10th Lecture (NCM 104 CD II) Care of Clients With Problems In

Care of Clients with Problems Problems In Inflammatory Inflammatory & Immunologic Response, Perception Perception & Coordination (NCM104)  Patients With Communicable Diseases II 

Vector Borne Diseases Malaria (Ague) 

 

Is an acute and chronic parasitic disease transmitted transmitted by the bite of  infected mosquitoes and Is confined mainly to tropical and subtropical subtropical areas The fever associated with this disease is called “Afternoon fever”

LOOKY HERE 

Topics Discussed Here Are: 1. V ec ect or or Bo Bor ne ne Di Di se se as as es es a. Malaria (A (Ague)  b. Dengu Denguee Feve Feverr (Bre (Breakb akbon onee Feve Fever/H r/Hemor emorrha rhagic gic Fever/Dandy Fever) c. Fila Filari rias asis is (Ele (Eleph phan anti tias asis is))

d.

2.

Leptospirosis (Weil’s Disease, Canicola Fever/Mud Fever) e. Lyme Disease f. Rock Rocky y Mou Mount ntai ain n Spo Spott tted ed Feve Fever  r  Sexu Sexuall ally y Tran Transmi smitte tted d Dise Diseas asee a. Gono Gonorrh rrhea ea (Cla (Clap/F p/Flo lores res Blan Blanca cas/G s/Glee leet) t)

 b. c.

Syphilis (Lues Venereal/Morbus Gallicus Acquir Acquired ed Immune Immune Defici Deficienc ency y Syn Syndro drome me (AIDS) (AIDS)

ETIOLOGIC AGENT - Protozoa of genus plasmodia genus plasmodia •

 Plasmodium falciparum (Malignant tertian)

•

 Plasmodium vivax (Benign tertian)

•

 Plasmodium malariae (Quartan)  Plasmodium ovale

•

INCUBATION PERIOD -  P. Falciparum = 12 DAYS -  P. Vivax = 14 DAYS -  P. malariae = 30 DAYS

Other CMs   

Easy fatigability fatigability Anemia Shock, due to bleeding (↓ Platelet)

MODE OF TRANSMISSION 1. Bite of an infected female Anopheles mosquito 2. 3. 4.

Bloo Blood d tra trans nsfu fusi sion on Rare Rare occasio occasions, ns, from from shared shared contamin contaminated ated needles needles Transpl Transplacen acental tal trans transmiss mission ion of of congen congenital ital malaria malaria

CLINICAL MANIFESTATIONS 1. 2. 3. 4.

Paroxysm Paroxysmss with shakin shaking g chills chills – Physiolog Physiologic ic compensa compensation tion (ATP (ATP is being being used) used) Rapi Rapidl dly y ris risin ing g feve fever, r, HA Profuse Profuse sweari swearing ng – Due Due to chilling chilling to to remove remove ATP ATP breakdo breakdown wn Myalgia Splenomegaly (↑ Heme breakdown due to parasites), Hepatomegaly Hepatomegaly 5. Splenomegaly 6. Orth Orthos osta tati ticc hypo hypote tens nsio ion n 7. Paroxysm Paroxysmss may last last for 12 12 hours, hours, may attac attack k daily or or every every 2 days 8. In ch children: a. Feve Feverr – Cont Contin inuo uous us  b. Convul Convulsio sions, ns, GI GI Sympto Symptoms ms – Prom Promine inent nt c. Splenomegaly 9. Cer Cerebra ebrall Ma Malari laria: a: a. Severe HA, Vomiting, Changes in sensorium  b. Jackso Jacksonia nian, n, Gran Grand d mal mal seizur seizuree Due to altered blood component going to the brain Due Will Will cause ↑ ICP

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REMEMBER   jcmendiola_Achievers2013

 Antipyretics with ANTICOAGULANT  effect are not given

PATHOPHYSIOLOGY  Anopheles mosquito gets the parasite from an infected person

Parasite multiplies in in the intestine of the mosquito ( Producing sporozoites) sporozoites)

Sporozoites discharged discharged into the saliva of the mosquito

Mosquito bites humans then injects the parasites (2 Phases of asexual cycle cycle within humans )

When sporozoites inoculate to the human blood Changed form into “exoerythrocytic” and carried to the liver 

Erythrocytic – Causes pathologic findings to human host

They invade hepatocytes

DIAGNOSTIC PROCEDURE 1.

Malarial Malarial Smear Smear – Blood Blood is stain stained ed on a film film and exam examined ined 2. Rapid Diagnostic Test (RDT) – Gives results within 10 – 15 minutes (Like a pregnancy test, but blood)

MANAGEMENT 1.

Medical REMEMBER  a. Anti Anti-m -maalari larial al dru drugs gs  Antibiotics are NOT given with Chloroquine Chloroquine – Except P. Except P. malariae  MALARIA, an  ANTI-MALARIAL Quinine drug is used instead  Sulfadoxine Sulfadoxine –  P.  P. falciparum Primaquine Primaquine –  P.  P. vivax and ovale  b. Erythroc Erythrocyte yte exchange exchange tran transfusi sfusion on – To repla replace ce blood blood componen components ts Nursi ursin ng Mana Manage geme ment nt a. Clos Closel ely y mon monit itor or clie client nt!! b. I&O Serum bilirubin, BUN creatnine, parasitic count Respiratory Respiratory and Renal symptoms – Determine ABGs and Plasma electrolyte c. Tepi Tepid d Spo Spong ngee Bat Bath! h! d. Heat Heat and and Hot Hot drin drinks ks duri during ng chil chillin ling g e. Comfort f. Drin Drink k ple plent nty y of of flu fluid idss g. Clot Clothi hing ng sho shoul uld d be kep keptt dry dry h. WOF: Neurologic toxicity  Due to Quinine i. Eval Evalua uate te the the deg degre reee of of ane anemi miaa  j.  j. WOF: WOF: Abn Abnor orma mall blee bleedi ding ng k. Consider SEVERE MALARIA as MEDICAL EMERGENCY  Monitor VS

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2.

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PREVENTION and CONTROL

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1. 2. 3. 4. 5.

All cases should be reported Screening of all infected persons from mosquitoes Breeding places must be destroyed Use of sprays / Effective insecticides Mosquito nets 6. Insect repellents 7. People living in malaria-infested areas SHOULD NOT DONATE BLOOD (For at least 3 years) 8. Blood donors are SCREENED

 NURSING DIAGNOSES -

Altered body temperature Activity intolerance Knowledge deficit Altered nutrition: Less than body requirements

Dengue Fever (Breakbone Fever/Hemorrhagic Fever/Dandy Fever/Infectious Thrombocytopenic Purpura )  Acute febrile disease caused by infection with one of the serotypes of dengue virus 

Dengue Hemorrhagic Fever  A SEVERE, or FATAL manifestation (Bleeding diathesis and hypovolemic shock) o

ETIOLOGIC AGENTS 1. Flavivirus 1, 2, 3, 4, a family of Togaviridae, small viruses that contain SINGLESTRANDED RNA 2. Arboviruses group B

MODE OF TRANSMISSION 1. Bite of  Aedes Aegypti a. Day-biting mosquito (Appears 2 hours AFTER SUNRISE, 2 hours BEFORE SUNSET)  b. Breed in stagnant water  c. Limited, low-flying movement d. Fine white dots at base of wings, white bands on legs 2.  Aedes albopictus a. May contribute to the transmission of the dengue virus in rural areas 3. Other contributory mosquitoes a. Aedes polynesis b. Aedes scutellaris simplex

INCUBATION PERIOD -

3 – 14 Days Commonly 7 – 10 Days

PREIOD OF COMMUNICABILITY 

Day before the febrile period to the end

 Mosquito is infective from Day 8 – 12 after the blood meal and remains infective throughout its life

SOURCES OF INFECTION 1. 2.

Infected persons Standing water 

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INCIDENCE 1.

Age

2. 3. 4.

a. Any age  b. But common among children (Peak: 4 – 9 y/o) Sex – Both Season – More frequent during rainy season Location – More prevalent in urban communities

PATHOPHYSIOLOGY

Infectious virus is deposited in the skin

Initial replication occurs at the site of  infection and in local lymphatic tissues Viremia (viruses on blood) occurs within a fe w days th th (Lasting until 4  – 5 day after onset of symptoms)  At the site of petechial rash, non-specific changes are noted, which include endothelial swelling , perivascular  edema and extravasation of blood

Marked ↑ in vascular permeability , hypotension, hemoconcentration, thrombocytopenia with ↑ platelet agglutination and or moderate DIC ↑ Permeability to vascular endothelium and loss of plasma from the intravascular space

CLINICAL MANIFESTATIONS 1.

2.

Pathophysiological abnormality like Hypovolemia

Dengue Fever  1. Prodromal symptoms: a. Malaise and anorexia (up to 12 hours)  b. Fever and Chills with frontal HA, ocular pain, myalgia, severe  backache and arthralgia 2. N/V 3. Fever – Non-remitting, persists for 3 – 7 days 4. Rash – Prominent on extremities and trunk (Face in some isolated cases) 5. Petechiae – Near end of the febrile period (Most common on lower extremities) Dengue Hemorrhagic Fever (DHF)  Severe form  Manifested by: a. Fever, hemorrhagic diathesis  b. Hepatomegaly, hypovolemic shock 

PHASES OF THE ILLNESS 1. Initial Febrile Phase (Lasting from 2 – 3 Days) a. Fever (39 - 40°C) with HA  b. Fever convulsions c. PALMS and SOLES = FLUSHED! d. (+) Tourniquet test e. Anorexia, Vomiting, Myalgia f. Maculopapular / Petechial rashes (Starts in distal portion of extremities, sparing the axilla and chest)

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g. Herman’s Sign = Skin appears PURPLE with blanched areas of varying sizes  PATHOGNOMONIC SIGN

2.

h. Generalized abdominal pain, hemorrhagic manifestations [(+) Tourniquet test,  purpura, epistaxis, gum bleeding] Circulatory Phase a. Fall of temperature with circulatory changes (3 rd – 5th Day)  b. Client becomes restless with cold clammy skin c. Cyanosis d. Thrombocytopenia with SHOCK! e. Bleeding diathesis leads to GIT Hemorrhage f. SHOCK = Due to loss of plasma (↑ Hct) g. Pulse: Rapid and weak; Narrow pulse pressure; ↓ BP h. May result to coma, MAC and DEATH within 2 days i. Therapy: Recovery 2 – 3 days

CLASSIFICATION ACCORDING TO SEVERITY (Halstead and Nimmanitya) Grade Signs and Symptoms Grade I 

  

Grade II 

 

Grade III 



Grade IV 

 

Fever  Hemorrhagic manifestation (+) Tourniquet Test All signs of Grade I Spontaneous bleeding (Nose, gums, GIT) Respiratory failure (Weak pulse, narrow pulse pressure, hypotension, cold clammy skin, restlessness) Profound shock  Undetectable BP and Pulse

COMPLICATIONS 1.

2.

3.

Dengue Fever  a. Epistaxis; menorrhagia b. GI Bleeding c. GI Disorder (Peptic Ulcer) DHF a. MAC  b. Hyperkalemia c. Tissue anoxia d. Hemorrhage into CNS / Adrenal glands e. Uterine bleeding f. Myocarditis Severe Manifestations a. Dengue Encephalopathy § ↑ Restlessness, apprehension / anxiety § Disturbed sensorium, convulsions § Spacity, hyporeflexia

DIAGNOSTIC TESTS 1. Tourniquet Test ©

Screening test Occlusion of arm veins for 5 mins © 2. Platelet Count (decreased) – Confirmatory test 3. Hemoconcentration - ↑ of 20% in Hct or steady rise in Hct 4. Occult blood

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5.

Hemoglobin determination

TREATMENT MODALITIES - There is no effective antiviral therapy for dengue fever (Entirely symptomatic) •

Analgesic Drugs – HA, ocular pain, myalgia IV Infusion – To prevent dehydration and replacement of plasma

•

Blood Transfusion – For severe bleeding

•

O2 Therapy – Clients with shock  Sedatives – To allay anxiety and apprehension

•

•

 NURSING MANAGEMENT 1. 2. 3.

4. 5. 6. 7.

Mosquito-free environment Rest during bleeding episodes VS are promptly monitored  NOSE BLEED = Trunk elevated, apply ice bag (Bridge of nose, forehead) Observe for signs of SHOCK – Slow pulse, cold clammy skin, prostration, ↓ BP Trendelenburg Position – To restore blood volume to head part Isolation not required – NOT INFECTIOUS!!

PREVENTION and CONTROL 1. 2. 3. 4.

Health Education! Early detection and treatment Treat mosquito nets with insecticides House spraying 5. Eliminate vectors by: a. Changing water / Scrubbing sides of flower vases (once a week)  b. Destroying breeding places c. Keeping containers covered 6. Avoid hanging too many clothes in the house 7. Case finding

 NURSING DIAGNOSES -

Altered body temperature Fear   Anxiety Knowledge deficit Activity intolerance

Filariasis (Elephantiasis)  

Parasitic disease caused by nematodes which are microscopic Threadlike African eye worm

CAUSATIVE ORGANISM - Wuchereria bancrofti – 4 – 5 cm long, affects lymph nodes and lymph nodes of legs, arms, vulva -

and breasts  Brugia malayi – Swelling of extremities confined to areas below knees and elbows  Brugias timori – Rarely affects genitals  Loa loa – Transmitted by the deer fly

MODE OF TRANSMISSION -

Mosquito bites

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PATHOPHYSIOLOGY Mosquito bites a person with lymphatic filariasis Microscopic worms circulating the person’s blood enter and infect the mosquito Microscopic worms enter lymph vessels where they grow into adults  Adult worm lives for 7 years in lymph vessels; they mate and release into bloodstream millions of microscopic worms (Microfilaria)

SYMPTOMS 1.

2. 3.

Begin with: On-and-off Chills • Headaches • Fever (3 months – 1 year) • Swelling, redness, pain in arms, legs or scrotum Areas of abscesses may appear due to dying worms / secondary bacterial infection

DIAGNOSTIC PROCEDURES Many mosquito bites over several months to years before filariasis takes place

 Adult worms die = First Symptoms Occur 

Damages kidney and lymph system

1.

Circulating Filarial Antigen (CFA) – Finger prick blood droplet 2. Larvae can be found in the blood 3. Patient’s History = Pattern of inflammation, signs of lymphatic obstruction

MODALITIES OF TREATEMENT 1.

Fluid collects and causes swelling in the arms, breasts, legs and for men the genital area

Swelling and decreased function of lymphatic system makes it difficult for the body to fight the infection

More bacterial infections in the skin, thus skin hardens and thickens (Elephantiasis)

2. Worms can obstruct the vessels causing the surrounding tissues to enlarge

3. In conjunctival filariasis, larvae migrate to the eyes and can sometimes be seen beneath the conjunctiva

4.

Blindness (Onchocerciasis)

 NURSING MANAGEMENT 1. 2. 3. 4. 5.

Health education – About mode of transmission Destruction of breeding places of mosquitoes Psychological and emotional support Personal hygiene Course of disease must be explained to client and family

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Ivermectin, albendazol, or Diethylcarbamazine (DEC) – Used in treatment and act by:  Eliminating the larvae  Impairing the adult worm’s ability to reproduce  Killing the adult worm Meds are given at low doses initially to prevent immunologic reactions due to large number of  dying parasites Surgery – To remove surplus tissue, drain the fluid, and minimize massive enlargement of the scrotum Elephantiasis of the legs = ELEVATE and ELASTIC BANDAGES DEC-fortified salt is helpful

PREVENTION and CONTROL   

Mosquito net Mosquito repellants between dusk and dawn Take yearly dose of meds that kills the worms circulating in the blood

 NURSNIG DIAGNOSES • • • •

Impaired physical mobility Knowledge deficit Impaired skin integrity Activity intolerance

Leptospirosis (Weil’s Diseases/Canicola Fever/Hemorrhagic Jaundice/Mud Fever/Swing Herd Disease)  

Zoonotic infectious bacterial diseases carried by animals, both domestic and wild Water / Food is contaminated by the infected which causes diseases when ingested / inoculated through the skin

ETIOLOGIC AGENT -  Leptospira interrogans – Spirochete genus of  Leptospira INCUBATION PERIOD -

6 – 15 DAYS

PERIOD OF COMMUNICABILITY   Leptospira – Urine (10 – 20 Days after onset)

SOURCE OF INFECTION  Rats –  L. icterohaemorrhagiae, L. bataviae  Dogs –  L. canicola  Mice –  L. grippotyphosa

MODE OF TRANSMISSION - Direct contact (Skin / mucous membranes)  ANIMALS, Human transmission is RARE •

Eyes, nose, mouth, semen / breaks in skin

CLINICAL MANIFESTATIONS 1.

2.

