerin does not control pain  Clopidogrel, prasurgrel, or ticagrelor if pt can’t be on aspirin or in addition to aspirin following stent placement o Clopidogrel is used for pt with unstable angina/non-ST elevation MI, or post-PCI  Used for 1 mo with bare metal stents, or 1 yr if drug eluting stents to prevent subacute stent thrombosis  Abciximab only for pts where invasive procedures planned (PCI catheter)  Percutaneous coronary intervention (PCI) vs coronary artery bypass surgery (CABG)  CABG: pts with multivessels atherosclerotic stenosis and impaired systolic function  Implantable cardioverter-defibrillator  Used for post-mi pts with severe LV dysfunction (ejection fraction 1mm in 2+ anatomically contiguous leads, no contraindications to thrombolytic therapy, pt 180/110 on >2 readings, bacterial endocarditis, diabetic retinopathy w/recent bleed, severe renal/liver disease, chronic warfarin therapy, stroke/TIA within 12 months  PCI is used for pts with acute STEMI w/in 2-3 hr of sx onset, ideally w/in 90 min; also used for pts when thrombolytics are contraindicated, are hypotensive, or in cardiogenic shock  Non-ST segment elevation MI (NSTEMI) Acute heart failure o Acute= over hours-days; cardiac decompensation with pulmonary edema & low cardiac output; can cause cardiogenic shock Chronic heart failure (CHF) o Chronic= months-years; hear it unable to meet the metabolic needs of the body while maintaining normal ventricular filling pressures o Causes: ischemia, HTN, valvular disease, alcohol abuse, cocaine, thyrotoxicosis  Myocardial injury: Adriamycin, alcohol use, cocaine, ischemic cardiomyopathy (atherosclerotic coronoary artery disease), rheumatic fever, viral myocarditis  Chronic pressure overload: aortic stenosis, HTN  Chronic volume overload: mitral regurgitation  Infiltrative diseases: amyloidosis, hemochromatosis  Chronic tachyarrhythmia or bradyarrhythmia o Sx: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, peripheral/pedal edema, elevated jugular venous pressure, crackles/rales in lungs pulmonary edema  NYHA functional classification (best predictor of mortality)  Class I: no limitation during ordinary physical activity  Class II: slight limitation of physical activity. Develops fatigue or dyspnea with moderate exertion  Class III: marked limitation of physical activity. Even light activity produces sx  Class IV: sx at rest. Any activity causes worsening o Dx: clinical diagnosis; BNP level (normal level excludes CHF as cause of dyspnea); echocardiography (transthoracic best initial; assess ejection fraction distinguishes systolic from diastolic dysfunction, valvular function), most accurate=multiple-gated acquisition scan (MUGA) or nuclear ventriculography;  Determining etiology: EKG, cardiac stress testing, CXR, holter monitor, cardiac catheterization (coronary angiography), CBC (anemia), thyroid function, endomyocardial biopsy (infiltrative disease or infection), swan-ganz right heart cath (distinguish CHF from ARDS)  TEE best at evaluating heart valve function and diameter  Nuclear ventriculography best for wall motion abnormalities  important to assess in pt on doxorubicin chemotherapy o Tx (general): salt restriction, diuretics, digoxin, vasodilators; ACE inhibitors, beta-blockers  f/u echo yearly o Diastolic dysfunction (backward failure)= impaired diastolic relaxation and decreased ventricular compliance o

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Sx: dyspnea, peripheral edema, ascites Dx: EF>40% Tx: beta blockers, diuretics; ACE inhibitors/ARB, hydralazine  NOT helpful: digoxin, spironolactone o Systolic dysfunction (forward failure)= low CO d/t impaired heart contraction (low ejection fraction)  #1 cause of CHF with systolic dysfunction is ischemic cardiomyopathy d/t coronary atherosclerosis or HTN, valve disease; alcohol, postviral (idiopathic) myocarditis, radiation, Adriamycin (doxorubicin), chagas disease, hemochromatosis (also restrictive cardiomyopathy), thyroid disease, peripartum cardiomyopathy, thiamine deficiency  Sx: fatigue, lethargy, hypotension  Dx: EF 100,4, vascular phenomena (arterial or septic pulmonary emboli, mycotic aneurysm, Janeway lesions), immunologic phenomena (GN, osler nodes, roth spots, positive rheumatoid factor), positive blood cultures not meeting major criteria o Tx: antibiotics for 4-6 wks  Best empiric: vancomycin + gentamicin  Vanco trough goal 15-20  Specific bugs  Strep penicillin G  staph aureus nafcillin + gentamicin; oxacillin, nafcillin, or cefazolin  staph epi or resistant staph vancomycin + gentamicin  MRSA or coagulase negative staph vancomycin  Viridans strep ceftriazone 4 wks  Enterococci ampicillin + gentamicin  HACEK organisms ceftriaxone  Fungal amphotericin + valve replacement  if prosthetic valve with staph infection add rifampin  If bugs resistant to treatment add aminoglycoside and increase duration of treatment  Valve excisions & replacement as needed: persistent infection, recurrent emboli, refractory to medical treatment  Fungal endocarditis: large friable vegetations w/ high risk of embolization  Dental prophylaxis: If heart defect + risk of bacteremia  Heart defects: prosthetic heart valve, previous infectious endocarditis, unrepaired cyanotic heart disease, heart transplant with abnormal valves causing regurg  Risk of bacteremia: dental work with blood, respiratory tract surgery  Amoxicillin; alternatives are ampicillin, cephalosporin, clindamycin, azithromycin, clarithromycin  Colonoscopy for strep bovis endocarditis d/t high risk of colon cancer or polyp allowing seeding of organism  Surgery if: CHF, ruptured valve, chordae tendinae, prosthetic vavle, fungal infections, abscess, AV block, recurrent emboli while on antibiotics acute pericarditis o acute inflammation of the parietal pericardium and superficial myocardium o causes: idiopathic, infectious, vasculitis (autoimmune, post-radiation), HSR/immune (dressler syndrome), disease of surrounding structure (ex. Transmural MI), metabolic (uremic, gaucher), trauma, neoplasm (breast, lung, lymph) o sx: nonexertional pleuritic chest pain (sharp, substernal, worse with inspiration & lying down; relieved by sitting forward; not relieved by nitroglycerin)  pericardial friction rub (harsh, high pitched, scratchy; best @ L. sternal border, variable intensity)  ECG: diffuse ST-segment elevation & PR depression (opposite in aVR and V1), low voltage diffusely o Complications: pericardial effusion, bleeding, tamponade, constrictive pericarditis o Tx:  Viral or inflammatory: aspirin or NSAIDs (indomethacin) for pain relief or ibuprofen+ colchicine; steroids for refractory sx  Dialysis for uremic pericarditis constrictive pericarditis o inflammation w/ granulation tissue forms a thickened fibrotic adherent sac that gradually contracts impairs diastolic filling o causes: radiation tx, cardiac surgery, or any cause of acute pericarditis (viral, uremia) o sx: chronic & slowly progressive weakness, fatigue, exertional dyspnea, pericardial knock (high-pitch early diastolic sound just after aortic valve closure), elevated JVP during inspiration distention of neck veins (Kussmaul sign)  appears like R. sided heart failure: chronic lower-extremity edema, hepatomegaly, ascites  ECG: low voltage o dx: CXR (cardiomegaly, calcified pericardium), MRI (shows thickening of pericardium), endomyocardial biopsy may be necessary o tx: resection of the pericardium Cardiac effusion/ tamponade o Tamponade: increased pressure w/in the pericardial space d/t accumulating effusion Impedes diastolic filling of the heart decreased CO cardiovascular collapse  If the fluid accumulates slowly, the sac can hold up to 2000 mL before causing problems; if it accumulates rapidly 10 mmHg with inspiration), hypotension, chest pain, dyspnea, jugular venous distention, distant cardiac sounds  Beck Triad (acute tamponade): hypotension, elevated JVP, small quiet heart

 ECG: low voltage diffusely, electrical alternans Diff dx: pericardial effusion causing cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy dx: CXR (cardiac enlargement) Tx: echo-guided pericardiocentesis or surgical pericardial window  Give IV fluids for supportive care while waiting for procedure (pts are preload dependent) aortic dissection o tear of the intima that allows longitudinal dissection false lumen or channel for blood flow  type A: involves ascending aorta or proximal aorta  type B: involves anything but the ascending aorta, usually starts distal to the L. subclavian artery branch  2/3 start in the ascending aorta a few cm above the aortic valve  intraluminal flap can occlude branch arteries; retrograde rupture into the pericardial sac cardiac tamponade; rupture into pleural space exsanguination; acute aortic regurg fulminant heart failure o risk factors: cystic degenerative of elastic media (Marfan, Ehlers-Danlos), HTN, aortic valve abnormalities (stenosis, bicuspid valve), coarctation of the aorta, pregnancy, atherosclerotic disease, cardiac sx or cath. o sx: sudden severe chest pain (sharp/tearing/ripping, radiates to back, not relieved by nitroglycerin)  complications: horner syndrome (compression of superior cervical ganglion), superior vena cava syndrome (d/t compression), hemopericardium, pericardial tamponade, aortic regurg, bowel ischemia, hematuria, HTN, hemiplegia (carotid a. dissection) o dx: CXR (widened mediastinum), unequal pulses or BP in the arms (d/t dissection along brachiocephalic artery), a new murmur of aortic insufficiency (early diastolic murmur; if the dissection near the aortic valve); confirm with TEE/CT with contrast/CTA/MRI o tx:  type A urgent surgery  type B medical management 1st (decrease MAP via vasodilation with sodium nitroprusside + beta blocker; or labetalol)  note: anticoagulation & thrombolytic therapy are contraindicated aortic aneurysm (dissecting hematoma) o risk factors: smoking, atherosclerosis/peripheral vascular disease, HTN o thoracic o abdominal aortic aneurysm (AAA)  dilation >1.5x normal (>3cm diameter); most occur below the renal a.  sx: midline pulsatile mass  dx: 1x screening via ultrasound is recommended for men 65-75 yo who have ever smoked  tx:  5.5 cm surgical excision of affected aorta with ducron graft replacement shock o cardiogenic shock: hypotension (160/100) o essential HTN (no identifiable cause) o causes of secondary HTN: renal/renovascular disease, endocrine (hyperaldosteronism, thyroid or parathyroid dz, cushing’s syndrome, pheochromocytoma, hyperthyroidism, acromegaly), drugs (OCPs, decongestants, estrogen, appetite suppressants, chronic steroids, TCAs, NSAIDs), coractation of the aorta, cocaine & other stimulants, sleep apnea o hypertensive emergency: HTN a/w acute end-organ damage (encephalopathy, MI, aortic dissection, pulmonary edema secondary to acute LV failure) o hypertensive urgency: asymptomatic severe HTN  tx: start anti-HTN tx, then recheck BP in 24-48 hrs (outpt tx for asymptomatic HTN); goal is to decrease BP in 24-48 hrs o increased systemic vascular resistance (afterload) concentric LVH; HTN also accelerates atherosclerosis  most damaging to the heart, eyes, CNS, kidneys  LVH w/ S4, MI, CHF, aortic dissection  retinal changes: arteriovenous necking, cotton wool spots=infarction of the nerve fiber layer in the retina, papilledema  intracranial hemorrhage, other types of stroke  nephrosclerosis (arteriosclerosis of afferent and efferent arterioles and glomerulus), decreased GFR o Dx: at least 2 readings >4 wks apart; evaluate for end-organ damage & cardiovascular risk factors  Assess for end organ damage & cardiovascular RFs: UA (protein, blood, glucose, microscopic exam), Hgb or HCT, WBC, serum K+, Ca2+, PO4, creatinine BUN, fasting glucose, lipid panel, ECG, TSH  PE: auscultate for bruits, fundoscopic exam, palpitation for kidney masses or enlarged aorta, look for edema & perfusion of legs, neuro exam  A cuff that is too small will falsely elevate BP  If pt is diabetic also check for microalbuminuria o Tx: pre-HTN (lifestyle changes), stage 1 (thiazide diuretic #1 choice, beta blocker next best; ACE inhibitor best for diabetes or CHF), stage 2 (2 drug tx; thiazide + beta blocker first choice)  Modify lifestyle: reduce salt intake, lose weight, avoid excessive alcohol consumption (has pressor action), exercise regularly, lowsaturated fat diet, stress management  Drug options: diuretic, antiadrenergic, vasodilator, ACE inhibitor, angiotensin receptor antagonist, Calcium channel antagonist  Beta blockers and thiazide diuretics decrease M &M, so they are 1st line agents o Thiazide diuretics (best for black pts w/o diabetes) o beta-blockers (decrease HR, CO, renin release) o avoid beta-blockers in hypertensive pts with CHF +volume overload (use ACE inhibitor instead to decrease afterload) o o o

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dyslipidemia o normal levels: total cholesterol 160

Low risk pt (190

dx: routine screening of average risk pt every 5 yrs (starting 35 yo M, 45 yo F; or age 20 if multiple CAD risk factors or DM) tx: lifestyle changes (diet low in saturation fat & cholesterol, exercise), lipid lowering drugs  diet: saturated fat 100.4 for >1hr  neutropenia: Abs neutrophil count 3 days add in vancomycin  if fever persists 5-7 days after vanco add antifungal (fluconazole or amphotericin B)  cancer pt should be immunized against pneumococcus and influenza  MMR and varicella zoster vaccines are contraindicated b/c they contain live virus  G-CSF (granulocyte colony stimulating factor) stimulates bone marrow to produce neutrophils; given prophylactically after chemo to reduce neutropenia lungs  physiology o VE=VT * f  Minute ventilation depends on tidal volume and respiratory frequency  Restrictive lung diseases decrease tidal volume compensatory increased frequency  Ex: idiopathic pulmonary fibrosis, obesity, kyphoscoliosis, pleural effusion, neuromuscular disease (myasthenia gravis, ALS, myopathy) o Oxygen/hemoglobin curve  P90%=60 mmHg, P75= 40 mmHg, P50=26 mmHg  Mental status changes occur below the P50 level o Hypoxemia= PaO2/FiO2 30 #1 sign of impending lung failure  Other signs of lung failure: use of accessory muscles (oblique mm. during exhalation; scalene, intercostals) o Pt needs to be on supplemental oxygen if PO2 40, inability to speak d/t dyspnea, accessory muscle use with fatigue despite maximal treatment, confusion, restlessness, agitation, lethargy, rising PaCO2, extreme hypoxemia  tx: intubation with ventilatory support o complications of chronic hypoxemia: pulmonary HTN, secondary erythrocytosis, exercise limitation, impaired mental functioning o dx: spirometry (FEV10.6, pleural fluid LDH >2/3 upper limit of normal for serum LDH  Pleural fluid LDH correlates with degree of pleural inflammation o Transudate: d/t alteration of oncotic forces; usually with low protein and LDH levels  Causes:  increased hydrostatic pressure: CHF or constrictive pericarditis  decreased oncotic pressure: nephrotic syndrome, cirrhosis w/ ascites (hepatic hydrothorax), malignancy, PE, hypothyroidism (myxedema)  decreased intrapleural pressure: atelectasis o Sx: diminished breath sound, dullness to percussion o Dx: CXR, diagnostic thoracentesis  Indications for thoracentesis: uneven pleural effusion or unilateral pleural effusion, evidence of infection (productive cough, fever, pleurisy), alarming signs (significant weight loss, hemoptysis, hypoxia), need to evaluate underlying lung parenchyma  Thoracentesis not done for pt with known CHF with B/L effusions (unless resistant to diuretics) or if effusion 500ml usually obscures the whole hemidiaphragm Fluid appearance Causes Clear yellow Transudative; CHF, cirrhosis, nephrotic syndrome Frank pus Infectious process, empyema Bloody Cause depends on HCT level in fluid *50% hemothorax (trauma, malignancy, PE w/infarction) Milky, turbid Chylothorax; triglycerides >110 mg/dL d/t disruption of thoracic duct, cholesterol effusion Dark green biliothorax o tx: therapeutic thoracentesis for effusion that is significant in size w/ pt dyspneic at rest (safely remove up to 1500 mL), tube drainage for “complicated parapneumonic effusion” to prevent fibrous peels; 1 wk trial of antibiotics if pt does not meet criteria for immediate drainage  indications for chest tube drainage (fluid characteristics): empyema, positive gram stain of fluid, presence of loculations, pH30, BP 10 mm, close contacts of TB pt or HIV pt >5mm is positive  Primary TB: ghon complex= calcified primary focus, Ranke’s complex= ghon complex+ calcified hilar lymph node  Secondary TB (reactivation) occurs in the most oxygenated portion of the lungs (apical/posterior segments)  AFB culture takes 4-8 wks on regular medium or 2-3 wks on liquid medium  Report to health department o Tx: 4 drug antibiotics (isoniazid+ rifampin + pyrazinamide + pyridoxine; alternatives include amikacin, ethambutol or streptomycin) for 2 mo, then 2 drug antibiotics for 4 more months (isoniazid + rifampin)  use pyridoxine (Vit B6) to prevent peripheral neuropathy  SE of treatment: hepatitis, hyperuricemia, thrombocytopenia  Note: oral OCPs decrease drug levels use barrier contraceptive during TB treatment  First 2 wks of treatment in respiratory isolation in hospital; then AFB every 8hrs until 3x (-), then d/c home to continue treatment for 6 mo  Prophylaxis for latent (primary) TB: 6-9 months of isoniazid +/- pyridoxine Lung cancer o #1 cause of cancer death in US o risk factors: smoking, radiation, environmental toxins (asbestos, radon)  asbestos can cause squamous cell, adenocarcinoma, or mesothelioma o sx: chronic nonproductive cough, hemoptysis, fatigue, decreased appetite, unintentional weight loss  scattered rhonchi, finger clubbing  phrenic nerve invasion diaphragmatic paralysis  laryngeal nerve invasion hoarseness  horner syndrome: ptosis, miosis, anhidrosis  occurs with apical/Pancoast tumor compression of superior cervical ganglion lack of sympathetic innervation  superior vena cava syndrome: obstruction of venous drainage edema of face and arm, formation of collateral veins in upper chest o small cell (oat cell) cancer  neuroendocrine origin; central location; early metastasis  causes paraneoplastic syndromes: SIADH, ectopic production of ACTH, Cushing syndrome, Eaton-lambert syndrome, peripheral neuropathy  lambert-eaton syndrome: d/t autoantibodies against voltage gated calcium channels in the presynaptic motor nerve terminal defective release of acetylcholine proximal muscle weakness, absent reflexes o tx: plasmapheresis, immunosuppressive drug therapy o non-small cell cancer: squamous, adenocarcinoma, large cell  squamous cell  central/hilar location, local extension instead of metastasis bronchial obstruction atelectasis, pneumonia  most likely to cavitate  can produce PTH-like hormone hypercalcemia  adenocarcinoma  peripheral location; metastasis early to bone/adrenal/CNS o a/w pulmonary scars/fibrosis & less related to smoking (most common pt is young female nonsmoker) o can cause thrombophlebitis  large cell  peripheral location; metastasis to CNS & mediastinum Superior vena cava syndrome, laryngeal n. paralysis hoarseness o dx: CXR, tissue dx, staging  “popcorn” or “bull’s eye” calcification of a solitary pulmonary nodule suggests a benign process; lack of calcification increases risk of malignancy  risk of malignancy increases with size (>2.5 is highly suspicious)  solitary nodules  in low risk pt (1cm, positive axillary lymph nodes  Tamoxifen prophylaxis for pts with multiple 1st degree relative with breast cancer GI pathology  Oral candidiasis o Tx: nystatin  Zenker diverticulum o Outpouching of pharyngeal constrictor mm. o Sx: dysphagia, halitosis, regurg of food particles aspiration pneumonia o Dx: barium study  avoid endoscopy or NG tube d/t risk of perforation o tx: surgical repair  Vascular rings & webs o Dx: barium study o Congenital anomaly; aortic arch vessels encircle the trachea and/or esophagus o Schatzk ring: peptic stricture of distal esophagus  Intermittent dysphagia to solids  Tx: pneumatic dilation o Plummer-vinson syndrome: located in proximal esophagus  a/w iron deficiency anemia; can transform to SCC  Sx: dysphagia  Tx: iron replacement  Scleroderma o Sx: reflux sx, progressive systemic sclerosis o Dx: manometry (inability to close LES) o Tx: PPI  Diffuse esophageal spasm or nutcracker esophagus o a/w emotional factors, functional GI disorders; may be precipitated by cold liquids o Sx: intermittent chest pain not related to exertion & dysphagia

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Dx: manometric studies (high amplitude peristaltic contractions; normal LES response; most accurate), esophagogram (corkscrew esophagus during spasm); r/o atypical coronary a. spasm or unstable angina (ECG, stress testing) Tx: antispasmodics (calcium channel blockers, nitrates), dietary modulation, psychiatric counseling

o Achalasia o Esophageal motility disorder; high lower esophageal sphincter tone o Sx: dysphagia to solids & liquids o Dx: barium swallow (bird beak sign at GE junction, dilation of the proximal esophagus), manometry (absent peristalsis; most accurate), CXR (widening of esophagus), upper endoscopy if alarming sx for cancer (weight loss anemia, blood in stool)  Histology: hypertrophied inner circular muscles with absent or degenerating neurons (ganglion cells( in the myenteric plexuses  air-fluid level seen on CT (incidental finding) o tx: mechanical dilations: pneumatic dilation, botulinum toxin injection (goof for 3-6mo), surgical sectional or myotomy esophageal varices o d/t portal HTN o sx: signs of liver disease (spider angioma, caput medusa, palmar erythema, asterixis), splenomegaly; vomiting blood +/- black stool o Dx: check vitals, hematocrit, platelet count, coag panel  Orthostasis: >10 increase in HR or >20 drop in BP from lying down to sitting up/standing o Tx: fluid resuscitation (#1), NG tube, octreotide, FFP, PRBCs, platelets, IV PPI, endoscopy (cautery, variceal band ligation or sclerotherapy), surgery  if hemorrhage: IV fluid resuscitation, consider intubation if ongoing hematemesis, prophylactic antibiotics, type & screen for possible transfusion, Somatostatin analog (octreotide)  Octreotide used when melena w/o hematemesis, with NG tube showing red blood  Decreases portal HTN  PRBCs if HCT 5 yrs GERD o Dx: biopsy o Tx:  Barrett (metaplasia) w/o dysphagia: PPI; f/u endoscopy every 2-3 yo  Low grade dysplasia: PPI; f/u endoscopy every 6-12 mo  High grade dysplasia: ablation via endoscopy (photodynamic therapy, radiofrequency ablation) esophageal cancer o squamous cell CA  usually occurs in the upper & middle esophagus  RF: alcohol, tobacco use, diet (nitrosamine, betel nuts, hot food/drinks, pickled foods), HPV, achalasia, Plummer-Vinson syndrome, caustic ingestions, nasopharyngeal carcinoma, dietary deficiency of beta-carotene/b1/zinc/zeleinum o Adenocarcinoma  Usually occurs in the distal 1/3 of the esophagus  RF: GERD (>20 yrs), Barrett’s esophagus (intestinal metaplasia of the lower esophagus), obesity, high dietary calorie & fat intake, smoking o Sx: dysphagia (solids liquids), weight loss, anorexia, odynophagia (mediastinal invasin), hematemesis, hoarse voice (recurrent laryngeal N. involvement), aspiration pneumonia, respiratory sx (involves tracheobronchial tree), tracheoesophageal or bronchoesophageal fistula, chest pain o Dx: barium swallow, upper endoscopy w/ biopsy, transesophageal u/s to determine penetration (staging), metastatic work-up (CT chest/abdomen, CXR, bone scan) o Staging  I: invades lamina propria or submucosa; nodes (-)  IIa: invades muscularis propria or adventitia; nodes (-)  IIb: invades up to muscularis propria; regional nodes (+)  III: invades adventitia (positive regional nodes) or tumor invades adjacent structures (positive or negative nodes)  IV: distant metastasis o Tx: neoadjuvant chemo+ radiation, esophagectomy (stage 0,1,2a), otherwise palliative tx (stent placement for dysphagia) Epigastric pain (general info) o Causes: non-ulcer dyspepsia (#1), gastric ulcer (worse with food; weight loss), duodenal ulcer (pain better with food), cancer (weight loss), pancreatitis (tenderness in PE), GERD (bad taste, cough, hoarse), gastroparesis (DM, bloating) o Dx: endoscopy o Tx: PPI (-prazole) >H2 blocker (-tidine), liquid antacids; misoprostol (prostaglandin analog; good for NSAID induced gastric damage, obsolete d/t PPI efficacy) Dyspepsia o Pain in the upper abdomen (esp. midline); can be a/w fullness, early satiety, bloating, nausea o Functional (non-ulcer) dyspepsia: sx >12 wks w/o evidence of ulcer on endoscopy  Dx of exclusion  If 55 yo or >45 yo with new dyspepsia, pt with cancer sx (weight loss, anemia, obstructive sx, dysphagia, etc.), pt that failed to respond to tx for PUD gastritis o gastritis= inflammation or erosion of gastric lining o causes: alcohol, NSAIDs, H.pylori, protal HTN, stress (burns, trauma, sepsis, multiorgan failure, mechanical ventilation, coagulopathy)  atropic gastritis a/w B12 deficiency o sx: painless GI bleeding (coffee ground emesis or Heme positive stool=5-10 mL blood, melena= 50-100 mL blood) acute erosive gastritis: severe hemorrhagic erosive lesion after exposure to injurious agents (aspirin, NSAIDs, alcohol)  hematemesis & abdominal pain o dx: upper endoscopy, H. Pylori testing (endoscopic biopsy, serology, urea breath test, or stool antigen) o tx: PPI, misoprostol for NSAID-induced (rarely used) Peptic ulcer disease (gastric or duodenal ulcers) o Causes: H. pylori infection (gram (-) bacteria; #1), NSAIDs (#2), zollinger Ellison syndrome (gastrinoma), stress (burns, head trauma), crohn disease, gastric CA  H. Pylori increases risk of: gastric adenocarcinoma, MALToma, chronic active gastritis  Zollinger Ellison syndrome: gastrin secreting tumor (usually pancreatic; >1000 pg/mL) increased acid production  Alcohol and tobacco delay healing o Sx: recurrent epigastric pain (dull, sore, gnawing)  Gastric ulcers  Sx: pain worse with food weight loss  Duodenal ulcers  Sx: burning pain that occurs on an empty stomach (b/c acid stimulation lasts 2-5 hrs after meal); pain relieved by antacids or eating o Complications: cancer, hemorrhage, perforation, gastric outlet obstruction o Dx: endoscopy (most accurate; biopsy for H. Pylori and cancer), or upper GI barium study; dx H.pylori (urease breath test, biopsy, stool H.pylori antigen test, or H. Pylori antibody test) o Tx:  If NSAID induced H2 blocker or PPI  H. Pylori PPI + clarithromycin + amoxicillin; f/u in 4-8 wks  If no response to tx, repeat H. pylori testing; if still (+) PPI+ 2 new antibiotics (metronidazole + tetracycline) + bismuth  If gastric ulcer, routinely repeat endoscopy to confirm healing  If not healing biopsy to r/o cancer 

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 Determine if tx failure d/t nonadherence to meds, alcohol, tobacco, or NSAID use Gastric cancer o Sx: dysphagia (cardiac region), persistent vomiting (blocking pyloric channel), early satiety (mass effect), pain d/t ulcer formation, bleeding anemia, weight loss o Dx: endoscopy Pancreatitis o Causes: alcohol, biliary tract disease (gallstones, biliary sludge=microlithiasis, sphincter of oddi dysfunction, ductal obstruction), ERCP, increased triglycerides >1000 mg/dL, hypercalcemia, infection (mumps, CMV), abdominal trauma, drugs (thiazides, pentamine, furosemide, sulfonamides, azathioprine, L-asparaginase, didanosine), cystic fibrosis, scorpion sting o Sx: acute epigastric abdominal pain radiating to the back, N/V; severe disease has hypotension & fever  Complications: phlegmon (solid mass of inflamed pancreas w/ patchy areas of necrosis), pancreatic necrosis, pancreatic abscess (2-3 wk later), pancreatic pseudocyst (inflammatory fluid + pancreatic secretions w/o an epithelial lining), vitamin B12 deficiency (anemia, hypersegmented neutrophils, neuropathy)  Suspect complications if peristent increased amylase, abdominal pain, mass, or fever  Pseudocyst spontaneously resolves w/in 6 wks if 3 increases mortality  Initial: age >55, WBC >16, glucose >200, LDH >350, AST >250  w/in 48 hrs of admit: HCT decrease >10 pts, BUN increase >5mg/dL after IV hydration, arterial PO2 6L o tx: “pancreatic rest” (NPO, NG suction if ileus & bowel distention or protracted vomiting), narcotic analgesia (meperidine), IV fluids, enzyme replacement, PPI  if >30% necrosis on CT or MRI antibiotics (imipenem) + needle biopsy to determine if infected  if infected surgical debridement  ERCP as need to place stents, remove obstructing stones and dilate strictures  most common cause of early death = hypovolemic shock Pancreatic cancer o 5th leading cause of cancer death; peak incidence 60 yo, 2/3 cases >65 yo o risk factors: male sex, age >50, black, smoking (#1), chronic pancreatitis, long standing diabetes, obesity, familial pancreatitis, family hx of pancreatic cancer o tx: neoadjuvant chemotherapy + pancreaticoduodenectomy (Whipple procedure); or palliative care (includes pancreatic & common bile duct stenting to relieve obstruction)  mean survival ~9 mo o adenocarcinoma  sx: painless jaundice d/t biliary obstruction (if tumor at head of pancreas)  Sx: painless jaundice, pruritus, weight loss, light-colored stools  Dx: CT scan, LRTs (cholestasis elevated alkaline phosphatase with elevated total & conjugated bilirubin) o Zollinger Ellison syndrome (gastrinoma)  Sx: ulcers (large >1-2cm, multiple, distal in the duodenum, recurrent after H.pylori eradication), diarrhea d/t acid inactivating lipase  Hypercalcemia if a/w MEN  Dx: endoscopy (confirm ulcers), fasting serum gastrin level (>1000 pg/mL); if inconclusive secretin stimulation test; if still inconclusive-> calcium infusion study (increases serum gastrin in pt with gastrinoma), serum chromogranin A (marker of neuroendocrine tumor) can confirm in difficult cases  Elevated gastrin level despite already high gastric acid output; persistent despite injecting secretin  Measure gastri pH to exclude the possibility of secondary hypergastrinemia d/t achlorhydria  r/o metastatic disease with Somatostatin receptor scintigraphy (nuclear octreotide scan) + endoscopic U/S  tx: surgical resection if focal; lifelong PPI if metastatic Tropical sprue o Hx of livingin in endemic areas (peurto rico) for ?1month o Sx: chronic fatty diarrhea, malabsorption of nutrients (vit B-12 & folic acid  megaloblastic anemia, glossitis, cheilosis, proterberant abdomen, allor, pedal edema), cramps, gas, fatigue, progressive weight loss  Hyperactive bowel sounds, borborygmi o Dx: small intestinal mucosal biopsy (blunting of villi, infiltration of chronic inflammatory celling including lymphocytes, plasma cella, and eosinophils) o Tx: TMP/SMX Celiac disease/sprue o Autoimmune intolerance to gluten; Intestinal villous atrophy o Sx: weight loss, bloating, flatulence, malnutrition (steatorrhea, deficiency of fat soluble vitamins A,D,E,K), dermatitis herpetiformis, iron deficiency anemia  Vit d deficiency calcium deficiency, osteoporosis  Vit K deficiency bleeding, easy bruising o Dx: anti-tissue transglutaminase, IgA antigliadin Ab, anti-endomysial Ab; small bowel biopsy (most accurate; flattening of villi), D-xylose test (measure urine excretion of sugar after 5 hrs; tests the gut absorption of this simple sugar) o Tx: gluten-free diet (wheat, oat, rye, barley) Lactose intolerance o Sx: increased stool osmolality  No weight loss or vitamin malabsorption o Dx: clinical after removing milk products for 1 days o Tx: avoid milk products except yogurt; oral lactase replacement Whipple disease

