Brainscape's Knowledge GenomeTM

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


See full index

Pathology > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

what is acute inflammation

A

how cells respond to attack, it is a sudden response if tissue is damaged

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

why is acute inflammation a sudden response to damaged tissue

A

to prevent the spread of infection e.g. bacteria & clears away dead tissue

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

list why and how acute inflammation occurs

A
  • response to injury
  • needs to be fast
  • limit risk of infection
  • not a precise science unlike humeral response
  • sets up pathway to wound healing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is meant by acute inflammation not being a precise science unlike humeral response

A

it is not targeted to B & T cells , so some healthy cells get killed in the process

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

what is the purpose of tissue responses to damage

A

to eliminate dead tissue which is necrotic (becomes phagocatised)

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

what is acute inflammations initial response to tissue damage

A

to be able to defend the body

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

list the relatively non specific responses of acute inflammation

A
  1. eliminate dead tissue (e.g. phagocytosis)
  2. protect against local infection (will be an area of neutrophils to defend the body)
  3. allow immune system access (increased vascular permeability in the area to allow T & B cells to come in & target specific pathogens & begin the healing process led by macrophages)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what happens when acute inflammation allows the immune system to access

A

increased vascular permeability in the area to allow T & B cells to come in & target specific pathogens & begin the healing process led by macrophages

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

how does acute inflammation eliminate dead tissue

A

phagocytosis

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

how does acute inflammation protect against local infection

A

will be an area of neutrophils to defend the body

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

list the causes of inflammation

A
  • infection
    virus
    fungi
    bacteria (eg conjunctivitis = acute inflammation of conjunctiva)
    parasites
  • mechanical injury (e.g. blunt trauma)
  • ischemia (causes an inflammatory response)
  • chemical (e.g. burns)
  • extremes of temperature
  • radiation (UV)
  • immune mechanisms (auto immune, may have acute inflammatory response e.g. seasonal hay fever)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

list the 5 cardinal features of acute inflammation

A
  1. rubor = redness
  2. calor - heat
  3. swelling (tumour)
  4. dolor = pain
  5. loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does rubor stand for

A

redness

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

what does calor stand for

A

heat

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

what is an example of swelling

A

tumour

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

what does dolor stand for

A

pain

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

what is an important clinical sign of acute inflammation

A

swelling (tumour)

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

what must be increased to allow access for an immune response

A

vascular permeability

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

at which stage does edema occur following an injury during acute inflammation

A

0-1.5 days

involved in the first wave of defence

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

what occurs during edema

A

swelling of vessels becomes more leaky, as the fluid leaks out and into the area of injury, which enables entry of neutrophils

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

when does the entry of neutrophils to the injured sight occur during acute inflammation

A

0-2.5 days

involved in the first stage of defence

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

what do the neutrophils do

A

fight off infections or dead cells, clearing the decks which paves away for the macrophages

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

what are monocytes

A

found in the blood stream

once migrate, gets activated and becomes M1 or M2 type macrophages

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

what do macrophages do

A

set up wound healing, so lays down collagen & recruits other cells to help heal the area

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

the initial mediators of acute inflammation must be fast and so can be derived from which two things

A
  1. cell membrane (a lot of initiated early inflammatory responses are derived from the cell membrane)
    or
  2. plasma (blood) - acute inflammatory response when get cut to decrease bleeding and protect the area & heal the wound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are the cell derived mediators of acute inflammation

A

from cells, secreted or synthesised i.e. histamine from mast cell.
usually platelets, neutrophils, monocytes/macrophages and mast cells but mesochymal cells also possible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what is histamine

A

a powerful vasodilator which increases the vascular permeability very early & brings neutrophils in to protect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the plasma derived mediator of acute inflammation

A

inactive precursors in circulation ie complement proteins and kinins
(polypeptides of inactive proteins which circulate in the blood plasma & once its exposed to oxygen or collagen or the outside world, proteins and kinins becomes activated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are cell derived histamine & serotonin stored in and released from

A
  • mast cells
  • basophils
  • platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the main purpose of mast cells, basophils and platelets

A

powerful vasodilators and increase vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is arachidonic acid

A

a fatty acid C-20 carbon chain found in the phospholipid membrane(/plasma membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what does arachidonic acid produce

A

eicosanoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is arachidonic acid present in

A

the membrane of the body’s cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what do eicosanoids contain

A
  • prostaglandins
  • thromboxanes
  • leukotrienes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what do prostaglandins do

A

produces a feeling of fever & detects pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what do thromboxanes do

A

‘Clotting’ regulates amount of permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what do leukotrienes do