Septic Stage Febrile (4 – 7 Days) • Abrupt onset of remittent fever, chills, HA, anorexia • • Abdominal pain and severe prostration • Respiratory distress Immune or Toxic Stage •

With or without Jaundice (4 – 30 Days)

•

If SEVERE: Death occurs in 9 th – 16th Day 1. Anicteric Phase (Without Jaundice) Low-grade fever with rash • 2. Icteric Phase (With Jaundice)  Wet Syndrome Hepatic and renal manifestations (Prominent) •

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LABORATORY DIAGNOSIS 1.

BUN and Creatinine 2. Agglutination – Test done after 2 nd /3rd Week  a. Microagglutination  b. Macroagglutination c. Indirect Hemoagglutination 3. Impaired liver and kidney Tests

PATHOPHYSIOLOGY

Cattle, swine and other livestock

Dogs

Rodents, wild animals

Contact with contaminated water and soil entry through the eyes, mouth, and broken skin

Man

ORGANS OF THE BODY INVADED BY THE ORGANISM 1. LIVER = After gaining entrance, it multiplies in the bloodstream and invades this organ causing JAUNDICE (Icteric – Gives an orange-colored skin) 2. KIDNEYS = Inflammation of the nephrons and tubular necrosis resulting in RENAL FAILURE 3. Leptospira = May affect the muscles, causing PAIN and or EDEMA

4. EYES = Conjunctivitis, orange-colored sclera due to Icteric TREATMENT (MANAGEMENT) 1.

2.

Medical a. Suppression of causative agent  b. Fighting possible complications 1. Aetiotropic Drugs – Penicillin, Doxycycline, Ampicillin, Amoxicillin Doxycycline – 100 mg PO q12 hrs (1 week) • 2. Peritoneal Dialysis – If client has kidney failure 3. Administration of F&E and blood as indicated Nursing a. Isolate (Proper disposition of urine)  b. Darken room (Irritating to client’s eyes) c. Skin care to ease pruritus – No ointments on skin, except Calamine Lotion d. Close surveillance e. Keep homes clean f. Eradicate rats and rodents g. Health education on modes of transmission

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h. Encourage OFI (Oral fluid intake) PREVENTION and CONTROL 1. 2. 3. 4. 5.

Sanitation in homes, workplaces and farms Need for proper drainage system and control of rodents (40% - 60% infected) Animals must be vaccinated (Cattle, dogs, cats and pigs) Infected human and pets should be treated Information dissemination campaign

 NURSING DIAGNOSIS • • • • • • •

Body image disturbance High risk for injury Anxiety Altered nutrition: Less than body requirements Impaired physical mobility Impaired skin integrity Knowledge deficit

B. burgdorferi is injected into skin by the bite of an infected tick Spirochetes multiply and migrates outward within the dermis

 Appearance of characteristic EM lesions

Lyme Disease  Activation of inflammatory response to bacteria

 Multisystem illness caused by tick borne spirochete (Closely mimics Rheumatic(?) Disease)

CAUSATIVE AGENT

Spirochetes avoid the immune response by ↓ expression of surface proteins, which may interfere with the function of immune factors

  Borrelia burgdorferi Neutrophils fail to appear in the developing EM lesion

INCUBATION PERIOD 

Permitting bacteria to survive and eventually spread throughout the body

3 – 32 Days

MODE OF TRANSMISSION -

Spirochetes spread via the bloodstream to the joints, heart, nervous system and distant skin sites

Tick bite / Contact with tick feces

PERIOD OF COMMUNICABILITY Joints -  Not communicable from person-to-person PATHOPHYSIOLOGY

Subjective joint pain, arthritis

CNS

Induce astrocytes to undergo astroliosis (Proloferation followed by apoptosis – Natur al death of neurons)

Heart

Spirochetes may induce host cells to secrete products toxic to nerve cells

Fatigue and malaise

Chronic secretion of  stress hormones

↓ Tryptophan in CNS

Dysregulation of hormones

Neurological dysfunction

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 AV Block (First Degree, Wenckebach, Complete Heart Block)

Myopericarditis chronic, cardiomyopathy, pericardial effusion

CLINICAL MANIFESTATIONS 1. Erythema Migrans = Annular skin lesions for a period of days to weeks and develops central clearing 2. Lesion – Warm to touch, not painful 3. Flulike symptoms 4. Inflamed, painful arthritis in large joint 5. Limb weakness, sensory lowers 6. Confusion, memory loss 7. Bell’s Palsy

DIAGNOSTIC TESTS 1. 2.

Blood, skin, CSF and joint fluid collection Observation of skin, myocardial, retinal and synovial lesions

MEDICAL TREATMENT 1.