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o Sx: arthralgias, ocular findings, neuro changes (dementia, seizures), fever, lymphadenopathy o Tx: ceftriaxone, TMP/SMX Inflammatory bowel disease (IBD) o Bimodal age distribution of presentation onset (20-30, 60) o Sx: anemia d/t iron deficiency or chronic GI blood loss; fatigue, weight loss, chronic ab pain, diarrhea, decreased weight, blood in stool, fever  Extraintestinal manifestations: arthralgias, uveitis, iritis, erythema nodosum, pyoderma gangrenosum, sclerosing cholangitis, increased risk of colon cancer, anemia o Dx: endoscopy, barium studies for small bowel  Screen for colon cancer after 8-10 yrs of colonic involvement with colonoscopy every 1-2 yrs o Tx:  acute exacerbaction steroids  chronic: 5-ASA derivatives (mesalamine) Asacol of UC, Rowasa fo UC limited to rectum, Pentasa for crohn  azathioprine and 6-MP (mercaptopurine) to wean pt off steroids  perianal disease ciprofloxacin and metronidazole  fistulae unresponsive to other treatment anti-TNF (infliximab); no response surgery  UC surgical resection curative  Crohn surgical resection only for obstruction o Crohn’s disease  Sx: transmural, skip lesions anywhere from mouth to anus; granulomatous; aphthous ulcers in mouth, weight loss, vague abdominal pain, linear ulcers with a “cobblestone” pattern  Complications: fistulas, abscess, obstruction (d/t stricture), non-healing ulcers  Extraintestinal sx: erythema nodosum, arthritis (polyarticular, asymmetric), ankylosing spondylitis, uveitis (photophobia, blurred vision, headache), cholelithiasis, fatty liver, nephrolithiasis (after small bowel resection or ileostomy) o Cholelithiasis d/t ileal bile salt malabsorption cholesterol rich lithogenic bile  Dx: abdominal CT, small bowel fluoroscopic study (“string sign” on barium x-ray), or endoscopy  Antisaccharomyces cerevesiae antibody (ASCA)  Tx: surgery used only for complications o Ulcerative colitis  Colitis=inflammation of the intestines (typically large bowel)  Diff dx: ischemic, infectious, radiation, IBD  Sx: lesions start in the rectum and proceed proximally; continuous only in the submucosa or mucosa; crypt abscesses, crampy abdominal pain, weight loss, low volume bloody mucoid diarrhea, tenesmus; hx of similar sx  Complication: toxic megacolon, hemorrhage o Toxica megacolon: >6cm diameter dilation, fever, increased WBCs, tachycardia, hypotension or altered mental status  Extraintestinal sx: erythema nodosum, pyoderma gangrenosum, uveitis, fatty liver, primary sclerosing cholangitis  Dx: stool samples to r/o infectious causes, colonoscopy w/ biopsy; “lead pipe” colon on barium x-ray  Infectious causes of bloody diarrhea: entamoeba histolytica, salmonella, shigella, camplobacter, c. diff, e.coli  Annual or biennial colonoscopy starting 8 yr after dx of pancolitis  Antineutrophil cytoplasmic antibody (ANCA)  Tx:  Mild-moderate & maintenance: sulfasalazine & other ASA compounds (mesalamine)  Moderate-severe: corticosteroids (only used until remission, then tapered down over 6-8 wks)  Refractory disease;: immune modulators (6-MP, azathioprine, methotrexate, TNF antibody (infliximab)) o Infliximab SE: increased risk of infection (esp. TB reactivation)  Total colectomy is curative; done for carcinoma or dysplasia, toxic megacolon, perforation  Toxic megacolon: NPO, NG suction, IV fluids, IV antibiotics, IV corticosteroids, surgical consult; total colectomy if refractory to medical tx Irritable bowel syndrome (IBS) o Sx: chronic dysmotility (bloating, cramping), pain (relieved by defecation or change in bowel movement, decreased at night), looser and more frequent stool with the onset of pain (intermittent diarrhea), constipation, passage of mucus, sense of incomplete emptying; extraintestinal sx (depression, sexual dysfunction, urinary changes) o Dx of exclusion o Tx: antispasmodic (dicyclomine=Bentyl, or hyoscyamine), TCA antidepressant (amitriptyline), lubiprostone (chloride channel activator to increase bowel movement frequency), protonix (pantoprazole), colase; stress reduction techniques (meditation), maintain food journal of irritants/relievers and for nutritional intake; increase fiber in diet  Constipation: Linaclotide (linzess; guanylate cyclase-C agonist)  diarrhea: antimotility agent (loperamide) Bowel ischemia o RFs: severe atherosclerotic disease, atrial fibrillation, hypotension o Sx: anion gap metabolic acidosis, acute onset abdominal pain, nausea, hypoactive bowel sounds, abdominal tenderness; blood diarrhea w/in 12-24 hrs ischemic colitis o Splenic flexure most commonly involved (watershed areas) Appendicitis o The most common cause of acute abdomen at any age is appendicitis Diverticulosis o Herniation of mucosa and submucosa through a weakness in the muscle lining of the colon (a/w meat-filled diet); pseudodiverticula b/c not all layers  Complications: acute diverticulitis, hemorrhage, obstruction; may have chronic sx similar to IBS (pain aggravated by eating, relief with defecation; bloating, constipation or diarrhea), LLQ pain  Dx: colonoscopy (most accurate) or barium studies o Diverticular hemorrhage is one of the most common causes of lower GI bleeding in pt>40 yo  Sx: painless passage of bright red blood; abrupt in onset & resolution

Tx: usually self-limited; give IV fluids and transufion as needed; if recurrent or chornic bleeding resection of affected colon segment o Diverticulitis  Hx of constipation and low fiber diet; d/t inspissated stool particles (fecalith) obstructing diverticula bacterial overgrowth  Sx: LLQ pain (or RLQ if cecum), fever, N/V, hypoactive bowel sounds, constipation; may have peritoneal irritation  Complications  Abscess: tender mass on exam, persistent fever & leukocytosis after treatment o Tx: conservative management if small, CT-guided percutaneous drainage or surgical drainage for large abscesses  Fistulas: majority are colovesical w/ male predominance; others are colovaginal, coloenteric, colouterine, coloureteral; rarely colocutaneous o Tx: single stage surgery with fistula closure and primary anastomosis o If colovesical fistula pneumaturia or fecaluria  Obstruction: ileus or pseudo-obstruction more likely than complete  Strictures: d/t recurrent diverticulitis; slow onset obstruction o Tx: trial of endoscopic therapy (bougienage, balloon, laser, electrocautery, or blunt dilating endoscope)  Stages:  I: small confined pericolic abscess  II: distant abscess (retroperitoneal or pelvic)  III: generalized suppurative peritonitis from rupture of abscess (non-communication w/ bowel lumen)  IV: fecal peritonitis d/t free communicating perforation  Differential dx: diverticulitis, painful diverticular disease w/o diverticulitis, acute appendicitis, Crohn disease, colon cancer, ischemic colitis, irritable bowel syndrome, GYN issues (ruptured ovarian cyst, endometriosis, ectopic pregnancy, PID)  Dx: CXR & ab x-ray (ID pneumoperitoneum, assess cardiopulmonary status), CBC (increased WBCs), CT scan (evaluate for abscess, fistula, perforation; pericolic fat stranding, bowel wall thickening >4mm)  Contrast enema is contraindicated; Endoscopy contraindicated during the acute phase o Endoscopy should be done >6wk after resolution of acute attack to exclude neoplasm  Tx:  Out-pt: broad spectrum antibiotics (TMP-SMX ,or ciprofloxacin + metronidazole, or clindamycin + gentamicin), clear liquid diet  In-pt: IV fluids, electrolyte balance, NPO, gradually advance diet, IV broad spectrum antibiotics (ampicillin+ aminoglycoside + metronidazole, or ampicillin-sulbactam, or ticarcillin-clavulanate; imipenem or meropenem used for severe/complicated case) o In-patient if: narcotics needed for pain, peritoneal signs, comorbid illness, inability to tolerate PO intake, complications that may require surgery  Emergent surgery: generalized peritonitis, uncontrolled sepsis, perforation, clinical deterioration  Elective resection: fistula, recurrent diverticulitis (>2 episodes requiring hospitalization) Polyposis syndromes o Familial adenomatous polyposis: defect in APC gene; thousands of polyps o Peutz-Jeghers syndrome  Multiple hamartomatous polyps, melanotic spots on lips & skin; increased frequency of breast/gonadal/pancreatic CA o Gardener syndrome: colon CA + (osteomas, desmoid tumors, other soft tissue tumors) o Turcot syndrome: colon CA + CNS malignancy o Juvenile polyposis: colon CA + multiple hamartomatous polyps Colon cancer o Screening: colonoscopy > barium enema, CT colonoscopy, capsule endoscopy > fecal occult blood testing  Routine every 10 yrs starting age 50  1 family hx: start 10 yrs before age of onset of family member’s cancer or by age 40  HNPCC: start age 25 with colonoscopy every 1-2 yrs  FAP: start sigmoidoscopy age 12 every year  Previous single adenomatous polyp: colonoscopy every 3-5 yrs  Previous hx of colon cancer: coloscopy at 1 yr and 3 yr post-resection, then every 5 years Diarrhea o Infectious causes of bloody diarrhea: entamoeba histolytica, salmonella, shigella, camplobacter, c. diff, e.coli o Clostridium difficile  Gram (+) spore forming  Pseudomembranous colitis; a/w antibiotic use (days-2ks after antibiotics use: clindamycin, cephalosporins, ampicillin)  Prominent in the sigmoid/rectal area  Sx: diffuse watery diarrhea, cramps, fever, abdominal tenderness  Dx: cytotoxin assay in the stool; stool C. diff antigen; endoscopy will show pseudomembranes (not required for dx)  Tx: IV/oral metronidazole or oral vancomycin  Recurrences: Metronidazole is used for 1st recurrence, oral vancomycin used for 2nd recurrence o Cryptosporidium parvum  Can cause diarrhea in immunocompetent and immunocompromised pt; pt with CD410 increase in HR or >20 drop in BP from lying down to sitting up/standing  Nuclear bleeding scan, angiography, capsule endoscopy  EKG to assess heart function in severe bleeding (may cause heart ischemia) o Tx: fluid resuscitation (#1), blood products  PRBCs if HCT 1500 mL of fluid needs to be present to present with flank dullness)  Signs of cirrhosis: spider telangiectasias, palmar erythema, gynecomastia, portal HTN esophageal varices, caput medusae, hemorrhoids; jaundice  Cancer: sister mary joseph nodule (umbilical nodule; indicated in gastric ca, colon ca, hepatocellular ca, lymphoma) Dx:  History: alcohol use, needle drug use, sexual hx, family hx of liver disease  Ultrasound  Abdominal paracentesis: Cell count & differential, [albumin], [total protein], culture; optional= [glucose], [LDH], gram stain, [amylase]; other tests= TB smear & culture, cytology, [triglyceride], [bilirubin]  Indication for paracentesis: new onset ascites, abdominal pain and tenderness, fever  Fluid appearance: Uncomplicated ascites; if clear yellow cirrhosis

Turbid/cloudy

Spontaneously infected fluid

Opalescent

Cirrhosis + elevated triglyceride

Milky

“chylous ascites”; Triglyceride >200-1000mg/dL d/t cirrhosis or cancer

Pink or bloody

*requires corrected neutrophil count: -1 neutrophils from absolute neutrophil count for every 250 RBCs; start empiric antibiotics if >250 *d/t “traumatic tap”, punctured collateral (from previous tap), cirrhosis, or cancer

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Bilirubin in fluid; if ascetic bilirubin>serum, consider ruptured gallbladder or perforated duodenal ulcer o

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SAAG (serum albumin-ascites gradient)  High gradient >1.1 g/dL (indicates portal HTN): cirrhosis, alcoholic hepatitis, massive hepatic metastases, heart failure/constrictive pericarditis, Budd-Chiari syndrome, portal vein thrombosis  Low gradient 2.5-3 g/dL  low protein (transudative) ascites has a higher risk of spontaneous bacterial peritonitis glucose: normally the same as serum; if low used up by WBCs, bacteria, malignant cells, gut perforation LDH ascetic fluid/serum ratio: >1 indicates infection or tumor Amylase: elevated from pancreatitis or gut perforation If suspected heart failure: CXR and echocardiogram Suspected cancer: FNA of palpable nodules Gut perforation into ascites: neutrophil count >250 cells/mm3, total protein >1g/dL, glucose 250); fluid cultures (most accurate)  Tx: cefotaxime  d/t recurrences, when ascites fluid albumin is low prophylactic norfloxacin or TMP/SMX Treatment  Cirrhosis: d/x alcohol, consider baclofen treatment, tx underlying liver dz when possible, salt-restricted diet, diuretics (spironolactone + furosemide)  Liver transplant for irreversible cirrhosis  Surgical options: serial therapeutic paracentesis, transjugular intrahepatic portosystemic shunts (TIPS)  Autoimmune hepatitis: glucocorticoid (prednisone) and/or azathioprine  Avoid: NSAIDs, ACE inhibitors/ARBs o Caution: beta blockers (increase risk of diuretic resistant ascites) but helps prevent variceal hemorrhage (must weigh benefits & risks)