A

‘Leaky’ increase vascular permeability

38
Q

what do steroids inhibit

A

phospholipase, which knock out the mechanism of arachidonic acid

39
Q

what do steroids suppress

A

initial acute inflammatory phase

40
Q

what do COX-1 & COX-2 inhibitors, ASPIRIN, indomethacin inhibit

A

cyclooxygenase

41
Q

what does prostacyclin cause & inhibit

A

vasodilation, inhibits platelet aggregation

42
Q

what does thromboxane cause

A

vasoconstriction, promotes platelet aggregation

43
Q

what also increases vascopermeability

A

prostaglandin H2 (PGH2)

44
Q

what does prostaglandin PGD2 & PGE2 cause

A

vasodilation
&
increased vascular permeability

45
Q

what does leukotriene regulate

A

vasoconstriction, bronchospasm, when increased vascular permeability, so that the cell does not become too leaky = start & stop mechanism

46
Q

list the three key points of arachidonic acid metabolism

A
  • thromboxane ‘clotting’
  • prostaglandins ‘pain’
  • leukotrienes ‘leaky’
47
Q

outline what thromboxane ‘clotting’ regulates

A

vasoconstriction
&
platelet aggregation

48
Q

outline what prostaglandins ‘pain’ regulates

A
  • platelet disaggregation
  • pain
  • vasodilation
49
Q

outline what leukotrienes ‘leaky’ regulates

A
  • vasoconstriction
  • neutrophil adhesion and chemotaxis
  • slow action on increased vascular permeability into the area
50
Q

what are cytokines

A

polypeptides (small proteins)

51
Q

what are two important cytokines that are produced by cells

A
  1. interleukin 1 (IL-1) & interleukin (IL-8)

2. tumour necrosis factor (TNF-alpha)

52
Q

list the things that interleukins and TNF are responsible for

A
  • increases leukocyte (white blood cells) adhesion to endothelial cells
  • increases body temperature - fever by regulating hypothalamus
  • degranulation of neutrophils
  • attracts neutrophils to damaged areas
53
Q

explain how interleukins & TNF are responsible for the degranulation of neutrophils

A

release their lysosomal content & reactive oxygen species to help destroy & liquify and pathogens

54
Q

explain how interleukins & TNF attracts neutrophils to damaged areas

A

they act as chemical signals to other neutrophils to come into area of attack & draw neutrophils in e.g. act as signals to bring in more neutrophils

55
Q

name a plasma derived mediators kinin

A
  • bradykinin = potent vasodilator
56
Q

what are and how do bradykinin (plasma derived kinin) work

A
  • they are small peptides derived from plasma precursors
  • are early short acting vasodilators that can cause pain
  • activates complement system

(they are inactive in the blood plasma, but when the plasma comes in contact with collagen, kinin becomes activated and causes short acting vasodilation)

57
Q

what initiates the kinin pathway

A

exposure of collagen to endothelial cells

58
Q

what is the complement system made up of

A

a series of small proteins which interact with each other in response to help neutrophils find bacteria & destroy them

59
Q

what is the complement system activated by

A

exposure to:

  1. antigen - antibody complexes
  2. mannose carbohydrates in oligosaccharides
  3. pathogens
60
Q

what are mannose found in

A

bacteria

61
Q

what is the complement activation for

A

to aid normal immune system

62
Q

what do effector functions e.g. C5a and C3a: inflammation act as

A

cytokines to recruit more neutrophils into the area

63
Q

when C3b is deposited onto the microbe, and once activated, what does it form

A

C3a

64
Q

what does C3b also form

A

a complex with other proteins & forms the membrane attack complex, which clears microbes through recognition as it goes around & slices microbes & goes into microbes and the microbe explodes or gets phagocytosed or breaks down C3a & C5a & recruits macrophage neutrophils

65
Q

list the cellular events in acute inflammation of neutrophils (how neutrophils get into area of infection)

A
  1. margination
  2. adhesion
  3. emigration
  4. chemotaxis (following C3a & C5a)
  5. phagocytosis and degranulation (of neutrophil)
66
Q

explain how margination occurs

A
  • changes in haemodynamic flow (the way blood circulates)
  • neutrophils align along the wall of endothelial cells (e.g. around edge of blood vessels or the bleeding person)
  • and to emigrate in and to an open blood vessel & a tissue where there is acute inflammation occurring
67
Q

explain how adhesion occurs

A
  • once neutrophil is centred of into the periphery, need to adhere to cell membrane of endothelial cell bu:
    1. E and P selections on endothelial cells
  • lightly tether the leukocyte to the endothelial cell (i.e. it catches the neutrophil as it passes by and enters it & then gets an up regulation of P selectin which = stronger hold of P & E selectins binding to the neutrophil)
  • binding to gylcoproteins on neutrophil
    once those are locked in place, you get…
    2. ICAM-1 on endothelial cell
  • (intracellular adhesion molecule-1) bind to integrins receptors on neutrophil
68
Q

what are the adhesion molecules E & P selectins

A

expressed on endothelial cells and bind to glycoprotein on surface of neutrophils

