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Phase 2a - Introductory Clinical Sciences > Inflammation and Healing > Flashcards

Inflammation and Healing Flashcards

1
Q

define inflammation

A

local tissue response to injury

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2
Q

name some beneficial effects of inflammation

A

Destruction of invading microorganisms.

Walling off of an abscess cavity - preventing spread of infection.

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3
Q

give examples of how inflammation may cause disease

A

An abscess in brain = space-occupying lesion, compressing surrounding structure.
Fibrosis from chronic inflammation - distort tissues, alter function.

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4
Q

define acute inflammation

A

the initial and often transient series of tissue reactions to injury

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5
Q

define chronic inflammation

A

subsequent and often prolonged tissue reactions following the initial response

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6
Q

what type of cell is characteristically recruited in acute inflammation?

A

neutrophil polymorph

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7
Q

list the possible outcomes of acute inflammation

A

suppuration (e.g. abscess)
organisation
progression to chronic inflammation
resolution

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8
Q

what is the vascular component of acute inflammation?

A

dilatation of vessels

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9
Q

what is the exudative component of acute inflammation?

A

vascular leakage of protein-rich fluid

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10
Q

list the causes of acute inflammation

A 
microbial infections;
hypersensitivity reactions;
physical agents;
chemicals;
bacterial toxins;
tissue necrosis (e.g. ischaemic infarction)
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11
Q

name some physical agents that may cause acute inflammation

A

trauma; ionising radiation; heat; cold

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12
Q

name some chemical agents that may cause acute inflammation

A

corrosives; acids; alkalis; reducing agents

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13
Q

describe how a microbial infection causes acute inflammation

A

viruses - death of individual cells by intracellular multiplication.
bacteria - release of exotoxins/endotoxins

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14
Q

how does a hypersensitivity reaction cause acute inflammation?

A

inappropriate/excessive immune reaction damages tissues

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15
Q

define tissue necrosis

A

death of tissues from lack of oxygen/nutrients resulting from inadequate blood flow (infarction)

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16
Q

what are the macroscopic appearances of acute inflammation?

A 
redness - rubor
heat - calor
swelling - tumor
pain - dolor
loss of function
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17
Q

what causes redness/rubor in acute inflammation?

A

dilatation of small blood vessels within the damaged area

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18
Q

what causes the heat associated with inflammation of peripheral parts of the body?

A

increased blood flow (hyperaemia) through the region - vascular dilatation and delivery of warm blood

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19
Q

what causes swelling associated with acute inflammation?

A

oedema - accumulation of fluid in extravascular space as part of fluid exudate.
also physical mass of inflammatory cells.

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20
Q

what causes the pain associated with acute inflammation?

A

stretching/distortion of tissues due to oedema.
pus under pressure in an abscess cavity.
chemical mediators (bradykinin, prostaglandins, serotonin)

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21
Q

what causes loss of function in acute inflammation?

A

movement of inflamed area is consciously and reflexly inhibited by pain.
severe swelling may limit movement.

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22
Q

If there are neutrophil polymorph’s present, is it acute or chronic inflammation?

A

acute

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23
Q

what are the three processes involved in acute inflammation?

A
  1. changes in vessel calibre and flow
  2. increased vascular permeability and formation of fluid exudate
  3. formation of cellular exudate - migration of neutrophil polymorphs into extravascular space
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24
Q

describe the changes in vessel calibre seen in acute inflammation

A

dilatation of arteriole
opening of pre-capillary sphincter
most capillaries full of blood

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25
Q

give some examples of chemical mediators that increase vascular permeability in acute inflammation?

A

histamine
bradykinin
nitric oxide

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26
Q

what is exudation?

A

net escape of protein-rich fluid from blood vessels

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27
Q

what proteins are present in the fluid exudate seen in inflammation?

A

immunoglobulins

coagulation factors - fibrin deposition

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28
Q

describe the process of neutrophil polymorph migration into tissues in acute inflammation

A
  1. margination of neutrophils
  2. pavementing of neutrophils
  3. pass between endothelial cells
  4. pass through basal lamina and migrate into adventitia
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29
Q

what is the main source of histamine?

A

mast cells, stored in granules in their cytoplasm

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30
Q

what stimulates histamine release?

A

C3a and C5a

lysosomal proteins released from neutrophils

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31
Q

what is the effect of histamine?

A

dilates vessel

increases vascular permeability

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32
Q

describe the role of tissue macrophages in acute inflammation

A

secrete chemical mediators that attract neutrophil polymorphs to the site

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33
Q

describe the role of the lymphatics in acute inflammation

A

channels dilate, and drain away the oedema fluid, limiting swelling.
antigens are carried to regional lymph nodes for recognition by lymphocytes.

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34
Q

what is the major role of neutrophil polymorphs in acute inflammation?

