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WBC with bilobate nucleus
Basophil
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Cromolyn sodium
- Prevents mast cell degranulation by stabilizing the cell membrane
- Used to treat asthma
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Cell that produces histaminase and arylsulfatase
Eosinophil
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CD14
Monocyte and macrophage marker
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WBC with kidney-shaped nucleus
Monocyte
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NK cell markers
CD16, CD56
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Class of antibodies to the A and B blood group markers
IgM (do not cross placenta)
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Class of antibodies to the Rh blood group marker
IgG (do cross placenta)
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Hemorrhagic disease of the newborn
- Caused by vitamin K deficiency, common in premies
- Treat with vitamin K injection
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Effect of factor X
- Converts prothrombin to thrombin
- Thrombin then converts fibrinogen to fibrin
- Fibrin forms clots, stabilized by factor XIII and Ca
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Hemophilia A
Factor VIII deficiency
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Hemophilia B
Factor IX deficiency
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What activates bradykinin?
Kallikrein, which is activated by factor XII
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vWF
- Links platelet Ib receptor to subendothelial collagen
- Binds factor VIII, protects it from degradation
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Ticlopidine, clopidogrel
Inhibit ADP-induced expression of GPIIb/IIIa
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Abciximab
Inhibits IIb/IIIa
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Epoxide reductase
- Activates vitamin K, allows it to act as a cofactor in the carboxylation reaction needed for production of clotting factors
- Inhibited by warfarin
-
Protein C
- Activated by protein S
- Inactivates factors V and VIII
- Factor V Leiden mutation produces a version of factor V that cannot be inactivated by protein C
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Basophilic stippling
- Thalassemias
- Anemia of chronic disease
- Iron deficiency
- Lead poisoning
-
Bite cells and Heinz bodies
G6PD deficiency
-
Defective enzyme in sideroblastic anemia
Ala synthase
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Target cell
- HbC disease
- Asplenia
- Liver disease
- Thalassemia
-
Hepcidin
- Hormone that regulates iron levels
- Synthesized in liver
- Acts on bone marrow macropages and intestinal epithelial cells
- Inhibits iron transport, and mediates iron sequestration in anemia of chronic disease
-
Folate deficiency
- Folate is needed to convert homocysteine to methionine
- Megaloblastic anemia with hypersegmented neutrophils and increased levels of homocysteine
-
B12 deficiency
- Megaloblastic anemia with hypersegmented neutrophils, increased homocysteine, and increased methalmalonic acid
- Peripheral neuropathy
- Can be due to malnutrition, malabsorption, pernicious anemia, or diphyllobothrium latum
-
Fanconi's anemia
- Caused by an inherited defect in DNA repair
- Presents with short stature, increased incidence of cancer, and aplastic anemia
- Often associated with AML
-
Pyruvate kinase deficiency
- Caused by an AR mutation
- Inability to make ATP causes RBCs to burst from osmotic stress
- Presents with hemolytic anemia in newborns
-
PNH
- Caused by impaired synthesis of GIP, which functions to anchor CD55 and CD59 to RBC membranes
- CD55/59 prevent RBCs from getting destroyed in the spleen
- Presents with intravascular hemolysis, due to complement-mediated RBC lysis
- Labs show increased urine hemosiderin
- Treat with eculizumab
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Warm agglutinin autoimmune hemolytic anemia
- Mediated by IgG
- RBC destruction in spleen
- Seen in pxs with SLE, CLL, and on methyldopa
-
Cold agglutinin autoimmune hemolytic anemia
- Mediated by IgM
- RBC destruction in liver
- Attacks of acute anemia triggered by cold temperatures
- Seen in patients with M. pneumonia or mono
-
Schistocytes on peripheral blood smear
Indicate mechanical destruction of RBCs
-
Hemolytic uremic syndrome
- Can be precipitated by E. coli infection
- Characterized by hemolytic anemia, thrombocytopenia and renal failure
-
Thrombotic thrombocytopenic purpura
- Due to mutant ADAMTS-13 metalloproteinase
- Failure to cleave vWF causes large vWF monomers to bounce around in the circulation and smash RBCs
- Presents with a triad of neurological symptoms, renal failure, thrombocytopenia, fever, and microangiopathic hemolytic anemia
-
Acute intermittent porphyria
- Due to a porphobilinogen deaminase deficiency
- Presents with abdo pain, pink urine, and polyneuropathies
- Treat with glucose and heme to inhibit ala synthase
-
Porphyria cutanea tarda
- Due to a uroporphyrinogen decarboxylase deficiency
- Most common porphyria
- Presents with tea-colored urine and blistering photosensitivity
- Exacerbated by alcohol
-
B6 deficiency
- B6 is needed to convert glycine and succinyl CoA into d-ala
- Deficiency can be induced by isoniazid, and causes sideroblastic anemia
-
Treatment for lead poisoning
- Dimercaprol in adults
- Succimer in children
-
Bernard-Soulier disease
- GP1b deficiency
- Platelets cannot adhere to subendothelial collagen
-
Glanzman's thrombasthenia
- GP IIa/IIIb deficiency
- Platelets cannot adhere to each other
- Normal platelet count
- Ristocetin triggers aggregation
- ADP does not trigger aggregation
-
ITP
- Caused by autoantibodies against GP IIb/IIIa
- Platelets are destroyed in the spleen
-
Poor aggregation in response to ristocetin but normal aggregation in response to ADP
Hemophilia B (factor IX deficiency)
-
Most common cause of hereditary hypercoagulability
- Factor V Leiden
- Factor V cannot be degraded by protein C
-
Prothrombin mutation
- Mutation in 3 prime untranslated region
- Associated with venous clots
-
Lepirudin, bivalirudin, argatroban
- Hirudin derivatives
- Direct thrombin inhibitors
- Use as an alternative to heparin in patients with HIT
-
Aminocaproic acid
Inhibit fibrinolysis, use to treat thrombolytic overdose
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