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129 Cards in this Set
- Front
- Back
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top 2 most numerous WBCs in blood
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1. PMNs 2. lymphs
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anisocytosis
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varying size RBCs
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pokilocytosis
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varying shape RBCs
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what component of eosinophils is involved in helminth protection
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major basic protein
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which cell type secrete histaminase in order to control reaction following mast cell degranulation
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eosinophils
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causes of eosinophilia (5)
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neoplastic, asthma, allergic processes, collagen vascular dz, invasive helminths
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who has lactoferin and what does it do
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contained in PMNs, interferes with Fe metabolism in bacteria
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dendritic cells
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proffesional APCs, express MHC II and FcR, main inducers of primary Ab response
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molecules common to E and I coag pathways
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10,5,2,1
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molecules of the intrinsic pathway (excl common)
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12,11,9,8
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what do GpIb and GPIIb/IIIa bind respectively
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GpIb binds to vWF which is bound to exposed subendo collagen; GIIb/IIIa binds to fibrinogen which connects platelets
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factor V leiden
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production of mutant factor V, cannot be degraded by protein C, incr risk of DVT (venous clots)
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ATIII deficiency
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RARE, reduced incr in PTT after admin of heparin; can be acquired in women on OCPs
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protein C or S def
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decr ability to inactivate V and VIII, incr risk of skin necrosis following warfarin admin
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which AA derivitive incr platelet aggregation and which decr it
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TxA2 incr aggregation, released by platelets; PGI2 (prostacyclin) decr aggregation and vasodilates (also helps inhibit aggregation), released by endothelium
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what causes incr #s of GpIIb/IIIa recetpros on platelets
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binding of ADP
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epoxide reductase
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activates Vit K, inhibited by warfarin
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which molecules are Vit K dependent and what does Vit K do to them
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factors 2,7,9,10, Protein C and S; adds gamma carboxyl group
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which factor is attached to vWF
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8
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antithrombin 3 inavtivates which factors
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2,7,9,10,11
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protein C and S
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protein S activates protein C which cleaves and inactivates factor 5a and 8a
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where is vWF made
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in endothelium and megakaryocytes
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alterations to coag cause by OCPs (3)
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incr F5 and 8, inhibit antithrombin III, incr fibrinogen
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most common cause of jaundice in first 24 hours of life
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ABO incompatibility (Mom probably O and baby is A or B, so anti-AB IgG crosses placent, causes mild anemia but no kernicterus)
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actions of bradykinin (3)
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vasodilation, incr permeability, incr pain
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D-dimers
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only detects breakdown of fibrin molecules which were crosslinked (F13), so proves there was a clot; seen in DIC, thrombi
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Ab's in blood type O pts
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anti A IgM, anti B IgM, anti AB IgG
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Ab to Rh
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is an IgG, can cross placenta which is why Rh incompatibility is dangerous
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crossmatch
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used to detect atypical Ab's directed against foreign Ag's on donor's RBCs, must be performed for each unit of donor blood; pt serum is mixed with a sample of RBCs from donor unit
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which blood type is associated with incr duodenal ulcers and which has incr gastric CA
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O has incr duodenal ulcers, A has incr gastric CA
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type and screen
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group (ABO), type (Rh), screen (Ab screen, indirect Coombs, detects atypical Ab's present in pts serum, ex: anti-D(Rh))
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most common contaminant of stored blood
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Yersinia entercolitica
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IgA deficienct individuals
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must receive blood or blood products without IgA or else they can develop a severe anaphylactic reaction if the have Ab's to IgA in their serum from some past exposure
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Rho-gam
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Anti-D (Rh) globulin, IgG, give during 28th week to all Rh- mothers, also given after birth if baby Rh+, does not cross placenta,