Anti-infective Drugs a. Tetracycline (Achromycin)  b. Chloramphenicol (Chloromycetin)

GENERAL MANAGEMENT 1. 2. 3. 4. 5.

IV Fluids and electrolytes Sedation – Paraldehydration or Chloral hydrate ↑ Protein, ↑ Caloric Diet Serum albumin transfusion Packed RBC for anemia 6. O2 for pulmonary complications 7. Fever control

Rocky Mountain Spotted Fever  Acute rickettsial infective disease transmitted to humans by infected ticks and manifested by severe systemic signs and a macular or papular rash

CAUSATIVE AGENT -

 Rickettsia rickettsii

INCUBATION PERIOD -

3 – 14 Days

MODE OF TRANSMISSION 

Bite from ticks,

 Contamination with tick feces

PERIOD OF COMMUNICABILITY   Not communicable from person-to-person

PATHOPHYSIOLOGY  NOTEBOOK 

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PROGRESSION - Rapid progressive systemic angiitis with severe systemic manifestations -

-

Vascular endothelial edema Fibrin and platelet deposition Microthrombi develops and obstructs and occludes small vessels Tissue infection Necrosis

CLINICAL MANIFESTATIONS 1. Petechial skin rash that becomes purpuric 2. Clouded sensorium  BADTRIP XD 3. 4. 5. 6.

Edema Hypotension Peripheral vascular circulatory collapse Myocardial involvement • Myocarditis – Focal vascular lesion plus mononuclear cell infiltration

DIAGNOSTIC PROCEDURES 1. 2.

Immunofluorescence of Skin Tissue Serologic 3. Indirect Fluorescent Antibody – Confirmatory 4. Complement Fixation 5. Blood Component

MEDICAL AND GENERAL MANAGEMENT - Same with Lyme Disease  LOL XD

Sexually Transmitted Disease Gonorrhea (Clap/Flores Blancas/Gleet)  Sexually-transmitted bacterial disease involving the mucosal lining of the genitourinary tract, rectum and pharynx

INFECTIOUS AGENT   Neisseria gonorrhoeae o o o o o

Gram-negative (-) coccus found in pairs  Non-spore former and non-motile Fragile and can’t survive long outside the body Readily killed by: Drying, sunlight, UV Light Can be killed with ordinary disinfectants

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INCUBATION PERIOD 

3 – 21 Days (Averages from 3 – 5 Days)

PERIOD OF COMMUNICABILITY -

Infected person remains communicable as long as the organism is present

MODE OF TRANSMISSION 1. 2. 3.

Contact with exudates from the mucous membranes (Usually sexual activity) Utero = Upon rupture of membranes Direct Contact – Contaminated vaginal secretion (During delivery) 4. Sexual Contact (Orogenital, Anogenital) Between opposite sexes / Same Sex • Infection with Neisseria gonorrhoeae 5. Fomites  FAIL 

PATHOPHYSIOLOGY

Becomes adherent to the urethral epithelium

Penetration of the mucosa

  Acute inflammatory response

Inflammatory edema of the gland ducts occurs

Polymorphonuclear  leukocytes in submucosa

Formation of  microabscesses

Larger abscesses form

Spread along mucosal surfaces

Can lead to STERILITY

Fallopian tubes

Endometrium

Peritoneal cavity

CLINICAL MANIFESTATIONS 1.

In Females a. Burning sensation and frequent urination  b. Yellowish purulent vaginal discharge c. Redness and swelling of genitals d. Itching of vaginal area e. Pain on urination f. Urethritis / Cervicitis = A few days after exposure (Can become STERILE) g. Endometritis salpingitis or pelvic peritonitis h. Pregnant women – May infect the eye of her baby during the passage through the birth canal 2. In Males (After 3 – 6 Days incubation period) a. Dysuria = With purulent discharge (Gleet) – 2 – 7 Days after exposure  b. Rectal Infection = Common to homosexuals c. Prevention of passage of urine d. Prostatitis e. Urethritis f. Pelvic pain and fever 

OTHER CLINICAL FEATURES VARY ACCORDING TO SITE INVOLVED

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1.

