Term
|
Definition
| severe and generalized edema with widespread subcutaneous tissue swelling |
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Term
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Definition
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Term
|
Definition
| finger pressure leaves a depression |
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Term
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Definition
| locally increased blood volumes. causes erythema. Active compared to congestion |
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Term
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Definition
| passive process compared to hyperemia. reduced outflow of blood |
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Term
| chronic passive hepatic congestion |
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Definition
| centrilobular regions are grossly red-brown. (nutmeg liver). Centrilobular area can undergo necrosis |
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Term
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Definition
| clinical disorders with an increased tendency to hemorrhage, often without significant injury |
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Term
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Definition
| hemorrhage contained within tissue |
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Term
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Definition
| minute 1/2mm hemorrhages into the skin |
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Term
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Definition
| >3mm hemorrhages often from vasculitis |
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Term
|
Definition
| subcutaneous >1cm hematomas |
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Term
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Definition
| Beneficial version of thrombosis |
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Term
| Antiplatelet effects of endothelial cells |
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Definition
| prostacyclin (PGI2) NO, ADPase |
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Term
| Anticoagulant effects of endothelial cells |
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Definition
| heparin-like molecules, thrombomodulin activates protein C to inactivate Va & VIIa, tissue factor pathway inhibitor |
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Term
| Fibrinolytic effects of endothelial cells |
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Definition
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Term
| Pro-platelet effects of endothelial cells |
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Definition
| vWF is essential to platelet binding |
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Term
| Procoagulant effects of endothelial cells |
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Definition
| Tissue factor: major activator of the extrinsic clotting cascade |
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Term
| Antifibrinolytic effects of endothelial cells |
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Definition
| inhibitors of plasminogen activators (PAIs) |
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Term
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Definition
| P-selectin: adhesion molecule, fibrinogen, fibronectin, factors V & VIII, platelet factor 4: anti-heparin, PDGF, TGF-beta |
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Term
| Platelet Dense (delta) granules |
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Definition
| ADP and ATP, calcium, hitamine, serotonin, epinephrine |
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Term
| Platelets' reaction step 1 |
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Definition
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Term
| Platelets' reaction step 2 |
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Definition
| secretion (release reaction): dense-bodies are released, negatively charged phospholipids appear. |
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Term
| Platelets' reaction step 3 |
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Definition
| aggregation: amplified by TxA2, thrombin stabilizes the platelet plug |
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Term
| Platelet Plug Stabilization step 1 |
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Definition
| thrombin binds protease-activated receptor causing aggregation and contraction and fusion of the platelet mass |
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Term
| Platelet Plug Stabilization step 2 |
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Definition
| thrombin converts fibrinogen to fibrin |
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Term
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Definition
| activated by ADP, binds fibrinogen when activated leading to aggregation |
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Term
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Definition
| inherited deficiency of GpIIb-IIIa |
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Term
| Thrombus associated inflammation |
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Definition
| stimulates neutrophil and monocyte adhesion due to chemotactic fibrin split products |
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Term
|
Definition
| Vascular Wall (endothelial cells) |
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Term