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shistiocyte
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also called helmet cell, is a fragmented RBC, can be seen in DIC, TTP, etc
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Bite cells
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seen in G6PD deficiency
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target cell (4)
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too much membrane; HbC dz, asplenia, Liver Dz, thalassemia
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basophilic stippling
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denatured rRNA, seen in thalassemias, anemia of chronic dz, Fe def, lead poisoning
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Heinz bodies
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denatured Hb, removal of these leads to bite cells, seen in a-thal and G6PD def
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Howell Jolly bodies
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basophilic nuclear remnants, seen in pts with functional hyposplenia or asplenia
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causes of microcytic anemia
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Fe def, thalassemias, lead poisoning (prob making Hb)
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decr serum hapteglobin (and what it does) and incr LDH
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indicates RBC hemolysis (haptoglobin binds free Hb and takes it to the spleen); use direct Coombs to distinguish if autoimmune
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roles of transferrin and ferritin
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transferrin transports Fe in plasma (most from Hb break down), ferritin stores Fe
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lead poisoning inhibits which enzymes and causes build up of what
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inhibits ferrochelatase and ALA dehydroenase in Hb synthesis; ALA and coproporphyrin build up
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signs of porphyria (5)
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painful abdomen (N/V), pink urine (can turn dark on standing), polyneuropathy, psych disturbances (agitation, paranoia), precipitated by drugs (ex: TPM-SMX)
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which enzymes are affected in acute intermittenent porphyria and what builds up
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uroporphyrinogen synthase; causes build up of porphobilinogen and ALA
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what is the rate limiting step in Hb synthesis, cofactor, location and reaction
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ALA synthase, requires B6 and occurs in mito; creates ALA from glycine and succinyl CoA
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2 components required for heme synthesis
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succinyl CoA and glycine, these are made into ALA
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where does the ferrochelatase reaction of heme synthesis occur
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in the mito, involves incorporation of Fe+2 into protophoryrin to make Heme
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serum Fe levels, TIBC (indirectly measures transferrin), ferritin and transferrin sat% (serum Fe/TIBC) in Fe def anemia
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decr Fe, incr transferrin, decr ferritin, decr sat
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serum Fe levels, TIBC (indirectly measures transferrin), ferritin and transferrin sat% (serum Fe/TIBC) in anemia chronic dz
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decr serum Fe, decr transferrin, incr ferritin, nl sat
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hepcidin
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inhibits release of Fe from macrophages and intestinal epithelial cells; is incr in inflammation (incr use of Fe in macros) and decr in Fe def and hypoxia
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mutation in SS
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single AA replacement in the 6th position on the B chain, glutamic acid is replaced with valine, creates abnormal hydrophobic globin chain interactions
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which form of Hb sickels in SS pts
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deoxy form
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what does the O2 dissociation curve look like for SS pts
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it is R shifted, symptoms of anemia may be mild compared to severity
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inheritence of SS and thals
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mostly AR
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genetic causes of a and b thal
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a is often due to gene deletions, b minor due to DNA splicing defects, major due to nonsense mutation and stop codon production
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what are HbH and Hb Barts
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seen in a-thal; HbH is B-tetramer and will show up on electrophoresis; Hb Barts is gamma-tetramer which occurs with lack of all 4 a chains, causes hydrops fetalis
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compensation in b-thal
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incr in fetal Hb (gamma chains) and incr in HbA2 (delta chains); also help to mop up excess a chains which are insoluble
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warm agglutinin autoimmune anemia
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IgG (or C3b); chronic, seen in SLE, CLL and with drugs (penicillin, methyldopa), mostly extravascular
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cold agglutinin autoimmune anemia
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IgM, acute; triggered by cold, seen with mycoplasma pneumoniae or mono
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direct vs. indirect coombs
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direct: pts RBCs, add serum with antibody, RBCs will agglutinate if covered with Ig; indirect: normal RBCs added to pts serum, agglutinate if Ab present in serum
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PNH symptoms, confirm test and 2 complications
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at night you becomes slightly acidodic and this incr complement; if you have abnormal GPI anchor or decr DAF then you develop mild intravascular hemolysis, confirm with the HAM test; incr risk of AML and of thrombi formation
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role of vasopressin in mild vWF def
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incr release of vWF from endothelium, can control bleeding in mild dz