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Diuretic-resistant ascites in pt w/ cirrhosis o Usual tx for ascites: salt restricted diet, diuretics (spironolactone & furosemide) o Differentiate from malignant ascites (peritoneal carcinomatosis), budd-chiari syndrome (hepatic vein thrombosis), chylous malignant ascites, nephrogenic ascites (tx renal transplant) o Dx: doppler U/s or CT scan ov liver & spleen + alpha-fetoprotein (r/o hepatocellular carcinoma or portal vein thrombosis) o Tx:  Repeat education about diet compliance (salt restricted)  Oral midodrine=vasopressorincreased renal perfusion, increase renal sodium excretion reduce ascites  5mg 3x/day; adjust dose every 24 hr to increase systolic BP 10-15 mmHg  Oral midodrine + parenteral octreotide is used to reverse type I hepatorenal syndrome  Serial paracentesis + salt restricted diet (2g/day) as a bridge to transplant or TIPS procedure  Replace albumin (6-8g albumin/L fluid removed) when >5 liters are removed  SE: protein & complement deficiency  TIPS (transjugular intrahepatic portosystemic shunt) procedure + diuretics  Relative contraindications to TIPS: spontaneous or problematic hepatic encephalopathy, alcoholic hepatitis, MELD score >18, advanced age, parenchymal renal disease  liver transplant is the only definitive therapeutic option if d/t portal HTN  AVOID/STOP: Beta blockers (reduce survival), NSAIDs (renal vasoconstriction), ACE inhibitors/ARBs  GI tract anatomy/physiology review o Layers: mucosa (surface epithelium, basal lamina, lamina propria= fibroblasts, nerves, BVs, connective tissue, immune cells), muscularis mucosa, submucosa (Meissner’s nerve plexus), muscularis externa/propria (muscularis inner circular, Auerbach’s myenteric nerve plexus, muscularis outer longitudinal), serosa (fat & BVs) o Esophagus: keratinized stratified squamous epithelium, submucosal mucous glands; upper 1/3 striated muscle, lower 1/3 smoothm. o Stomach: body= columnar mucous cells, antrum= cuboidal o Small bowel: columnar cells w/ brush border (microvilli)  Duodenum: brunner’s glands  Ligament of Treitz separates duodenum from jejunum  Jejunum: wider (4cm), thicker, more vascular, larer villi, thick circular folds  Ileum: prominent lymphoid (peyer’s patches), less circular folds o Colon: goblet & absorptive columnar cells o L. Colon: oval ringed lumen; transvers & right colon triangular shaped lumen; crescent moon shape for appendix opening Liver & gallbladder  Liver related tests o Bilirubin  Biliary stasis  jaundice, pruritus, light-colored stools  Jaundice is clinically noticeable when serum bilirubin >2-2.5 mg/dL

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Dx: cholestasis elevated alkaline phosphatase with elevated total & conjugated bilirubin; U/S of biliary system; extrahepatic dilatation w/o evidence of stones CT scan or ERCP to detect occult stones or structures and r/o malignant causes (cholangiocarcinoma, pancreatic CA, ampullary of vater cancer)  Conjugated (direct) bilirubin: enzymatically bound to glucuronic acid  Only conjugated bilirubin can be filtered & renally excreted  Elevated: hepatocellular disease (elevated ALT & AST, abnormal clotting factor & albumin synthesis) or biliary obstruction (elevated alkaline phosphatase) o Acute hepatocellular necrosis (viral and drug hepatis, hepatotoxins, acute heart failure) o Obstruction: primary sclerosing cholangitis  Unconjugated (indirect) bilirubin: reversibly & noncovalently bound to albumin  Causes of elevation: hemolysis, Gilbert syndrome o ALT & AST  Normal levels ~30 (M) or ~20 (F)  Elevated: liver failure, hepatitis, rhabdomyolysis, MI  Note: level of LRTs do not correlate to the severity of the disease; liver biopsy is needed to assess severity Primary Sclerosing cholangitis o Autoimmune intrahepatic & extrahepatic large bile duct obstruction  occurs in younger males; a/w inflammatory bowel disease (esp ulcerative colitis) o sx: jaundice or sx of biliary obstruction (pruritus)  complications: stricture, infection (cholangitis), cholangiocarcinoma, cirrhosis o dx: elevated alkaline phosphatase, bilirubin, and GGTP; ERCP (most accurate; beading, narrowing, or strictures), beading of bile ducts  biopsy is not essential to dx o tx: cholestyramine or ursodeoxycholic acid Primary biliary cirrhosis o Autoimmune destruction of intrahepatic bile ducts (small & medium sized) bile stasis, cirrhosis  Most common in 35-60 yo F; a/w other autoimmune diseases (rheumatoid arthritis)  Decreased ability to absorb and store fat-soluble vitamins o Sx: pruritus, fatigue, jaundice, steatorrhea, hepatosplenomegaly; xanthomas and xanthelasmas; osteoporosis  Complications: cirrhosis o Dx: increased alkaline phosphatase (2-5x), serum bilirubin (normal), anti-mitochondrial antibodies; liver biopsy (most accurate) o Tx: ursodiol (ursodeoxycholic acid; reduces cholesterol absorption, reduces cholestasis), cholestyramine (bile acid Sequestrant; relieves itching) Biliary colic o Usually a/w cholelithiasis  Risk factors: fat, female, 40s (fertile) o Sx: acute onset severe RUQ pain (precipitated by fatty meal, ~30-60 min), N/V o Dx: elevated bilirubin & alkaline phosphatase (mild if non obstructive, bilirubin >3g/dL if obstruction), RUQ ultrasound Acute cholecystitis o Stone impacted in the cystic duct; infection with enteric flora (e.coli, klebsiella) o Sx: fever, increased WBC, peristent RUQ pain o Dx: ultrasound (gallbladder wall thickening, pericholecystic fluid); scintigraphy via HIDA (hepatobiliary iminodiacetic acid) scan if questionable dx (nonvisualization of gallbladder indicates obstruction) o Tx: NPO, IV fluids, IV antibiotics, cholecystectomy w/in 48-72 hrs Cholangitis o Intermittent obstruction w/reflux of bacteria up the biliary tree o Tx: if septic urgent decompression w/ surgery or ERCP Budd-Chiari o Hepatic vein thrombosis Hepatitis o Causes: viral (hepatitis, CMV, EBV, HSV 1), toxic, autoimmune (ANA, anti-LKM=liver kidney microsome), hemochromatosis, Wilson’s disease, alpha-1 antitrypsin disease o Sx: N/V, diffuse abdominal pain, fever, myalgias, fatigue, arthralgias, jaundice, dark urine  Chronic if sx >6mo o Dx: ALT>AST  transaminase >1000 IU/L viral or toxic hepatitis or ischemia (“shock liver”)  alcoholic hepatitis: transaminase 10 g) or chronic use  drug is normally metabolized by liver P450 toxic metabolite that is bound by glutathione  dx: nomogram (plot serum acetaminophen level against time of last ingestion) to determine if N-acetylcysteine is needed  tx: oral activated charcoal, N-acetylcysteine (started w/in 10 hrs & continued for 72 hrs)  observation only if nomogram shows levels below the danger zone o Hep A  Fecal-oral transmission  Sx: arthritis, vasculitis, cryoglobulinemia  Dx: anti-hep A IgM  Tx: self-limited in weeks  prevention: Hep A vaccine (2 doses 6 mo apart) if traveling to an endemic area or pt with chronic liver disease; HAIg w/in 2 wks post-exposure + vaccine; vaccinate close contacts

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Hep E    Hep B  

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Hep D  Hep C  

Fecal-oral transmission Pregnancy women have an increased risk of severe hepatic necrosis and liver failure Tx: self-limited w/in weeks Complications: cirrhosis, hepatocellular CA, polyarteritis nodosa Dx: HBsAg, HBeAg (indicates viral replication/infectious)  Chronic hep B: surface antigen positive for >6 mo; e-antigen often positive; hepatitis B DNA level by PCR is the best way to determine viral replication activity o Liver biopsy determines the degree of inflammation and fibrosis Tx: interferon (acute infection), lamivudine (chronic infection)  Prevention: hep B vaccine (3 doses w/in 6 mo), HBIg post-exposure + vaccine o Anti-HBsAg w/o IgG indicates vaccination induced immunity no Ig needed post-exposure  Chronic hep B (any 1 of the following): adefovir, lamivudine, telbivudine, entecavir, tenofovir, interferon o Interferon SE: arthralgias, thrombocytopenia, depression, leukopenia o Adefovir SE: renal dysfunction Defective RNA virus that requires Hep B to replicate (either co-infection or later superinfection)

Transmission: blood transfusion, IV drug use Complications: cirrhosis, hepatocellular CA, polyarteritis nodosa, cryoglobulinemia, membranoproliferative glomerulonephritis (secondary to cryoglobulinemia), B-cell lymphoma, plasmacytoma, autoimmune diseases (Sjogren’s syndrome, thyroiditis), lichen planus, porphyria cutanea tarda, idiopathic thrombocytopenic purpura  Dx: anti-hep C Ab (ELISA), hep C RNA assay (PCR)  Hep C PCR RNA viral load is the most accurate way of determining disease activity  Liver biopsy determines the degree of inflammation and fibrosis  Tx: ribavirin, pegylated interferon alpha, proteases (Telaprevir, boceprevir); vaccinate against hep A & B  wait 3-4 months post-exposure before starting treatment to see if there is spontaneous clearance; goal is to reduce viral load to prevent complications o note: start treatment if elevated ALT, detectable HCV RNA and histologic evidence of chronic hepatitis of at least moderate grade  If pregnant w/ hepatitis: Test newborn @12-18 mo for hep C RNA  Protease inhibitors o check viral load at 4,8, and 12 wk & 6mo after tx.  If 0 viral load then treatment is only needed 24 wks total (only 12 of which is with protease inhibitor), if higher then treat for 36-48 wks o Telaprevir requires eating w/ 2g fat to slow absorption  Started with IFN & ribavirin o Bocepravir is started 4 wks after starting IFN & ribavirin  Interferon SE: flu-like sx, depression, psychosis, pancytopenia  Ribavirin SE: hemolysis anemia  Note: no longer required to f/u LRTs as part of tx  Chronic hep C: interferon + ribavirin o Vaginal birth and breast feeding are both fine for pts with hepatitis virus Alcoholic liver disease o Dx of exclusion; liver biopsy (most accurate); AST>ALT; binge drinking gives a sudden rise in GGTP Non-alcoholic fatty liver disease o Range: steatosis, steato-hepatitis, advanced fibrosis in non-alcoholic pts o a/w obesity and DM2  MOA most likely insulin resistance increased fat accumulation in the hepatocytes (increased rate of lipolysis and elevating circulating insulin levels); intrahepatic fatty acid oxidation increase in oxidative stress local incrase in Proinflammatory cytokines TNF-alpha liver inflammation, fibrosis, cirrhosis o Dx: liver biopsy (macrovesicular fat deposition with displacement of the nucleus to the periphery) Alpha-1 antitrypsin deficiency o Occurs in young (50%), decreased TIBC, liver biopsy (determines iron concentration; most accurate); mildly elevated AST and alkaline phosphatase  EKG may show conduction defects; echocardiogram may show dilated or restrictive cardiomyopathy  Abdominal MRI and HFE (C282y) gene testing can be used to confirm the diagnosis instead of liver biopsy  Prussian blue= stain for RBC cell iron o Tx: phlebotomy, iron chelation (deferoxamine, deferasirox), liver transplant, treat complications  Iron chelators are used for pt that can’t be managed with phlebotomy or are anemic w/ hemochromatosis from overtransfusion  Acute liver failure o Tx: transplant or self-resolution  Mucomyst (acetylcysteine) is sometimes used although no research evidence of it’s benefit  Fulminant liver failure o Sx: rapidly progressive encephalopathy, coagulopathy, elevated bilirubin, ascites, peripheral edema, hypoglycemia, hyperammonemia, lactic acidosis o Tx: fatal w/o emergency liver transplant  Chronic liver disease/ cirrhosis o Sx: ascites, elevated estrogen (gynecomastia, testicular atrophy, palmar erythema, spider angiomas); portal HTN varices (esophageal/gastric), hemorrhoids, caput medusae (distended abdominal wall veins); hypoglycemia (liver stores glycogen), hyperbilirubinemia, jaundice, coagulopathy (decreased clotting factors), hypoalbuminemia edema, leukonychia (white nails); asterixis, encephalopathy; thrombocytopenia d/t splenic sequestration  Elevated estrogen is d/t decreased production of steroid hormone binding globulin  Coagulopathy: liver produces all clotting factors (except factor 8)  Tx: FFP and platelets if bleeding occurs  Esophageal varices  Tx: propranolol, banding via endoscopy  Hepatic encephalopathy  d/t increased ammonia inhibitory neurotransmission via GABA receptors in CNS o precipitated by alkalosis, hypokalemia, hypovolemia, GI bleeding, constipation, dehydration, large protein loads, hypoxia, sedatives, hypoglycemia, infection  Sx: decreased mental function, asterixis (flapping tremor), rigidity, hyperreflexia, fetor hepaticus (musty breath)  Tx: lactulose or lactitol (nonabsorbable disaccharides); neomycin or rifaximin (antibiotics), ornithine-aspartate infusion, or oral sodium benzoate; diet changes (decrease protein intake (6 mo required before pt eligible for transplant  MELD score (modified end-stage liver disease): patients risk of dying while waiting for a liver transplant o Based on INR, bilirubin, creatinine, if pt has dialysis >2x/wk kidney & other urology  physiology o

