Exam 1 High Yield Flashcards
Causes of microcytic anemia
Iron deficiency anemia of chronic disease thalassemias lead poisoning sideroblastic anemia
Causes of normocytic anemia
sickle cell anemia
Causes of macrocytic anemia
alcohol abuse
B12 deficiency
folate deficiency
Chemotactic pathway factors
C5a
Opsonizing pathway factors
C3b
Anaphylatoxic (histamine)
C3a, C4a, C5a
Lytic
C9
IgG
Binds toxins to phagocytic cells
activates complement (but not as good as IgM)
2 IgG’s bind C1q
Passes placenta
Responds after IgM, but bigger/faster/stronger on 2nd exp.
Any presence in
IgD
Extra long hinge region
Presence on cell surface indicates mature B cell (in addition to sIgM)
MW 180,000
IgE
Extra constant domain (4 total) Lots of sugar (carbs) Type I (immediate hypersensitivity) Resistance to worms/parasites Fc binds mast cells and basophils MW 190,000
IgM
Pentamer Mu has extra constant domain Excellent at activating complement Can't get into tissues or bind phagocytes Small secretory component 1 IgM binds C1q Responds first (before IgG) MW 900,000/100 mg/dL (too viscous if high)
IgA
Secreted in mucus membranes as dimer
Protected by secretory component
Uses alternative pathway in blood
MW 4,000,000/200 mg/dL
CBC values/labs for thalassemia (alpha or beta)
Decreased MCV, MCH, MCHC
Normal RDW
Increased RBC #/production (compensatory), lysis (unconj bilirubin, LDH, AST)
Splenomegaly, bilirubin gallstones, anemia (?)
Dx’ing alpha thalassemia
2 gene deletion: microcytosis
3 gene deletion: anemia, microcytosis
Hgb electrophoresis: NORMAL
Types of alpha thalassemia
1 gene deletion: silent carrier
2 gene deletion: trait (trans and cis, Africa and Asia)
3 gene deletion: Hb H Disease
4 gene deletion: hydrops fetalis