A

PHAGOCYTOSIS

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35
Q

describe the steps of phagocytosis

A
  1. adhesion of particle to cell surface (opsonisation facilitates)
  2. ingestion of particle by sending out pseudopodia
  3. fusion of lysosomes with the phagosome - phagolysosome
  4. intracellular killing of microorganism
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36
Q

list the five terms used to describe special macroscopic appearances of acute inflammation - as dependent on the type of tissue involved and the type of agent provoking the inflammation.

A 
serous
suppurative (purulent) inflammation
membranous inflammation
pseudomembranous inflammation
necrotising (gangrenous) inflammation
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37
Q

describe some beneficial effects of acute inflammation

A

dilution of toxins - allows them to be carried away in lymphatic.
entry of antibodies - phagocytosis, toxin neutralisation.
transport of drugs (antibiotics) to inflamed area
fibrin formation impedes movement of microorganisms.

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38
Q

describe some harmful effects of acute inflammation

A

vascular damage.
swelling - e.g. airway obstruction
inappropriate inflammatory response - type 1 hypersensitivity reactions (e.g. hayfever)

39
Q

what factors determine the outcome of acute inflammation?

A

type of tissue involved.
amount of tissue destruction.
both of these depend on nature of injuring agent.

40
Q

what is the usual result of acute inflammation?

A

resolution

41
Q

what causes acute inflammation to progress to suppuration?

A

excessive exudate

42
Q

what causes acute inflammation to progress to organisation?

A

excessive necrosis

43
Q

what causes acute inflammation to progress to chronic inflammation?

A

persistent causal agent

44
Q

what conditions favour resolution of acute inflammation?

A

minimal cell death/tissue damage.
occurred in organ with regenerative capacity (e.g. liver)
rapid destruction of causal agent
rapid removal of fluid/debris - good local vascular drainage.

45
Q

what is pus?

A

a mixture of living/dying/dead neutrophils and bacteria, cellular debris and possibly globules of lipid

46
Q

what conditions favour progression of acute inflammation to organisation?

A

large amounts of fibrin.
lots of necrotic tissue.
exudate and debris not removed/discharged

47
Q

what are the systemic effects of inflammation?

A 
pyrexia.
constitutional symptoms.
weight loss.
reactive hyperplasia of reticuloendothelial system.
haematological changes.
amyloidosis.
48
Q

what are the predominant cells seen in chronic inflammation?

A

lymphocytes, plasma cells and macrophages

also fibroblasts and multinucleate giant cells

49
Q

list the causes of chronic inflammation

A

primary chronic inflammation
transplant rejection
progression from acute inflammation
recurrent episodes of acute inflammation

50
Q

give some examples of causes of primary chronic inflammation

A

TB, leprosy, viral infections - resistance to phagocytosis.
endogenous - necrotic adipose tissue, bone
exogenous - silica, asbestos, sutures, prostheses
autoimmune diseases
chronic IBD eg ulcerative colitis
primary granulomatous diseases - Crohn’s, sarcoidosis

51
Q

what are the macroscopic appearances of chronic inflammation?

A 
chronic ulcer
chronic abscess cavity
thickening of wall of a hollow viscus
granulomatous inflammation
fibrosis
52
Q

describe the cellular infiltrate seen in chronic inflammation

A

lymphocytes, plasma cells and macrophages.
possibly a few eosinophil polymorphs, but no neutrophil polymorphs.
some macrophages may form neutrophil giant cells.

53
Q

describe the differences between macrophages and neutrophil polymorphs

A

macrophages can ingest a wider range of materials.
neutrophil polymorphs last 3 days - destroy themself when they ingest microorganisms.
Macrophages are long-lived - if they can’t kill ingest microorganisms, they will harbour them.

54
Q

give some examples of organisms that can survive inside macrophages

A

mycobacteria - M tuberculosis and M leprae.

histoplasma capsulatum.

55
Q

what are macrophages derived from? what system does this make them part of?

A

blood monocytes.

mononclear phagocyte system aka reticuloendothelial system.

56
Q

define a granuloma

A

aggregation of epithelioid histiocytes

57
Q

what cell types does a granuloma contain?

A

epithelioid histiocytes

also possible - lymphocytes and histiocytic giant cells

58
Q

give some examples of granulomatous disease

A

Tuberculosis
leprosy
Crohn’s disease
sarcoidosis

59
Q

describe the morphology of an epithelioid histiocyte

A 
vague histological resemblance to epithelial cells.
large vesicular nuclei
eosinophilic cytoplasm. 
elongated.
arranged in clusters.
60
Q

name a major secretory product of epithelioid histiocytes

A

angiotensin-converting enzyme

can use ACE levels as a marker for systemic granulomatous disease (e.g. sarcoidosis)

61
Q

what does association of granulomas with eosinophils indicate?

A

parasitic infection (e.g. worms)

62
Q

What type of granuloma is seen in TB?

A

granuloma with caseating necrosis

63
Q

what type of cells make multinucleate giant cells in granuloma?

A

histiocytes

64
Q

list some common causes of granuloma

A

TB, leprosy, fungi, parasites, syphilis.
materials that resist ingestion - keratin, necrotic bone, talk, silica.
beryllium
Crohn’s disease; sarcoidosis; Wegener’s granulomatosis

65
Q

what causes formation of histiocytic giant cells?

A

accumulation of matter that is indigestible by macrophages.

especially when foreign particles are too large to be ingested by a single macrophage.

66
Q

describe the appearance of Langhans giant cells

A

horseshoe arrangement of peripheral nuclei at one pole of the cell - characteristic in TB

67
Q

what type of giant cell is characteristic in TB

A

Langhans giant cell

68
Q

describe the appearance of foreign body giant cells

A

large cells with nuclei randomly scattered throughout cytoplasm

69
Q

what must be present for there to be a granuloma?

A

EPITHELIOID HISTIOCYTES - giant cells are commonly seen in granulomas, but without epithelioid histiocytes, it’s not a granuloma

70
Q

describe the appearance of Touton giant cells

A

central ring of nuclei, peripheral to which there is lipid material

71
Q

list some of the roles of chronic inflammation in systemic/organ-specific diseases

A

myocardial fibrosis after MI.
initiation and propagation, and progression, of cancer e.g. ulcerative colitis, tissue response to asbestos fibres.
atheroma development.
tissue injury associated with neurodegenerative disorders e.g. MS

72
Q

differentiate between resolution and repair

A

Resolution - initiating factor removed, tissue undamaged/able to regenerate.
Repair - initiating factor still present, tissue damaged and unable to regenerate.

73
Q

define repair

A

replacement of damaged tissue by fibrous tissue.

collagen is produced by fibroblasts.

74
Q

list types of cell that regnerate

A 
hepatocytes
pneumocytes
all blood cells
gut epithelium
skin epithelium
osteocytes
75
Q

what cell types don’t regenerate?

A

myocardial cells

neurones

76
Q

describe the appearance of coagulative necrosis

A

firm, pale area with ghost outlines on microscopy

77
Q

describe the appearance of colliquative necrosis. where is this seen?

A

dead area is liquefied.

seen in the brain.

78
Q

what disease shows caseous necrosis? what is the appearance of this?

A

TB.

pale yellow semi-solid material.

79
Q

define gangrene, and its appearance

A

necrosis with putrefaction.
follows vascular occlusion or certain infections.
black.

80
Q

what is fibrinoid necrosis?

A

a microscopic feature in arterioles in malignant hypertension

81
Q

list the types of necrosis

A 
coagulative
colliquative
caseous
gangrene
fibrinoid
fat necrosis
82
Q

what causes fat necrosis?

A

trauma.

pancreatitis.

83
Q

give an example and explanation of complete restitution

A

complete restoration following loss of part of a regenerative cell population - e.g. healing of a minor skin abrasion.

84
Q

define organisation of tissues

A

repair of specialised tissues by formation of fibrous scar.

85
Q

how does organisation occur?

A

production of granulation tissue, laid on a scaffold of fibrin, and removal of dead tissue by phagocytosis.

86
Q

describe the formation of granulation tissue

A

capillary endothelial cells grow and proliferate into damaged area - open into vascular channels, arranged as loops.
fibroblasts divide, secrete collagen/matrix, and acquire bundles of muscle fibres - myofibroblasts, function as SMCs.
contract to reduce wound size.

87
Q

what does granulation tissue consist of?

A

loops of capillaries supported by myofibroblasts.

possible inflammatory cells.

88
Q

what causes wound contraction? what is its purpose?

A

contraction of myofibroblasts in granulation tissue. collagen is secreted, forming a scar.
reduces volume of tissue for repair - but this produces a scar

89
Q

describe “healing by first intention”

A

apposed wound margins are joined by fibrin deposition, which is then replaced by collagen and covered by epidermal growth

90
Q

describe “healing by second intention”

A

wound margins are unapposed due to extensive tissue damage.
tissue defect fills with granulation tissue.
epithelial regeneration to cover surface.
granulation tissue contracts - scar formation

91
Q

list some complications of scarring/wound contraction

A

stenosis (narrowing) - if tissue damage goes around the lumen of a tube
obstruction of a tube due a stricture
permanent shortening of a muscle - contracture
burns can result in a lot of contraction - cosmetic damage, impaired motility

92
Q

describe abscess formation

A
  1. pus accumulates in a tissue
  2. becomes surrounded by a ‘pyogenic membrane’
  3. this consists of sprouting capillaries, neutrophils and occasional fibroblasts
  4. this will eventually result in granulation and scarring
93
Q

what challenge does an abscess present for treating bacterial infection?

A

bacteria within abscess cavity are relatively inaccessible to antibodies and antibiotic drugs

94
Q

describe the difference between a bacterial endotoxin and an exotoxin

A 
exotoxin = synthesised inside the cell
endotoxin = associated with cell wall

Phase 2a - Introductory Clinical Sciences (6 decks)

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