Term
| Three triggers for thrombus formation. |
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Definition
| Direct injury to vessel walls, stagnation of blood flow, hypercoagulative state (autoimmune or genetic) |
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Term
| What are the two factors that can initiate the clotting cascade? |
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Definition
| Hageman factor (inflammatory response), tissue factor 8 (released by platelets) |
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Term
| Role of platelets in thrombus formation. |
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Definition
| Activating thrombin and fibrinogen, recruitment of other platelets |
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Term
| Which serine protease cleaves fibrinogen to fibrin? |
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Definition
|
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Term
| Two chemical mediators of cyclooxygenase pathway are involved in regulating thrombus formation? |
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Definition
| Thromboxane and prostacyclin |
|
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Term
| How does an endothelial cell negatively regulate thrombus formation? |
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Definition
| Nitric oxide and prostacyclin secretion, physical barrier between plateletes and collagen/vWF. |
|
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Term
| What is the major source of venous emboli? |
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Definition
| Stasis (reduction in turbulent flow) |
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Term
| Aterial emboli are primarily associated with what disease process? |
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Definition
|
|
Term
| What does infarction mean? |
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Definition
| Necrosis as a result of ischemic event |
|
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Term
| How does congestive heart failure lead to generalized edema? |
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Definition
| Reduction in blood pressure (shock) - seeping of fluid out of capillaries because of loss of blood flow/pressure |
|
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Term
| Five types of shock and what do they have in common? |
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Definition
| Cardiogenic, hypovolemic (hemorrhage), septic, anaphylactic, neurogenic (brain damage) - all have a reduction in blood pressure/volume, increase in vasodilation and vascular permeability |
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Term
| How can you bleed to death from disseminated intravascular coagulation? |
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Definition
| Pseudo-hemophiliac state - all clotting proteins and platelets are consumed |
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Term
|
Definition
| Thinning of blood vessel lumen by deposition of fats and cholesterol |
|
|
Term
| What is the unifying hypothesis for atherosclerosis pathogenesis? |
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Definition
| Cholesterol leaked into blood vessels, oxidized cholesterol activates macrophages, cytokines released, fibroinflammatory response, "foam cell" necrosis (oxidized cholesterol not easily digested), "positive feedback" of macrophages and necrotic core formation |
|
|
Term
| What type of inflammation occurs in atherosclerosis? |
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Definition
|
|
Term
| Structure of an atheroma. |
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Definition
| Necrotic core, foam cells and inflammatory factors, neovascularization, fibrous cap |
|
|
Term
| How can an atheroma lead to an infarct? |
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Definition
| Platelets form thrombi when cap ruptures, thrombi becomes embolytic, thrombus gets stuck in heart |
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Term
| What can we learn about atherosclerosis and ischemic heart disease resulting in myocardial infarction from the genetic condition known as familial hypercholesterolemia? |
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Definition
| Cholesterol unable to be uptaken, causing increase in LDL, decrease in HDLs/VHDLs, direct atherosclerosis as a result of lack of cell uptake of cholesterol - DRAMATIC effect (5-6x serum LDL) |
|
|
Term
| What are the four principle effects of ischemic heart disease? |
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Definition
| Myocardial infarct, angina, chronic congestive heart failure, and sudden death |
|
|
Term
| What is the primary cause of myocardial infarction? |
|
Definition
|
|
Term
| What are the four major risk factors for IHD? |
|
Definition
| Hypertension, cigarette smoking, diabetes, blood cholesterol level |
|
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Term
| Describe the events occurring in the damaged myocardium from 12 hours to 3 months following a myocardial infarction. |
|
Definition
| Necrosis of myocardial cells, leukocyte chemotaxis, inflammatory response, fibrosis formation (3 months for myocardial fibrosis) |
|
|
Term
| What are the top three cancers in terms of incidence? |
|
Definition
| 1) Breast/prostate, 2) Lung, 3) Colon/rectum |
|
|
Term
| What are the top three cancers in terms of mortality? |
|
Definition
| 1) Lung, 2) Breast/prostate, 3) Colon/rectum |
|
|
Term
| What are the three general features that distinguish benign from malignant neoplasms? |
|
Definition
| Invasion, metastasis, and appearance |
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|
Term
|
Definition
| A reversion of differentiation in cells - characteristic of malignant neoplasms |
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|
Term
|
Definition
| Variable in size, shape, and appearance of cells and/or nuclei - characteristic of malignant neoplasms |
|
|
Term
|
Definition
| Abundance of DNA in cancer cells, indicating malignancy |
|
|
Term
|
Definition
| Cellular abnormality is restricted to the originating tissue (early neoplasms) |
|
|
Term
| Explain the clonal origin of neoplasms |
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Definition
| Neoplastic growth comes from the cancerous transformation of a single cell |
|
|
Term
| What type of cancer protein is Ras? |
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Definition
| Ras is a family of genes encoding small GTPases involved in cell growth, differentiation, and survival. |
|
|
Term
| What is the significance of Ras? |
|
Definition
| Single most common oncogenic mutation location - can be transformed by a point mutation, causing the growth signal to never stop. |
|
|
Term
| What are the three mechanisms for altering protooncogenes to oncogenes? |
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Definition
| 1) Change in protein structure (increase in activity or loss of regulation), 2) Increase in protein concentration (gene amplification, increased mRNA stability, gene duplication), 3) chromosomal translocation (incrased gene expression) |
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|
Term
| How does Rb work normally and in carcinogenesis? |
|
Definition
| Rb normally prevents excessive cell growth by inhibiting cell cycle progression. In carcinogenesis, it is inactivated, allowing the cell to escape G0 and enter the cell cycle |
|
|
Term
| How does p53 work normally and in carcinogenesis? |
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Definition
| Normally, p53 activates DNA repair proteins, induces growth arrest (usually for the purpose of repair), and initiates apoptosis. In carcinogenesis, p53's activity is either severely reduced or lacking altogether |
|
|
Term
| How does APC work normally and in carcinogenesis? |
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Definition
| Normally, APC helps control how often a cell divides, how it attaches to other cells, or whether a cell moves within or away from a tissue. In carcinogenesis, APC causes misregulation of cadherins, altered cell migration, and chromosome instability |
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|
Term
| What is meant by the "Two-hit hypothesis" and "Loss of heterozygosity"(LOH)? |
|
Definition
| Only one working allele of a tumor suppressor gene is necessary for its function, so both must be mutated for the cancer phenotype to appear. |
|
|
Term
| What are the five types of DNA repair mechanisms? |
|
Definition
| Homologous recomination, mismatch repair, nucleotide excision repair, DNA crosslink repair, non-homologous end joining |
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|
Term
| A genetic defect in which DNA repair mechanism is the most common cancer predisposition? |
|
Definition
|
|
Term
| How is the reactivation of telomerase thought to be related to cancer? |
|
Definition
| The lengthening of the DNA strands brought about by telomerase helps maintain the immortality of cancer cells (telomerase activation in >90% of all tumors) |
|
|
Term
| What are the three categories of carcinogens? |
|
Definition
| Viral, chemical, and physical |
|
|
Term
| How can HPV infection lead to cervical cancer? |
|
Definition
| Viral replication and gene integration leads to p53 binding and degradation by E6 protein and Rb (blocks cell cycle progression) inhibition by E7 |
|
|
Term
| What is the difference between a tumor initiator and a tumor promoter? |
|
Definition
| Initiators contribute to the transformation of normal cells, promoters amplify carcinogenic effects of initiators |
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|
Term
|
Definition
| Reproducible, dose-dependent reaction reflecting direct action of the compound or its metabolites on a tissue |
|
|
Term
| What are the four characteristics that influence toxicity? |
|
Definition
| Absorption, distribution, metabolism, excretion |
|
|
Term
| The majority of complications associated with use of oral contraceptives are related to what vascular process? |
|
Definition
| Deep vein thrombosis (and thromboembolism) |
|
|
Term
| How is the vascular endothelium damaged during hyperthermia? |
|
Definition
| Altered vascular permeability, edema, blisters, general vasodilation, inefficient cardiac function, altered respiration, and ultimately death |
|
|
Term
| How is the vascular endothelium damaged during local hypothermia? |
|
Definition
| Endothelium lining of venules and capillaries damages small vessel permeability - activating an inflammatory response and the formation of localized edema and blisters |
|
|
Term
| Which types of burns allow for regeneration and why? |
|
Definition
| First and second - the basal cells (the source of regenerating epithelial surface cells) remain intact |
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|
Term
| What is a common sign of reversible alcohol induced injury in the liver? |
|
Definition
| Fatty liver. As a side note, cirrhosis is irreversible |
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