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ITP
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peripheral platelet destruction, anti-GpIIb/IIIa Ab's; usually follows URI; PT and PTT normal, incr bleeding time, microhemorrhage
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TTP
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deficiency of vWF-cleaving metalloprotease, leads to incr platelet aggregation and thrombi, schistiocyte formation, incr LDH, incr ind bili, neuro and renal symptoms dominate
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vWF def
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most common bleeding disorder, causes defective platelet adhesion and decr F8 survival; normal platelet count and PT, incr bleeding time, nl/incr PTT (F8)
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what does PT test and which drug uses this to monitor
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extrinsic, 1,2,5,7,10; INR is standardized, warfarin
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what does PTT test and which drug uses this to monitor
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intrinsic, all but 7 and 13; heparin
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glazmanns thrombasthenia
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decr in GpIIb/IIIa leads to defect in platelet aggregation; incr bleeding time, minor bleeding
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bernard soulier
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decr GpIb, also have decr # of platelets, defect in platelet to collagen binding, incr bleeding time, mild bleeding
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hemophilia A and B
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both x-linked recessive, cause late rebleeding and hemoarthrosis, incr PTT; A is lack of F8, more common; B is lack of F9
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markers for R-S cells
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CD 15 and 30, B-cell origin
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strongest predictor of prognosis in Hodgkins
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stage
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what type of Ig do most MM pts make
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IgG, then IgA
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mycoses fungoides
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chronic cutaneous T-cell lymphoma (CD4), presents with severe puritis and psoriasis like lesions; Sezary syndrome is when these cells enter the blood
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prognostic factor in NH lymph
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histiologic type
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small lymphocytic lymphoma
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neoplasia of small mature B cells, elderly, like a tissue phase of CLL, low grade
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follicular lymph
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from germinal cell (B-cell), adults, t(14:18), constitutive bcl-2 expression, difficult to cure but indolent, often waxing and waning
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diffuse large cell lymph
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germinal cells (mostly B, some T), older adults and some children, aggressive (can infiltrate BM, GI, SC) but many curable, most common NH lymph
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mantle cell lymphoma
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adults, B cells, CD5+, t(11;14), poor prognosis, often BM infiltration, low grade
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lymphoblastic lymphoma
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children, immature T cells, commonly presents with ALL and mediastinal mass, very aggressive
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Burkitt's lymphoma
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similar to L3 ALL, leukemic phase and BM involvement common, children, EBV, t(8;14), c-myc next to heavy chain, starry sky
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t(11;22)
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Ewing sarcoma
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t(14;18)
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follicular lymphoma, bcl-2
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t(15;17)
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M3 type of AML
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t(2;5)
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anaplastic large cell lymphoma
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t(11;14)
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mantle cell lymphoma
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leukomoid reaction and ex's
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incr WBC with L shift, incr leukocyte alk phos; appendicitis (PMNs), whooping cough (lymphs)
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where does ALL spread to and what marker do leukemic cells have
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CNS and testes; retain Tdt+ (marker of pre-t/b cells)
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most common ALL
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C-ALLA, Cd-10+, B-cell
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aurer rods
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peroxidase+ enzymatic cytoplasmic includsions, commonly seen in AML, treatment leads to release of these which causes DIC
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which AML type invades gums
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M5
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smudge cells
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CLL, fragmented lymphs
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hairy cell leukemia
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mature B-cell tumor in elderly, have filamentous hair like projections, stain TRAP+
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which leukemia has warm Ab autoimmune HA
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CLL
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age ranges for ALL, AML, CLL, CML
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ALL: <15, AML 15-60, CML 30-60, CLL >60
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JAK2 mutation
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seen in myeloproliferative disorders (-CML), allows for growth receptor activation without GF stimulus
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levels of RBCs, WBCs and platelets in PCV
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incr in all
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which anti-coag can be used in pregnancy
