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Pathology Test 1 > Inflammation > Flashcards

Inflammation Flashcards

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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
chronic injury examples
viral and chronic infection, persistant injury, autoimmune dz
26
possible pathway of an acute injury/inflammation (seq of events)
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)
27
sequence of events for chronic inflammation
injury - chronic inflammation - healing/organization - fibrosis
28
3 events in acute inflammation
1. vd vasc changes, neutrophil, limited injury
29
4 events in chronic inflammation
1. angiogenesis 2. PMNs in 3. fibrosis (scar) 4. progressive cell and tissue injury
30
what is ischemic injury resulting in death?
INFARCTION!!!!
31
what is the only way you won't surmount an infection?
if you are compromised
32
morphological patterns of acute inflammation (4)
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
what is the morphology of the following acute injury/inflammation: ulcers, abcess, blister, pericarditis
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
give an example of each of the following acute inflammation morphological changes: ulcer supperative serous fibrous
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
what is the pathophys of acute appendicitis?
increase in PMNs all over appendix and this has lots of lytic enzymes and will burst
36
you will see a lot of ________ in bacterial infection
neutrophils
37
you will see a lot of ________ in viral infection
lymphocutes and b cells
38
you will see a lot of ________ in parasite infection
eosinophils
39
first responders to chronic inflammation
macrophage
40
what do activated macrophages do in chronic inflammation?
1. eliminate microbes and necrotic tissue 2. initiate repair process 3. make tissue injury in chronic inflame 4. accumulate and persist (=granuloma)
41
why don't granulomas form with acute infection?
they form in chronic bc they hang around persist and accumulate where as in acute they move away or die
42
granuloma
collection of macrophages surrounded by lymphocytes
43
path from monocyte to macrophage and 2 fates
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
cross talk between macrophages and T cells in chronic inflammation
macrophages present antigens to activate t cell t cell releases cytokines to activate macrophage
45
what can you deduce if you see lung tissue with lymphocytes?
viral interstitial pneumonia
46
what if there are eosinophils "at the scene" ?
parasite or allergic rxn (IgE) - major basic protein granules
47
what if mast cells are "at the scene?"
in both acute and chronic - release histamine, LKT, IL1, TNF and allergic IgE…. anaphylaxis.
48
why do granulomas form?
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
example of granulomatous inflammation
necrotizing granuloma in caseous necrosis in TB
50
the two avenues by which you "heal" s/p inflammation
1. regeneration - cells proliferate and replace | 2. repair - replace with scar and fibrous collagen
51
labile cells
continuously dividing - skin/hematopoetic
52
stable cells
quiescent - sit in Go and if called upon they will proliferate (liver smooth muscle kidney panc fibroblasts endothelial cells)
53
permanent cells
nondividing - skeletal muscle and cardiac
54
parachymal cells and ECM
parenchyma cells are the functioning ones inside like hepatocytes. ECM is CT blood vessels collagen etc - "stroma"
55
when must you lay down scar tissue/granulation tissue?
if you injure both the parachemal cells and the ECM. you will have granulation tissue (scab)
56
what is granulation tissue? what is it made of? who makes it?
granulation tissue is a temporary tissue on the way to making a scar. it is made of capillaries and fibroblasts. fibroblasts produce collagen.
57
5 steps in replacement of injured cells with fibrous tissue
1. inflammation 2. angiogenesis 3. migration and proliferation of fibroblasts 4. fibrosis 5. scar remodeling "I AM FUCKING SMART"
58
angiogenesis
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
VEGF
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
fibrosis
deposit of collagen and ECM by fibroblasts
61
scar remodeling
inc synthesis and dec degredation collagenase will thin out the scar. new balance between degrad. and synthesis. controlled by MMP's
62
cytokines r/t collagen
increase synthesis
63
metalloprotenase r/t collagen
decrease collagen degradation
64
wound healing by first intention
epithelial regeneration surmounts fibrosis
65
wound healing by second intention
infarct or ulcer where inc loss of parenchyma cells and cannot restore original architecture
66
lymphocytes
B AND T CELLS!!!!
67
what are the four zones of an ulcer?
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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