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2A CLINICAL SCIENCES > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What is inflammation?

A

The local physiological response to tissue injury/infection

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2
Q

Beneficial effects of inflammation

A

Destruction of invading microorganisms
Walling off an abscess cavity -> preventing spread of infection

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3
Q

Acute inflammation

A

Neutrophil mediated inflammation

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4
Q

Chronic inflammation

A

Macrophage/lymphocyte-mediated inflammation

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5
Q

Disadvantageous effects of inflammation

A

Abscess - brain - space-occupying lesion -> compression of vital structures

Fibrosis due to chronic inflammation - distort tissues -> permanently alter tissue function

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6
Q

What cells are involved in inflammation?

A

Neutrophil polymorphs
Macrophages
Lymphocytes
Endothelial cells
Fibroblasts

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7
Q

Neutrophil polymorphs

A

2-3 day lifespan
Polylobed nucleus
Perform phagocytosis
Cytoplasmic granules containing lysosomes that digest phagocytosed bacteria
Stick to endothelial cells, squeeze through gaps & migrate to tissues

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8
Q

How are neutrophil polymorphs involved in inflammation?

A

-first on scene of acute inflammation
-phagocytosis
-release chemicals which attract inflammatory cells, eg. macrophages
-usually die on scene of inflammation - phagocytosed by macrophages

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9
Q

Macrophages

A

Weeks-months/years
Phagocytic - bacteria, debris
Carry debris to lymph nodes
May present antigen to lymphocytes -> induce 2. immune reaction

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10
Q

Lymphocytes

A

Years
Minimal cytoplasm - do not produce many proteins therefore minimal ER
Produce chemicals which attract other inflammatory cells and antibodies (from B lymphocyte plasma cells)
Immunological memory for past infections & antigens

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11
Q

Plasma cells

A

B-cell antibody producing - produce antibodies
Lots of ER

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12
Q

How are endothelial cells involved in inflammation?

A

-line capillary blood vessels in areas of inflammation
-normal conditions - produce NO to prevent adherence - however become sticky in areas of inflammation so inflammatory cells adhere to them (pull apart inflammatory cells)
-become porous to allow inflammatory cells to pass into tissues
-grow in areas of damage to form new capillary vessels

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13
Q

Fibroblasts

A

Long lived cells
Spindle shaped
Lots of ER - to produce collagen, fibrin

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14
Q

How are fibroblasts involved in inflammation?

A

-late in inflammation
-form collagenous connective tissue in areas of chronic inflammation & repair

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15
Q

Features of acute inflammation

A

-sudden onset
-short duration
-usually resolves
-fluid leaks into tissues - oedema

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16
Q

Stages of acute inflammation:

A

VASCULAR PHASE
-vasodilation - BF to area increases
-endothelial cells swell then contract -> increasing vascular barrier permeability
-exudation of fluid - leakage of protein-rich fluid from vascular space -> interstitial space -> oedema

CELLULAR PHASE
-neutrophil polymorph - arrive, phagocytose, release lysosomes, release chemicals which attract other inflammatory cells, eg. macrophages
-macrophages - arrive, phagocytose, release lysosomes

OUTCOMES
-resolution/suppuration/organisation/progression to chronic inflammation

17
Q

What are the potential outcomes of acute inflammation?

A

Resolution
Supparation
Organisation
Progression to chronic inflammation

18
Q

What is resolution?

A

The complete restoration of the tissues to normal after an episode of acute inflammation

19
Q

What is suppuration?

A

The formation of a pus:
-living, dying & dead neutrophils & bacteria
-cellular debris
-globules of lipid

(an abscess)

20
Q

What is organisation as an outcome of acute inflammation?

A

Tissue replacement by granulation tissue as part of the process of repair

21
Q

What 3 processes are involved in the acute inflammation response?

A

1)changes in vessel calibre & flow
2) increased vascular permeability & formation of the fluid exudate
3)formation of the cellular exudate - emigration of the neutrophil polymorphs into the extravascular space

22
Q

What are the characteristic features of inflammation?

A

Redness - 2. to vasodilation & increased BF
Heat - localised increase in temp., also due to increased BF
Swelling - due to increased vessel permeability - fluid loss from vascular space -> interstitial space
Pain - causes by stimulation of local nerve endings from mechanical & chemical mediators

23
Q

Causes of acute inflammation

A

Microbial infections, eg. viruses
Hypersensitivity reactions, eg. parasites
Physical agents, eg. trauma/radiation
Chemicals, eg. corrosives/acids
Bacterial toxins
Tissue necrosis, eg. ischaemic infarction

24
Q

Acute appendicitis as an example of acute inflammation

A

-unknown precipitating factor
-neutrophils appear
-vasodilation
-inflammation of serosal surface (outer lining of organs)
-pain
-appendix surgically removed or inflammation resolves
or
-appendix bursts with generalised peritonitis & possible death

25
Q

How can chronic inflammation arise?

A

-it can follow acute inflammation
-it can begin as ‘chronic’ inflammation, eg. infectious mononucleosis

26
Q

What is acute inflammation?

A

The initial & often transient series of tissue reactions to injury

27
Q

What is chronic inflammation?

A

The subsequent & often prolonged tissue reactions following the intitial response

28
Q

Features of chronic inflammation

A

-slow onset
-long duration
-can resolve if there is no tissue damage (eg. viral infection like glandular fever)
-may never resolve
-often ends up with repair & formation of scar tissue
-can cause fibrosis (thickening/scarring of tissue)

29
Q

Causes of chronic inflammation

A

Primary chronic inflammation
Progression from acute inflammation
Transplant rejection
Recurrent episodes of acute inflammation

30
Q

Tuberculosis as an example of chronic inflammation

A

-no initial acute inflammation
-mycobacteria ingested by macrophages
-macrophages often fail to kill the mycobacteria
-lymphocytes appear
-macrophages appear
-fibrosis occurs

31
Q

What is a granuloma?

A

A collection of epithelioid histiocytes (macrophages) surrounded by lymphocytes
-cell collections (used macrophages surrounded by lymphocytes)
-type of chronic inflammation
-may be due to mycobacterial infection
-may be seen around foreign material in tissue

32
Q

Granulation tissue

A

An important component of healing & comprises small blood vessels in a connective tissue matrix with myofibroblasts

33
Q

Granuloma vs granulation tissue

A

-granuloma is a mass of granulation tissue typically produced in response to infection, inflammation, or the presence of a foreign substance - it is an organised collection of macrophages that forms in response to chronic inflammation
-granulation tissue is a new connective tissue & small BVs that form on the surfaces o a wound during the healing process

34
Q

Examples of mycobacterial infections

A

TB
Leprosy
Crohn’s
Sarcoidosis

35
Q

What can be used to treat inflammation?

A

-aspirin
-ice
-antihistamine
-steroid cream - NOT on bacterial infection

36
Q

Why is aspirin used to treat inflammation?

A

Eg. ibuprofen
Prostaglandin synthetase - enzyme producing prostaglandins
Prostaglandins - chemical mediators of inflammation
Ibuprofen inhibits prostaglandin synthetase

37
Q

Why is ice used to treat inflammation?

A

-cold prevents capillary sphincters opening
-thus, preventing blood flowing to capillaries
-VASOCONSTRICTION

2A CLINICAL SCIENCES (14 decks)

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