Hemodynamics Flashcards
1
Q
Nitric oxide
A
- Macrophage produce NO through 2 NO synthase enzymes
- Causes vasodilation & NO free radicals are toxic to microbal & mammalian cels
- Reduces leukocyte adhesion
- Reduces platelet adhesion
- Endothialial stimulation = Ca+2 influx & endothelial NOS activation
2
Q
Congestion of Liver
A
- Cardiac failure (right heart = venous congestion)
- Damming of blood in the IVC
- Central veins & sinusoids are DISTENDED with blood
- Hepatocytes around the central vein (necrosis & degeneration)
- Hepatocytes on the periphery of portal area better O2 (hepatic arteriloles)
- Periportal hepatocytes (periphery) show FATTY change
- Histology: central areas are red & depressed COMPARED w/surrounding tan parenchyma = NUTMEG liver pattern
- Cetrilobular necrosis w/degenerating hepatocytes = enlarged liver
3
Q
Hemorrhage
A
- LOW platelet count
- Purpura: small on dots on surface of skin
- Due to = Trauma or vascular inflammation (vasculitis)
- Ecchymoses: Subcutaneous hematomas (bruises) larger Surface area
- LARGE hemmorrhages w/in body cavities-
- Hemopericardium = Blood in the pericardial sac
- Can cause cardiac temponade
- Hemoperitoneum = Blood in between inner lining of abdominal wall & outer of abdominal organs
- Causes: trauma, abdominal aortic aneurysm, HIGH does of anti-coags
- Hemothorax= Blood in pleural cavity
- Causes: narrowing pulse pressure, hypotension
4
Q
Thrombosis
A
- Intravascular mass formed from Blood components adhered to Vessel wall
- Vrichow triad
- Endothelial injury
- Statis or turbulence flow
- Blood hypercoag
- Endothelial injury:
- ulcerated plaques in atherosclerosis
- Vascular injury = Vasculitis
- Causes: Hypertension, turbulent flow, scarred valves, bacterial endotoxins
- Stasis or turbulent flow - Prolonged bed rest, aneuysms (abdominal)
5
Q
Hemostatic Process (Primary)
A
- Reflex vasoconstriction
- ECM collagen exposed from basement membrane
- Endothelin release causes secondary vasoconstriction
- Platelet adhesion DUE to vWF = shape change & granule release
- Granule = ADP & TxA2 = FURTHER platelet aggregation = hemostatic plug (END of primary hemostatis)
6
Q
Hemostatic process (secondary)
A
- Tissue factor & platelet phospholipids = THROMBIN activation
- Results in Fibrin polymerization-cementing platelets into secondary hemostatic plug
- Fibronogen to Fibrin = Crosslinked - STABLE
- Antithrombic events:
- Release of t-PA (fibronolytic)
- Thrombomodulin (blocks coag cascade)-binds with thrombin->protein C proteolysis F 5 & 8
- antithrombin 3 inactivates thrombin along w/heparin like mols & F10,9,12,11
- NO, PGl2, ADP from endothelium=INHIBIT platelet aggregation
7
Q
Def in Platelet adhesion & aggregation
A
- Glanzmann thrombasthenia:
- Def in Gp2b-3a complex - originally Gp1b ADP induces confromational change
- Gp2b-3a allows for Fibronogen to bridge platelet (adhesion)
- Bernard-soulier syndrome:
- Def. in Gp1b binds w/vWF which allows platelet adhesion to damaged endothelium
8
Q
Hypercoagulability
A
- NOT common cause of thrombosis
- Causes: Hereditary
- Mutations in factor 5 gene (Leiden)
- Prothrombin gene-correlates w/elevated lvls of homocysteine (hardening of major arteries)
- Def oF antithrombin 3, Protein C & S
- Causes: Aquired
- Oral contraceptive
- Cardiac failure
- Heparin induced thrombocytopenia syndrome (HIT) = LOW platelet, PF4 antibodies to heparin form CHECK PTT/Intrisic pathway
- Antiphosolipid syndrome = can cause miscarriage and can form clots in arterial and venous system
9
Q
Intrinsic & extrinsic
A
- Intrinsic = PTT (heparin decreases)
- Hageman factor - HMWK collagen - 12A
- 11, 9, 8 Associated w/Thrombin
-
Extrinsic = PT (Coumadin decreases)
1. Tissue injury - Thromboplastin - F7 - Common pathway- Factor 10
- activated by Ca+2 influx from BOTH intrisic & extrinsic
- F 5, 2, 1-(fibronogen)
- Fibrinogen to Fibrin to CROSS-linked fibrin - active Factor 13 = Stabilizer
10
Q
Prolonged Bleeding Time
A
- Tests Platelet function UP to the formation of temp plug (primary hemo)
- PROlonged BT=
- Aspirin/NSAID - Plt count normal
- Bernard-soulier- Thrombocytopenia (low), GIANT platelets (Big Suckers)
- Glanzman’s disease - No fibronogen bridging - Low platelet, renal failure, scurvy
- vWB disease- combined platelet and coag defect
11
Q
Prothrombin Time
A
- Used to measure effectiveness of extrinsic pathway - formation of fibrin clot - meshwork (secondary hemo)
- Factors 7, 10, 5, 2, 1
- Normal - 11-15 seconds
- Helpful for checking on patients warfarin response - anticoag time
- PROLONGED PT - liver disease
- Detect Factor 7 def
- Normal Thrombin time - 9-13 seconds Measures fibrinolytic pathway (fibronogen-fibrin)
12
Q
Partial Thromboplastin Time
A
- Measures intrinsic pathway (til formation of fibrin-meshwork)
- Factors 12, 11, 9, 8, 10, 5, 2, 1
- Norm = 25-40 seconds
- Measure pts on heparin therapy
- Detect factors def in intrisic pathway
- Normal Thrombin time - 9-13 seconds Measures fibrinolytic pathway (fibronogen-fibrin)
- Test:
- Kaolin-Activation of contact-depen Factor12
- Cephalin-Sub platelet phospholipid
13
Q
Reasons for Bleeding Disorders
A
- Increased fragility of BV:
- Patachiae, purpuras (appear in bacterial infection that activate hagmans factor or DEF of Vit C)
- Platelet, bleeding time, coag (PT, PTT) are normal
- Platelet def & dysfunction
- Derangement of coag-PT, PTT prolonged, BT normal, Hemm in joints, LL (trauma)
- Combo of all these factors
14
Q
Henoch-Schonlein purpura
A
- Seen in childhood
- Following upper resp infection
- Infective endocarditis
- Pathogenesis:
- systemic hypersensitivity disease
- widespread inflammatory rxn of capillaries & small vessels
- Symptoms:
- Purpuric rash
- Abdominal colic (intense cramping)
- Polyarthralgia (pain in multiple joints)
- Acute glomerulonephrtis (RBC urine)
- Skin Signs: Deposition of IgA (found in mucus membranes tears, saliva, Resp, GI)-Fibrin deposits
- Platelet, bleeding, coag = NORMAL
15
Q
Disseminated Intravas Coag (DIC)
A
- Complex systemic thrombohemorrhagic disorder (small blood clots throughout)
- Causes a hemostatic defect
- Results from utilization of coag factors & platelets (Consumption Coag)
- Pathogenesis:
- NOT a primary disorder - secondary to other causes:
- Obstetric complication, infections, neoplasms, MASSIVE tissue injury
- Release or entry of tissue factors (coagulants) OR extensive endothelial injury
- Results in formation of coag sequence-FORMATION of micro thrombi (microcirculation)
- CAUSES ischemia