Quiz 1_Learning Objectives Part 2_Spencer Flashcards Preview

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Flashcards in Quiz 1_Learning Objectives Part 2_Spencer Deck (68)
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50. Define arteriosclerosis.

Thickening and loss of artery elasticity

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51. Highlight the differences between arteriosclerosis clinical entities:
Atherosclerosis:
Arteriosclerosis
Monkeberg medial calcific sclerosis

a. Atherosclerosis: thickening of large arteries, lumen narrowing
b. Arteriolosclerosis: thickening of small arteries/arterioles, lumen narrowing
c. Monkeberg medial calcific sclerosis: calcific deposits in muscular arteries, usually >50 yo, doesn’t encroach on lumen

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52. Define atherosclerosis

Thickening of large arteries accompanied by lumen narrowing

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53. Discuss the stages in the natural history of atherosclerosis

i. Initial lesion with a few macrophages/foam cells
ii. Fatty streak lesion with intracellular lipid accumulation
iii. Intermediate lesion with small extracellular lipid pools
iv. Atheroma lesion with more extracellular lipid, can be symptomatic
v. Fibrosis/calcification with lipid core, can be symptomatic
vi. Complicated lesion with surface defect or hemorrhage/hematoma/thrombus, symptomatic

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54. Review the gross anatomy and histology of each atherosclerosis stage

54. Review the gross anatomy and histology of each atherosclerosis stage

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55. Discuss the consequences on cardiovascular function and clinical outcomes of each atherosclerosis stage with emphasis on the complicated stage.

Stenosis: progressive plaque growth leading to ischemia
Occlusion: total closure of the lumen caused by thrombosis on plaque; can result in hemorrhage into plaque (not sure exactly what this means?) or atheroembolus. This results in severe clinical symptoms such as MI, cerebral infarct, gangrene (not sure how the bacteria shows up).
Aneurysm: occurs as a result of mural thrombosis, embolization, wall weakening and leads to rupture/massive hemorrhage

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56. Review the endothelial injury hypothesis of atherosclerosis pathogenesis

This hypothesis is essentially that atherosclerotic development is initiated by endothelial wall injury. The lesion is then exploited by oxidized LDL, macrophages, T-lymphocytes, and the arterial wall constituents.

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57. Review the risk factors of atherosclerosis and their contribution to endothelial activation

Being an old guy with family history with low HDL/LDL ratio with hypertension who smokes and has diabetes. Apparently also being type A.

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58. Diagram the intrinsic, extrinsic and “new” coagulation pathways.

Memorize page 539 of Silverthorn book.

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59. Explain how PT and PTT tests are performed.

PT tests the extrinsic pathway proteins: factors VII, X, II, V, and fibrinogen.
7, 10, 2, 5, fibrinogen. They take the plasma, add citrate to prevent clotting, add tissue factor and phospholipids, and then add exogenous calcium and measure the time to coagulate.
PTT (partial thromboplastin time) looks at the intrinsic pathway proteins (factors XII, XI, IX, VIII, X, V, II, fibrinogen). 12, 11, 9, 8, 10, 5, 2, fibrinogen. The lab takes blood, adds ground glass (negatively charged particles) to activate XII, phospholipids, calcium, and then measures the time to clot.

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60. Name the four stages of hemostasis and explain what is occurring in each.

0. injury occurs
1. vessel wall undergoes reflex constriction via endothelin release
2. platelets aggregate on the subendothelial matrix, facilitated by VWF
3. coagulation cascade to form clot, facilitated by TF, thrombin, phospholipids, fibrin
4. thrombic/antithrombic events including t-PA, thrombomodulin, trapped PMNs/RBCs, polymerized fibrin

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61. Explain the “3 A’s” associated with the role of platelets in hemostasis.

Adhesion: VWF/GpIb → platelets adhere to subendothelial matrix
Activation: degranulation of dense bodies → release Ca and ADP → amplify aggregation
Aggregation: GbIIb/IIIa-fibrinogen cross-linking, surface phospholipid on platelets → platelet contraction → plug/aggregation.

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62. Name three functions of von Willebrands factor.

1. facilitate adhesion between platelet GpIb and subendothelium (esp if blood is fast-flowing)
2. facilitate aggregation using platelet GpIIb/IIIa
3. facilitate factor VIII binding by protecting it from cleavage and recruiting it to hemorrhage site

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63. Explain the roll of factor XIII in coagulation.

Factor XIII shows up late in the game and stabilizes fibrin polymers that actually form the fibrin gel that clots the lesion.

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64. Name the three inherent anticoagulant systems/mechanisms in the blood.

Antithrombin system: antithrombin III + heparins
Protein C system: thrombomodulin, protein C, protein S
Fibrinolytic system: plasminogen activators, plasmin, plasminogen activator inhibitors, plasmin neutralizers

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65. Identify four types of hemophilia and the factors that are deficient in each.

VWF disease: VWF
Hemophilia A: factor VIII
Hemophilia B: factor IX
Hemophilia C: factor XI

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66. Name the three components of “Virchow’s triad” active in thrombosis.

Endothelial injury: could be from bacterial endotoxins, radiation, cigarette smoke, etc

Hypercoaguability: can be genetic for example protein C, S defects, or can be secondary to factor such as bedrest, MI, tissue damage, cancer

Abnormal blood flow: turbulence, stasis…activated factors are not swept away by fresh blood, helps activate endothelial cells

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67. Explain the abnormality present in factor V Leiden hypercoagulability.

2-15% of Caucasians carry Leiden mutation in factor V (60% in Pt with Hx DVT). Mutaion renders factor V resistant to cleavage by protein C → much highter risk of venous thrombosis.

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68. Discuss the etiological, clinical, and laboratory findings associated with DIC.

DIC = disseminated intravascular coagulation; sudden/insidious onset of fibrin thrombi in microcirculation. Visible microscopically. Cause insufficient circulation. Consumes platelets/coagulation proteins. Paradoxically can cause bleeding catastrophe. Lab findings are thrombocytopenia, long coagulation test time, D-dimer (evidence of fibrin degradation), fragmented RBCs. Etiology = sepsis, necrosis, malignancies (esp leukemia), OB. Can break DIC cycle with heparin/treatment of underlying illness.

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69. Calculate an INR from a patient’s PT value and the normalized PT value.

INR = patient PT/normalized PT.

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70. Explain the mechanism behind three forms of antiplatelet.

Aspirin/NSAID: irreversibly block COX-1 in platelets
Clopidogrel: block ADP receptor
Abcixomab/tirofiban: block GPIIb/IIIa

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71. Vasoactive Amines:

histamine? Triggered by IgE cross-linking, C3a, C5a, IL-1, IL-8

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72. Plasma Proteins

zymogens, require proteolytic cleavage to be active

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73. Eicosanoids:

from arachidonic acid cascade; local short-range hormones, forms in lipid bodies

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74. Platelet Activating Factor:

increase vascular permeability, cell adhesion/aggregation, chemotactic for PMNs; uses serpentine GPCRs

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75. Cytokines:

typically produced by WBCs, many mediate inflammatory processes; example = TNF-alpha and IL-1 (signal via NF-kb)

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76. Chemokines:

activate via serpentine/G proteins; attract multiple types of cells; modulate integrin-based adhesion

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77. Nitric Oxide:

Ca-induced release from endothelial cells → vasodilation; can be antimicrobial but also damages host

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78. Lysosomal constituents:

chops up proteins

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79. Free Radicals:

breaks down tissue infected area to curb spread of pathogen