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heparin
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reversile of heparin
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protamine sulfate, is + charged and binds to heparin which is -
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which molecule causes the neuro damage in B12 def
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propnoyl CoA
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methylmalonic acid and homocyteine levels in B12 and folate def
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B12: both incr, folate: only homocysteine
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corrected retic
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Hct/45 X retic count; tells you if BM is responding appropriately
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polychromasia
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stage before retics, usually not in peripheral blood but presence indicates incr BM activity; if present, you need to divide retic count in 2
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sideroblastic anemias
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defect in heme synthesis but Fe is still delivered to mitochondria but cant get out (sideroblast); are located in BM, stain with Prussian blue; seen in B6 def (INH, decr ALA synthase), Lead, alcohol (mito toxin); incr Fe, incr %sat, decr TIBC, incr ferritin
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intravascular hemolysis
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often IgM mediated (activates MAC), releases Hb into blood which binds hapteglboin and is phagocytosed by macros to preserve Fe; usually no jaundice but can have Hb-uria
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pt who complains of itching after a shower
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PCV, this is beacause they have incr #s of all cell types, including mast cells
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allergic blood transfusion reaction
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most common, immediate type I HS, itching, hives, anaphylaxis
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febrile blood transfusion reaction
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type II, recipient has anti-HLA Ab's against donor WBCs due to previous blood donatio or pregnancy
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hemolytic blood transfusion reaction
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1. give wrong ABO, immediate intravascular hemolysis (complement and MAC), shock, type II, chills, SOB, hemoglobinuria; 2. pt has Ab against donor RBC Ag which was not originally in the serum during the crossmatch but was coded for in memory b-cells, takes days to weeks to form
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EBV is mostly associated with which Hedgkins lymphoma
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mixed cellularity
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systemic mastocytosis
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mast cell proliferation, incr histamine release leads to syncope, flushing, uticaria and diarrhea
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what are contained in dense and alpha granules in plateletes
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dense: ADP, Ca++; alpha: vWF, fibrinogen
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platelet activating factor
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acts via IP3 to incr Ca++ which strengthens the platelet plug
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spherocytes (2)
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have decr membrane; hereditary spherocytosis and autoimmune HA (macrophages remove the membrane covered with Ig's or complement)
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normocytic anemia causes
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acute hemorrhage, enzyme defects (ex: G6PD def), RBC membrane defects, BM disorders (aplastic anemia), Hb-opathies, autoimmune HA, anemia of chronic dz
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heme oxygenase
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takes heme released from RBCs and converts it first to biliverdin (causes bruises to turn green) and then bilirubin
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transferrin saturation
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serum Fe/TIBC
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Hb electrophoresis in a-thal minor
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normal because ALL types of Hb are decreased but proportions stay the same; if there is HbH (as in a-major) that will show up
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long term treatment of B-thal major and potential complication
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blood transfusions, can develop cardiac failure secondary to hemochromotosis
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what do fetuses with erythroblastosis fetalis die of
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high output cardiac failure
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CBC findings, clinical findings and treatment for hereditary spherocytosis
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incr MCHC, incr RDW, normocytic, incr osmotic fragility; fluctuating jaundice, gallbladder probelms; treat with splenectomy
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good prognosis of Hodkins associated with what levels of RS and lymphs
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incr lymphs and decr RS associated with good prognosis
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Waldenstroms macroglobinemia
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usually men >50 with a lymphoplasmocytoid lymphoma which produces a monoclonal IgM; symptoms of hyperviscocity, no lytic lesions
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polyclonal gamopathy
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benign, many clones making Igs, seen in chronic inflammation (like RA)
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plasmacytoma
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plasma cell proliferation with IgG M-spike, involves soft tissues (ex: lungs, nasopharynx)
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common complication of CLL
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infection because abnormal B cells can't differentiate so you get decr Igs
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PCV findings
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headaches, blurred vision, dyspnea, ruddy cyanosis, spenomegaly, hemorrhage or thrombosis, gout, hypercellular BM, serum EPO often decr; treatment is phlebotomy to incude Fe def anemia
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