Block 5 Case 4

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Direct Coombs test:: To identify hemolysis.
Add RBCs to Coombs serum (antibodies against human IgG and C3), if agluttination occurs the RBCs had antibodies bound.
Indirect Coombs test:: To check transfusion compatibility. Add donor RBCs to patient's serum. Then add Coombs serum. If antibodies from patient's serum attacked the RBCs, agluttination occurs.
Monospot test:: IgM heterophile antibodies are produced in response to EBV infection. Take a drop of patient's serum and add to horse RBCs. If agglutination occurs, test is positive for EBV.
Serum anti-HAV:: 1 week after symptoms IgM detected, lasts 6 months.
4 weeks after symptoms IgG detected, lasts years.
HBsAg:: Hepatitis B surface antigen: If positive, marker of active infection. >6mo, chronic. Persisent, carrier.
HBsAb:: Hepatitis B surface antibody: appears 4 weeks after HBsAg disappears. Indicates immunity due to infection or vaccine.
HBcAb:: Hepatitis B core antibody: appears between HBsAg and HBsAb. Marker of infection or prior infection. NOT seen if vaccininated.
HCAb:: Hepatitis C antibody: indicates prior or current exposure.
Normal RBC lifespan, turnover rate: 120 days, 1% turnover/day
8 lab tests in hemolytic anemia: Declining Hct
Reticulocytosis
Low haptoglobin
Hemoglobinuria
Urine hemosiderin
Elevated indirect bilirubin
Elevated serum LDH
Smear abnormalities
Classes of hemolytic anemia (intrinsic and extrinsic):: Intrinsic: membrane defects, glycolytic defects, oxidation vulnerability, hemoglobinopathies
Extrinsic: Immune, microangiopathic, infection, hypersplenism
Acute renal failure: RIFLE: Risk: Cr*1.5, GFR -25%
Injury: Cr*2.0, GFR -50%
Failure: Cr*3.0, GFR -75%
Loss: Complete loss of kidney fcn for >4weeks
End stage: Loss > 3months
Creatinine change/day in total renal failure:: 0.5 mg/dL
3 classes of acute renal failure:: Prerenal: adaptive response to volume depletion, no kidney dmg
Intrinsic: cytotoxic or structural damage
Postrenal: urine obstruction
Hyaline casts seen in :: concentrated urine, febrile disease, diuretic therapy.

Not indicative of disease
Red cell casts seen in :: Glomerulonephritis
White cell casts seen in:: Pyelonephritis, interstitial nephritis
Renal tubular casts seen in:: Acute tubular necrosis, interstitial nephritis
Coarse, granular casts seen in:: Nonspecific... maybe acute tubular necrosis
Broad, waxy casts seen in:: Chronic renal failure... indicates stasis in enlarged collecting tubules.
DIC: 5 steps: Exposure of blood to procoagulants (TF, cancer procoagulant)
Formation of fibrin in blood
Fibrinolysis
Depletion of clotting factors
End organ damage
DIC: 4 diagnostic studies and criteria: PT, PTT, platelet count, fibrinogen levels
2/4 - possible
3/4 - probably
4/4 - most likely
DIC: 2 confirmatory tests: D-Dimer: detects cross linked fibrin
Fibrin degredation products: detects plasmin cleaved fibrinogen or fibrin.
DIC: treatment in bleeding vs thromosis: Bleeding: FFP for factors/platelets
Clotting: IV heparin
CMV: family, pathogenesis, conditions, treatment: Herpesvirus
Infects cells, contained by immunesystem, but dormant in leukocytes.
Mild mono, pneumonia, hepatitis, retinitis in ICPs
Ganciclovir
EBV: family, pathogenesis, conditions, treatment: Herpesvirus
Infects B cells by C3d receptor. Lies dormant.
Mono, Burkitt's lymphoma
No antiviral.
Brucella: ID, pathogenesis, Conditions, treatment: Gram - coccobacillus
Gets phagocytosed, moves to RE system creating granulomas/abscesses
Undulant fever
TMP/SMX
C. difficile: ID, pathogenesis, conditions, treatment: Gram + rod
Antibiotics destroy normal intestinal flora, grows.
Pseudomembranous colitis.
Stop antibiotics, start metro/vanco
Ehrlichia: ID, pathogenesis, conditions, treatment: Small gram -
tick bite, infection of WBCs, multiply in vesicles --> inclusion body
Ehrlichiosis
Doxycycline
Leptospira: ID, pathogenesis, treatment: Spirochete
Systemic spread, flulike symptoms, resolves, 2nd phase -- IgM response and meningitis.
Penicillin, Erythromycin
Parvo B19: family, associated conditions, treatment: Parvoviridae
Fifth's disease, aplastic anemia crisis
No antivirals
Salmonella: ID, pathogenesis, conditions, treatment: Gram - rod
Large innoculum, penetrades mucosal barrier --> inflammation fever, diarrhea
Gastroenteritis
Rehydration... no Antibiotics
Toxoplasma gondii: class, pathogenesis, conditions, treatment: protozoa
Cysts from cat feces, phagocytosed by macrophages, dormant in tissue and cysts
Mono in normal, Brain, eye, liver, encephalitis in ICPs.
Sulfonamides + Pyrimethamine
AIDS: protozoal infections: Cryptosporidiosis: chronic diarrhea
Pneumocystosis: PCP most common!
Toxoplasmosis: pneumonia or CNS infection
AIDS: fungal infections: Candidiasis: thrush, invasive
Cryptococcosis: CNS infection
Coccidiodomycosis: disseminated, meningitis
Histoplasmosis: meningitis, granulomas
AIDS: bacterial infections: mycobacteria: MAC, TB etc
Nocardiosis: pneumonia, meningitis
Salmonella: chronic diarrhea
AIDS: viral infections: CMV: pulmonary, intestional, CNS
HSV: ulcerations
VZV: skin vesicles
EBV: neoplasms
JCVirus: progressive multifocal leukoencephalopathy
AIDS: Neoplasms: Kaposi sarcoma: HHV8
B cell non-hodgkin: EBV
Uterine/cervix/anal cancer: HPV
AIDS testing: standard test: Serum/plasma
Enzyme immunoassay (EIA) detects antibodies to HIV1,2. IE, must wait for antibodies to develop! (2-12weeks).
Sens 99% Spec 99%
Follow up with Western blot.
AIDS testing: Rapid: Rapid EIA
Confirm with Western blot.
Counsel patients about meaning of "preliminary results". Test needs to be confirmed!
AIDS testing: 4 other tests: Home sample collection
Oral fluid
Urine based
p24 antigen
HIV virus: physical components: Spherical, core contains 2 copies of RNA, 3 viral enzymes (protease, rev. transcriptase, integrase).
Envelope has gp120 on a gp41 stalk.
HIV virus: types, prevalence: HIV1, HIV2.