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Definition
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Term
|
Definition
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Term
|
Definition
| Converts fibrinogen to fibrin. activates protease activated receptors (PARs) |
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Term
| Extrinsic Clotting Cascade |
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Definition
| exogenous trigger, most physiologically relevant. PT. Requires tissue factor, also initiated by calcium. factors VII, X, II, V, fibrinogen. |
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Term
| Intrinsic Coagulation Cascade |
|
Definition
| required exposing factor XII (Hageman factor) to thrombogenic sufaces. PTT. Initiated by negative particles. factors XII, XI, IX, VII, X, V, II |
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Term
|
Definition
| activation is initiated by cleavage of the extracellular end. A 'tethered' peptide thus released triggers the 'clipped' receptor. |
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Term
| Endogenous Anticoagulant Classes for Clotting Control |
|
Definition
| Antithrombins, Proteins C & S, TFPI |
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Term
|
Definition
| inhibit thrombin and IXa, Xa, XIa, XIIa, (Antithrombin II and heparin) |
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Term
|
Definition
| Vit K dependent, inactivate Va & VIIIa |
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Term
|
Definition
| inactivates tissue factor/VIIa complexes |
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Term
|
Definition
| moderates the size of a clot. greatly plasmin. blocked by PAIs |
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Term
|
Definition
| product of plasminogen cleavage. breaks down fibrin, produces FSPs, activated by Plasminogen Activators |
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Term
|
Definition
| Most important is t-PA, Plasminogen can also be activated by XII. Also u-PA and streptokinase. |
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Term
|
Definition
| Fibrin split products or degradation products. Includes D-dimers. Mild anticoagulant effect. products of plasmin cleavage of fibrin |
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Term
|
Definition
| An FSP clinically useful for diagnosing thrombotic states including DIC, DVT, PE |
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Term
|
Definition
| Most clinically relevant plasminogen activator, largely confines activity to recent thrombosis due to fibrin affinity. |
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Term
|
Definition
| Urokinase-like PA: can activate plasmin in the fluid phase. |
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Term
|
Definition
| exogenous bacterial plasminogen activator |
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Term
|
Definition
| Plasminogen activator inhibitors, increased by thrombin and cytokines |
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|
Term
| Three primary abnormalities that lead to thrombosis |
|
Definition
| endothelial injury, turbulent blood flow, hypercoagulability |
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Term
|
Definition
| stasis is a major contributor in the development of venous thrombi. Promotes endothelial activation, platelet/endothelium proximation, prevent factor dilution |
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Term
|
Definition
| single nucleotide mutation in factor V, caucasians common. Causes hypercoagulable state |
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Term
|
Definition
| 3' intron mutation. almost 3x thrombin levels. Causes Hypercoagulability |
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Term
|
Definition
| Causes hypercoagulability, prehaps causes thioester linkages. either deficiency of cystathione beta-synthase or more commonly 5,19-methylenetetrahydrofolate reductase. |
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Term
| Rare inherited primary hypercoagulability |
|
Definition
| antithrombin III, proteins C & S |
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Term
|
Definition
| Heparin-induced thrombocytopenia: Thrombophilic state. caused by unfractionated heparin. Antibodies targed heparin/platelet factor 4 complex. Causes DIC-like condition |
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Term
| Antiphospholipid Antibody Syndrome |
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Definition
| Previously lupus anticoagulant syndrome: antibodies to epitopes on plasma proteins. Signs: recurrent thromboses, repeated miscarriages, cardiac vegetations, thrombocytopenia. False-positive syphilis. Primary and Secondary Forms. |
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Term
| Catastrophic Antiphospholipid Antibody Syndrome |
|
Definition
| widespread small-vessel thrombi, cardiovascular surgery becomes difficult. treat with anticoagulation and immunosuppression. |
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Term
|
Definition
| Laminations alternating platelet and fibrin layers. Signifies flowing blood at source |
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Term
|
Definition
| occur in the heart chambers or in the aortic lumen |
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Term
|
Definition
| Frequently occlusive. Decreasing frequency: coronary, cerebral, femoral |
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Term
|
Definition
| Venous Thrombosis (Red or stasis thrombi): invariably occlusive, long cast of the lumen, relatively few platelets. Can cause varicose ulcers. |