fractional excretion of sodium: ratio of sodium excreted vs filtered in the kidneys  FeNa= 100x(UNa/PNa)/(UCr/PCr)  =100x [(urinary sodium x plasma creatinine)/ (plasma sodium x urinary creatinine)]  Creatinine represents the GFR o Normal urine output 1.0ml/kg/hr (kg of ideal body weight) o Glomerular filtration rate (GFR): inversely related to serum creatinine (increased creatinine indicates a decreased GFR) o Glomerular arteriole control  Afferent: Prostaglandin dilates  Efferent: angiotensin II constricts o Kidney “filter”= fenestrated capillary, glomerular basement membrane, podocytes Best initial test for any kidney disorder is urinalysis, BUN, and creatinine o Urine analysis/ microscopy: protein, white cells (direct microscopy exam) or leukocyte esterase (dipstick), RBCs, specific gravity, pH, nitrites  Proteinuria >300 mg/day; nephrotic level proteinuria >3g/day  normally 30-50 mg/24 hrs of Tamm-Horsfall protein is excreted; standing and increased physical activity increase urinary protein excretion  Microalbuminuria: 50-300 mg/day o >300 mg/D is detectable on urine dipstick; urine dipstick only detects albumin (not other proteins; other proteins detected with immunoelectrophoresis) o ACE inhibitor/ARB should be started for any degree of proteinuria in a diabetic pt (delays development of renal insufficiency)  f/u persistent proteinuria with a kidney biopsy; severe proteinuria indicated glomerular damage  determining total protein excretion in a day: UA (best initial), protein: creatinine ratio> 24 hr urine collection o 1+ protein ~ 1 g/24 hr in UA (2+=2g/24 hr, etc.) o protein: creatinine is faster and technically easier to perform  ratio indicates g protein/24 hrs (ratio of 1.2 indicates 1.2 g protein/24 hrs)  Protein(tam Horsfall protein) based casts indicate tubular injury (intrinsic renal damage)  RBC casts glomerular nephritis, WBC casts renal parenchymal inflammation/infection, fatty casts nephrotic syndrome, granular (“muddy brown”) casts ATN; broad waxy casts CKD  Hyaline casts (only tam Horsfall protein) are physiologic; d/t dehydration, extreme exercise, low flow state, etc.  >5 squamous cells indicates a poor sample (not clean catch)  nitrites: indicates presence of gram (-) bacteria on dipstick o Hematuria  Diff dx:  Intrarenal: kidney trauma, renal stones/crystals, pyelonephritis, renal cell CA, vascular injury (vasculitis, renal thrombosis)  Extrarenal: trauma (foley placement), infectious (urethritis, prostatitis, cystitis), nephrolithiasis, neoplasm (prostate, bladder)  Dx: distinguish hematuria from hemoglobinuria/myoglobinuria (rhabdomyolysis) Polycystic kidney disease o Autosomal dominant o Sx: bilateral flank masses, flank pain, HTN, hematuria Bartter’s syndrome o Autosomal recessive: defect in salt reabsorption in the thick ascending limb of the loop of Henle hyperplasia of the juxtaglomerular apparatus increased renin increased aldosterone hypokalemia Acute glomerulonephritis/ nephritic syndrome o Inflammatory renal diseases o Causes  Primary renal disorders: membranoproliferative GN types 1&2, mesangioproliferative GN, crescentic GN (anti-GBM, ANCA), fibrillary GN, proliferative GN (IgA nephropathy)  Secondary renal disorders: SLE, postinfectious/poststrep, hep C or B related GN (cryoglobulin-induced), vasculitis related (wegner, Churg-Strauss, polyarteritis nodosa, microscopic polyangiitis, Henoch-Schonlein purpura), infective endocarditis related GN o Sx: HTN & edema (d/t volume retention), hematuria, renal failure, low proteinuria (3.5 g/24 hr), hypoalbuminemia (300 is detectable on urine dipstick)  SLE: ANA  multiple myeloma or amyloidosis: serum & urine electrophoresis  viral: HIV, Hepatitis testing o Tx: diet changes (strict salt restriction, low protein diet), diuretics (thiazide, loop; ACE or ARB if diabetes),  Diabetic nephropathy: ACE inhibitor, tight glycemia control (goal AbA1c= 6.5-7.0), BP control (goal 25% w/in 3 months  Risk factors: acute drop in BP, ACE inhibitor, radio-contrast, atheroemboli following catheter procedure o Sx: weight gain, edema  Uremia: fatigue, weakness, nausea & early morning vomiting, itchiness, confusion, pericarditis, coma  Azotemia: increased BUN w/o sx  oliguria: 90 + proteinuria, 2= 90-60, 3= 30-60, 4=15-30, 5=50% lowing of creatinine clearance (10 WBCs), urine culture (most accurate)  No further dx is needed when symptomatic with WBCs in urine  Urine culture and imaging studies are done for frequent episodes or failure to respond to tx o Tx: TMP/SMZ, ciprofloxacin, cephalexin, or nitrofurantoins (esp pregnant pt)  treat for 3 days in uncomplicated cases; treat 7 days if anatomical abnormality genital pathology  female o chlamydia trachomatis screening in sexually active women radiation; hormonal therapy  complications of prostatectomy: erectile dysfunction, urinary incontinence  hormonal therapy shrinks current lesions (not preventative for recurrences); flutamide, GNRH agonists, ketoconazole, orchiectomy  infectious o condylomata acuminata (anogenital warts)  d/t human papilloma virus (HPV)  sx: verrucous, papilliform, skin colored or pink lesions in the anogenital region  tx: chemical or physical agents (trichloroacetic acid, 5-florouracil epinephrine gel, podophyllin), immune therapy (imiquimod, interferon alpha), surgery (cryosurgery, excisional procedures, laser treatment)  podophyllin: topical antimitotic agent that causes cell death; teratogenic Endocrine  Adrenal insufficiency o Acute sx: orthostatic hypotension, chronic abdominal pain, weakness  Hyponatremia, hyperkalemia, acidosis, hypoglycemia, fever, tachycardia, azotemia (d/t volume depletion from decreased aldosterone), eosinophilia (d/t decreased cortisol) o Chronic sx: malaise, weight loss, chronic fatigue, anorexia, N/V, hypoglycemia, hypotension, hyperpigmentation if primary disease o Dx: cortisol level, ACTH stimulation test with cosyntropin (ACTH analog) if abnormal, get ACTH level; CT scan for primary dz, MRI for secondary dx  Cortisol levels are normally highest in the morning, then lower throughout the day; elevated during illness, or after surgery/trauma  Morning cortisol 20 microgram/dL intact function  ACTH stimulation test: 250 microgram ACTH given, then measure cortisol at time 1,30 min, 60 min; normal if >7 microgram/dL increase or max level >18 microgram cortisol  Insulin-glucose tolerance test= gold standard for testing the hypothalamic-pituitary axis  Chronic adrenal insufficiency: cosyntropin stimulation test with cortisol and ACTH levels (#1)  Cortisol low, ACTH high primary adrenal insufficiency  Cortisol and ACTH low secondary or tertiary adrenal insufficiency  Increase in cortisol level >20 mcg/dL 30-60 min after the administration of 250 mcg of cosyntropin r/o primary adrenocortical insufficiency (addison’s disease) o Tx:  Acute tx: IV saline + glucose, corticosteroids (hydrocortisone 100 mg q6-8 hr; at high dose it provides both corticosteroid & mineralocorticoid activity)  Long term tx: glucocorticoids (hydrocortisone 25-30 mg/day) +/- mineralocorticoids (fludrocortisone 0.1-0.2 mg/day; needed if primary insufficiency)  Glucocorticoid SE: diabetes, HTN, obesity, osteoporosis, cataracts  Note: if pt on steroids chronically and is having surgery hydrocortisone IV before surgery & q6hr for 24 hr after (stress dose of corticosteroids to prevent acute primary adrenal insufficiency) o Addison’s disease (primary adrenal failure)  Low cortisol & aldosterone  Causes: autoimmune destruction (#1), TB adrenalitis, chronic granulomatous infection (Histoplasma, Coccidioides), B/L adrenal hemorrhage (sepsis, DIC), metastases (lung, breast, stomach), x-linked adrenoleukodystrophy; CMV or MAI infection in AIDs pt  Sx: N/V, abdominal pain, diarrhea or constipation, weight loss, hyperpigmentation, decreased BP, vitiligo

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Hyponatremia (d/t mineralocorticoid deficiency & increased vasopressin d/t lack of cortisol), hyperkalemia (a/w mild hyperchloremic acidosis) o Secondary adrenal insufficiency  Low ACTH secretion from pituitary; low cortisol but normal aldosterone  Causes: chronic exogenous use of corticosteroids (#1), autoimmune, metastatic cancer, infiltrative disease amenorrhea o primary amenorrhea (no menses by age 16)  differential dx: pregnancy, mullerian or vaginal agenesis, androgen insensitivity, turner syndrome o secondary amenorrhea/ oligomenorrhea:  amenorrhea: 3mo w/o menses in a women with previously regular menses  oligomenorrhea: infrequent interval >40 days or 25), signs of metabolic syndrome (HTN, low HDL, triglyceride >250 mg/dL), 1 st degree relative with diabetes, hx of gestational diabetes  Start screening 45yo and repeat every 3 yrs; kids with risk factors screening at 19yo and every 2 yrs o Sx: polyuria, polydipsia, nocturia; Macrovascular complications (coronary artery disease, stroke, peripheral vascular disease), microvascular complications (retinopathy, nephropathy, neuropathy)  Diabetic retinopathy: dot hemorrhages, hard exudates; eventual blindness  Diabetic retinopathy occurs before nephropathy  Diabetic neuropathy  Sx: peripheral sensory problems; loss of proprioception imbalance; numbness and tingling  Increased risk of epidural abscesses cord compression  Dx: spine MRI  Diabetic nephropathy  Tx: ACE inhibitor or ARB  Gastroparesis  Occurs >10 yrs after onset of diabetes; anatomic neuropathy dysmotility; inability to sense stretch of the GI tract  Sx: chronic abdominal discomfort, bloating, constipation, anorexia, N/V, early satiety  Dx: clinical; nuclear gastric emptying study if no response to treatment  Tx: erythromycin, domperidone, or metoclopramide to increased GI motility; improve glycemic control, small frequent meals, bethanechol  Diabetic ketoacidosis  Precipitants: infection, pregnancy, MI  Glucagon stimulates hepatic gluconeogenesis and glycogenolysis; lipolysis is enhances release of free fatty acids oxidation causes ketones  Sx: polyuria, polydipsia, weight loss, mental status changes, vision blurring; kussmaul breathing (deep & rapid to compensate for metabolic acidosis), N/V, abdominal pain, fatigue, malaise; signs of dehydration o Complications: cerebral edema (d/t rapid correction of hyperglycemia or rapid hypotonic fluid administration), ARDS, thromboembolism, fluid overload, acute gastric dilatation o Cardiovascular collapse= most common cause of death in DKA  d/t acidosis, hypovolemia & electrolyte deficiencies  Anion gap metabolic acidosis, hyperglycemia, hypovolemia (d/t osmotic diuresis), ketone bodies in serum; depletion of total body K+, Mg2+, and phosphate o may appear as hyperkalemia b/c K+ moving out of cell as H+ moves in, but urinary losses cause overall depletion  Tx: hydration, insulin, potassium, bicarbonate (only used if pH 18, anion gap 100 mg/dL), serum osmolarity >320-370 osm, neuro sx (seizures, coma)  Tx: fluid resuscitation with normal saline, insulin  Nontraumatic amputations of the lower extremities o Dx: fasting serum glucose >126 (2x; most specific), glucose tolerance testing (>200 mg/dL; most sensitive), random glucose >200 mg/dL + sx of diabetes  Impaired fasting glucose/impaired glucose tolerance tests (prediabetes): fasting glucose 100-126 mg/dL, oral glucose tolerance test (75 g load) 140-200  HbA1c to monitor glycemic control o Tx: lifestyle modification, glucose control with meds, office visits every 3-6 mo (with HbA1c check), yearly ophthalmologic exam, semi-annual dental visits, yearly urine screens to detect microalbuminuria, yearly foot exams (if neuropathy present, every 3 mo)  Lifestyle modification: low sugar & fat diet, exercise, strict glycemic control, smoking cessation, target Bp 50%), decreased TIBC, liver biopsy (determines iron concentration; required for dx)  Abdominal MRI and HFE (C282y) gene testing can be used to confirm the diagnosis instead of liver biopsy  Prussian blue= stain for RBC cell iron o Tx: phlebotomy, iron chelation (deferoxamine, deferasirox), liver transplant, treat complications  Iron chelators are used for pt that can’t be managed with phlebotomy or are anemic w/ hemochromatosis from overtransfusion Vitamin excess/deficiencies Vitamin Excess deficiency D *decreased Ca2+ & phosphate Thiamine *seen in alcoholics & fad diets *sx: poor short term memory, lower extremity paresthesias, decreased vibratory position sense; tachycardia, hypotension Fluid balance in body o Water deficit= Total body water x [(serum Na/140)-1]  Total body water= cofactor *weight  cofactor 0.6 for men, 0.5 for women & elderly men, 0.45 for elderly women  TBW decreases with age & obesity (fat is low on water content)  Water distribution: 2/3 ICF, 1/3 EFC (1/4 plasma 85% venous, 15% arterial, ¾ interstitial fluid)  Hours to correct= (serum Na-140)/0.5

