Inflammation Flashcards

1
Q

name a vascular change that occurs in inflammation

A

vasodilation

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

what mediates vasodilation in inflammation?

A

histamine

nitric oxide

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

what vessels undergo vasodilation in inflammation?

A

arterioles first, then capillaries

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

name five cellular changes that occur during inflammation

A
stasis 
white cell margination 
rolling 
adhesions
migration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is white cell margination?

A

when white cells move peripherally due to slowed rate of blood flow because of vasodilation

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

why do blood cells stick to vessel walls in inflammation?

A

the vessels express proteins on their luminal surface which have matching proteins on the WBC’s

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

what proteins cause blood cells to stick to the vessel walls in inflammation?

A

selectins (bind to VCAM)
integrins (bind to ICAM)
VCAM
ICAM

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

what does ICAM and VCAM stand for?

A

vascular cell adhesion molecule

intracellular adhesion molecule

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

what effect do chemokines have on blood cells sticking to the lumen?

A

they increase the affinity of the ligands, making the bonds longer lasting

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

what two things increase expression of selectin in inflammation?

A

histamine

thrombin

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

what two things increase endothelial cell expression of VCAM and ICAM in inflammation?

A

TNF

IL-1

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

what does vascular permeability due to inflammation cause?

A

loss of proteins

change in osmotic pressure, as water follows the proteins out

this results in swelling

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

name two ways that blood vessels can become permeable

A

endothelial cell contraction resulting in gaps between cells

direct injury

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

what substances cause endothelial cell contraction?

A

histamine
bradykinin
substance P
leukotrienes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what do blood cells do after they leave the vessel and what is this called?

A

they follow a chemical gradient

chemotaxis

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

what are the three phases in phagocytosis?

A

recognition + attachment

engulfment

killing + degradation

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

what do phagocytes use to engulf foreign material?

A

extensions of the cytoplasm called pseudopods

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

what do phagocytes produce that kill pathogens?

A

reactive oxygen species

reactive nitrogen species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

name an ROS made by phagocytes

A

NADPH oxidase

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

name an RNS made by phagocytes

A

nitric oxide synthase

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

what are clinical features of inflammation?

A

rubor
calor
tumor
dolor

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

what is rubor?

A

redness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is calor?

A

heat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is tumor?

A

swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is dolor?

A

pain

26
Q

what cell characterises acute inflammation?

A

neutrophil

27
Q

name four possible outcomes of acute inflammation

A

resolution
suppuration
organisation
chronic inflammation

28
Q

what two outcomes of inflammation can progress to fibrosis?

A

suppuration

chronic inflammation

29
Q

what does the outcome of acute inflammation depend on?

A

the site of injury
the type of injury
the duration of injury

30
Q

what is resolution?

A

the complete restoration of the tissue to normal

31
Q

when is resolution likely to occur?

A

when there is:

  • minimal cell death
  • capacity for tissue repair
  • a good vascular supply
  • easily removed injurious agent
32
Q

what is suppuration?

A

production of pus

33
Q

what is a walled off space filled with pus called?

A

empyema

34
Q

why do abscesses and empyemas need to be removed?

A

they have no blood supply so cells needed for repair and antibiotics cannot reach the area

35
Q

what is organisation?

A

scarring of damaged tissue

36
Q

when does organisation occur?

A

lots of necrosis
lots of fibrin produced
poor blood supply
tissue damaged can regenerate

37
Q

what outcome is more likely if damage goes beyond the basement membrane and why?

A

organisation

if it is not damaged it acts as a scaffold for resolution

38
Q

what is the common response to injury in all tissues?

A

formation of granulation tissue

39
Q

how is granulation tissue formed?

A

capillaries and myofibroblasts infiltrate area

deposit collagen and smooth muscle that tissues can build on top of

40
Q

why does granulation tissue appear very red?

A

due to the new vascular supply forming

41
Q

what can organisation of a large area cause?

A

loss of function and contraction as normal cells are replaced with fibrosis

42
Q

what happens if the regenerative capacity of the liver is overwhelmed?

A

the liver becomes cirrhotic and can fail, meaning it can’t remove toxins from the blood and make proteins

43
Q

what characterises chronic inflammation?

A

the presence of a lymphocyte

44
Q

what is a granuloma?

A

an aggregate of epithelioid histiocytes

45
Q

what can cause granulomas to form?

A

foreign body’s
endogenous substances (bone, keratin)
exogenous substances (talc, asbestos)
infections

46
Q

what do granulomas caused by mycobacterium TB cause?

A

caseous necrosis

47
Q

what is infarction?

A

death of tissue after loss of oxygen

48
Q

what does the heart require to contract?

A

ATP

therefore it also needs oxygen

49
Q

what fails if no ATP is produced?

A

the sodium potassium pump

the calcium pump

50
Q

what happens when the sodium potassium pump fails?

A

hyperkalaemia

swelling

51
Q

what happens when the calcium pump fails?

A

hypercalcaemia

52
Q

what does hypercalcaemia stimulate?

A
ATPase
phospholipase
proteases 
endonuclease 
increased mitochondrial permeability
53
Q

how long is the window before serious damage occurs in MI?

A

20 minutes, after which damage is irreversible and cell death starts via necrosis

54
Q

what can be seen that identifies an MI in the first 20 mins?

A

only changes on an ECG

55
Q

what are the first changes due to MI that can be seen microscopically?

A

pyknosis
redness
shrunken, dark nucleus
presence of contraction bands

56
Q

what happens within the first day after an MI?

A

cell contents leak and initiate the complement cascade

causes acute inflammation, which can cause gross changes

57
Q

what are the three types of necrosis?

A

caseous
liquefactive
coagulative

58
Q

when is there the greatest risk of cardiac rupture post MI?

A

3-7 days after

59
Q

what replaces neutrophils in cardiac tissue?

A

macrophages

these create a yellow appearance and can be seen on microscopy

60
Q

when can’t an MI be dated and why?

A

if it happened more than 6 weeks ago

collagen is laid down after 2 weeks and is completed at 6 weeks