Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology-Medical-Prof > Inflammation > Flashcards

Inflammation Flashcards

1
Q

Inflammation definiton ?

A

response of vascularized tissues that delivers leukocytes and molecules of host defence from the circulation to the sites of infection and cell damage in order to eliminate the offending agents

page-73

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

can inflammation occure in avascular tissue ??

A

cornea
=keratitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bad effect of inflammation ?

A
  1. hypersensitivity
  2. allergy
  3. autoimmune disease
  4. rheumatoid arthritis
  5. atherosclerosis

74

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Cardinal signs of inflammation ?

A
  1. rubor=Redness
  2. tumor=swelling
  3. calor =heat
  4. dolor =pain
  5. functio laesa /loss of function

76

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Pathogenesis of cardinal features ?

A
  1. Rubor=Vasodilation=Histamine & NO=Redness=Hyperamia
    2.Tumor=Swelling=Exudation =Edema=Extravascular accumulation of fluid=inc granulation tissue
    3.Calor=Heat=Inc blood flow
    4.Dolor=Pain=sweeling & edema=compress nerve ending
    5.Function laesa =pain & tissue destruction =fibroplasia & metaplasia

76

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Inflammation classification ?

A

1.Acute inflammation
=serous i
=fibrinous i
=purulent i
=ulcer

2.Chronic inflmmation
=chronic specific
=chronic non-specific

76

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Acute inflammation definiton ?

A

the initial rapid response to infection & tissue damage is AI

77

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of Acute inflammation ?

A
  1. Infection
  2. Immune response
  3. Ischemia
  4. Trauma
  5. tissue necrosis
  6. foreign bodies

77

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Componenets of Acute inflammation ?

A
  1. Dilatation of blood vessels
  2. inc blood flow
  3. inc permeability of microvasculature
  4. plasma protein and leukocyte leave the circulation
  5. Emigration of leukocyte from the microcirculation
  6. Leukocytes accumulate in the focus of injury

77

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Cells of AI?

A
  1. Polymorphoneuclear leokocyte-Neutrophil
  2. Macrophage
  3. Eosinophil
  4. Leukocyte

77-78

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fates/Outcome of Acute Inflammation ??

A
  1. Complete resolution
    =removal of cellular debris & microbs by macrophage
    =resorption of edema fluid by lymphatics

2.Healing by connective tissue replacement
=Scarring & Fibrosis

3.Progression to chronic inflammtion

78

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Morphological types of AI ?

A
  1. Serous Inflamamtion
    =pleural & pericardial effusion , ascites
    =exudation of cell poor fluid into spaces created by cell injury /body cavities

2.Fibrinous inflammation
=Pricarditis,Meningitis
=vascular leaks are large to pass Large molecules

3.Purulent inflammation
=Abscess,Boil
=Production of pus/purulent exudates
=Abscess —- localized collections of pus

4.Ulcers
=local defect/excavation of the surface of an organ/tissue that is produced by sloughing /shedding of inflammed necrotic tissue
=Peptic ,stomach,duodenum

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Whicha acute inflammation is more complicated ?

A

Fibrinous inflammation

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Events of ACute inflammtion ??

A
  1. Vascular events
  2. Cellular events
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Vascular events of Acute Inflammation ?

A
  1. Transient vasoconstriction
  2. Persistent vasodilation of arterioles
    =vasodilation
    =Histamine + NO
    =inc blood flow
    =Rubor & Calor
    3.Inc vascular permeability of the microvasculature
    4.Slowing of blood flow -Stasis
    =Combined Vasodilation +Inc vascular permeability

80-81

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Inc vascular permeability-Mechanism ?

A
  1. Contraction of endothelial cells
    =inc gap between endothelial cells
    =most common & rapidly/immediatley
    =Histamine+Bradykinin+Leukotriens

2.Endothelial injury
=direct damage to endothelium
=burn-toxin-mirobes
=necrosis and detachement

3.Leukocyte mediated endothelial injury-
=Leukocyte adhere to the endothelium and release proteolytic enzyems

4.Transcytosis
=Transport of fluid and proteins through the endothelial cells
=Vascular endothelial growth factor-VEGF

5.leakage from new blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cells of acute inflammation?

A

neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

chronic inflammation where neutrophil is the inflammaotry cells ?

A
  • chronic pyogenic osteomyelitis
  • chronic irritation & damage in the lungs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

chronic inflmmation cells ?

A

lymphpocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

acute I where lymphocytes are cells ?

A

acute viral infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

exogenous chemotactic substances ?

A

bacterial products

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

endogenous chemotactic substances ?

A

87
C5a
IL-8
LTB4

23
Q

Vasodilators chemical mediators ?

A

Prostaglandin
\histamine
nitric oxide 92

24
Q

pain mediators > 92

A

prostaglandin
bradykinin

25
Q

fever mediators ?

A

IL-1
TNF
prostaglandin

26
Q

Inc vascular permeability?? 92

A

C5a
C3a
leukotrienes -C4 D4 E4
PAD
bradykinin

27
Q

physiological giant cells
113

A

megakaryocytes of bone marrow
osteoclastic giant cell in bone
syncytotrophoblast of the placneta

28
Q

pathological giant cells ?

A

lagnhans
osteoclastic giant cell
aschoff giant cells
reed sternberg giant cell
multinucleate giant cell

29
Q

fate of granuloma ?

A

cold abscess
dystrophic calcification
formation of sinus tract

30
Q

soft vs hard tubercle ? 110

A

soft tiubelce— central caseartion necrosis

31
Q

hallmark of TB ?

A

soft tubercle

32
Q

key features of granuloma ?

A

modified activated macrophages
= epithelioid cells

33
Q

langerhans cell ?

34
Q

Morphology of granuloma ?

35
Q

granuloma def ?

A

microscopic aggregation
of epithelioid cell / epithelial like cells
surrounded by collar of lymphpocytes

36
Q

which stain for granuloma ??

37
Q

granulomatous I ?

A

106
form of chronic I characterized by collections of activated Macrophages + t lymphocytes + necrosis

38
Q

exudate vs transudate ?

39
Q

exudate cause ?

A

inc vascular permeability

40
Q

transudate cause ?

A

inc hydrostatic pressure
dec plasma colloidsl osmotic pressure

41
Q

character of exudate ?

A

high -== protein + specific gravity

42
Q

exudate defiantion ?

43
Q

acute phase protein name ? 114

A

C-reactive protein
serum amyloid A = SAA
fibronogen

44
Q

pathogenesis of TB ?

45
Q

which giant cell in TB ?

A

langhans giant cell

46
Q

cat scratch disease agent ?

A

bartonella henselae

47
Q

frustrated phagocytosis ?

48
Q

phagocytosis def ?

49
Q

phagocytosis M/A ?

50
Q

why ESR rise in acute phase response ?

A

rise fibrinogen
form rouleaux - stack that sediment rapidly

51
Q

what is epithelioid cells ?

52
Q

activated M vs Epithelioid cell ?

53
Q

which mediator is must for necrosis in TB ?

54
Q

Ecosanoids fucntion ?

Pathology-Medical-Prof (35 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions