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Hi Yield 4.4 - 6.0

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mhewett's version from 2016-07-17 18:34

Section 4.4 HIV & AIDS

Question Answer
HIV destroysCD4 T cells
What are the 3 stages of HIV?1) Acute stage - ab in 3-4 weeks and will have general viral sx
2) Latent period - asymptomatic for 3-10 yrs
3) AIDS
How is AIDS defined?+ HIV test AND: <200 CD4 T cells or defining opportunistic illnesses
What are the direct complications of HIV?fever, weight loss, cachexia, night sweats
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Section 5.0 Bleeding Disorders

Question Answer
What are the 2 modes of clot formation in the human body?1) platelet activation and aggregation
2) clotting cascade activation
What is the intrinsic pathway?starts with factors in the bloodstream
XII --> XI --> IX (+ VIII)--> X
What is the extrinsic pathway?starts with factors released by injured cells
tissue factor --> VII --> X
What is the common pathway?X (+ V) --> II (thrombin) --> I (fibrinogen) --> fibrin CLOT (+ XIII) --> stabilized fibrin clot
What is bleeding time?tests how long it takes to form a clot with platelets; so platelet function
What is PT for?extrinsic and common pathway factors (VII, V, II, I +/- X)
What is PTT for?intrinsic and common pathway factors (all but VII, XIII)
What is TT for?common pathway factors (II, I)
What does VWF bind to?VIII and platelets
What is hemophilia A?lack of factor VIII
What is hemophilia B?lack of factor IX
Vit K deficiency results in what nonfunctional factors?II, VII, IX, X
What are 4 things that cause vit K deficiency?fat malabsorption, abx, newborns, coumadin
What happens in DIC?spontaneous activation of the coagulation cascade causing intravascular coagulation and organ ischemia, and later mucosal bleeding.
What is ITP?disorder of decreased platelet numbers
What is child ITP?acute (post viral infection); self limited
What is adult ITP?chronic (d/t anti-structural platelet Ab); tx corticosteroids
What is TTP?spontaneous platelet aggregation causing systemic platelet clot formation and consumption of platelets.
What are the s/sx of TTP?thrombocytopenia, schistocytes, hemolysis, fever, ischemic organ damage
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Section 5.1 Hemolytic Anemias

Question Answer
What is spherocytosis?a chronic disease characterized by hemolysis of spheroidal RBCs, anemia, and splenomegaly; d/t deficiency in spectrin
What is spectrin?determines shape of RBCs
Why does G6PD deficiency cause hemolytic anemia?G6PD normally removes radicals (there are lots of enzymes in the body that do this but in RBC's, it's the only one (PPP) -> thus causing RBC lysis d/t excess radicals --> hemolytic anemia)
What are the enzymes of the hexose monophosphate pathway shunt utilized to eradicate organic peroxides?G6PD --> glutathione reductase --> glutathione peroxidase
What causes sickle cell anemia?a single AA substitution (valine for glutamate) in the beta globin chain (at the 6th AA position), so it's more prone to crystallization under certain conditions.
What conditions cause sickling?hypoxia, acidosis, dehydration
What is a sickling crisis?any sickling event of RBCs resulting in occlusion of blood vessels by the sickled RBCs
What is hemoglobin made up of?a heme unit (binds O2), 2 alpha globin chains (req for O2 to bind), 2 beta globin chains
What is a-thalassemia characterized by?characterized by microcytic anemia & splenomegaly
What are the genetics of a-thalassemia?humans get 2 a-thalassemia alleles from each parent; so normal ppl have 4 alleles for this
What are the different types of a-thalassemia?1 lost - asymptomatic
2 lost - mod microcytic anemia
3 lost - severe microcytic anemia
4 lost - lethal; tetramers of gamma (Bart's hemoglobin) and beta chains
What is B-thalassemia characterized by?jaundice, leg ulcers, splenomegaly
What is minor B-thalassemia?missing 1 allele; mod microcytic anemia
What is major B-thalassemia?aka Cooley's anemia; missing both alleles; don't need B globins to survive but will have severe microcytic anemia
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Section 5.2 Immune-Mediated Hemolysis