Urethra a. Dysuria  b. Urinary frequency and incontinence c. Purulent discharge d. Itching e. Red and edematous meatus 2. Vulva a. Occasional itching  b. Burning and pain c. More severe BEFORE PUBERTY and AFTER MENOPAUSE 3. Vagina a. Engorgement, redness and swelling  b. Profuse purulent discharge 4. Liver – RUQ Pain 5. Other possible symptoms – Pharyngitis, Tonsilits, Rectal Burning

DIAGNOSTIC EXAM 1. Females = Culture of specimen (Cervix and Anal Canal): 24 – 72 Hours 2.

M ales = Gram Staining

TREATEMENT MODALITIES 1.

Uncomplicated Gonorrhea (Adults) •

Ceftriaxone 125 – 250 mg, IM single dose

•

2.

Doxycycline 100 mg, orally (For 7 days) Pregnant Women •

Ceftriaxone 125 – 250 mg, IM single dose PLUS… Erythromycin 500 mg, orally (For 7 days) • 3. Aqueous Procaine Penicillin = 4 million units IM after (-) Skin test 4. Disseminated Gonococcal Infection (Adults and Adolescents) •

Ceftriaxone 1 gram IM or IV q24 hours

•

Spectinomycin 2 grams IM q12 hours (If allergic to B-lactam antibiotics) 5. Therapy may be switched to the following regimens to complete one full week of  antimicrobial therapy Cefixime 400 mg PO, BID • Ciprofloxacin 500 mg PO, BID • CI: Children, adolescents, and pregnant lactating women  •

Gonococcal Conjunctivitis – Ceftriaxone 1 gram, single dose, IM and irrigation of infected eye with NSS

 NURSING MANAGEMENT 1. Ask the client if he / she has drug sensitivities and WOF AE during therapy (Before therapy) 2. Explain that client is still infectious and can transmit Gonococcal infection until cultures  prove (-) 3. Standard precautions 4. Confidentiality 5. Isolated until recovered from disease 6. Gonococcal arthritis = Apply moist heat 7. Infants born to mothers (+) positive for g onorrhea: 1% Silver Nitrate • •

Or any ophthalmic prophylaxis on both eyes at birth

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8. Report all gonorrheal cases 9. Refrain from sexual intercourse until treatment is completed SIGNS OF GONOCOCCAL OPTHALMIA NEONATORUM -

-

Lid edema Bilateral conjunctival edema Purulent discharge (2 – 3 Days after birth) Corneal Ulceration and Blindness = IF LEFT UNTREATED

PREVENTION and CONTROL 1. Sex Education (Schools, and community) 2. 3.

Case findings Incidence of gonorrhea must be reported so contacts can be treated

 NURSING DIAGNOSES • • • • •

Altered sexuality pattern Social isolation Knowledge deficit Altered urinary isolation Risk for infection

Syphilis (Lues Venereal/Morbus Gallicus) 

Chronic, infectious sexually-transmitted disease that usually begins in the mucous membranes and quickly becomes systemic

ETIOLOGIC AGENT -

Treponema pallidum •

Spirochete – Can pass through mucosa / cracks / placentas

SOURCES OF INFECTIONS 1. 2. 3. 4.

Discharges = Lesions of the skin or mucous membranes Semen, blood, tears and urine Mucous Discharges = Nose, eyes, genital tract or bowels Surface lesions

INCUBATION PERIOD 

10 – 90 Days (Average is 3 Weeks)

PERIOD OF COMMUNICABILITY 

Variable and indefinite

MODE OF TRANSMISSION 1.

Direct Transmission – Contact with an infected person 2. Indirect Contact – Articles freshly soiled with discharges / blood 3. Congenitally through the placenta 4. Syphilitic baby to a wet nurse / Anyone carelessly handling diapers

PATHOPHYSIOLOGY  GAWA

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CLINICAL MANIFESTATIONS 1.