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Term
|
Definition
| gelatinous with dark red dependent portion and yellow 'chicken fat' upper portion. |
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|
Term
| Libman-Sacks endocarditis |
|
Definition
|
|
Term
|
Definition
| Deep Vein Thrombosis: larger leg veins, often embolize, asymptomatic in half. Virchow's Triad |
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Term
|
Definition
Hypercoagulability
Hemodynamic changes (stasis, turbulence)
Endothelial injury/dysfunction |
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Term
|
Definition
| Migratory Thrombophlebitis: procoagulants (mucin, VIII, tissue factor) from tumors cause thromboembolism. |
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Term
|
Definition
| Disseminated Intravascular Coagulation (consumption coagulopathy): widespread fibrin thrombi in the microcirculation, often causes circulatory insufficiency |
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Term
|
Definition
| Pulmonary Embolus that straddles the pulmonary artery bifurcation |
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Term
|
Definition
| embolus that gains access to the systemic circulation through atrial/interventricular defect |
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Term
|
Definition
| After fractures of long bones. Pulmonary insufficiency, neurologic symptoms, anemia, thrombocytopenia, tachypnea, dyspnea, tachycardia, petechial rash |
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Term
|
Definition
| Most than 100 cc of air required |
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Term
|
Definition
| A form of air embolism caused by sudden decreases in atmospheric pressure. Includes 'the bends', 'the chokes', caisson disease. Treated with high pressure. |
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Term
|
Definition
| gas bubbles cause edema, hemorrhage, and focal atelectasis or emphysema. Severe embolus causes 'the chokes' respiratory distress |
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Term
|
Definition
| More chronic form of 'the bends' including ischemic necrosis of the femoral heads, tibia and humeri. |
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Term
|
Definition
| 1 in 40,000 but mortality is 80%. Permanent neurological deficit in 85% of survivors. Dyspnea, cyanosis, shock. |
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Term
|
Definition
| Occur with venous occlusions, loose tissues, dual circulations, sluggish veins, re-established flow. Lungs. |
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Term
|
Definition
| solid organs with end-arterial circulation including heart, spleen and kidney or where density limits collateral flow. |
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Term
|
Definition
| poorly defined and slightly hemorrhagic |
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|
Term
| Ischemic Coagulative Necrosis |
|
Definition
| After 4 to 12 hours (living). From reparative response beginning in the margins. Replaced by scar. Brain instead undergoes liquifactive necrosis. |
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Term
|
Definition
| Caused by infected vegetations or microbes seeding necrotic tissue. Infarct is converted into an abscess. |
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Term
|
Definition
| Determinants: vascular supply (collaterals?), rate (slow occlusion?), hypoxic vulnerability (neurons/ myocytes?), pO2: (cyanosis?) |
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Term
|
Definition
| Caused by hemorrhage, trauma, burns, MI, PE, sepsis. Hypotension, hypoperfusion, hypoxia. |
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Term
|
Definition
| Mortality near 20%. Mostly Gram-Positive. Systemic vasodilation, hypoperfusion. DIC. Bacteria cause inflammation, endothelial activation, metabolic abnormalities, immune suppression, organ dysfunction. |
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|
Term
| Inflammation in Septic Shock |
|
Definition
| TLRs trigger inflammation in response to microbial materials. Complement cascade is activated producing anaphylotoxins, chemotactic fragments, and opsonins. |
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Term
|
Definition
| Toll-like receptors: cause immune cells to produce TNF, IL-1, IFN-gamma, IL-12, IL-18 |
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|
Term
| Endothelial Activation in Septic Shock |
|
Definition
| Cause thrombosis, vascular permeability, vasodilation. Anticoagulant factors are diminished. Hypoperfusion. NO is increased. |
|
|
Term
| Metabolic Abnormalities in Septic Shock |
|
Definition
| Insulin resistance and hyperglycemia which decreases neutrophil function. Glucocorticoid deficit. |
|
|
Term
| Immune Suppression in Septic Shock |
|
Definition
| Cytokine soup and from apoptotic cells |
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Term
|
Definition
| kidneys, liver lungs and heart. Due to metabolic changes and hypoperfusion |
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|
Term
|
Definition
| Nonprogressive: neurohumoral mechanisms to maintain pressure |
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|
Term
|
Definition
| Progressive: hypoxia, lactic acidosis causing dilation, peripheral pooling worsens output, DIC, organ damage begins |
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|
Term
|
Definition
| Irreversible: lysosomal enzyme leakage, NO synthesis affects heart, renal shutdown w/ tubular necrosis, death |
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