Hematology/Oncology Flashcards
Erythrocytosis
Anisocytosis
Poikilocytosis
Reticulocyte
- Erythrocytosis = polycythemia = increased RBCs
- Anisocytosis = varying sizes
- Poikilocytosis = varying shapes
- Reticulocyte = immature RBC
Spectrin
supplies the biconcavity/flexibility of RBCs
1/3 of platelets are stored in?
Spleen (lifespan = 8-10 days)
Causes of polycythemia/erythrocytosis?
- Any time have increased EPO (hypoxia, renal cell carcinoma, HCC, pheochromocytoma, hemangioblastoma)
- Down’s babies at birth
- Polycythemia vera –> have increased RBCs, but normal EPO
Barr bodies
=inactivated X in neutrophils
–>seen in all women + KF men
When do you see hypersegmented polymorphic neutrophils?
-Vitamin B12/Folate deficiency
Neutrophil chemotactic factors?
- Leukotriene B4
- IL-8
- C5a
CD14 = cell marker for?
Macrophages
Causes of Eosinophilia?
- DNA-CAAPA:
- Drugs
- Neoplastic
- Asthma (and Churg-Strauss)
- Collagen Vascular diseases
- Allergic processes
- Addison’s (adrenal insufficiency)
- Parasites (invasive)
- Acute Interstitial Nephritis
Phagocytes:
- in brain
- in tissue
- in liver
- in joints
- brain = microglia
- tissue = macrophages
- liver = kupffer cells
- joints = A-cells
Mast cells vs Basophils?
Both are similar, mediate allergic rxn
- Basophils in Blood
- Mast cells in tissue
-mast cells are involved in type 1 hypersensitivity rxns
Langerhans cells
- dendritic cells on skin and mucous membranes
- act as professional APCs
- possess Birbeck granules = racquet-shaped intracytoplasmic granules
Main inducers of primary antibody response?
Dendritic cells = professional APCs
clock-face chromatin
Plasma cells (B cells differentiate into plasma cells; plasma cells produce lots of antibody specific to a particular antigen)
plasma cell neoplasm?
Multiple Myeloma –> make a whole bunch of one particular type of B cell, all making one type of antibody (so see monoclonal antibody spike)
CD3
on ALL T-cells
- ->Th also have CD4
- ->Cytotoxic also have CD8
anti-AB antibodies (Ig type?)
-IgM –> don’t cross placenta
anti-Rh antibodies (Ig type?)
=IgG –> can cross placenta and cause hemolytic disease of newborn (erythroblastosis fetalis) if fetus is Rh+
Blood type A (example)
- have A antigen on RBC surface
- B antibody in plasma
erythroplastosis fetalis
- cause?
- symptoms?
- hypersensitivity type?
- how to prevent?
- type 2 hypersensitivity rxn
- cause: Rh- mother exposed to Rh+ fetal blood during delivery; makes anti-Rh IgG –> can cross placenta in subsequent pregancies, causing hemolytic disease of newborn in next fetus who is Rh+
- Symptoms in infant: hepatosplenomegaly, severe anemia, jaundice, demise/death
- Treat/Prophylaxis = give mother Rhogam = Rho (D) Ig at first delivery to prevent all future erythroblastosis
Deficiency of Factor VIII?
Hemophilia A
“Aight”
Deficiency of Factor IX?
Hemophilia B
“Benine”
Vitamin K deficiency?
decreased synthesis of “diSCo 1972”
- proteins C and S
- Factors X, IX, VII, II (10, 9, 7, 2)
*Vitamin K normally catalyzes carboxylation of glutamic acid residues on proteins involved with blood clotting
Vitamin K antagonist?
Warfarin
–>acts by inhibiting Epoxide Reductase (vitamin K–>activated vitamin K)