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Goljan Lecture Notes > Chapter 3: Inflammation & Repair > Flashcards

Chapter 3: Inflammation & Repair Flashcards

1
Q

What are the cardinal signs of inflammation? What are they caused by?

A

rubor (redness) and calor (heat) - d/t histamine-mediated vasodilation of arterioles

tumor (swelling) - d/t histamine-mediated increase in ventral permeability

dolor (pain) - PGE2 sensitizes specialized nerve endings to the effects of bradykinin

functio laesa (loss of function)

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2
Q

What degrades bradykinin?

A

ACE

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3
Q

What is a complication of an ACE inhibitor?

A

ACE inhibitor inhibits the metabolism of bradykinin –> increases vessel permeability –> angioedema

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4
Q

What are the sequential cellular steps involved in acute inflammation?

A
  1. emigration (includes margination, rolling of neutrophils, firm adhesion in venules d/t expression of intern adhesion molecules such as beta2-integrins)
  2. transmigration (diapedesis) of neutrophils
  3. chemotaxis
  4. phagocytosis via opsonization
  5. intracellular microbial killing
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5
Q

What inactivates beta2-integrins and produces neutrophilic leukocytosis?

A

catecholamines and corticosteroids

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6
Q

Name some chemotaxis mediators

A

C5a
leukotriene B4 (LTB4)
bacterial products
IL-8

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7
Q

What is the purpose of exudates?

A
  1. dilates bacterial toxins

2. provides opsonins

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8
Q

Macrophages and dendritic cells that have encountered microbes produce which cytokines to activate the endothelial cells of nearby venules to produce selectins?

A

TNF and IL-1

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9
Q

What are the two main opsonins?

A

IgG and C3b

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10
Q

In acute inflammation, what is the main cell present?

A

neutrophil

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11
Q

In chronic inflammation, what is the main cell present?

A

macrophage/monocyte

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12
Q

How does a neutrophil or monocyte kill bacteria or fungi?

A

O2-dependent myeloperoxidase (MPO) system

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13
Q

What is the process of the MPO system?

A

NADPH oxidase enzyme complex converts molecular O2 to superoxide FRs –> releases energy (respiratory burst)

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14
Q

How can you diagnose chronic granulomatous disease?

A

no color change from clear to blue when conducting an NBT dye test

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15
Q

What are macrophages in the CNS called?

A

microglial cells

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16
Q

What are macrophages outside the CNS called?

A

dendritic cells

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17
Q

What is the MC precipitation of hemolysis in G6PD deficiency?

A

infection

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18
Q

What causes Chronic Granulomatous Disease?

A

Deficiency in NADPH oxidase

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19
Q

What else should you know about CGD?

A

X-linked R
NBT dye test is negative (doesn’t change color b/c no respiratory burst)
missing peroxide b/c no NADPH oxidase

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20
Q

What kind of bacteria CAN pts with CGD kill?

A

catalase negative (e.g. Strep. pyogenes)

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21
Q

What kind of bacteria CAN’T pts with CGD kill?

A

catalase positive (e.g. Staph)

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22
Q

G6PD deficiency results in a lack of what molecule?

A

NADPH –> therefore this interferes with normal function of the O2 dependent MPO system

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23
Q

What is the most important chemical mediator in acute inflammation?

A

histamine

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24
Q

What does histamine do to arterioles?

A

vasodilates

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25
Q

What does histamine do to venules?

A

increases vessel permeability

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26
Q

What amino acid makes serotonin?

A

tryptophan

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27
Q

What effect does serotonin have on vasculature?

A

vasodilator and increases vascular permeability

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28
Q

What are the 2 anaphylatoxins? What do they do?

A

C3a and C5a

Stimulate mast cells to release histamine –> vasodilation and increased vessel permeability

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29
Q

What is made by endothelial cells and is a potent vasodilator?

A

NO

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30
Q

What is the function of IL-1?

A

associated with fever b/c stimulates the hypothalamus to make PG’s –> stimulates thermoregulatory system to produce fever

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31
Q

What enzymes is blocked by corticosteroids?

A

phospholipase A2

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32
Q

What enzymes are blocked by aspirin?

A

COX 1 and 2 irreversibly

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33
Q

What medication blocks the enzyme 5-LOX?

A

Zileuton

34
Q

What medication blocks receptors for LTB4, LTC4, LTD4, and LTE4?

A

Montelukast

35
Q

If taking a corticosteroid, would you see an increase or decrease in neutrophils?

A

You would see an INCREASE in neutrophils on CBC b/c corticosteroids block the adhesion molecule LTB4 from being formed.

36
Q

What affect does epinephrin have on adhesion molecule synthesis and neutrophil count?

A

DECREASES adhesion molecule synthesis

neutrophil count INCREASES

37
Q

MCC of skin abscess

A

S. aureus

38
Q

What is fibrinous inflammation?

A

exudate that covers serial surfaces (heart, lungs, peritoneum)

39
Q

What is serous inflammation?

A

thin watery exudate (e.g. blister, viral pleuritis)

40
Q

What percent of peripheral blood lymphocytes are T cells?

A

60%

41
Q

What is the ratio of helper to suppressor T cells (CD4:CD8)?

A

CD4:CD8 = 2:1

42
Q

What is a unique characteristic of eosinophils?

