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Pathology Test 1 > Inflammation > Flashcards

Inflammation Flashcards

1
Q

5 pillars of inflammation

A

tumor, calor, dolor, rubor, function loss

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2
Q

types of acute inflammation

A

serous, fibrinous, supperative, ulceration

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3
Q

types of chronic inflammation

A

lymphphacytic, plasma cellular, eosinophillic, granulomatous, fibrous

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4
Q

acute v. chronic basics

A

acute- often related to trauma, fluid and plasma protein exudation and PMNs – NEUTROPHILS!!!!!!! are FIRST RESPONDERS!!!!!!!! (sometimes pus)

chronic: persistent infection, foreign bodies, immune reactions. **LYMPHOCYTES AND MACROPHAGES!!!!!!** PLASMA CELLS, granulation tissue and fibrosis

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5
Q

exudate

A

protein rich fluid — INC SPECIFIC GRAVITY

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6
Q

transudate

A

protein pour fluide (ie. blister)

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7
Q

first event in acute inflammation

A

vasodilation and increased blood flow to the sight (rubor, valor)

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8
Q

what is the second step in acute inflammation and what causes it?

A

second step - histamine serotonin LKT bradykinin - endothelial contraction

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9
Q

third step in acute inflammation

A

leukocyte cellular events

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10
Q

3 steps of acute inflammation

A
  1. vd 2. inc perm 3. leuk cellular events
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11
Q

what are the 6 steps of “leukocyte cellular events?”

A
  1. margination
  2. rolling
  3. adhesions (RBCs pool when blood slows)
  4. diapedesis
  5. chemotaxis
  6. phagocytosis

MRADCP

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12
Q

what happens to blood after vd?

A

IT SLOWS DOWN!!!! pools

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13
Q

selectins

A

mediate adhesions in MIGRATION AND ROLLING - the looser connection

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14
Q

expression of selectins is regulated by ______

A

cytokines

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15
Q

integrins

A

when TNF and IL1 are released from activated macrophages integrins (CAM1, VCAM1 and PECAM1) created the TIGHTER connection or adhesion

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16
Q

chemotaxis is mediated by_______

A

c5a and LKTb4

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17
Q

order of things that infiltrate into the lung

A
  1. fluid
  2. proteins and fibrin
  3. neutrophils
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18
Q

pneumonia histologically

A

you will notice inc rbcs in the alveolar septum r/t pooling. also in what should be the clear air space there is eosinophilic pink fluid from capillaries and later there will be protein, neutrofils

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19
Q

chronic granulomatous dz

A

no ROS/burst - organisms surround by histocytes. defects in neutrophillic fxn leads to recurrent bacterial infections

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20
Q

chediak-higashi syndrome

A

impaired fusion of lysozymes to phagocytes and decreased secretion of secretory granules by cytotoxic lymphocytes

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21
Q

where do LKT come from and what is the fxn?

A

leuk and mast cells. inc vasc perm, inc chemotaxis, inc adhesin

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22
Q

where do cytokines come from?

A

macrophages, lymphocytes, endothelial cells and mast cells

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23
Q

where do anaflotoxins come from?

A

plasma and liver

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24
Q

common causes of acute inflammation with regard to injuries

A

infarct, bact infection, toxin, trauma

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25
Q

chronic injury examples

A

viral and chronic infection, persistant injury, autoimmune dz

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26
Q

possible pathway of an acute injury/inflammation (seq of events)

A

injury then to either (chronic) or
acute inflammation
that can go three places:
1. resolution
2. abcess —-> heal/organization —-> fibrosis
3. or directly to fibrosis (collagen and lose fxn)

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27
Q

sequence of events for chronic inflammation

A

injury - chronic inflammation - healing/organization - fibrosis

28
Q

3 events in acute inflammation

A
  1. vd vasc changes, neutrophil, limited injury
29
Q

4 events in chronic inflammation

A
  1. angiogenesis
  2. PMNs in
  3. fibrosis (scar)
  4. progressive cell and tissue injury
30
Q

what is ischemic injury resulting in death?

A

INFARCTION!!!!

31
Q

what is the only way you won’t surmount an infection?

A

if you are compromised

32
Q

morphological patterns of acute inflammation (4)

A

ulcers - local defect of surface, slough off necrotic tissue

abcess- supperative protein rich pus exudate

serous inflammation - protein poor exudate like a blister. will resorb into lymphatics

fibrous inflammation - has exudate - ie. pericarditis

33
Q

what is the morphology of the following acute injury/inflammation:

ulcers, abcess, blister, pericarditis

A

ULCER - (ulcer) local defect of surface, slough off necrotic tissue

ABCESS- supperative protein rich pus exudate

BLISTER - serous inflammation - protein poor exudate like a blister. will resorb into lymphatics

PERICARDITIS fibrous inflammation - has exudate - ie. pericarditis

34
Q

give an example of each of the following acute inflammation morphological changes:

ulcer
supperative
serous
fibrous

A

ULCER - (ulcer) local defect of surface, slough off necrotic tissue

ABCESS- supperative protein rich pus exudate

BLISTER - serous inflammation - protein poor exudate like a blister. will resorb into lymphatics

PERICARDITIS fibrous inflammation - has exudate - ie. pericarditis

35
Q

what is the pathophys of acute appendicitis?

