Term
| What portion of the heart becomes infarcted with LAD occlusion? |
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Definition
| anterior wall + anterior septum of LV |
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Term
| What portion of the heart becomes infarcted with RCA occlusion? |
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Definition
| poster wall, posterior septum, papillary muscles of the LV |
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Term
| What portion of the heart becomes infarcted with LCA occlusion? |
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Definition
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Term
| When do you begin to see gross changes in the heart after infarct? |
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Definition
4 hours
4-24 hours = dark discoloration due to coagulative necrosis |
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Term
| What are the three main phases of morphologic changes post-MI? |
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Definition
Coagulative necrosis = 1 day
Inflammation = 1 week
Healing/granulation tissue = 1 month |
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Term
| What do you see grossly and microscopically <4 hours post-MI? |
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Definition
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Term
| What do you see grossly and microscopically 4-12 hours post-MI? |
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Definition
| beginnings of coagulation necrosis: eosinophilia of the fibers, pyknosis of the nuclei, fibers start to get smaller. |
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Term
| What do you see grossly and microscopically 12-24 hours post-MI? |
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Definition
gross: dark mottling
microscopic: ongoing coagulation necrosis, pyknosis of nuclei |
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Term
| What do you see grossly and microscopically 1-3 days post-MI? |
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Definition
gross: mottled, but becoming lighter
microscopic: NEUTROPHIL infiltrate, NO NUCLEI (GHOST CELLS), losing mycocytes |
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Term
| What do you see grossly and microscopically 3-7 days post-MI? |
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Definition
gross: yellow pallor = dead myocardium
microscopic: myocyte disintegration, phagocytosis of dead cells, macrophages joining the party to help remove dead cells, neutrophil necrosis |
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Term
| What do you see grossly and microscopically 7-10 days post-MI? |
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Definition
gross: hyperemia at border as granulation tissue enters
microscopic: well-developed phagocytosis and EARLY GRANULATION TISSUE (fibroblasts, collagen, neovascularization) |
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Term
| What do you see grossly and microscopically 10-14 days post-MI? |
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Definition
gross: red-gray borders
microscopic: mature granulation tissue |
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Term
| What do you see grossly and microscopically 2-8 weeks post-MI? |
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Definition
gross: gray-white granulation tissue (SCAR)- starts endocardial and moves outward
microscopic: increased collagen deposition, loss of cellularity |
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Term
| When are you most at risk for arryhthmias post-MI? |
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Definition
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Term
| When are you most at risk for acute fibrinous pericarditis post-MI? |
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Definition
2-3 days
Occurs after acute TRANSMURAL MI.
Presents as chest pain and friction rub.
Grossly, it would normally be yellowish but the inflamed pericardium now turns redish pink |
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Term
| When are you most at risk for rupture of the ventricular free wall, interventricular septum, or papillary muscle post-MI? |
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Definition
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Term
| What lab tests are done to detect cardiac enzymes post MI? |
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Definition
1. myoglobin - first to rise - in 30-60 min
2. CK-MB
3. Troponin I - most specific cardiac marker, appears at 4 hours, peaks at 24 hours, hangs around for a week |
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Term
| What is the autoimmune pericarditis that presents several weeks post-MI? |
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Definition
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Term
| How long do we have to intervene post-MI before there is irreversible damage/coagulative necrosis? |
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Definition
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Term
| What % of coronary artery is occluded in stable angina? What are stable plaques composed of? |
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Definition
>75%
mostly fibrous cap, small lipid core |
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Term
| What % of coronary artery is occluded in unstable angina? What are unstable plaques composed of? |
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Definition
50-75%
small fibrous cap, lipid-rich core |
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Term
| Hemostasis is dependent on what 3 major entities? |
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Definition
Virchow's Triad:
1. Blood vessel endothelium
2. Platelets
3. Coagulation and fibrinolytic systems |
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Term
| What is the difference between primary and secondary hemostasis? |
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Definition
primary= forming a weak platelet plug
secondary = stabilizing platelet plug, mediated by coagulation cascade |
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Term
| What are the 4 steps of primary hemostasis? |
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Definition
Step 1- transient vasoconstriction (reflex neural + endothelin release)
Step 2 - platelet adhesion to the surface of disrupted vessel (vWF binds exposed collagen, platelets bind vWF via GPIb receptor)
Step 3 - Platelet degranulation (ADP from dense granules promotes exposure of GPIIb/IIIa receptor on platelets and TXA2 promotes platelet agg)
4 - Platelet aggregation (via GPIIb/IIIa, form a weak platelet plug using fibrinogen) |
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Term
| What are in platelet light granules? (alpha) |
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Definition
PF4, PDGF (most important)
also contain fibrinogen, fibronectin, Factors V and VIII, TGFB |
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Term
| What are in platelet dense granules? (beta) |
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Definition
| ADP, Ca2+, histamine, serotonine, epi |
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Term
| What triggers secondary hemostasis? What does it result in? |
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Definition
| tissue factor (Factor VII) released from the site of injury activates the plasma coagulation cascade, forming thrombin which converts fibrinogen to fibrin which is crosslinked by Factor XIIIa forming a stable plug |
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Term
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Definition
| integral membrane protein expressed on the surface of endothelial cells that combines with thrombin to form a complex that activates protein C, a naturally occurring anticoagulant that degrades Factor Va and VIIIa |
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Term
| What does the Heparin-like molecule do? |
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Definition
Complexes with Antithrombin III to:
1. inactivate thrombin
2. inactivate factors Xa and IXa |
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Term
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Definition
prothrombin time
-evaluates pts ability to clot
-measures extrinsic pathway
-often done before surgery |
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Term
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Definition
paritial thromboplastin time
-detects presence of clotting disorder
-measures intrinsic pathway
-used to determine if heparin therapy is effective |
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Term
| What coagulation factors are in the prothrombin group? what do these factors have in common? |
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Definition
Factors II, VII, IX, X
-All of these proteins contain gamma-carboxy glutamic acid which is needed for the binding of calcium. All are synthesized in the liver and are Vit K dependent |
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Term
| Is mucosal bleeding (such as epistaxis) a disorder of primary or secondary hemostasis? |
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Definition
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Term
| Is deep tissue bleeding into muscles and joints (hemarthrosis) a disorder of primary or secondary hemostasis? |
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Definition
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Term
| Is rebleeding after surgical procedures (eg. disorder of primary or secondary hemostasis? |
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Definition
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Term
Name the Hemostasis Disorder described:
-IgG autoantibodies against platelet antigens (eg. GPIIb/IIIa)
-thrombocytopenia due to antibody-bound platelets being consumed by the spleen |
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Definition
| Immune Thrombocytopenic Purpura (ITP) |
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Term
| What molecule does heparin complex with in HIT? What happens after that? |
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Definition
Platelet Factor 4 (from light granules)
Abs generated against heparin-PF4 complex also attack the platelets, consuming them. The fragments of destroyed platelets may activate remaining platelets leading to thrombosis. |
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Term
Name the Hemostasis Disorder described:
-large, uncleaved vWF multimers leading to abnormal platelet adhesion and microthrombi
-a type of microangiopathic hemolytic anemia |
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Definition
TTP
Thrombotic thrombocytopenic purpura |
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Term
Name the Hemostasis Disorder described:
-classically seen in kids with E coli O157:H7 dysentery
-a type of microangiopathic hemolytic anemia |
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Definition
HUS
Hemolytic Uremic Syndrome |
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Term
Name the Hemostasis Disorder described:
Genetic GP1b deficiency (impaired platelet adhesion) |
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Definition
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Term
Name the Hemostasis Disorder described:
Genetic GPIIb/IIIa deficiency (impaired platelet aggregation) |
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Definition
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Term
| How does aspirin impair platelet aggregation? |
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Definition
| aspirin irreversibly inactivates cyclooxygenase which decreases TXA2 which normally aggregates platelets |
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Term
Name the Hemostasis Disorder described:
-decreased Factor VIII
-normal PT
-inc PTT
-normal bleeding time
-normal platelet count |
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Definition
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Term
Name the Hemostasis Disorder described:
-point mutation in Factor 5a
-inherited
-hypercoagulability |
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Definition
APC Resistance aka Factor V Leiden
Factor V cannot be inactivated by activated Protein C which normally digests both 5a and 8a |
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Term
| How do you tell the difference between Hemophilia A and VWD? Both have decreased factor VIII. |
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Definition
VWD will have an abnormal ristocetin test(ristocetin causes vWF to bind GP1b, but without vWF there will be impaired platelet agglutination)
Bleeding time will be elevated in VWD because vWF-GP1b is not functional, however we dont use bleeding tests anymore to differentiate |
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Term
| What factors does activated Vit K gamma activate? |
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Definition
| II, VII, IX, X, proteins C and S |
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