A

They have Charcot-Leiden crystals (seen in sputum of asthmatic pts)

43
Q

What is the effector cell in a Type II hypersensitivity reaction?

A

Eosinophils

44
Q

What is the effector cell in a Type I hypersensitivity reaction?

A

mast cells

45
Q

What is the benefit of a fever?

A

O2 binding curve shifts to the right

decreased bacterial/viral reproduction

46
Q

What disease is associated with pseudomembranous inflammation?

A

C. difficile

47
Q

Name the markers on the following cell types:
Helper T cell
Cytotoxic T cell
Marker for Ag recognition site for all T cells
Marker for histiocytes
Marker only on B cells (name virus that utilizes this marker)
Marker found on all leukocytes

A

Helper T cell - CD4
Cytotoxic T cell - CD8
Marker for Ag recognition site for all T cells - CD3
Marker for histiocytes - CD1
Marker only on B cells (name virus that utilizes this marker) - CD21 (EBV)
Marker found on all leukocytes- CD45

48
Q

What mediators cause fever?

A

IL-1 and PGE2

49
Q

What is the cause of osteomyelitis?

A

S. aureus

50
Q

What is the common cause of cellulitis?

A

Group A Strep. pyogenes

51
Q

What are causes of fibrous pericarditis?

A
  1. SLE
  2. first week of MI then again in 6 wks later (Dresser’s Syndrome)
  3. Coxsackie virus
52
Q

MC organism producing infxn in 3rd degree burns

A

Pseudomonas auruginosa (pus is green d/t pyocyanin)

53
Q

Those who suffer from poor wound healing should be checked for what deficiency?

A

Zn deficiency

54
Q

What is the pathogenesis of Marfans?

A

Defect in fibrillin –> poor wound healing

55
Q

What is the pathogenesis of Ehlers-Danlos?

A

defect in collagen d/t breaking down –> poor wound healing

56
Q

What is pathogenesis of Scurvy?

A

Vitamin C deficiency –> defect in hydroxylation of lysine and proline –> no crossbridging –> abnormal collagen –> poor wound healing, hemorrhaging, hemarthroses

57
Q

What type of collagen is the initial collagen in wound repair?

A

Type III collagen

58
Q

What day does granulation tissue begin to form?

A

Day 3

59
Q

What enzyme breaks down type III collagen and replaces it with type I collagen?

A

collagenase (tensile strength returns to 80% normal w/in 3 months)

60
Q

What causes keloid formation?

A

excess Type III collagen deposition

61
Q

In white individuals, what is keloid formation often due to?

A

3rd degree burns

62
Q

What do surgeons inject into sounds in order to prevent excessive scar tissue formation?

A

glucocorticoids

63
Q

MCC of impaired wound healing

A

infections

64
Q

MC pathogen causing sound infection

A

S. aureus

65
Q

How does diabetes increase susceptibility to infection?

A

decrease blood flow

increase tissue glucose levels

66
Q

What is the difference between a keloid and hypertrophic scar?

A

Keloid- raised scars extending beyond borders of original wound

Hypertrophic scar- raised scar remaining in confines of original wound

67
Q

Scenario: Chronically draining sinus tract of the skin, the physicians tried to put abs on it (didn’t work). There was an ulceration lesion at the orifice of this chronically draining tract. What is it?

A

squamous cell carcinoma

68
Q

What cell is involved in lung injury repair?

A

Type II pneumocyte

69
Q

What cell in the brain proliferations in response to injury and which one removes the debris?

A

Astrocytes proliferate

Microglial cells remove debris

70
Q

In peripheral nerve transection, which cell is key to reinnervation?

A

Schwann cells

71
Q

Cardiac muscle damage is permanent or temporary? What kind of repair occurs?

A

permanent damage

repair by fibrosis

72
Q

What immunoglobulin is predominantly seen in acute inflammation?

A

IgM

73
Q

What cells and immunoglobulins are seen in chronic inflammation?

A

absolute monocytosis

increased serum IgG

74
Q

What findings on blood smear are seen in severe inflammatory conditions?

A

toxic granulation

Dohle bodies

75
Q

What findings would you see with corticosteroid therapy?

A

increased plasma neutrophils

decreased B and T cells

76
Q

What cell types are seen in each scenario?

Acute inflammation
Acute allergic reactions
Viral infections
Chronic inflammation

A

Acute inflammation - neutrophil
Acute allergic reactions- eosinophil
Viral infections - lymphocytes
Chronic inflammation - monocytes/macrophages but also see a lot of plasma cells and lymphocytes

77
Q

A granuloma results from an acute or chronic infection?

A

chronic

78
Q

What cytokine (released by a T helper cell) activates a macrophage?

A

gamma INF

79
Q

What two cells are key players in granuloma formation?

A

T helper cell and macrophage (Type IV hypersensitivity)

80
Q

What cell is responsible for a positive PPD test?

A

T helper cell

81
Q

What two areas of the kidney are most susceptible to tissue hypoxia?

A
  1. straight portion of proximal tubule b/c most of oxidative metabolism located there
  2. medullary segment of thick ascending limb
82
Q

What happens to the ESR when you have increased immonoglobulins? Why?

A

immunoglobulins decrease the negative charge that normally keeps RBCs from sticking to each other –> clumping of RBCs –> increased ESR

*seen in cold agglutination with IgM and multiple myeloma (cryoglobulins)

Goljan Lecture Notes (4 decks)

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