A

increase in PMNs all over appendix and this has lots of lytic enzymes and will burst

36
Q

you will see a lot of ________ in bacterial infection

A

neutrophils

37
Q

you will see a lot of ________ in viral infection

A

lymphocutes and b cells

38
Q

you will see a lot of ________ in parasite infection

A

eosinophils

39
Q

first responders to chronic inflammation

A

macrophage

40
Q

what do activated macrophages do in chronic inflammation?

A
  1. eliminate microbes and necrotic tissue
  2. initiate repair process
  3. make tissue injury in chronic inflame
  4. accumulate and persist (=granuloma)
41
Q

why don’t granulomas form with acute infection?

A

they form in chronic bc they hang around persist and accumulate where as in acute they move away or die

42
Q

granuloma

A

collection of macrophages surrounded by lymphocytes

43
Q

path from monocyte to macrophage and 2 fates

A

circulating monocyte - adherent monocyte - emigrating monocyte

into tissue = macrophage

if activated by cytokines and GF it will go into repair mode where i twill promote scar formation

if activated by INF2 / T cells it will go into inflammation tissue injury

44
Q

cross talk between macrophages and T cells in chronic inflammation

A

macrophages present antigens to activate t cell

t cell releases cytokines to activate macrophage

45
Q

what can you deduce if you see lung tissue with lymphocytes?

A

viral interstitial pneumonia

46
Q

what if there are eosinophils “at the scene” ?

A

parasite or allergic rxn (IgE) - major basic protein granules

47
Q

what if mast cells are “at the scene?”

A

in both acute and chronic - release histamine, LKT, IL1, TNF and allergic IgE…. anaphylaxis.

48
Q

why do granulomas form?

A

because you try to digest something and you simply can’t. macrophages come in and encase it and lymphocytes gather outside. looks like a single cell with multi nuclei lined by lymphocytes…. - often due to foreign body like a suture. “granulomatous inflammation”

49
Q

example of granulomatous inflammation

A

necrotizing granuloma in caseous necrosis in TB

50
Q

the two avenues by which you “heal” s/p inflammation

A
  1. regeneration - cells proliferate and replace

2. repair - replace with scar and fibrous collagen

51
Q

labile cells

A

continuously dividing - skin/hematopoetic

52
Q

stable cells

A

quiescent - sit in Go and if called upon they will proliferate (liver smooth muscle kidney panc fibroblasts endothelial cells)

53
Q

permanent cells

A

nondividing - skeletal muscle and cardiac

54
Q

parachymal cells and ECM

A

parenchyma cells are the functioning ones inside like hepatocytes. ECM is CT blood vessels collagen etc - “stroma”

55
Q

when must you lay down scar tissue/granulation tissue?

A

if you injure both the parachemal cells and the ECM. you will have granulation tissue (scab)

56
Q

what is granulation tissue? what is it made of? who makes it?

A

granulation tissue is a temporary tissue on the way to making a scar. it is made of capillaries and fibroblasts. fibroblasts produce collagen.

57
Q

5 steps in replacement of injured cells with fibrous tissue

A
  1. inflammation
  2. angiogenesis
  3. migration and proliferation of fibroblasts
  4. fibrosis
  5. scar remodeling

“I AM FUCKING SMART”

58
Q

angiogenesis

A

second step in forming scar tissue - it is regulated by VEGF from the macrophage. causes vd, migration and proliferation of endothelial cells, inhibits remodeling and proliferation in capillaries, forms mature smooth muscle

59
Q

VEGF

A

angiogenesis courtesy of macrophage

second step in forming scar tissue - it is regulated by VEGF from the macrophage. causes vd, migration and proliferation of endothelial cells, inhibits remodeling and proliferation in capillaries, forms mature smooth muscle

60
Q

fibrosis

A

deposit of collagen and ECM by fibroblasts

61
Q

scar remodeling

A

inc synthesis and dec degredation

collagenase will thin out the scar. new balance between degrad. and synthesis. controlled by MMP’s

62
Q

cytokines r/t collagen

A

increase synthesis

63
Q

metalloprotenase r/t collagen

A

decrease collagen degradation

64
Q

wound healing by first intention

A

epithelial regeneration surmounts fibrosis

65
Q

wound healing by second intention

A

infarct or ulcer where inc loss of parenchyma cells and cannot restore original architecture

66
Q

lymphocytes

A

B AND T CELLS!!!!

67
Q

what are the four zones of an ulcer?

A
  1. base and margins (thin layer of necrotic tissue)
  2. nonspecific inflammation (neutrophils)
  3. granulation tissue (3-5 days)
  4. fibrous collagenous scar tissue

Pathology Test 1 (1 decks)

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