MOD Ch4 Flashcards
Filariasis
Helminth infection (Wuchereria), can cause localized edema
Pulmonary Edema
Chronic lung congestion can lead to “heart failure” cells (hemosiderin-laden macraphages)
Hepatic congestion
Often from advanced heart failure. Leads to “nutmeg liver” due to hepatocyte necrosis from ischemia in a centrilobular pattern.
Steps of hemostasis
- Vasoconstriction
- Primary hemostasis
- Secondary hemostasis
Primary hemostasis steps
- Adhesion
- Activation
- Aggregation
Primary hemostasis, adhesion
Weibel-Palade bodies release von Willebrand factor, which allows for adhesion.
Von Willebrand disease
No VWF, normal platelet count
Bernard Soulier syndrome
No Gplb receptor (visible under microscope: giant platelets)
Primary hemostasis, activation
GpIIb-IIIa change to form fibrinogen links.
Secretion initiated by thrombin, release by ADP and thromboxane A2 (which is inhibited by aspirin)
Primary hemostasis, aggregation
GpIIb–IIIa complex allows cross-linking
Glanzmann thromasthenia
GpIIb-IIIa deficiency
Thrombocytopenia
Loss or less production of platelets (platelet count may be low, but platelets are functional)
Vitamin K dependent clotting factors
II, VII, IX, X
Coumadin
aka Warfarin, blocks Vitamin K dependent clotting factors
Factor V Leiden mutation
Factor V mutation that makes factor V resistant to cleavage by Protein C
–> inability to inhibit coagulation
Heparin induced thrombocytopenia
Antibodies to PF4-heparin complexes leads to a prothrombotic state.
- exposure to unfractionated heparin
- PF4-heparin complexes form
- IgG crosslinks platelet Fc receptors and PF4-heparin complexes
- platelet activation and aggregation
Antiphospholipid antibody syndrome
Antibodies against plasma proteins that bind to phospholipids
Sx: vascular, obstetric (unexplained miscarriages)
Primary: has an immune disorder
Secondary: does not have an immune disorder
Septic emboli
Endocarditis–> valve vegetations break loose
Sx: Janeway lesions, Roth spots, Splinter hemorrhage
