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Pathology > Q & A Chapter 2 > Flashcards

Q & A Chapter 2 Flashcards

1
Q

What are two factors that differentiate acute inflammation from chronic inflammation?

A

Time and type of cell response

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2
Q

What is the cell response for acute inflammation?

A

Neutrophils

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3
Q

What is the cell response for chronic inflammation?

A

Lymphocytes, plasma cells or macrophages

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4
Q

What are the 5 cardinal signs of inflammation?

A

Calor (Heat), Rubor (redness), Dolor (Pain), Tumor (Swelling), loss of function

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5
Q

What is the hallmark of acute inflammation?

A

Edema

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6
Q

What is the end result of acute inflammation?

A

Degradation/removal of the harmful stimuli

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7
Q

What causes the redness, heat and swelling associated with acute inflammation?

A

Vascular events cause vasodilation so there is increased blood flow to the site of inflammation

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8
Q

What causes vasodilation in acute inflammation?

A

Histamine acts on H1 receptors of post capillary venules and causes the formation of endothelial cell gaps

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9
Q

What type of edema is present in inflammation?

A

Exudate edema (rich in cells and proteins)

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10
Q

What mediates angiogenesis?

A

Vascular endothelial growth factor (VEGF)

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11
Q

What are two causes for endothelial injury/damage?

A

Burns and bacterial toxins

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12
Q

What are the three steps of acute inflammation?

A
  1. Rolling
  2. Adhesion
  3. Diapedesis
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13
Q

What are the factors needed for step 1: rolling?

A

Selectins on the endothelium; Sialyl-Lewis sugar groups on the leukocytes

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14
Q

What is the disorder associated with a mutation in the Sialyl-Lewis sugar groups?

A

LAD-2: Leukocyte adhesion deficiency

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15
Q

What are the factors needed for step 2: adhesion?

A

Beta-integrins binding to ICAM-1 (intracellular adhesion molecules) and VCAM-1 (vascular cell adhesion molecules)

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16
Q

What is the disorder associated with integrin mutations?

A

LAD-1: Leukocyte adhesion deficiency (mainly a defect in beta-2 integrins)

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17
Q

What are the factors needed for step 3: diapedesis?

A

PECAM-1 (Platelet endothelial cell adhesion molecule), AKA CD31 on the epithelium and leukocytes

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18
Q

What are the three steps of phagocytosis?

A
  1. Recognition and attachment
  2. Engulfment
  3. Killing
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19
Q

What is the enzyme associated with the oxygen dependent pathway of killing?

A

NADPH Oxidase- has cytoplasmic and membrane bound components

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20
Q

What are the steps associated with the oxidative burst?

A
  1. Oxygen is converted into superoxide and other free radicals
  2. Chloride binds to the free radicals with the help of myeloperoxidase (in azurophilic granules)
  3. Formation of hypochloride and hypochlorous acid
  4. Hypochlorus acid is used to kill bacteria
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21
Q

Where is myeloperoxidase found in cells?

A

In azurophilic granules

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22
Q

What is the disorder associated with a mutation in the plasma membrane components of NADPH oxidase?

A

X-linked Chronic Granulomatous Disease

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23
Q

What is the disorder associated with a mutation in the cytoplasmic components of NADPH oxidase?

A

Autosomal Recessive Chronic Granulomatous Disease

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24
Q

Which is the more potent mechanism for killing pathogens?

A

Oxygen dependent mechanism

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25
Q

Which leukocyte function defect is the most common? what causes it?

A

Bone marrow suppression, caused by chemicals/drugs OR infections

26
Q

What are the preformed chemical mediators of inflammation?

A

Histamine from mast cells; serotonin from platelets and enterochromaffin cells

27
Q

What is the precursor to the chemical mediators that are synthesized “on demand”?

A

Arachidonic acid

28
Q

What are the three arachidonic acid metabolites?

A

Lipoxines, leukotrienes, prostaglandins

29
Q

What are two chemical mediators that are highly hyperalgesic?