 Infusion rate= water deficit/hours to correct Calculating maintenance fluids  100 mL/kg for 1st 10 kg, 50 mL/kg for next 10 kg, 20 mL/kg for every 1 kg remaining  divide total by 24 for hourly rate  4mL/kg for 1st 10 kg, 2 mL/kg for next 10 kg, 1 mL/kg for every 1 kg remaining  gives hourly maintenance level  give fluid to maintain urine output at 0.5-1 mL/kg/hr o Fluid replacement therapy  Normal saline (0.9%; 154 mOsm/L): used for dehydration, blood loss  Replace blood loss with crystalloid at a 3:1 ratio (either NS or LR)  D5 ½ NS: maintenance fluid (often given with 20mEq of KCl/L of fluid)  D5W: used to dilute powered medications, sometimes for correcting hypernatremia  Lactated ringer’s solution: replacement of intravascular volume  Do not use if hyperkalemia (solution contains K+) Serum osmolarity= (2*Na) + (BUN/2.8)+ (glucose/18) o Normal 280-295 mOsm/kg o plasma hypertonicity (>295 mOsm/kg): stimulates Osmoreceptors in the hypothalamus produces thirst; also stimulates posterior pituitary to release ADH (act on V2 receptors in kidney collecting ducts to increase water absorption) Hyponatremia o Serum Na+ 295 mOsm/kg): hyperglycemia, exogenous solutes (radiocontrast, mannitol)  Corrected [Na]: for every 100 glucose over 100, add 1.6 Na+  Osmotic shift of water out of cells o Low serum osmolarity (20 mEq/L + urine osm 20 mEq/L + urine osm >300: SIADH  Hypervolemic: CHF, hepatic failure, nephrotic syndrome (renal failure) o Tx:  normal saline used for mild or slowly developed hypovolemic hyponatremia  water restriction for asymptomatic euvolemic pt  hypotonic hyponatremia  mild (Na+ 120-130): withhold free water  moderate (Na+ 110-120): loop diuretics given with saline  severe (Na+ 8mmol/L during the first 24 hrs d/t risk of central pontine demyelination Hypernatremia o Na+ >145 mmol/L o Sx: altered mental status, restlessness, weakness, focal neuro deficit, dry mucous membranes, decreased salivation o Hypovolemic  Causes (water loss>Na+ loss): dehydration, diaphoresis, diarrhea, respiratory losses, diuretics, osmotic diuresis d/t glycosuria, renal failure  Tx: IV normal saline (0.9%) until volume deficit is restored, then 5% dextrose in half-normal saline (0.45%)  Correct no more than 1mEq/L/hr  Mild cases can be started with D5W 0.45% saline o Euvolemic  Causes: diabetes insipidus, insensible respiratory (tachypnea)  Diabetes insipidus: complete (urine osmolality 15mg/dL or 60 yo+ RF  T-score compares bone density with the normal density of a young woman  Osteopenia: T score 1.5-2 SD below  Osteoporosis: T score >2 SD below o Tx: calcium & Vit D (best initial); bisphosphonate (-dronate), estrogen or raloxifene for postmenopausal women, teriparatide (PTH analog), calcitonin nasal spray  Bisphosphonate SE: osteonecrosis of the jaw, pill esophagitis  Teriparatide SE: osteosarcoma, hypercalcemia  arthritis o general info  sx: joint swelling, redness, warmth, tender to palpation, limited rand of motion in all planes (active & passive)  diff dx: infectious (staph aureus, N. gonorrhea, TB, lyme, fungal), crystal (gout, pseudogout), trauma, osteoarthritis, rheumatoid arthritis, hemochromatosis  non-inflammatory arthritis diff dx: osteoarthritis, fibromyalgia, hypothyroidism, neuropathic pain, depression  viral causes are acute (5), pauciarticular asymmetric arthritis or DIP joints only; inflammation of joints, periosteum, along tendons, and bone insertion points “sausage digits” (also seen with Reiter syndrome)  Rheumatic fever: symmetric polyarthritis, 6-8 wks  Reactive arthritis: follows a GI or GU infection w/ salmonella, shigella, campylobacter, Yersinia, or chlamydia  Reiter syndrome: arthritis, uveitis, urethritis o Can follow chlamydia infection; a/w HLA-B27  Ankylosing spondylitis: occurs in young men; morning stiffness, worse w/rest; sacroiliitis w/sclerosis around sacroiliac joints  dx: aspiration of joint fluid for gram stain, culture, cell count, crystal analysis; radiograph, possible biopsy  non-inflammatory exudate: WBC 10 yr after acute intermittent gout; chronic swelling & discomfort ath increases in time, subcutaneous tophaceous deposits of monosodium urate o tx: acute tx + allopurinol; surgery if nerve compression, joint deformity, or chronic skin ulceration + infection pseudogout (calcium pyrophosphate deposition disease)  d/t accumulation of calcium pyrophosphate dehydrate crystals  risk factors: hemochromatosis, hyperparathyroidism  a/w DM, hypothyroidism, Wilson disease  sx: affects large joints (knees, wrists)  dx: joint aspiration=arthrocentesis (short & rhomboid weakly positive birefringent crystals (blue in polarized light), elevated WBC count); x-ray (calcification of cartilaginous structures and degenerative joint disease); chondrocalcinosis or linear calcium deposits in joint  tx:  acute attack: NSAIDs; if no response intraarticular steroids (triamcinolone)  if recurrent attacks colchicine prophylaxis rheumatoid arthritis  autoimmune; inflammatory; a/w HLA types; joint deformity d/t chronic synovitis pannus formation damage to all structures surrounding the joint (cartilage destruction and erosion of periarticular bone, damage to ligament & tendons)  more common in young women; onset age 30-50 yo  sx: bilateral symmetric erosive polyarticular arthritis (multiple small enflamed joints; PIP, MCP, wrist, knee, ankle), morning stiffness that gets better with use (>30 min stiffness), ulnar deviation of MCP joints, radial deviation of wrist, swan-neck deformities, boutonniere deformity, rheumatoid nodules, Bouchard nodes (PIP enlargement)  extraarticular sx: vasculitis lesions ischemic ulcers, keratoconjunctivitis sicca (Sjogren syndrome), sicca syndrome (dry mucous membranes), episcleritis, interstitial lung disease (pleural effusion, nodules of lung parenchyma), cardiac (pericarditis), neuro (myelopathy, spinal cord compression from subluxation of disk), carpal tunnel syndrome, anemia of chronic disease, baker cyst (d/t inflamed synovial fluid excess fluid production), cervical joint involvement (esp C1/C2 subluxation; neck pain, stiffness, hyperreflexia), fatigue, fever, increased risk of developing osteopenia & osteoporosis  felty syndrome: RA, splenomegaly, neutropenia; leucopenia, lymphadenopathy, thrombocytopenia  Caplan syndrome: RA, pneumoconiosis (restrictive lung disease), lung nodules  arthritis affects >3 joints: elbow, wrists, MCP or PIP joints (DIP spared), knee, ankle, or MTP  rheumatoid nodules: subcutaneous nodules on extensor surface of proximal ulna or other pressure points (juxtaarticular regions)  dx: increased ESR, rheumatoid factor (IgM anti-IgG), ANA titer, x-ray; arthrocentesis to obtain synovial fluid if dx unclear (r/o infection or crystal disease); anti-cyclic citrulinated peptide (anti-CCP), normocytic anemia  diagnostic criteria (6+ = RA): joint involvement (up to 5 pts), elevated ESR or CRP (1 pt), duration >6 wks (1 pt), RF for anti-CCP (1pt)  x-ray: periarticular bone & cartilage destruction (periarticular osteopenia) w/loss of joint space & joint margin erosions; joint space narrowing, subchondral polysclerosis, marginal osteophyte formation, cyst formation o obtain cervical x-ray before any surgery to assess for cervical subluxation (intubation risk)  tx:  acute sx (pain control): NSAIDS or COX-2 inhibitors (celecoxib), low dose corticosteroids (if NSAIDs not effective before DMARDS onset of action)  disease modifying anti-rheumatic drugs (DMARDs): Drug Side effects methotrexate (#1) Toxic to liver, bone marrow, lungs hydroxychloroquine (for mild disease) Toxic to retina (screen with dilated eye exam) sulfasalazine Bone marrow toxic, hemolysis with G6PD deficiency, rash, oligospermia TNF antagonists (etanercept, infliximab, adalimumab) Reactivation of TB, infection Rituximab (removes CD20 lymphocytes) Infection Gold salts (oral or parenteral gold) Nephrotic syndrome o other DMARDs: leflunomide, abatacept, penicillamine  If refractory to other tx immunosuppressives (azathioprine, leflunomide, cyclosporine, cyclophosphamide) Juvenile rheumatoid arthritis or adult still disease  Sx: high spiking fever (>104F) in a young pt + rash (salmon colored, chest & abdomen); splenomegaly, pericardial effusion, mild joint sx  Dx: clinical; anemia, leukocytosis  Tx: aspirin or NSAIDs; if no response steroids Osteoarthritis (degenerative joint disease)  Loss of articular cartilage in weight bearing joints; noninflammatory  sx: arthritis (pain worsens with activity), mild morning stiffness ( RA> osteoarthritis  synovial lining has no BM, so bacteria and antibiotics easily cross  sx: warm, red, immobile joint, often palpable effusion; if bacteremia fever & chills  dx: arthrocentesis (WBC>50,000 cells, neutrophils predominant; gram stain, fluid culture), blood cultures; get x-ray or CT scan for possible prosthetic joint infection  tx: empiric tx with ceftriaxone + vancomycin  gram (-) bacilli: quinolones, aztreonam, cefotaxime, piperacillin, aminoglycosides  gram (+) cocci: oxacillin, nafcillin, cefazolin, piperacillin + tazobactam o resistant gram (+) cocci: linezolid, daptomycin, tigecycline  prosthetic joint infection: remove the joint, treat for 6-8 wks with antibiotics, then replace the joint o gonococcal arthritis  #1 infectious arthralgia in pt 50,000)  tx: IV ceftriaxone, cefotaxime, or ceftizoxime as empiric tx; quinolones only if sensitive  if recurrent gonorrhea infection test for terminal complement deficiency seronegative spondyloarthropathies o usual onset in male F 20-30 yo  sx: low back pain and stiffness that radiates down the buttocks (pain relieved by activity), flattening of normal lumbar curvature (eventually fusion of vertebral joint via bridging syndesmophytes; “bamboo spine”), decreased chest expansion, enthesopathy of achilles tendon  other possible sx: transient arthritis, of knee/hip/shoulders, anterior uveitis, AV block, aortic insufficiency, increased risk of aortic regurg (secondary to scarring of aortic valve cusps, increased risk of vertebral fracture with minor trauma (d/t decreased bone mineral density)  dx: x-ray of sacroiliac joint (best initial; narrowing of sacroiliac joints, bilateral sacroilitis), MRI (most accurate); elevated ESR  tx: exercise, NSAIDs; if ineffective anti-TNF (etanercept, adalimumab, infliximab) o psoriatic arthritis  sx: preceding psoriasis, sacroiliac joint involvement, sausage digits from enthesopathy, nail pitting  dx: elevated ESR, x-ray of joint (“pencil in a cup” deformity, bony erosion, irregular bone destruction), elevated uric acid (d/t increased skin turnover)  tx: NSAIDs methotrexate (severe dz or if NSAIDs not effective) anti-TNF o reactive arthritis (Reiter syndrome)  secondary to IBD, sexually transmitted infection, GI infection (Yersinia, campylobacter, salmonella)  sx: joint pain, ocular sx (uveitis, conjunctivitis), genital sx (urethritis, balanitis); keratoderma blennorrhagicum (looks like pustular psoriasis)  “can’t pee, can’t see, can’t climb a tree”  dx: clinical; tap hot swollen joints to r/o infections  tx: NSAIDs; if ineffective sulfasalazine bursitis o soft tissue swelling & tenderness; joint movement limited by active movement but not passive movement fibromyalgia o young women with chronic musculoskeletal pain and tenderness with trigger points of focal tenderness at trapezius, medial fat pad of the knee, and lateral epicondyle o sx: pain at many sites (neck, shoulders, back, hips); stiffness, numbness, fatigue, headaches, sleep disorder o dx: clinical o tx: amitriptyline (best initial), milnacipran, pregabalin; trigger point injections with local anesthetic  milnacipran: inhibitor of Serotonin and NE reuptake polymyositis and dermatomyositis o polymyositis: proximal muscle weakness (esp getting up, walking up stairs); some have pain & tenderness o dermatomyositis: malar involvement, shawl sign (erythema of face, neck, shoulders, upper chest, and back), heliotrope rash (swollen purple eyelids), gottron papules (scaly patches on the back of hands, esp PIP and MCP joints), proximal muscle weakness w/ normal sensation and reflexes  a/w cancer in 25% (ovary, lung, GI, lymphoma)  muscle involvement d/t damage of muscle fibers (inflammation, necrosis, fiber atrophy, or antibody-mediated damage) o dx: CPK and aldolase (best initial), muscle biopsy (most accurate); anti-Jo antibody a/w lung fibrosis  possible positive/elevated: ANA, rheumatoid factor, ESR, CRP  MRI show patchy muscle involvement; electromyography is often abnormal o Tx: steroids; if not responsive methotrexate, azathioprine, IV immunoglobulin, or mycophenolate  Hydroxychloroquine helps with skin lesions carpal tunnel syndrome o compression of the median nerve as it passes under the flexor retinaculum  a/w overuse of the hand/wrist, pregnancy, DM, rheumatoid arthritis, acromegaly, amyloidosis, hypothyroidism o sx: pain along the median nerve distribution in hand (palmar side of thumb, index finger, half of ring finger; pain worse at night), atrophy of the thenar eminence 

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 tinel sign: tapping median nerve reproduces sx  phalen sign: flexion of the wrists at 90 degrees reproduces sx o dx: clinical; electromyography or nerve conduction testing o tx: wrist splints, avoid manual activity, NSAIDs; steroid injection if splints & NSAIDs not effective; surgical decompression curative dupuytren contracture o hyperplasia of palmar fascia contracture of 4th & 5th fingers o RFs: genetic, alcoholism, cirrhosis o Tx: triamcinolone injection; surgical release Rotator cuff injury o Rotator cuff tendonitis/ impingement  d/t repetitive activity above shoulder height  Sx: shoulder pain aggravated by activities such as reaching or lifting the arm over the head  Dx: neer test (passive motion of the arm above the head pain and guarding), improvement of ROM after lidocaine injection into the joint o Rotator cuff tear  d/t trauma (falling on an oustreated hand) or as the end result of chronic impingement and tendonitis  Sx: inability to flex or abduct the shoulder; limited mid arc abduction and external rotation;, pain in shoulder when lying on it, tenderness at supraspinatus insertion o Dx: MRI o Tx: NSAIDs, rest, physical therapy; if ineffective steroids; if ineffective or complete tear surgery Patellofemoral syndrome o Anterior knee pain secondary to trauma, imbalance of quadriceps strength, or meniscal tear o Sx: pain walking up/down stairs, pain worse when walking after sitting a prolonged period but decreases after walking  Crepitus, joint locking, instability o Dx: clinical o Tx: physical therapy and strength training with cycling  No knee brace or surgery Achilles tendonitis o Sx: posterior heel pain on the achilles tendon insertion site or on the tendon itself; pain with palpation and passive dorsiflexion of the ankle o Tx; rest, analgesics, stretching/strengthening exercises Retrocalcaneal bursitis o Bursae are located between the posterior calcaneus and the achilles tendon, and between the achilles tendon and the skin o Sx: posterior heel pain secondary to chronic irritation of the underlying bursae Plantar fasciitis o d/t repetitive use or excessive loading (ex. Training for marathon) o Sx: gradual onset pain at the bottom of the foot near calcaneus (point tenderness at fascia insertion on the calcaneus; worse in the morning and after prolonged sitting, improves with walking) o Dx: clinical (marked tenderness over the medial calcaneal tuberosity, increased pain with passive dorsiflexion of the toes) o Tx: stretching exercises, arch supports (orthotics), NSAIDs, night splinting; if ineffective steroids; surgical release (rarely needed) Calcaneal stress fracture o Occur in athletes in running or jumping sports; pt with RF for osteopenia o Sx: diffuse heal pain that is worse by medial and lateral compression Tarsal tunnel syndrome o Tarsal tunnel is on the medial aspect of the help; formed by the flexor retinaculum traversing over the talus and calcaneus o Sx: pain that worsens with use; pain, burning, tingling, or numbness that can radiate to the plantar heel or to the distal sole and toes  Sx exacerbated by percussion of the tarsal tunnor or with dorsiflexion and eversion of the foot low back pain o differential dx:  musculoskeletal low back or leg pain: lumbar sprain or strain, degenerative disk disease, herniated disk, spinal stenosis, trauma, congenital disease (kyphoscoliosis), spondylitis  referred or visceral pain: pelvic disease, renal disease, aortic aneurysm, GI disease  non-mechanical low back pain: neoplasia, infection, inflammatory arthritis, paget disease, cauda equina syndrome o dx: H& P (test strength, sensation, refluxes), Patrick maneuver (hip external rotation + knee flexion over the other leg making a 4 while examiner pushes on flexed knee & opposite side of pelvis helps distinguish pain from sacroiliac joint), x-ray, CT scan or MRI  red flags to indicate imaging: >50 yo, hx of cancer, unexplained weight loss, pain >1mo, nighttime pain causing difficulty sleeping, no response to previous tx, neuro sx  1) x-ray: assess lytic lesions and compression fractures  2) MRI>CT: assess for cancer, infection, disc disease o tx:  any acute mechanical back pain w/o neuro deficit 4-6 wks of early mobilization, NSAIDs, muscle relaxants  MRI or CT if not responsive or sudden neuro deficit o musculoskeletal pain  lumbosacral strain #1 cause of back pain; starts after physical exertion  sx: local tenderness & contraction of the paraspinal muscles  pain doesn’t radiate, normal neuro exam, (-) straight leg test  tx: encourage continuing usual activities, avoid twisting motions or heavy lifting, NSAIDs or other non-narcotic analgesics, narcotics only if severe pain & only use short term, muscle relaxant, massage, acupuncture, weight loss, back strengthening exercises; f/u in 4 wks  if symptoms do not improve in 6 wks, consider imaging studies, referral to surgeon  prevention: keep the back straight while lifting an object, bend at the knees, avoid sleeping on stomach, regular exercises that avoid repetitive twisting and bending o cauda equina syndrome  sx: low back pain, saddle anesthesia, bowel or bladder dysfunction; erectile dysfunction, possible lower extremity weakness & loss of reflexes d/t compression of multiple sacral nerve roots  tx: surgical emergency; surgical decompression o sciatica  d/t herniated disk, usually L4-L5 or L5-S1