Question Answer
What is immune-mediated hemolysis?aka autoimmune hemolytic anemia; development of ab against one's own RBC's
What are the 2 types of autoimmune hemolytic anemia and how are they named?warm and cold ; named by what temp the anti-RBCs are most active
What are the risk factors for warm agglutinin (ab) disease?drugs (methyldopa, dopa, high dose penicillin or cephalosporin), malignancies (lymphoma, leukemia), SLE
What are the risk factors for cold agglutinin (ab) disease?mycoplasma pneumonia, mononucleosis, lymphoma, 50% are idiopathic
How do you identify whether a pt has ab to RBCs?Coombs test (direct, indirect)
What does the direct Coombs test detect?immune-mediated hemolysis by identifying ab bound DIRECTLY to RBCs
What does the indirect Coombs test identify?free floating ab directed against RBCs; test of choice for isoimmunization in Rh- females
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Section 5.3 Other Anemias

Question Answer
What causes microcytic anemias?lead poisoning, iron deficiency, thalassemia
What causes normocytic anemia?(normal sized RBCs but just don't have enough); bone marrow disease/damage, renal failure
What causes macrocytic anemia?(usually from a metabolic issue) hypothyroidism, liver disease; megaloblastic (a type of macrocytic but also immature RBCs) - B12/folate deficiency/chemotherapeutic agents/D. latum infection
What causes megaloblastic anemia?d/t defective DNA synthesis
What are clinical findings of megaloblastic anemia?leukopenia, hypersegmented neutrophils, thrombocytopenia
What does B12 deficiency cause that folate deficiency does not?neurologic symptoms
What is plummer-Vinson?microcytic anemia d/t low grade, long-term iron-deficiency (no iron -> can't make hemoglobin -> microcytic anemia)
What does plummer-Vinson result in?manifestations of iron deficiency (atrophic glossitis, koilonychias, pallor), esophageal webs (dysphagia for solids, not liquids)
What is fanconi anemia?inability to remove oxygen radicals from bone marrow; AR
What are clinical findings of fanconi anemia?microcephaly, short stature, petechiae/bruises, cafe au lait spots, macrocytic anemia, thromboycytopenia, recurrent aplastic anemia, deformed/absent radius bones, small/deformed/absent thumbs
What are pts with fanconi anemia at high risk of getting?leukemia, lymphoma
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Section 5.4 Red Blood Cells

Question Answer
What are Heinz bodies?denatured hemoglobin visible w/in RBCs; associated with G6PD deficiency
What are Howell-Jolly bodies?nuclear fragments in RBCs; looks like basophilic (blue granules). Indicative that RBCs are leaving bone marrow while still immature.
What is basophilic stippling?mult tiny blue polka dots w/in RBCs; indicative of lead poisoning
What are reticulocytes?immature RBCs that are released early from the bone marrow in response to hemorrhage or similar events; blue lace-like patterns are visible w/in the RBCs (and represent remnants of ribosomal RNA)
What are siderocytes?extra iron in RBCs; represents iron not bound to hemoglobin. These are "pappenheimer bodies". Result of iron overload secondary to deranged bone marrow function
What is polycythemia?erythrocytosis = high RBCs.
What is primary polycythemia?aka polycythemia vera; bone marrow disease; type of myeloproliferative disorder.
What is secondary polycythemia?caused by hypoxia (COPD), living at high altitudes, RCC, anabolic steroids
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Section 5.5 Neutropenia

Question Answer
What does neutropenia mean?low number of neutrophils (it's a type of granulocytopenia)
What causes decreased production of neutrophils?bone marrow disease, chemo and other drugs that affect bone marrow, HIV-1 infection, Vit B12 or folate deficiency
What causes increased destruction of neutrophils?Felty's syndrome (variant of RA that includes immune-mediated destruction of neutrophils via anti-neutrophil ab.
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Section 5.6 Leukocytosis

Question Answer
What does leukocytosis mean?high number of white blood cells (WBCs = neutrophils, eosinophils, lymphocytes, monocytes)
What causes neutrocytosis?(neutrophils are always first when there is any ifnlammation or infection) acute inflammation, acute infection, bacterial infection, certain cancers that promote inflammation (like pheos), leukemia of mature neutrophils (CML)
What causes eosinocytosis?type I hypersensitivities, helminthic infections
What causes lymphocytosis?granulomatous diseases (tb, wegener's granulomatosis, sarcoid), viral infections (T cells respond to viruses and T cells are lymphocytes), pertussis, leukemias of mature lymphocytes (CLL)
What causes monocytosis?granulomatous diseases, infectious mononucleosis
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Section 5.7 Leukemias

