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Hematology General 3


Most common cause of anemia worldwide Fe def anemia
HUS vs TTP HUS: no neuro sxs, more renal > TTP
Most common congenital coagulopathy von Will (1% prevalence)
Dz = increase in ultra-high molecular wt multimers of von Willebrand factor TTP
HYPOproliferative anemia due to: Marrow damage, Fe def, dec'd stimulation
HYPERproliferative anemia due to: BM failure to compensate for blood loss or RBC destruction
Enzyme disorder: adequate Fe but can't get it into Hgb; Fe accumulates in ? Sideroblastic anemia; in RBC mitochondria
Causes of B12 def Diet (vegans); malabsorption: inadequate intrinsic factor prodn (70%), terminal ileum dz (sprue, Crohns), tapeworm, drugs
B12 def vs folic acid def B12: meat/dairy; to 5000 mcg in liver (3 yrs); Folic acid: fruit/veg; 5-20 mg stored (few mos)
Due to spectrin pro in cytoskeleton Hereditary spherocytosis
Triad: anemia, splenomegaly and jaundice Hereditary spherocytosis
Acquired stem cell disorder making RBC membrane prone to lysis by complement PNH
In PNH, increased risk of: leukemia/myelofibrosis
Episodic hemolytic anemia related to oxidative stress (hereditary) G6PD def
2 RBC conditions w/pigment gallstones Hereditary spherocytosis, sickle cell
Acquired hemolytic anemia due to IgM autoantibody Cold agglutinin dz
Evans syndrome (immune thrombocytopenia) AIHA
Engorged retinal veins seen in: P vera; waldenstrom
Causes of decreased plt function: membrane defects Glanzmanns; Bernard-Soulier
HIT mechanism Heparin combine w/PF4; this plus Abs => plt activation => limb or life threatening thrombosis
Extrinsic & intrinsic coag pathways converge to form: factor Xa
All clotting factors (except FVIII) made in: Liver
fx of liver dz on coag 1st: dec in FVII (short half-life) prolongs PT; then dec in other factors => prolonged aPTT; dz causes splenomegaly => thrombocytopenia
Vitamin K is a necessary co-factor in the g-glutamyl carboxylation of: Factors II, VII, IX, X; also Protein C and Protein S
vit K def is seen in: HDN (tx w vit K); malabsorption (vit K, A,D,E fat soluble); malnutrition; antibx use
Causes of prolonged aPTT: Def of intrinsic (FXI, FVIII, FIX ) & common pathway factors; Heparin & DTI tx; Inhibitors to coag factors
Prolonged aPTT; doesn't correct w/mixing study FVIII inhibitor
Protein C or Protein S Def: predisposition to: recurrent venous thromboses
Dz: mutation makes it resistant to inactivation by Activated Protein C Factor V Leiden
Recurrent arterial or venous thromboses; 2nd trimester miscarriages; thrombocytopenia; valvular heart dz; suggests: Anti-Phospholipid Syndrome
Acral ischemia: DIC
thromboxane A2 is: potent stimulator of plt aggregation & vasoconstriction
fibrin is digested by plasmin
Dz’s causing ITP SLE, CLL, virus (HIV/Hep C)
von W defect is in: platelet adhesion only
vWF is synthesized in: endothelial cells & megakaryocytes
Fn of vWF: mediate platelet adhesion to damaged vessel site
Glanzmann rare autosomal rec; def in IIb/IIIa, plts can’t agg; high BT
Bernard-Soulier Syndrome Rare autosomal rec; low/abn plt vWF receptor; giant plts, thrombocytopenia, prolonged BT
The ___ pathway initiates coag process; then _____ pathway enhances _____ formation in clot Extrinsic; intrinsic; thrombin
First factors to be affected in hepatic dysfunction Vit K dependent factors (2, 7, 9 & 10) + factor 5
HIT occurs when? 4-10 days post hep infusion
Distinguish liver dz coagulopathy from vit K def Vitamin K def only: 5 is normal, 7 is low; Liver dz only: both 5 & 7 are low
Created by: Adam Barnard Adam Barnard