sx: pain in distribution of lumbar or sacral nerve roots +/- motor or sensory deficits; back pain w/radiation down the back of the leg or lateral foreleg  L4: dorsiflexion of foot, knee reflex, inner calf sensation  L5: dorsiflexion of toe, inner foot sensation  S1: eversion of foot, ankle reflex, outer foot sensation  dx: straight leg test to 45-60 degrees  tx: encourage continuing usual activities, avoid twisting motions or heavy lifting, NSAIDs or other non-narcotic analgesics, narcotics only if severe pain & only use short term, muscle relaxant, massage, acupuncture, weight loss, back strengthening exercises; f/u in 4 wks  steroid injection can be tried if no response to conservative management  if symptoms do not improve in 6 wks, consider imaging studies, referral to surgeon o spondylolysis  defect in part interarticularis (congenital or secondary to stress fracture)  ankylosing spondylitis: occurs in young ( CT with intrathecal contrast)  give glucocorticoids first before dx testing if obvious cord compression in order to decrease cord pressure  malignancy  cancers that metastasize to bone: lung, breast, prostate, lymphoma, GI, melanoma  multiple myeloma: increased calcium, mild renal failure (increased Cr), anemia  sx: systemic complaints (fever, decreased weight), pain at night or that is not relieved by lying supine; new onset of pain in pt >50yo  dx: lateral and AP x-ray of spine, ESR, CBC  tx: chemo for lymphoma, radiation for solid tumors  TB osteomyelitis of spine (Pott disease)  Sx: chronic and slowly progressive pain, fever, night sweats  Epidural abscess  Usually d/t staph aureus  Dx: elevated ESR, fever  Tx: steroids, anti-staph antibiotic (vancomycin or linezolid empiric tx; if sensitive, change to beta lactam (oxacillin, nafcillin, cefazolin) + gentamicin; surgical drainage for large collections o Lumbar spinal stenosis (neuropathic claudication)  Narrowing of the spinal canal pressure on the cord (esp in back extension d/t cord compression on ligamentum flavum); pt >60 yo; a/w degenerative joint disease (degenerative central canal stenosis)  Enlarging osteophytes at facet joints and hypertrophy of the ligamentum flavum  Sx: pain with walking (esp downhill= back extension; radiates to butt and lateral thighs), may have unsteady gait & leg weakness when walking  Dx MRI  Tx: weight loss, steroid injections; surgical correction to dilate the spinal canal  Osteomyelitis o Agents: staph aureus (#1), salmonella (sickle cell pt)  Risk factors: IV drug use, sickle cell, immunocompromised  Children obtain infection via hematogenous spread  adults obtain infection via contiguous (nearby) infection (often a/w vascular insufficiency and diabetes) o diabetes ulcer from peripheral neuropathy or vascular disease; may have a draining “purulent sinus tract” in the lesion o sx:  vertebral osteomyelitis: tenderness to gentle percussion over the spinous process; back pain. Low grade fever, elevated ESR o dx: x-ray (best initial), biopsy (most accurate); MRI if initial x-ray is normal (bone scan if MRI contraindicated); ESR can be used to f/u response to therapy, elevated platelets (inflammatory marker); +/- fever or elevated WBC  use MRI 1st for vertebral osteomyelitis o tx: wait for cultures and treat appropriately; long-term IV antibiotics +/- surgery  staph: oxacillin, cefazolin, nafcillin, or ceftriaxone if sensitive; vancomycin or linezolid if resistant  gram (-) bacilli such as E.coli: fluoroquinolones (ciprofloxacin)  SE: interfere with bone growth (contraindicated in pregnancy and kids), achilles tendon rupture dermatology  acanthosis dermatosis (grover disease) o pruritus, erythematous-brown keratotic papules over the anterior chest, upper back, and lower rib cage  acanthosis nigricans o symmetrical hyperpigmented velvety plaques in the axilla, groin, and neck  a/w insulin resistance (diabetes mellitus, addison’s disease, polycystic ovarian syndrome, obesity); GI malignancy in older pts  acrochordons (skin tags) o multiple skin tags a/w insulin resistance, pregnancy, or crohn’s disease (perianal)  actinic keratosis o pre-malignant lesion (predisposes to SCC); occur in sun-exposed areas o dry scaly flat papules with an erythematous base; sandpaper-like texture; hyperkeratosis can become prominent “cutaneous horns” o dx: acanthosis (thickening of epidermis), parakeratosis (retention of nuclei in stratum corneum), dyskeratosis (abnormal keratinization), hyperkeratosis (thickening of stratum corneum)  angioedema o d/t C1 esterase inhibitor deficiency increased C2b and bradykinin  hereditary or d/t ACE inhibitor use (-pril); C1q normal in hereditary and low in acquired, C4 down in all forms o sx: rapid onset of non-inflammatory edema of the face/limbs/genitals, laryngeal edema, edema of the bowel colicky abdominal pain  episodes usually follow an infection, dental procedure, or trauma  atopic dermatitis o usually in infancy; involves cheeks, forehead, limbs 

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o sx: pruritus is usually the only sx basal cell carcinoma o most common malignant tumor of the eyelid (thinning or loss of eyelashes in the region of the tumor; bleeding and ulceration can occur)  tx: surgical excision using microscopically controlled margins (Mohs technique)  spread from a periocular BCC into the orbit can occur tx= enucleation of the eye o slow-growing papule with pearly rolled border, and overlying telangiectasia o dx: invasive clusters of spindle cells surrounded by palisaded basal cells blue nevi o smooth-surfaced, dome-shaped melanocytic papules that develop from macules; 60 yo  triggers: furosemide, NSAIDs, captopril, penicillamine, antibiotics o pruritic disease; tense blisters in flexural areas; urticarial plaques  does NOT involve mucous membranes o dx: IgG and C3 deposits at the dermal-epidermal junction (against the hemidesmosomes); subepidermal bulla with eosinophils capillary hemangioma o can be found in deep tissues and the viscer (sp. Liver)  thin walled BVs with narrow lumens willed with blood and separated by connective tissue; vessels are lined by endothelium that rapidly proliferates during the growth phase of the tumor o strawberry (infantile, capillary) hemangioma  variant of capillary hemangioma=most common benign vascular tumor in children; appear w/in the first few days-weeks of birth and grow rapidly during the first 1-2 yrs of life  superficial: bright red compressible plaques with sharply demarcated borders  deeper: duskier blue appearance  tx: reassurance; most self-resolve by 5-8 yo cavernous hemangiomas o soft blue compressible masses up to a few cm in size  large dilated vascular spaces; can appear on skin, mucosa, deep tissues, and viscera  a/w with von Hippel-Lindau disease when in the brain or viscera cherry hemangioma/ senile hemangiomas o most common benign vascular proliferation in adults; appear 30-40 yo o small bright red cutaneous papules  dilated capillaries and post-capillary venules in the papillary dermis that do not repress spontaneously cold injuries o frostbite  tx: rapid rewarming with warm water contact (irritant, allergic) dermatitis o type 4 HSR: a/w hx of exposure to irritant substance (plant uroshiol (poison ivy/oak/sumac=woody scrub, ginko fruit, mango skin), cosmetics, formaldehyde, fragrances, preservatives, rubber, nickel)  initial sensitization occurs w/in 10-14 days of exposure o pruritus, erythema, edema, vesicles & bullae; can be secondarily infected (impetiginized by staph or strep) o tx: avoid exposure, calamine lotion, topical antihistamines, topical corticosteroids, oral steroids dermatitis herpetiformis o a/w gluten sensitive enteropathy (celiac sprue or celiac disease), HLA B8/DR3/DQw2 o pruritic papules and vesicles on elbows, knees, buttocks, posterior neck, scalp o dx: anti-endomysial antibodies o tx: dapsone erythema multiforme o a/w recent herpes simplex infection o most acral in distribution hypersensitivity reactions o antibody mediated (type 2): immune hemolytic anemia, Rh hemolytic disease of the newborn o immune complex- mediated (type 3): serum sickness o cell-mediated (type 4): tuberculin skin test, allergic contact dermatitis  latent period of 1-2 days before dermal inflammation ichthyosis vulgaris o normal skin at birth with gradual progression ot dry scaly skin; skin is dry & rough with horny plates of the extensor surfaces of the limbs; condition worsens in the winter d/t dryness; “lizard skin” Kaposi sarcoma o a/w HHV8 infection o Reddish purple dark vascular plaques or nodules on cutaneous or mucosal surfaces keratoacanthoma o low-grade malignancy; pathologically resembles SCC o solitary, firm, round, skin colored or reddish plaque nodule with central keratin plug (“vocano-like” nodule) lentigo simplex o round or oval macule with even pigmentation; d/t intraepidermal melanocyte hyperplasia lichen planus o inflammatory; pruritic violaceous flat-topped papules with fine white streaks on the surface (wickham’s striae) lichen simplex chronicum o d/t chronic scratching, picking, or rubbing of the skin o thickened plaques on the skin with increased skin markings and hyperpigmentation, or thickened papules with excoriated centers melanoma o most common malignancy in women 25-29 yo o risk factors: fair skin, hx of blistering sunburns, family hx, dysplastic nevus syndrome, atypical nevi and >100 typical nevi o solitary lesion; mole that has changed in size or color, and becomes symptomatic (pruritic, painful, bleeding)  asymmetry, border irregularities, color variations, diameter >6mm, enlargement

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o dx: excisional biopsy w/ narrow margins o tx: if depth 1mm sentinel lymph node study miliaria (heat rash) o superficial aggregated small vesicles, papules, or pustules over the trunk; burning & itching neurocutaneous diseases o tuberous sclerosis  sx: neuro sx (seizures, progressive psychomotor retardation, slowly progressive mental deterioration), skin sx (adenoma sebaceum, shagreen patches, ash leaf patches), retinal lesions, cardiac rhabdomyomas  adenoma sebaceum: reddened facial nodules  shagreen patches: leathery plaques on the trunk  ash lead patches: hypopigmented areas  tx: seizure control o neurofibromatosis (von Recklinghausen disease)  sx: neurofibromas, 8th CN tumors, café au lait spots (cutaneous hyperpigmented lesions), meningioma and gliomas  neurofibromas: soft, flesh colored lesions attached to peripheral nerves  tx: 8th CN lesions may need surgical decompression to help preserve hearing o sturg-weber syndrome  sx: port-wine stain of face, seizures, CNS (homonymous hemianopsia, hemiparesis, mental subnormality)  dx: skull x-ray (calcification of angiomas)  tx: control seizures pellagra o d/t niacin deficiency o sx: dermatitis, diarrhea, dementia pemphigus vulgaris o blistering of skin & mucous membranes; (+) nikolsky’s sign o dx: IgG deposits intercellularly in the epidermis (autoantibodies against desmoglein) o tx: steroids, immunosuppressive agents (azathioprine, prednisone, methotrexate) porphyrias o porphyria cutanea tarda  deficiency of uroporphyrinogen decarboxylase (in heme synthesis pathway)  painless blisters, increased skin fragility on the dorsal surfaces of the hands, facial hypertrichosis & hyperpigmentation  triggers: ethanol, estrogens, hep C infection  dx: elevated urinary porphyrin  tx: phlebotomy, hydroxychloroquine, interferon alpha psoriasis o salmon colored patches, silvery scales over the extensor surfaces of the elbows, knees, scalp, and trunk pyoderma gangrenosum: a/w inflammatory bowel disease rosacea o most common 30-60 yo o rosy hue (flushed skin) with telangiectasia over the cheeks, nose, and chin; papules and pustules may be present  flushing precipitated by hot drinks, heat, emotion o tx: topical metronidazole for the papules/pustules seborrheic dermatitis o a/w parkinson’s disease, HIV o acute or chronic papulosquamous dermatitis; dry/waxy scales and underlying erythema  usually involves: scalp, central face, presternal, interscapular area, umbilicus, and body folds o tx: topical antifungal agents seborrheic keratosis o seen in elderly pts o greasy brown crust-like lesions with a stuck on appearance spider angiomas o a/w pregnancy, liver disease, pt with estrogen supplements (OCPs) o dilated cutaneous arterioles; central papule with radiating blanching capillaries squamous cell carcinoma o aggressive, metastasizes frequently  risk factors: exposure to sunlight (#1), arsenic, aromatic hydrocarbons, chronic osteomyelitis, chronic scars vitiligo o total depigmentation d/t autoimmune destruction of melanocytes  a/w other autoimmune diseases: pernicious anemia, autoimmune thyroid disease such as grave’s or chronic autoimmune thyroiditis, type 1 DM, primary adrenal insufficiency, hypopituitarism, alopecia areata  peak age 20-30 o macular depigmentat that involves acral and peri-orifical areas drug induced rashes/reactions o agents: PCNs, sulfa drugs (thiazides, furosemide, sulfonylureas), allopurinol, phenytoin, lamotrigine, NSAIDs o morbilliform rash=mild o erythema multiforme: multiple target lesions that can be confluent; can also be d/t herpes or mycoplasma  tx: prednisone o phototoxic drugs: tetracyclines (esp. doxycyline)  exaggerated sunburn reaction with erythema, edema, and vesicles over sun-exposed areas o >30% of the body surface area is involved o steven johnson syndrome (erythema multiforme major) & toxic epidermal necrolysis (TEN)  immune complex mediated HSR  drugs: sulfonamides (TXM-SMX), NSAIDs, anticonvulsants (phenytoin), barbiturates  Steven johnson syndrome  sudden onset mucocutaneous lesions over 2 sites (usually oral and conjunctival); epidermal necrolysis syndrome; includes mucosal surfaces; target appearance of lesions; fever, tachycardia, hypotension, altered consciousness, conjunctivitis, seizures, coma can occur