A

Prostaglandin E2 and Bradykinin

30
Q

Which chemical mediator is associated with thrombus formation?

A

Thromboxane A2 –> greater than prostacyclin; can see thrombus formation–> in the coronary arteries see MI, in the carotid arteries see stroke

31
Q

Which chemical mediator is important in the pathogenesis of bronchial asthma?

A

Leukotrienes

32
Q

What chemical mediator is important in fever mediation?

A

Prostaglandins

33
Q

What will deficiency of C2 and C4 lead to?

A

Autoimmune disorders

34
Q

What will deficiency of C3 lead to?

A

Severe fatal infections

35
Q

What will deficiency of C5-C9 lead to?

A

Susceptibility to Neisseria organisms –> Gonorrhea and meningitis

36
Q

What will deficiency of C1 inhibitor lead to?

A

Hereditary angioneurotic edema

37
Q

What occurs in paroxysmal nocturnal hemoglobinuria?

A

Uncontrolled complement activation due to lack of inhibitors

38
Q

What are the effects of bradykinin?

A

Increased vascular permeability, contraction of smooth muscles (esp lungs), vasodilation of blood vessels, hyperalgesic and chemotactic for neutrophils

39
Q

What are the effects of thrombin in inflammation?

A

Secretes nitric oxide, stimulates thromboxane A2, stimulates cyclooxygenase enzymes

40
Q

What are the effects of nitric oxide?

A

Vasodilation, inhibition of platelet aggregation

41
Q

What does aspirin inhibit?

A

Thromboxane A2 – also prevents blood clots

42
Q

What are the main causes of chronic inflammation?

A

Persistent infections, autoimmune diseases, prolonged acute inflammation

43
Q

What cells are physically present in granulomas?

A

Macrophages

44
Q

What cells are responsible for the formation of a granuloma?

A

T-helper 1 cells

45
Q

What is the cytokine that is important for granuloma formation?

A

Interferon-gamma secreted by Th1 cells

46
Q

What is a granuloma?

A

Collection of epitheloid macrophages

47
Q

What makes up an immune granuloma?

A

Virus, bacteria, protozoa, fungus surrounded by macrophages (can be giant cells)

48
Q

What are giant cells?

A

Epitheloid macrophages that have fused together

49
Q

What are some causes of foreign body granulomas?

A

Beryllium, suture material, silicon breast implants leakage

50
Q

Are there giant cells in foreign body granulomas?

A

YES- but they do not have a horseshoe nucleus and you can see the foreign material in it

51
Q

What occurs in sarcoidosis?

A

Formation of a noncaseating granuloma in response to a lung pathology

52
Q

What population mainly gets sarcoidosis?

A

Mainly African females

53
Q

What is the septic shock triad?

A

Liver failure–> Hypoglycemia;
Cardiovascular failure –> Hypotension; Desseminated intravascular coagulation –> endothelial cell damage causes multiple clots in the circulation

54
Q

What initiates fever?

A

Pyrogens

55
Q

What are exogenous pyrogens?

A

Bacterial substances

56
Q

What are endogenous pyrogens?

A

TNF-alpha, IL-1 and IL-6

57
Q

Where do pyrogens act?

A

Cross the blood-brain barrier and act on the hypothalamus to reset the temperature centre

58
Q

What drives the liver to produce acute phase proteins?

A

Cytokines– particularly TNF-alpha, IL-1 and IL-6

59
Q

What are three substances produced by the liver in response to cytokines?

A

C-reactive protein; fibrinogen; serum amyloid A

60
Q

Why do you have increased leukocytes in inflammation?

A

They migrate from the bone marrow reserve pool

61
Q

What is the most important inflammatory cytokine that causes loss of appetite and weight loss?

A

TNF

62
Q

What happens when inflammation is defective?

A

Wounds will not heal; you have increased susceptibility to infection and increased tissue damage

Pathology (4 decks)

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