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Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

list the five cardinal signs of inflammation

A
  1. redness
  2. swelling
  3. heat
  4. pain
  5. loss of function
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2
Q

what is acute inflammation dominated by?

A

neutrophils

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3
Q

define suppurative

A

pus

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4
Q

define purulent

A

pus

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5
Q

define fibrino

A

lots of fibrin

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6
Q

fill out the chart regarding acute inflammation

A
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7
Q

is fibrinous acute or chronic?

A

ACUTE

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8
Q

is fibrous acute or chronic?

A

CHRONIC

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9
Q

what is the goal of acute inflammation?

A

dilute toxins, isolate, eliminate, repair

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10
Q

list the three things inflammation can act as.

A
  1. primary mechanism of pathologic change
  2. secondary contributor and propagator of disease
  3. precursor to chronic inflammation/fibrosis
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11
Q

how does the body know there’s an injury? (exogenously vs endogenously)

A

exogenous - microbes, foreign body, injury
endogenous - autoreactive, hypersensitivity reactions

activation of innate immune system

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12
Q

list the main mediators of acute inflammation

A

PGE2, complement, cytokines IL-1, IL-6, TNF

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13
Q

function of IL-8?

A

activates neutrophils

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14
Q

list the fever cytokines

A

IL-1, TNF, IL-6

PGE2

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15
Q

list/describe the phases of acute inflammation

A
  1. Fluidic (exudative) - inc blood flow from histamine, leaky vessels/permeability inc, emigration of leukocytes
  2. cellular - deliver leukocytes to injury, leukocyte adhesion cascade
  3. reparative phase - resolution, healing via fibrosis, abscess formation, chronic inflammation
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16
Q

generally describe leukocyte adhesion cascade

A

margination > rolling > adhesion > diapedesis (migration) > chemotaxis (neutrophil activation)

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17
Q

How does the following drugs affect acute inflammation?

steroid, COX 1 and 2 inhibitors, and leukotrine receptors antagonists

A

steroids - inhibits phospholipases > arachidonic acid cannot be made

COX 1 and 2 inhibitors - inhibit COX > not prostaglandin synthesis > no vasodilation or inc vascular permeability

leukotrine receptors antagonists - leukotrine B4 cannot bind > no bronchospasm or inc vascular permeability

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18
Q

list the outcomes/goals of the complement cascades

A

formation of C5a and C3a - attract leukocytes for inflammation
formation of C3b - opsonizes pathogen, induce phagocytosis
formation of membrane attack complex (MAC) - creates pore in microbial surface

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19
Q

list the important acute phase proteins

A
20
Q

list the “positive” APP. what do they mean?

A

c-reactive protein
serum amyloid A
mannose-binding protein
fibrinogen
*increase in inflammation

21
Q

list the “negative” APP. what do they mean?

A

albumin
*decrease in inflammation

22
Q

define pyrexia

A

fever

*hyperthermia does NOT equal pyrexia

23
Q

what prostaglandin is a driver of fever and when reduced can reduce fever?

A

PGE2

24
Q

define edema

A

excess fluid in tissues

25
Q

define effusion

A

vascular leakage aka when fluid leaks into body cavities and NOT tissues

26
Q

ID the pathology

A

pleural effusion

27
Q

define transudate/serous exudate

A

clear watery fluid
low concentration of plasma protein or leukocytes > injury is rather mild or peracute

histology - affected tissues spread apart by watery fluid

28
Q

define exudate

A

extravascular fluid rich in protein/cells
cloudy

29
Q

transudate or exudate?

A

transudate

30
Q

ID transudate vs exudate.

A

exudate - hemorrhagic

31
Q

ID pathology

A

serosanguinous effusion
aka exudate

32
Q

ID pathology

A

pyothorax

33
Q

ID pathology

A
34
Q

define chylous ascites

A

milky fluid in peritoneal cavity due to blockage of lymphatic drainage

35
Q

list type I hypersensitivity pathologic lesions

A

vascular dilation
edema
smooth muscle spasm
mucus production
inflammation

36
Q

what is the type I hypersensitivity immune component

A

IgE > mast cell release vasodilators

37
Q

list type II hypersensitivity pathologic lesions

A

cell lysis
inflammation

38
Q

what are the type II hypersensitivity immune component

A

IgG and IgM > activate complement

39
Q

list type III hypersensitivity pathologic lesions

A

necrotizing vasculitis (fibrinoid necrosis)
inflammation

40
Q

what are the type III hypersensitivity immune component

A

IgG and IgM

41
Q

list the type IV hypersensitivity pathologic lesions

A

perivascular cell infiltrates
edema
cell destruction
granuloma formation

42
Q

what is the type IV sensitivity immune component

A

T lymphocyte mediated

43
Q

what are examples of type 4 hypersensitivity diseases?

A

contact dermatitis, transplant rejections, tuberculosis, chronic allergic diseases, Johne’s disease (granulomatous enteritis)

44
Q

define immunodeficiency disease

A

failure of immune system to protect host

45
Q

primary vs secondary immunodeficiency

A

primary - congenital or genetic defect in immune system
secondary - immune system weakened by external factors

Pathology (12 decks)

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