HIV1 is common in US.
HIV virus: cell entry and lifecycle: gp120 binds to CD4 on T cells.
gp120 binds to coreceptors CCR5/CXCR4.
Conformation allows gp41 to insert into cell membrane, fusion.
RNA undergoes reverse transcription --> cDNA is integrated into host genome and becomes latent.
T cell is activated by antigen or cytokines, transcription begins, virus produced, cell death.
3 stages of HIV infection:: Acute syndrome: high virus, viremia, flu-like symptoms, resolves in 2-4 weeks.
Chronic phase: Intact immune system, latent phase. General asymptomatic.
Full blown AIDS: fever, fatigue, weight loss, breakdown of host defense. Occurs 7-10yrs after infection.
Histoplasmosis: pathogenesis: Airborne spores deposited in alveoli.
Germinate into yeast, macrophages/neutrophils eat.
Transported to lymphnodes, access blood stream.
Granuloma formation in spleen or systemic infection.
Histoplasmosis: general symptoms: Hepatosplenomegaly.
Lymphadenopathy.
Fever, weight loss, malaise.
Histoplasmosis: Diagnosis: Serum culture gold standard.
Serum/urine antigen detection also good if disseminated.
Serologic antibody tests less sensitive.
Giemsa stained blood can show yeast.
Histoplasmosis: treatment in mild vs severe and AIDS vs non-AIDS: Mild, itraconazole 6-18mo
Severe, AmphB until stable, then like mild.

AIDS:
Mild, itraconazole for life.
Severe, AmphB until stable, then like mild.
HIV transmission facts:: Heterosexual sex most common mode worldwide, and for US women.
Risk of HIV infection in screened blood: 1/800,000.
Risk due to needle stick: .3%, mucous membrane exposure: .09%
No transmission through skin, saliva, tears, sweat, urine.
HIV transmisison during pregnancy:: Can occur during pregnancy, delivery, breast feeding.
Give prophylactic HAART to mother during pregnancy, labor, delivery and to baby else 25% risk of infection to baby.
C-section can help.
Classes of ART agents:: Reverse transcriptase inhibitors
HIV-1 protease inhibitors
Entry inhibitors
Reverse transcriptase inhibitors: nucleoside reverse transcriptase inhibitors (NRTIs) and NNRTIs.: NRTI: enter cells, phosphorylate and produces synthetic substrate for reverese transcriptase, competitively inhibiting it and ending elongation.
NNRTI: Non-competitive inhibition by binding to p66 subunit and modifying reverse transcriptase.
HIV-1 protease inhibitors: Prevents proteolytic cleavage of gag/pol proteins (code for structure and ezymes). Stops virion from assembling.
Entry inhibitors: Interfere with receptor binding or entry process. (Enfuvirtide stops gp41 interaction, blocking fusion.)
HIV: when to treat: No treat if CD4 T cell > 350.
Offer if 201-350
Treat if < 200!

OR treat if any history of AIDS defining illness.
HIV: therapy combos: NRTI + NNRTI or protease inhibitor. Multidrugs very important to stop resistance!!
Highest risk HPV strain in cervical ca.: 16,18
Cervical cancer staging: 0: CIN III, in situ
1: Confined to cervix
2: extends to upper 2/3 vagina, but not pelvic wall
3: pelvic wall, lower 1/3 vagina
4: mets, bladder, rectum etc
Amphotericin B: side effects: Shake and bank: rigors and fever. Lasts 30min, meperidine may help.
Nephrotoxic effects.
Anemia.

Lipid formulations less nephrotoxic, more shakenbake.

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