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17 Cards in this Set
- Front
- Back
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HIV adn AIDS
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HIV destroys CD4 Tcells
HIV1, HIV2 transmitted via semen, blood, vaginal secretion and breast milk 3 stages: acute stage: takes 3-4 weeks to develop anti-HIV antibodies, usually generalized viral syndrome (fever, weight loss, cachexia, ight sweats) Latent period: asymptomatic, virus are still dividing, last 3-10 years. Advanced symptomatic infx (AIDS): AIDS=(+) HIV test and: 1: <200 CD4 Tcells/ul, or 2: AIDS-defining opportunistix infx (pneumocystitis pneumonia, toxoplasmosis, cmv retiniits, myobacterium avium complex, progressive multifocal leukoencephalopathy (PML), or cryptococcal meningitis, 2: AIDS-associated malignancies (kaposi's sarcoma, brain lymphoma, invasive cervical cancer, or certain non-hodgkin's lymphomas), or 3: HIV-complicating infx (HIv dementia, HIV enceephalopathy, extrapulmonary TB, chronic isosporiasis, cryptosporidiasis, disseminated histopplasmosis, chronic,or pulmonary HSV, disseminated coccidioidomycosis, or esophageal or respiratory candidiasis |
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bleeding time
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platelet fnx
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PT (prothrombin time)
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extrinsi, common pathway (2, 5, 7, 1)
measure coumadin |
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PTT (partial thromboplastin time)
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intrinix, common pathways (all factors except 7, 13)
measure Heparin |
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TT (thrombin time)
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common pathway (factors 2,1)
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Von Willebrand Disease (VWD)
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deficiency of (VWF)
VWF carries/binds factor VIII>causes a factor VIII functional def. Autosomal dominant Tx: VWF or humate (purified factor VIII) +/- desmopressin which serves to release factor VIII that is collected and stored in endothelial cells signs/symps: -bleeding from small cuts, easy bruising -increased menstrual bleeding -increased PTT and bleeding time labs: increase bleeding time increase PTT |
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Hemophilia A
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lack of factor VIII
Tx=factor VIII excessive bleeding x-linked recessive LABS: increased PTT, normal PT and bleeding time |
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Hemophilia B/christmas B
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lack of factor IX
Tx: factor IX excessive bleeding x linked recessive LABS: Increased PTT normal PT and bleeding time |
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Vitamin K def
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cause nonfunctional factors 2, 7, 9, 10
excessive bleeding may be due to : fat malabsorption (in cystic fibrosis, chronic pancreatitis>blocking of pancretic duct>decrease lipase>decrease fat soluble vitamins. long term antibiotics: destroy gut flora>gut flora are athe primary providers of vitamin K Newbors: lack gut flora>no vit K>hypocoagulable for the 3-5 days. vit K doesn't cross placenta, missing in breast milk. every baby gets a vit K shot. coumadin therapy: prevent the vit K dependent activation of factors 2, 7, 9, 10. Use PT as the measure coumadin given wiht heparin to counteract the inhibition of protein c and S by coumadin at the strat of therapy. |
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idiopathic thrombocytopenic purpura
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petechiae, purpura, mucosal bleeding due to decrese platelets
In children: acute (post viral infx), usually self limited In adults: chronic, due anti-structural platelet (type 2 Hypersensitivity). TX: corticosteroids LABS: prolonged bleeding time |
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Thromobotic thrombocytopenic purpura
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unknown specific cause or secondary to clopidogrel, quinine, and interferon alpha
spont. platelet aggregation wiht resutling systemin platelet clot formation and consutmption of platelets. untreated>fatal TX: plaspmapheresis signs and symps: severe thrompcytopenia shistocytes: helmet cells, triangular cells evidence of hemolysis: Low HGB high reticulocyte count polychromasia on blood smear high LDH (indicates ischemic organ damage) fever ischemic organ damage |
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High LDH
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marker for ishemia
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spherocytosis/familial spherocytosis/chronic familial icterus/spherocytic anemia
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chomolysis of speroidal RBCs, anemia, splenomegaly
deficiency in spectrum TX: splenectomy>decrease anemia, increase risk of infx by encapsulated bacteria (H. influenza, N. meningitidis, S. pneumonia) |
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G6PD deficiencey
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x linked recessive
more common in blacks in RBC's: pentose pO4 pathwawy is the sole means for producing NADPH, so RBC is very sensitive to oxidative damage in G6PD deficiency excess radicals casued by FAVA beans, sulfa drugs, quinine derivatives, viral infx THE MOST COMMON ENZYMOPATHY |
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Sickle Cell Anemia
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autosoma recessive, yields HBS
more in Blacks, confers resistance to malaria SINGLE AMINO ACID SUBSTITUTION: BETA GLOBIN CHAIN- GLUTAMAT 6 -->VALINE making it more prone to crystalizzation sickling in deoxygentated state (hypoxia, acidosis, dehydration sickling crisis=occlusion of blood vessel (painful)-->repeated events cause autosplenectomy |
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alpha thallasemia
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decreased synthesis of alpha globin chains
alpha chains are mandatory for survival so as protection humans get 2 alpha thalassemai alleles from each parent so normal person have a 4 alleles (normally humans inherit one allele from each parten tfor a particular gene allowing each person to have 2 allesl for a gene) MIcrocytic anemai and splenomegaly 1 alpha-allele lost: asympto. 2 alpha-allele lost: moderate microcytic anemia 3 alpha-allele lost: severy microcytic anema 4 alpha-allele lost: lethal; tetramers of gamma and beta chains--> Hgb cant carry o2 --> called Hgb BARTS |
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beta thalassemai
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decrese synthesis of beta globin chains
cause: jaundice, leg ulcers, splenomegaly major beta thalassemai (missing 2 alleles)= cooley's Anemia-->SEVERE MICROCYTIC ANEMA Minor beta-thalassemia (missing 1 allele)= moderate microcytic anemia |
