Term
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Definition
| Hydroperitoneum, fluid in the peritoneum |
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Term
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Definition
| Severe and generalized edema with widespread subcutaneous swelling |
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Term
| Review the causes of edema that produce transudate. |
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Definition
| Increased hydrostatic pressure can be caused by cardiac failure, renal failure(through activation of renin-angiotensin which increases blood volume by retaining Na+) and reduced osmotic pressure which is caused by nephrotic syndrome(leaks albumin), hepatic failure(doesn't make albumin), malnutrition |
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Term
| exudate appears in what type of edema? |
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Definition
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Term
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Definition
Congestion = lack of sufficient outflow. Filled with DEOXYGENATED blood.
hyperemia = increased inflow due to excercise or inflammation. Filled with OXYGENATED blood. |
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Term
| List the range and size of hematomas |
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Definition
| petechiae(1-2mm), purpura(>3 mm), ecchymoses(>1-2 cm) |
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Term
| List the change in color of bruises and what pigmentous endogenous substance causes them |
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Definition
| Hemoglobin is reddish-blue and is degraded to bilirubin which is blue-green and turns into hemosiderin which is gold-brown |
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Term
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Definition
| a potent endothelial derived vasoconstrictor responsible for immediate constriction of arterial vessel following injury |
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Term
| Describe primary hemostasis |
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Definition
| Primary hemostasis is the activation of platelets into flat discs that secrete their granules to recruit more platelets forming the initial hemostatic plug. |
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Term
| Describe secondary hemostasis |
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Definition
| Secondary hemostasis involves the membrane bound pro-coagulant Tissue Factor(Factor III or thromboplastin) that acts with factor VII to activate the coagulation cascade which results in thrombin production. Thrombin cleaves fibrinogen into the insoluble fibrin and also recruits more platelets to solidify the initial plug. |
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Term
| describe what tissue plasminogen activator(t-PA) does. |
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Definition
| t-PA along with thrombomodulin serves to inhibit the coagulation pathway once a clot has formed to confine the hemostatic process to the site of injury. |
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Term
| What cytokines cause leakiness in inflamed blood vessels? |
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Definition
| Histamine, Bradykinin, Leukotrienes |
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Term
| Describe how thrombomodulin works |
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Definition
| Thrombomodulin activates protein C which turns Thrombin from a pro-coagulant into an anti-coagulant. |
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Term
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Definition
| Endothelial injury and turbulent flow are reciprocative while both can lead to hypercoagulability. All three eventually cause thrombosis |
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Term
| What is the Leiden Mutation? |
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Definition
| A substitution in factor V gene causing it to be resistant to cleavage by protein C(what anti-coagulative pathway is this?). This leads to a much higher rate of Deep Vein Thrombosis. The mutation is highly prevalent in the caucasion population. |
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Term
| Heparin Induced Thrombocytopenia and Thrombosis |
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Definition
| Antibody response to heparin treatment that creates factor 4+heparin immune complexes thereby reducing platelet count. |
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Term
| Describe 5 causes of red infarcts |
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Definition
| Occur with venous occlusions(testis, ovaries), lungs(loose tissues), and tissue with dual circulation(lungs, intestines). It is also present in tissue that was previously obstructed with poor venous outflow and also when arterial supply is repaired to normal after ischemic damage(such as after angioplasty). |
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Term
| Describe causes of white infarcts |
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Definition
| Happens in arterial occlusions in solid organs with end-arterial supply(heart, kidney, spleen) and where tissue is dense to prevent seepage of blood into necrotic area |
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Term
| Describe time scale of necrosis. |
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Definition
| Acute vascular occlusion difficult to detect if it happens right before death. Tissue takes 4-12 hours to show necrosis with inflammation defining the borders within 1-2 days |
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