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Physiology > Inflammation > Flashcards

Inflammation Flashcards

1
Q

What are the causes of acute inflammation?

A

Microbial infections

Hypersensitivity reactions

Physical and chemical agents

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2
Q

How do you recognise acute inflammation?

A

Red- dilation of blood vessels

Hot- increased blood flow

Swollen- mainly due to oedema

Painful- stimulation of nerve endings by pressure and chemical mediators

Loss of function

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3
Q

What are the two initial reaction phase of acute inflammation?

A

Vascular and exudative phase

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4
Q

What happens in the vascular phase?

A

Dilation and increased permeability

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5
Q

What happens in the exudative phase?

A

Fluid and cells escape from permeable venules

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6
Q

What is the characteristic cell of acute inflammation?

A

Neutrophil polymorph

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7
Q

What happens to capillary sphincters during inflammation?

A

They relax allowing a greater blood flow into the capiilaries

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8
Q

What happens to the plasma proteins in inflammation?

A

Net flow out of the blood

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9
Q

What are the features of the exudate phase?

A

High protein content (immunoglobins,)

Fibrinogen- fibrin (acutely inflamed organ surfaces covered by fibrin)

High turnover, continuously removed via lymphatics

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10
Q

What is transudate in respect to the exudate phase?

A

The normal state the body is in.

No net flow out, normal vascular permeability, low protein content

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11
Q

What is increased vascular permeability?

A

Produced by chemical mediators (histamine, bradykinin)

Involves stimulation of endothelial cell

Only in post capillary venules

Through transient, intercellular gaps

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12
Q

What happens to the lymphatic system in acute inflammation?

A

Lymphatics dilate, drain fluid from exudate, antigens carried to lymph nodes- recognised by lymphocytes

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13
Q

What are the functions of neutrophils?

A

Kills organisms, degrade necrotic tissue, ingest offending agents, produce chemical mediators, produce toxic oxygen radicals, produce tissue damaging enzymes

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14
Q

What is transmigration?

A

Cells adhere to the vessel walls, squeeze through the endothelial walls into the tissue

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15
Q

What is chemotaxis?

A

The process neutrophils use to find antigens. The receptors are filled as the neutrophil moves along the concentration gradient

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16
Q

What are the 4 enzymatic cascade systems that plasma contain?

A

Complement system, the kinins, the coagulation factors, fibrinolytic system

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17
Q

How do neutrophils do their function?

A

Movement, recognition of and adhesion to micro-organisms, phagocytosis, intracellular killing of micro-organisms

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18
Q

Why are neutrophils filled with pre-made granules?

A

So toxic agents can be released in minutes

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19
Q

What is phagocytosis?

A

The cell taking thing inside to destroy them

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20
Q

What is opsoniation?

A

Opsonins coating receptors on leucocytes and greatly enhancing phagocytosis

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21
Q

Some examples of major opsonins?

A

Fc fragment of IgG

C3b

Collectins- plasma proteins that bind to micrbial cell walls

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22
Q

Examples of acute inflammation

A

Serous- protein rich fluid exudate

Catarrhal- mucus hypersecretion

Fibrinous-exudate contains plentiful fibrin

Haemorrhagic- severe vascular injury

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23
Q

Explain the suppuration type of inflammation

A

Formation of pus-neutrophils, bacteria, cellular debris

Nearly always caused by an infective agent

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24
Q

What is in abscess?

A

A collection of pus surrounded by a membrane of sprouting capillaries, neutrophils and fibroplasts

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25
Q

Where may deep seated abscesses drain?

A

Along a sinus tract or fistula

26
Q

Describe ulceration as a form of inflammation

A

A local defect or excavation which has been produced by the sloughing of inflammatory necrotic tissue

27
Q

What are the beneficial effects of acute inflammation?

A

Dilution of toxins

Entry of antibodies

Fibrin formation

Transport of drugs

Delivery of nutrients and oxygen

Stimulation of the immune response

28
Q

What are the harmful effects of acute inflammation?

A

Digestion of normal tissues

Swelling

Inappropriate inflammatory response

29
Q

What is type 1 hypersensitivity?

A

The classic allergic response. Mast cells release large amounts of histamines through degranulation

30
Q

What is pyrexia?

A

An increase of temperature due acute inflammation

31
Q

What are some constitutional symptoms of acute inflammation?

A

Malaise, anorexia and nausea

32
Q

What are the haematological changes of acute inflammation?

A

Increased erythrocyte sedimentation rate

Anaemia

Leukocytosis

33
Q

What is fibrosis?

A

The thickening and scarring of connective tissue

34
Q

What factors favour resolution?

A

Minimal cell death and tissue damage

Regenerative tissue

Rapid destruction of the agent

Rapid removal of fluid and debris by vascular drainage

35
Q

What is the end result of organisation?

A

Replacement of destroyed tissue by granulation tissue

36
Q

What factors favour organisation?

A

Large amounts of fibrin

Substantial necrosis

Exudate and debris cannot be removed

37
Q

What is a classic example of granulation tissue?

A

Capillary loops and macrophages

38
Q

In granulating tissue what is the inflammatory exudate replaced by?

A

Capillaries, macrophages, fibroblasts and collagen

39
Q

What is granulation tissue regulated by?

A

Growth factors, TNF, EGF, FGF

40
Q

What is TB and Leprosy and example of?

A

Primary chronic inflammation caused by resistence of infective agent to phagocytosis and intracelullar killing

41
Q

What is chronic tophaceous gout with crippling gouty arthritis an example of?

A

Primary chronic inflammation caused by foreign body reactions to endogenous materials

42
Q

What is asbestos an example of?

A

Primary chronic inflammation caused by foreign body reactions to exogenous materials

43
Q

What rheumatoid arthritis an example of?

A

Primary chronic inflammation caused by an autoimmune disease

44
Q

What is ulcerative colits an example of?

A

Primary chronic inflammation caused by specific diseases of unknown aetiology

45
Q

What is sarcoidosis an example of?

A

Primary chronic inflammation caused by granulomatous

46
Q

What factors favour progression from acute to chronic inflammation?

A

Indigestible substances

Deep seated suppurative inflammation where drainage is delayed or inadequate

Recurrent episodes of acute inflammation and healing

47
Q

What is osteomyelitis?

A

A chronic abcess which is extremely difficult to eradicate

48
Q

What is chronic cholecystitis?

A

Replacement of wall by fibrous tissue , lymphocytes rather than neutrophils predominate

49
Q

What does chronic inflammation look like?

A

Chronic ulcers, chronic abscesses, thickening of the wall of a hollow viscus, granulomatous inflammation, fibrosis

50
Q

How do you identify a chronic ulcer?

A

Mucosa breached, base lined by granulation tissue and punched through other tissue layers

51
Q

What cells are more common in chronic inflammation?

A

Lymphocytes, plasma cells, macrophages, multinucleate giant cells

52
Q

What are macrophages?

A

Phagocytic capabilites

Can harbour viable organisms resistant to lysosmal enzymes

Produce a range cytokines

53
Q

What is a granuloma?

A

An aggregate of epitheloid macrophages

54
Q

What is a histiocyte?

A

Macrophage in connective tissue

55
Q

What causes granulomatous disease?

A

Specific infections, foreign bodies, specific chemicals, drugs

56
Q

Exudate vs transudate?

A

High protein content from increased vasc perm vs low protein from normal vasc perm

57
Q

Acute vs chronic inflammation

A

Distinguished by dynamics and character process

58
Q

What is granulation?

A

Important healing process with small blood vessels and connective tissue

59
Q

What is fibrin?

A

Deposited in acute inflammation

60
Q

What is “fibrous”?

A

Typical scar tissue with collagen

Physiology (6 decks)

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