Primary Syphilis a. One or more chancres (Painless) that erupt in the genitalia, anus, nipples, tonsils / eyelids (Painless, start as papules, then erode)  b. Chancres have endurated, raised edges, and clear bases (Disappears after 3 – 6 weeks even without therapy) c. Chancres are often overlooked in females 2. Secondary Syphilis  Development of mucocutaneous lesions and generalized lymphadenopathy (Days – 8 weeks after onset) a. Macular, popular, pustular or nodular   b. Lesions = Uniform size, well-defined and generalized c. Erupt between rolls of fat on: Trunk, arms, palms, soles, face and scalp d. Perineum, vulva, rolls of fats in the scrotum, lesions enlarge and erode,  pink/grayish-white lesions (Condylomata lata) e. HA, anorexia, malaise, weight loss, N/V, sore throat, slight fever  f. Alopecia (Temporary) g. Nails – Brittle and pitted 3. Latent Syphilis a. No clinical symptoms – But serologic test is reactive  b. 2/3 of clients asymptomatic until death  4. Late Syphilis a. Destructive but non-infectious stage  b. Three Subtypes: i. Late, Benign Syphilis 1. 1 – 10 Years after the infection 2. Gumma = Chronic, superficial nodule or deep granulomatous lesion (Solitary, asymmetric, painless, endurated) a. Can be found in any bone ii. The Late Syphilis 1. Involves the Liver = Epigastric pain, tenderness, enlarged SPLEEN, anemia 2. Upper Respiratory Tract = Perforation of the nasal septum /  palate 3. Bones / Organs = Destroyed which lead to death (Severe cases) iii. Cardiovascular Syphilis 1. Develops about 10 years after infection

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2. Asymptomatic but may suffer from aortic regurgitation and aneurysm 5.

Congenital Syphilis a. Fetus Ö Overwhelmed by infection and die Ö Will be expelled by the uterus (Miscarriage / stillbirth)

 b. Macerated appearance (Collapsed skull and protuberant abdomen) c. Skin = Livid red color, number of bullae filled with hemorrhagic fluid d. Autopsy = Spleen and Liver ENLARGED, Pancreatitis, thickening of intestines e.

May still show alterations in fetal development at various stages

CLINICAL MANIFESTATIONS 1.

Early Congenital Syphilis a. Lesions of the skin and mucous membranes

 b.

2.

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“Syphilitic Pemphigus” – Bullous rash

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Loss of weight, wrinkling of skin “ Old man look ”

 Syphilitic papules – Skin at the base of nails, nails may be loosened and shed (Syphilitic Nonychia) Mucous patches = Lips, mouth, throat, nasal passages  Liver and Spleen Protuberant abdomen (Enlargement of the liver and spleen)  Liver cells are immature and imperfectly formed 

 Hepatic insufficiency = Failure of protein metabolism Late Congenital Syphilis a. Interstitial Keratitis – Commonest late lesion 4 – 60 years old or even later   

Circomcorneal Vascularization, followed by vascular infiltration

 Severe lesions – Corneal scarring (Opacities lead to slight impairment / complete blindness)

DIAGNOSTIC PROCEDURES 1. 2. 3. 4.

Dark Field Illumination – Most effective if lesions present Fluorescent Treponemal Antibody Absorption Test VDRL Slide Test and Rapid Plasma Reagent Test CSF Analysis

MODALITIES OF TREATMENT 1.

Early Syphilis – Penicillin G benzathine IM (2.4 million units) 2. More than a year duration – Penicillin G benzathine (2.4 million units/week x 3weeks) 3. Allergy to Penicillin  Oral Tetracycline / Doxycycline (15 days for early, 30 days for late) 4. Abstain from sexual contact until infection has healed (Can’t during treatement)

 NURSING MANAGEMENT 1. Stress – Importance of completing the treatment even after the symptoms subside 2. 3.

Instruct infected individuals to inform their partner to be treated Universal precaution 4. Secondary Syphilis – Keep lesions dry 5. Cardiovascular Syphilis – WOF signs of ↓ CO (↓ Sensorium and UO and hypoxia) and  pulmonary congestion

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6.  Neurosyphilis – Assess LOC, mood, coherence; WOF: Ataxia 7. Encourage to undergo VDRL Testing after 3, 6, 12, and 24 months if any relapse 8.

Report all cases

PREVENTION and CONTROL 1.

Report Cases 2. Control prostitution 3. Require sex workers to have regular check-ups  LOL 4. Proper sex education 5. Contact tracing

 NURSING DIAGNOSES 1. 2. 3. 4. 5. 6.

Altered sexual pattern Self-esteem disturbance Social isolation Knowledge deficit Impaired skin integrity Anxiety

Acquired Immune Deficiency Syndrome (AIDS)  

Aids involves an immune deficiency HIV – Causes AIDS Retrovirus belonging to the family of lentiviruses o Lentiviruses = ‘Slow Viruses’ o

MODIFIED CLASSIFICATION (STAGES) OF HIV INFECION

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Clinical Stage 1: Asymptomatic – CD4 Count of