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o respiratory epithelium involvement  respiratory therapy  100, systolic BP staph  risk factors: lymphatic obstruction, local trauma or abscess, fungal infections, DM, alcoholism  sx: bright red hot swollen lesion (fiery red tender painful plaque w/ well demarcated edges); leukocytosis, fever, chills if bacteremia  complications: sepsis, local spread, necrotizing fasciitis  tx: uncomplicated IM or oral PCN or erythromycin, otherwise same as cellulitis o cellulitis  infection of dermis & subcutaneous tissue  agents: staph>strep (group A=beta hemolytic=pyogenes)  chronic fungal foot infection can serve as a nidus for bacterial cellulitis (should be eradicated in recurrent cellulitis)  Means of bacterial invasion Likely pathogen wounds, abscesses staph aureus local trauma, breaks in skin step pyogenes (group A strep) acute sinusitis haemophilus influenzae immersion in water pseudomonas aeruginosa, aormonas hydrophila, vibrio vulnificus  risk factors: breaks in skin venous stasis diseases, lymphedema, diabetic ulcers  sx: warm red swollen tender skin, +/- fever  orbital involvement= medical emergency  signs of toxicity: high grade fever w/ rigors & chills, malaise, fatigue, confusion  Tx: staph PCN or cephalosporin; start IV antibiotics until signs of infection improvement, then follow up oral antibiotics for 2 weeks  if signs of toxicity IV nafcillin or cefazolin; oral dicloxacillin for mild cellulitis o hair follicle infections: folliculitis, furuncles, carbuncles  agents: staph aureus  folliculitis: pus is limited to the epidermis  furuncle (boil): small abscess  carbuncles: collection of furuncles; diabetic pt at increased risk acne o comedones (blackheads & whiteheads)  nodulocystic & scarring o tx:  mild: topical retinoids or topical benzyl peroxide  if ineffective topical erythromycin or clindamycin  mild-moderate: topical vit A (tretinoid, adapalene, tazarotene) or benzyl peroxide + topical antibiotic (erythromycin, clindamycin, tetracycline)  if ineffective oral antibiotic (minocycline or doxycycline)  moderate-severe: oral doxycycline against Propionibacterium acnes + oral vit A (isotretinoin)  vit A SE: teratogenic (oral or topical), hyperlipidemia (oral)  nodulcystic & scarring acne (oral isotretinoin)

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cutaneous abscesses o collection of pus w/in the dermis and deeper skin tissues; painful, tender, fluctuant red nodules (start as pustule surrounded bya rim of erythematous swelling) o agents: usually polymicrobial of skin & adjacent mucous membrane flora o tx: incision & drainage with dry dressing  Gram stain, culture, and systemic antibiotics are rarely necessary herpes zoster (shingles) o d/t varicella zoster virus latent infection (initial infection=chicken pox); latent infection in the sensory dorsal root ganglia o sx: pain precedes vesicular eruption by ~48 hrs; eruption along the affected dermatome; eruption lasts 2-3 wks o tx: acyclovir herpetic whitlow o infection of the hand with HSV1 or 2 o sx: throbbing pain in distal pulp space; non-purulent vesicles on the volar surface; systemic sx (fever, lymphadenopathy) can occur o dx: multinucleated giant cells seen on Tzanck smear o tx: self-limiting; oral acyclovir and topical bacitracin to prevent secondary infection Impetigo o Superficial skin infection o Agents: staph aureus, strep pyogenes (group A beta-hemolytic strep) o Sx: weeping, crusting, oozing, draining of skin; pruritis honey colored macules, vesicles, and bullae (skin blisters that enlarge and rupture) o Tx:  Mild: topical mupirocin, bacitracin, or repatamulin  Severe: oral dicloxacillin or cephalexin molluscum contagiosum o agent: poxvirus  a/w cell-mediated immunodeficiency (HIV, corticosteroid use, chemotherapy) o multiple dome shaped lesions with central umbilication; pink translucent quality and may be arranged in a linear fashion d/t spread of virus to adjacent skin by scratching (can cause conjunctivitis if lid margins infected)  kids (trunk & extremities), adults (face, lower abdomen, genitals), STD (penis, pubis, inner thighs) o tx: curettage or liquid nitrogen pityriasis rosea o a/w human herpesvirus 7 (HHV7) o oval fawn colored plaques 200 and no AIDS defining illness): influenza, hep B, Hep A (if men who has sex with men), pneumococcus; Td booster every 10 yrs  if not vaccinated as a child, pt should also receive: MMR, varicella (zoster once >60 yo)  avoid live vaccines (except MMR and varicella/zoster): BCG, anthrax, oral typhoid, intranasal flu, oral polio, yellow fever vaccines o Normal CD4 count is 600-2500 cells/mm3  CD4 12 or 100.4 (38 C) or < 96.8 (36 C), RR> 20 or PaCO2 3 days add in vancomycin  if fever persists 5-7 days after vanco add antifungal (fluconazole or amphotericin B)  other vaccination o all pt >18 yo should receive 1x TDaP booster instead of the Td booster (every 10 yrs) o pneumococcal vaccine is administered 1x @65 yo, or for pt with chronic condition (lung/CV, renal, asplenia, immunocompromised, DM) as a vaccine with booster 5 yrs later if given before age 65 Biostatistics + + A B C D  negative predictive value (NPV): the probability of being free of a disease if the test result is negative o a pt with a high probability of having a disease will have a low NPV; the prevalence of the disease is directly related to the pre-test probability of having the disease  normal (bell-shaped) distribution: 68%=1SD from the mean, 95%=2 SD, 99.7%=3 SD  case-control study o used to compare the exposure of people with the disease (cases) to the exposure of the people without the disease (controls) o compare results using an exposure odds ratio  if the prevalence of the disease is low, the odds ratio approximates the relative risk  cohort study o people are followed over time for the occurrence of the disease o measure: relative risk or relative rate, median survival  RR>1 indicates a positive association between the risk factor and the outcome, RR0.1 secsodium bicarbonate (narrows QRS complex by alleviating depressive action on sodium channels)

warfarin Vitamin K, fresh-frozen plasma  Neuroleptic malignant syndrome o Drug induced idiosyncratic reaction  Drugs: dopaminergic antagonists (haloperidol and other typical neuroleptic agents, atypical neuroleptics)  Sx start w/in 2 weeks of starting the precipitating drug o Sx: fever (hyperthermia), muscle rigidity, autonomic instability (diaphoresis), altered mental status (confusion) o Dx: elevated creatine kinase, leukocytosis, electrolyte abnormalities o Tx: immediate cessation of the causative drug, dantrolene (muscle relaxant), bromocriptine (dopamine agonist), amantadine (antiviral with dopaminergic properties)  Chemical damage to eye #1 step is to wash the eye with copious amounts of water >15 min o Acid exposure has higher chance of recovery; alkaline exposure causes permanent corneal damage  Alcohol: 12 Oz beer, 8 Oz wine, 5 oz liquor are all equivalent to 14 g alcohol; recommended weekly limit is 40 g Pharmacology  Side effect overview o Ototoxic: cisplatin, carboplatin, aminoglycosides o Optic neuritis: ethambutol, hydroxychloroquine o Peripheral neuropathy: phenytoin, isoniazid, vincristine, heavy metals, chronic alcoholism o Thyroid dysfunction: amiodarone, lithium  ACE inhibitors (-pril) o Inhibit conversion of angiotensin I angiotensin II (vasoconstrictor) o Action in heart: reduces preload & afterload, prevents remodeling  Drug of choice for CHF d/t survival advantage o SE: cough, hyperkalemia, angioedema, acute renal failure, dry cough, urticarial skin rash, altered sense of taste, leukopenia, pancytopenia, hypotension  Contraindicated: pregnancy, renal failure, bilateral renal artery stenosis  Acetazolamide o Carbonic anhydrase inhibitor decreases serum bicarbonate production, hypokalemia  Acyclovir

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o SE: crystalline nephropathy (prevent/treat with aggressive IV hydration) Angiotensin receptor antagonist (ARBs; -sartan) o MOA: Competitive inhibition of angiotensin II receptor o SE: leukopenia, pancytopenia, hypotension, hyperkalemia, acute renal failure  Contraindications: pregnancy, bilateral renal artery stenosis Aspirin o Se: tinnitus, sensorineural hearing loss (high dose 6-8 g/day) Azathioprine o Purine analog; converted to 6-mercaptopurine; inhibits purine synthesis o SE: diarrhea, leukopenia, hepatotoxicity Benzodiazepines o Lorazepam (atovan) has no decreased respiratory drive (so can be given continuously or at higher doses)  Uses: alcohol withdrawal o Avoid in elderly patients (exacerbates mental status changes and increases fall risk) Beta-blocker (atenolol, metoprolol) o Action in heart: prevent and reverse adrenergically mediated intrinsic myocardial dysfunction and remodeling o Kidney: decreases renin synthesis/release o SE: bronchospasm, bradycardia, depression, sleep disturbances (insomnia), fatigue, may increase TGs and decrease HDL (hyperlipidemia), sedation, erectile dysfunction  May mask hypoglycemia sx in diabetic pts on insulin  Contraindications: asthma, 2nd or 3rd degree heart block Buproprion o Use: smoking cessation Calcium channel blockers (amlodipine, nifedipine, diltiazem, verapamil) o Blockade of L-channels, reducing intracellular calcium vasodilation  Contraindications: heart failure, significant heart block o Dihydropyridines (amlodipine, nifedipine)  SE: tachycardia, flushing, hyperkalemia, edema o Non-dihydropyridines (diltiazem, verapamil)  SE: heart block, constipation Carvedilol o Alpha & beta blocker colchicine o SE: diarrhea, bone marrow suppression neutropenia; contraindicated in renal insufficiency Clonidine o Alpha-2 agonist o SE: postural hypotension, drowsiness, dry mouth, rebound hypertension with abrupt withdrawal Clozapine o SE: agranulocytosis (monitor CBC q 1-2 wks) Cyclophosphamide o SE: acute hemorrhagic cystitis, bladder cancer, sterility, myelosuppression  MESNA and increased fluid intake help to avoid bladder SE (d/t acrolein) Cyclosporine o MOA: calcineurin-inhibitor; inhibits transcription of IL-2 and other cytokines (mainly inhibits T-helper lymphocytes) o SE: nephrotoxicity (azotemia, hyperuricemia, hyperkalemia, hypophosphatemia, hypomagnesemia; HUS rare), HTN (renal vasoconstriction and sodium retention; tx calcium channel blocker), neurotoxic (headache, visual changes, seizures, mild tremor, akinetic mutism), glucose intolerance, infection, malignancy (increased risk of squamous cell carcinoma of the skin and lymphoproliferative disorders), gingival hypertrophy, hirsutism, GI (anorexia, N/V, diarrhea) Digoxin o Verapamil decreases the renal clearance of digoxin o SE: anorexia, N/V, bidirectional ventricular tachycardia, accelerated junctional rhythms Fluphenazine o Typical antipsychotic; injected every 2-3 wks in schizophrenics with poor copmlicant  More potent than haloperidol o SE: hypothermia (inhibits shivering mechanism and/or autonomic thermoregulation) Hydralazine o MOA: arterial vasodilation o SE: reflex tachycardia, headache, angina, SLE-like syndrome  Contraindications: severe coronary artery disease Isoniazid o SE: liver damage Leucovorin o Folinic acid (derivative of tetrahydrofolic acid); antidote to methotrexate; folate rescue for bone marrow and GI mucosa cells Loop diuretics (furosemide) o MOA: inhibit Na-K-2Cl carrier in thick ascending limb or loop of henle o Se: sensorineural hearing loss, hypokalemia, metabolic alkalosis (d/t excretion of H+), prerenal renal failure (d/t decreased circulating blood volume), rash, hyperuricemia, hyperglycemia, hypocalcemia  Contraindications: gout, hypokalemia Macrolides o Azithromycin  SE: prolonged QT interval Metformin o SE: severe lactic acidosis  Stop metformin if Cr>1.3-1.4 Metoclopramide o Dopamine receptor antagonist; prokinetic (increased peristalsis, increased strength of gastric contractions, relaxation of the pyloric sphincter)

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o Tx: nausea, gastroparesis o SE: agitation, loose stools, extrapyramidal sx (tardive dyskinesia, dystonic reactions, parkinsonism) Mycophenolate o MOA: reversible inhibitor of inosine monophosphate dehydrogenase (rate-limiting enzyme in de novo purine synthesis) o SE: bone marrow suppression Nitroprusside o Vasodilator; direct arterial & venous dilator o SE: weakness, fatigue, nausea, muscle twitching, cyanide toxicity Neuromuscular blocking agents o Succinylcholine  Depolarizing neuromuscular blocker; rapid onset (45-60 sec), rapid offset (6-10 min)  SE: hyperkalemia arrhythmias  Contraindications: hyperkalemia, crush/burn injuries >8hrs old (d/t risk of rhabdomyolysis), pts with demyelinating syndrome (Guillain-barre), pts with tumor lysis syndrome o Atracurium  Metabolized in plasma and hydrolyzed by serum esterases  Safe to use in pt with renal and liver disease o Pancuronium  Excreted mostly unchanged in the urine o Mivacurium  Excreted mostly unchanged in the urine o Rocuronium  Clearly mostly by the liver Potassium sparing diuretics (spironolactone) o MOA: competitive inhibition of aldosteronerenal sodium loss o SE: hyperkalemia, gynecomastia, diarrhea  Contraindication: renal failure Proton pump inhibitors (omeprazole) o SE: increased gastrin levels Tacrolimus o Calcineurin-inhibitor (similar to cyclosporine); inhibits IL-2 transcription; macrolide antibiotic produced by fungi o SE: nephrotoxicity (azotemia, hyperuricemia, hyperkalemia, hypophosphatemia, hypomagnesemia; HUS rare), HTN (renal vasoconstriction and sodium retention; tx calcium channel blocker), neurotoxic (headache, visual changes, seizures, mild tremor, akinetic mutism), glucose intolerance, infection, malignancy (increased risk of squamous cell carcinoma of the skin and lymphoproliferative disorders), GI (anorexia, N/V, diarrhea)  Most common: neurotoxic, diarrhea, glucose intolerance  Unlike cyclosporine, it does not cause gum hypertrophy or hirsutism Tetracyclines o Doxycycline  SE: phototoxicity (exaggerated sunburn reaction with less sun exposure time) Thiazide diuretics (hydrochlorothiazide, chlorthalidone) o MOA: inhibit Na-Cl transporter in the early distal tubule  sodium diuresis, volume depletion, possibly lower peripheral vascular resistance o SE: hypokalemia, hyponatremia, hypercalcemia, hyperuricemia, hyperglycemia (carbohydrate intolerance), elevation of cholesterol & triglyceride levels (hyperlipidemia), metabolic alkalosis, hypomagnesemia, orthostatic hypotension, photosensitivity  Contraindications: DM, gout, hypokalemia Toradol (ketorolac) o NSAID that can only be given 110), nonhemorrhagic stroke w/in 2 mo, surgery w/in past 10 days, thrombocytopenia (14 days and do not have an increase risk of bleeding  other options for tx= catheter extraction, catheter fragmentation, surgical thrombectomy