69
Q

which out of E & P selections are the sticky ones

A

P selectin

70
Q

what are P selectins stored in

A

weibel-palade bodies of endothelial cells

71
Q

P selectins which are stored in the weibel-palade bodies relocate to the plasma membrane after…

A

stimulation by histamine and thrombin

72
Q

what are P selectins released by

A

histamine and thrombin

73
Q

what happens to P selectins if, theres a mast cell or increase basophil regulation

A

it increases P selectins which are regulated by histamine

74
Q

what are weibel-palade bodies

A

cigar shaped organelles in endothelial cells that store P-selectins

75
Q

what happens when endothelail cells which contain weibel-palade bodies are activate by histamine & thrombin

A

redistribution of P-selectin (i.e. it relocates to the cell membrane & can bind to neutrophils)

76
Q

explain how emigration.migration occurs

A
  1. requires firm adhesion by leukocyte and endothelial cell (P selectin, E selectin & ICAM1)
  2. migration is mediated by PECAM-1
    - platelet endothelial cell adhesion molecule
  3. leukocyte passes between endothelial cells
  4. leukocyte lies between endothelial cells - it releases collegenase/elastases to digest the endothelial basement membrane & get into the tissue
77
Q

what does PCAM-1 do

A

opens up tight junctions between the endothelial cells and allows neutrophils to pass between the endothelial cells and enables passing between boundaries, allowing neutrophils into the extracellular space

78
Q

explain how the continuation of migration - chemotaxis works

A
  1. once in the endothelial cells, leukocytes migrate towards chemical signals
    - CHEMOTAXIS
    - examples of chemical signals are:
    fragments of complement system (C5a),
    prostaglandins and leukotrienes (products of arachidonic acid metabolism)
79
Q

summerise the cellular events in acute inflammation of neutrophils

A
  • leukocyte roles down and binds to P & E selectins which forms a cross linking which enables blocked sequence to be open
  • so the integrin receptors break open due to E & P selectin by an intracellular signal which allows the integrin receptor to bind to ICAM1
  • E & P selectin also grips the neutrophil & puts it next to the endothelial cell
  • once got the whole integrity of ICAM1 with the P selectin holding the neutrophil down, it releases and manufactures PECAM-1 (CD31) on the endothelial adhesion molecule which breaks open the tight junctions and enables the neutrophil to squeeze through endothelial cells/emigrate from inside the blood vessel to tissue outside and looks for cytokines it can follow e.g. interleukins or C5a or C3a
  • and carries neutrophils to area of injury
80
Q

what happens once the neutrophil reaches the area of injury

A

once the neutrophil has escaped the compound, it is going to destruct and wants to kill bacteria, it is a non specific response so an acute immune response. so it will ingest any cell it comes across e.g. a C3b attached to a bacteria respiratory burst produces a lot of free radicals, so it depends on a good blood supply as its oxygen dependent

81
Q

what disadvantage does neutrophils of a diabetic have

A

less ability to fight off bacteria because they don’t have a good oxygen supply

82
Q

name the two types of mechanisms for bacterial killing

A
  1. oxygen dependent (respiratory burst)

2. oxygen independent (phagocytosis)

83
Q

list the steps of phagocytosis ‘the clear up’

A
  • neutrophils or monocyte arrives at site of injury
  • need to recognise the foreign material or dead cells
  • need to ingest the debris and bacteria
  • need to engulf the material
84
Q

what are opsonins

A

factors that coat bacteria to enable recognition by neutrophils/macrophages for ingestion

85
Q

what are the two key opsons

A
  • immunoglobulin (IgG)

- C3b and component of complement

86
Q

what happens in order for phagocytosis to ensue

A

neutrophil recognises IgG or C3b then phagocytosis ensues

87
Q

list the phases of phagocytosis

A
  1. chemotaxis and adherence of microbe to phagocyte
  2. ingestion of microbe by phagocyte
  3. formation of a phagosome
  4. fusion of the phagosome with a lysosome to form a phagolysosome (which encapsulates organism we want to phagocytose)
  5. digestion of ingested microbe by enzyme
  6. formation of residual body containing indigestible material
  7. discharge of waste materials
    (indigestible waste material gets left behind and becomes scar tissue, and can end up in lymphatics and spleen/plasma which = pus discharge)
88
Q

what are lysosomal contents

A

contents of neutrophils and monocytes that are contained in intracellular vesicles to protect the cells

89
Q

what do lysosomal contents e.g. granules contain

A
  1. lactoferrin - binds Fe (iron) and so reduces mitotic rate of bacteria
  2. lysozyme - attacks cell wall or gram negative bacteria
  3. collagenases - denature collagen & breaks up cellular degree
  4. ellastases
90
Q

what does the oxygen dependent mode of killing (the respiratory burst) produce

A

ROS (reactive oxygen species)

91
Q

what can hypochlorous acid do

A

it is potent and can wipe out most bugs so for neutrophils to produce more hypochlorous acid can help to further protect the body from infection

Pathology (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions