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Pathology Quiz 1 > Quiz 1_Learning Objectives Part 2_Spencer > Flashcards

Quiz 1_Learning Objectives Part 2_Spencer Flashcards

1
Q
  1. Define arteriosclerosis.
A

Thickening and loss of artery elasticity

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2
Q
  1. Highlight the differences between arteriosclerosis clinical entities:
    Atherosclerosis:
    Arteriosclerosis
    Monkeberg medial calcific sclerosis
A

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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3
Q
  1. Define atherosclerosis
A

Thickening of large arteries accompanied by lumen narrowing

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4
Q
  1. Discuss the stages in the natural history of atherosclerosis
A

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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5
Q
  1. Review the gross anatomy and histology of each atherosclerosis stage
A
  1. Review the gross anatomy and histology of each atherosclerosis stage
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6
Q
  1. Discuss the consequences on cardiovascular function and clinical outcomes of each atherosclerosis stage with emphasis on the complicated stage.
A

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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7
Q
  1. Review the endothelial injury hypothesis of atherosclerosis pathogenesis
A

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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8
Q
  1. Review the risk factors of atherosclerosis and their contribution to endothelial activation
A

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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9
Q
  1. Diagram the intrinsic, extrinsic and “new” coagulation pathways.
A

Memorize page 539 of Silverthorn book.

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10
Q
  1. Explain how PT and PTT tests are performed.
A

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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11
Q
  1. Name the four stages of hemostasis and explain what is occurring in each.
A
  1. injury occurs
  2. vessel wall undergoes reflex constriction via endothelin release
  3. platelets aggregate on the subendothelial matrix, facilitated by VWF
  4. coagulation cascade to form clot, facilitated by TF, thrombin, phospholipids, fibrin
  5. thrombic/antithrombic events including t-PA, thrombomodulin, trapped PMNs/RBCs, polymerized fibrin
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12
Q
  1. Explain the “3 A’s” associated with the role of platelets in hemostasis.
A

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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13
Q
  1. Name three functions of von Willebrands factor.
A
  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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14
Q
  1. Explain the roll of factor XIII in coagulation.
A

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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15
Q
  1. Name the three inherent anticoagulant systems/mechanisms in the blood.
A

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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16
Q
  1. Identify four types of hemophilia and the factors that are deficient in each.
A

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

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17
Q
  1. Name the three components of “Virchow’s triad” active in thrombosis.
A

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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18
Q
  1. Explain the abnormality present in factor V Leiden hypercoagulability.
A

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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19
Q
  1. Discuss the etiological, clinical, and laboratory findings associated with DIC.
A

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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20
Q
  1. Calculate an INR from a patient’s PT value and the normalized PT value.
A

INR = patient PT/normalized PT.

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21
Q
  1. Explain the mechanism behind three forms of antiplatelet.
A

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

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22
Q
  1. Vasoactive Amines:
A

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

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23
Q
  1. Plasma Proteins
A

zymogens, require proteolytic cleavage to be active

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24
Q
  1. Eicosanoids:
A

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

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25
Q
  1. Platelet Activating Factor:
A

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

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26
Q
  1. Cytokines:
A

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

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27
Q
  1. Chemokines:
A

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

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28
Q
  1. Nitric Oxide:
A

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

29
Q
  1. Lysosomal constituents:
A

chops up proteins

30
Q
  1. Free Radicals:
A

breaks down tissue infected area to curb spread of pathogen

31
Q
  1. NF-κB:
A

the central inflammatory component in many species; typically retained in cytoplasm but gets activated into acting as a gene transcription factor for inflammatory response proteins. Activation process is downstream from pathogen recognition pathways. Inhibited by aspirin (separate from aspirin’s COX inhibition).

32
Q
  1. Toll-Like Receptors:
A

sentinel microbe-recognizing receptors located in the periphery on macrophages and DCs

33
Q
  1. State the 5 cardinal signs of inflammation
A

Swelling, redness, heat, pain, loss of function

34
Q
  1. Identify types of stimuli that lead to inflammation
A

Bacteria, dead tissue, foreign bodies (eg splinter), antibody-complement (C3a, C5a), trauma

35
Q
  1. Name the major differences between acute and chronic inflammation
A

Acute is characterized by edema/exudate, PMNs, MΦs, not-specific
Chronic is characterized by fibrosis, tissue destruction, lymphocytes, and is immunospecific

36
Q
  1. Identify the stages in endothelial adhesion and transmigration
A

Rolling → adhesion → transmigration

37
Q
  1. Name the four general families of adhesion molecules and give specific examples of each.
A

Selectins (example P-selectin, where P is for platelets or L-selectin (L is for leukocytes))
Immunoglobulins (example ICAM-1 (intercellular adhesion molecule)
Glycoproteins (example PSGL-1)
Integrins (example LFA-1)

38
Q
  1. Identify which adhesion molecule family is generally complimentary to members of which other family.
A

Selectins select a glycoprotein

Immunoglobulins interested in integrins

39
Q
  1. Name the endogenous and exogenous chemoattractants important in neutrophils chemotaxis
A

Exogenous (from bacteria/pathogens): bacterial lipids and peptides
Endogenous (host-derived): C5a, LTB4, IL-8

40
Q
  1. Explain the neutrophilic mechanism for killing and degradation of bacteria
A

recognition → engulfment → killing/degradation
PMNs recognize an opsonized/antibody-coated target based on the Fc fragment of IgG, the C3b component of complement, or collectins.
This recognition allows engulfment to occur.
Upon engulfment, PMNs kill the pathogen intracellularly using superoxides/H2O2, myeloperoxidase, azurophilic granules, HOCl.

41
Q
  1. Identify categories of disease caused by inappropriate activation of the inflammatory response
A
  1. Identify categories of disease caused by inappropriate activation of the inflammatory response
42
Q
  1. Name three causes of chronic inflammation
A

Autoimmune reactions, viral infections (CD8+ cells), intracellular bacterial infections (eg TB, leprosy), acute inflammatory reactions that have persisted

43
Q
  1. Identify the characteristic cell types found in acute and chronic inflammation.
A

Acute is characterized by PMNs; chronic is characterized by lymphocytes. Both seem to have MΦs.

44
Q
  1. Describe the pathogenesis of granulomatous inflammation
A

Granulomas are nodular types of chronic inflammation. They frequently have giant cells (monocytes/macrophages). Good example is TB. A granuloma is just a collection of MΦs and frequently results in a collar of lymphocytes forming around the node. Giant cells (fused) can occur.

45
Q
  1. Fluid collections: exudates vs. transudate
A

Exudate is higher density protein, eg pus. Transudate is lower density protein so is more clear. Edema results from hypertension or lymphatic blockage or low oncotic pressure.

46
Q
  1. Chemotaxis
A

Movement of a cell based on following a chemical gradient

47
Q
  1. Selectin, Integrin
A

Selectin is used first to get the leukocyte near the epithelium and to correctly select/identify it. Integrins are then used to pull the leukocyte into the epithelium.

48
Q
  1. Phagocyte oxidase, inducible NO synthase
A

Not exactly sure, but I think phagocyte oxidase is just an enzyme that facilitates making HOCl to kill pathogens. NO synthase makes NO to kill bacteria (note that in excess it can also be lethal to host).

49
Q
  1. Serous, fibrinous and purulent (suppurative) exudates
A

Serous: thin fluid from plasma or secretions from peritoneal, pleural, pericardial cavities. If this fluid collects it is called an effusion (eg blister). Memory: “a serious eff-in’ blister”.

Fibrinous: occurs with greater vascular permeability when fibrinogen passes vascular barrier. Histologically characterized by eosinophilic meshwork of threads. Clear it via fibrinolysis/macrophages. This can be converted to scar tissue. Note that this can occur on the pericardium.

Purulent/suppurative: characterized by pus or puruluent exudate with PMNs, liquefactive necrosis, edma. Typically triggered b pyogenic bacteria such as staphylococci. Textbook example is appendicitis. The localized collection of purulent inflammatory tissue is an abscess. Memory: staph infections suppurt pur abscesses. Appendicitis is suppur painful.

50
Q
  1. Ulcer
A

Local defect or excavation of the surface of an organ from the sloughing of inflamed necrotic tissue. Example is peptic ulcer in stomach/duodenum. Look for intense PMN infiltration. Can lead to fibrosis, scarring, accumulation of of lymphocytes/macrophages/plasma cells.

51
Q
  1. Tertiary lymphoid organ
A

Essentially the site of an inflammatory process where lymphocytes gather

52
Q
  1. Granuloma
A

A granuloma is an outcome of chronic inflammation. It occurs when cells try to contain an offending agent. So, you end up with an aggregation of macrophages that are surrounded by monocytes/giant cells. Textbook example is tuberculosis.

53
Q
  1. Define “resolution” of inflammation
A

Resolution is the healing after the injurious stimulus is removed. Inflammation should be resolved and normal function should return. This process includes removing cellular debris and absorption of edema by lymphatics.

54
Q
  1. Give an example of complete resolution
A

Poison ivy vesicles that do not scar?

55
Q
  1. Name 4 outcomes of acute inflammation
A

Resolution: healing from removing stimulus, regeneration of parenchyma, resolution of inflammation.

Abscess formation: cluster of PMNs (compare to ulcer which is a necrotic surface), liquefactive necrosis, edema. Can see in brain. Could include bacterial infection from vascular spread, or from outside injury. Renal would show darker area on CT. Example PID → tubo-ovarian abcesses → ectopic pregnancy.

Fibrosis: scarring from replacing parenchyma with connective tissue. Smallpox is more PMN/abscess involving both epi and dermis; chickenpox is more just epidermis/serous. Pulmonary fibrosis is sequel of chronic interstitial inflammation. Example hep B lymphocytes → fibrotic nodule in liver parenchyma = cirrhosis.

Chronic inflammation:
Histological: lymphocytes, plasma, macrophages
Temporal: how long does it stay around?
AIDS Pt cannot clear what should be an acute infection so it becomes chronic.

56
Q
  1. Name four sequalae of acute inflammation
A

Serous: tin/watery, accumulation of fluid within mesothelial space like peritoneal/pericardial; skin blister (serous fluid within epidermis, caused by virus/burn). Vesicles smaller, bulla larger. In bulla, fluid can be between dermis and epidermis.

Fibrinous: increased vascular permeability → larger molecules enter extravascular space. Can be caused by cancer. Can result in body cavity lining deposition. Example pericarditis.

Suppurative: pus-like exudate composed of neutrophils, liquefactive necrosis, edema. Caused by certain bacteria. Example appendicitis, brain abscess. Histologically look for PMNs with lobed nuclei. Inflammation leads to necrosis.

Ulcers: local defect or excavation of tissue that results from the sloughing off of necrotic tissue. Textbook example is peptic ulcers in the GI tract. This can result in fibroblastic proliferation if it turns chronic. Characterized by intense PMN infiltration during acute phase.

57
Q
  1. Necrosis (p. 14-24)
A

a. Coagulative: most common; denaturation of cell proteins dominates. Myocardial, renal, pulmonary infarcts common example.
b. Liquafactive: extensive acute inflammation; often from bacterial/fungal infections. Tissue is largely digested. Abscess and cerebral infarction common examples.
c. Caseous: typically associated with TB; combination of liquefactive and coagulative necrosis
d. Gangrenous: bacterial colonization in a tissue that has already undergone necrosis.
e. Enzymatic/Fat necrosis (pancreas)

58
Q
  1. Apoptosis (p. 25-32):
A

pathway of cell death induced by a suicide program

59
Q
  1. Steatosis (p. 33-4):
A

abnormal accumulation of triglycerides within parenchymal cells.

60
Q
  1. Hemachromatosis (p. 861-3):
A

excessive accumulation of body iron.

61
Q
  1. Hemosiderosis (p. 36-7):
A

hemosiderin (hemoglobin-derived, golden pigment which stores iron) is deposited in tissues as a result of systemic overload of iron.

62
Q
  1. Ischemia:
A

inadequate blood supply to a tissue

63
Q
  1. Infarction:
A

tissue death as a result of poor blood supply

64
Q
  1. Cirrhosis:
A

degeneration, thickening, and fibrosis of liver parenchyma

65
Q
  1. Xenobiotics:
A

biologically active chemical that is not endogenous.

66
Q
  1. Carbon tetrachloride (CCl4):
A

compound metabolized by liver to form a free radical that is toxic to cells.

67
Q
  1. Centrilobular necrosis (liver):
A

necrosis around the central vein in the liver.

68
Q
  1. Lipid peroxidation:
A

oxidative degradation of lipids; free radicals “steal” electons.

Pathology Quiz 1 (6 decks)

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