Question Answer
What is leukemia?neoplastic WBCs in the blood
What are the precursors to granulocytes (neutrophils, basophils, eosinophils) and monocytes?myeloid cells
What does it mean to have acute or chronic leukemia?refers to maturity of cell type - so acute means immature cells; chronic means cancerous cell type is mature
What is the difference between lymphocytic and myelogenous leukemias?lymphocytic is free floating in blood; myelogneous is everything but lymphocytes
What is ALL?most common malignancy in children; overabundance of lymphoblasts (lymphocytes); causes lymphadenopathy and impaired bone marrow function (--> anemia, thrombocytopenia, granulocytopenia)
What is AML?all ages; causes impaired bone marrow function; can see Auer rods
What is CML?peak 30-40 yo (25-60); insidious onset; causes impaired bone marrow function; associated with Philly chromosome (9:22 making bcr-abl); low LAP (leukocyte alk phos)
What is CLL?>50 yo; males; + smudge cells; causes lymphadenopathy and impaired bone marrow function; variant is Sezary Syndrome
What is Hairy Cell Leukemia?middle aged white males; #1 sign is splenomegaly, hepatomegaly rare; only affects B cells (develop hair-like projections); causes impaired bone marrow function; + TRAP and CD25
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Section 5.8 Lymphomas

Question Answer
What are the 2 types of lymphomas?Hodgkin's disease and non-Hodgkin's lymphomas; differentiated by the presence of Reed Sternberg cells
What is Hodgkin's Disease?leukocytosis of PMNs; + RS cells; high # of RS cells --> poor prognosis
What is non-Hodgkin's lymphomas?widespread adenopathy, neutrocytosis, hypercalcemia, hepatosplenomegaly; spreads to multiple different distant nodes
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Section 5.9 Plasma Cell Neoplasms

Question Answer
What are plasma cell neoplasms?tumors of ab producing B cells
Monoclonal gammopathybenign; excess Ig is functional; potential to convert to mult myeloma
Multiple myelomamalignant; produces excess IgG/IgA and light chains; produces IL6 and IL1 (osteoclast activating factors) --> lytic/punched out lesions; can also see bence jones proteins, amyloidosis, hypercalcemia, anemia, leukocytopenia, inc susceptibility to infections, M spike
Bence Jones proteins seen inmult myeloma
Waldenstrom'saka primary macroglobulinemia; males; comprised of flame cells; hyperviscosity syndrome
what are flame cells?eosinophilic neoplastic plasma cells
what is hyperviscosity syndrome?inc in viscosity of blood d/t overproduction of IgM thickening the blood causing fatigue, weakness, skin/mucosal bleeding, headache, visual problems, neurologic problems
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Section 5.10 Phlebothrombosis

Question Answer
What is phlebothrombosis?clots in the veins
What are the risk factors of phlebothrombosis?virchow's triad - blood stasis, hypercoagulability, endothelial cell damage
What is Trousseau's syndrome?migratory venous thrombosis; more common in those with any of virchow's triad
What is the most common inheritable disorder causing hypercoagulability?Factor V Liden
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Section 6.0 Arteriosclerosis (5a)

Question Answer
What are the 4 types of arteriosclerosis?atherosclerosis, monckeberg's, arteriolosclerosis (hyperplastic), arteriolosclerosis (hyaline)
What causes atherosclerosis?high LDL cholesterol
What type of cells can be seen in atherosclerosis?foam cells (cholesterol laden macrophages)
What type of aa does atherosclerosis affect?large and medium sized arteries (aorta, carotids, iliac, coronary)
What layer does atherosclerosis affect?intima (endothelium, inner lining)
What occurs in Monckeberg's?benign calcium deposits in media to produce lumps
What type of aa does Monckeberg's affect?radial and ulnar a
What causes hyperplastic arteriolosclerosis?malignant htn (SBP>210 or DBP>150)
What type of aa does hyperplastic arteriolosclerosis affect?small arteries and arterioles
How is hyperplastic arteriosclerosis characterized histologically?onion skin hyperplasia
What causes hyaline arteriolosclerosis?inflammation and "use"
What type of aa does hyaline arteriosclerosis affect?small arteries and arterioles
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