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Pathological Processes > S2) Acute Inflammation > Flashcards

S2) Acute Inflammation Flashcards

1
Q

What is inflammation?

A

Response of living tissue to injury

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2
Q

Causes of acute inflammation (5)

A

Microbial infections

Hypersensitivity reactions

Physical agents

Chemicals

Tissue necrosis

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3
Q

Clinical signs of AI (5)

A

Rubor = redness

Tumor = swelling

Calor = heat

Dolor = pain

Loss of function

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4
Q

4 stages of vascular response

A

1) Arterioles vasoconstrict
2) Arterioles and capillaries vasodilate causing heat and redness

3) Permeability of blood vessels increases
- exudate formed

4) Stasis caused by increased concentration of RBCs and increased viscosity of the blood

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5
Q

Where is histamine released from?

What does it do? (3)

A

Mast cells, basophils and platelets

Vasodilation, increased permeability and pain

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6
Q

Transudate vs exudate

A

Transudate caused by change in hydrostatic pressure

Exudate has a high protein content

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7
Q

How does the exudate leave the vessels? (5)

A

Contraction of epithelia

Cytoskeletal reorganisation

Direct injury

Increased transcytosis eg vegF channels

Leukocyte dependent injury

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8
Q

Which two mediators cause epithelia to contract

A

Histamine and leukotrienes

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9
Q

4 stages of neutrophil infiltration

A

1) Margination caused by stains
2) Rolling - intermittent sticking
3) Adhesion
4) Emigration

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10
Q

How do neutrophils migrate from the vessels? (2)

A

Relaxation of tight junctions

Digestion of basement membrane

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11
Q

4 stages of neutrophil movement inside tissue

A

1) Chemotaxis - attracted by C5a, LTB4 and bacterial peptides
2) Receptor binds to ligands
3) Cytoskeleton rearranges
4) Pseudopod forms (cytoplasm filled projection)

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12
Q

What do neutrophils do? (4)

A

1) Contact, recognition and internalisation
2) Facilitated by opsonins
3) Cytoskeletal changes
4) Phagosomes fuse with lysosomes to make secondary lysosomes

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13
Q

What are the two mechanisms of destruction?

A

Oxygen dependent

Oxygen independent

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14
Q

Describe oxygen independent mechanisms (3)

A

Lysozymes and hydrolases

Bactericidal permeability increasing protein (BPI)

Cationic proteins (defensins)

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15
Q

Which chemical mediators increase blood flow? (2)

A

Histamine and prostaglandins

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16
Q

Which chemical mediators increase vascular permeability? (4)

A

Histamine
Leukotrienes
Serotonin
Bradykinin

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17
Q

Which mediators cause neutrophil chemotaxis? (3)

A

C5a, LTB4 and bacterial peptides

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18
Q

How does the following combat injury:

Exudate (3)

A

Delivers protein to areas of injury eg mediators and fibrinogen

Dilutes toxins

Increases lymphatic drainage

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19
Q

How does the following combat injury:

Infiltration of cells

A

Removes organisms and debris

20
Q

How does the following combat injury:

Vasodilation

A

Increases delivery and temperature

21
Q

How does the following combat injury:

Pain and loss of function

A

Enforces rest, reducing chance of further damage

22
Q

4 local complications of acute inflammation?

A

Swelling can block tubes eg bile duct or intestine

Exudate can compress pericardium causes cardiac tamponade

Loss of fluid eg in burns

Pain

23
Q

How is fever caused?

A

Macrophages produce pyrogenic cytokines (TNF, interleukin 1) when stimulated by excess pyrogens

Cytokines cause increase in synthesis of prostaglandin E2

Anterior hypothalamus set point increases

24
Q

How is prostaglandin synthesis inhibited?

A

Aspirin or NSAIDS inhibit cyclo-oxygenase which produces prostaglandins from arachadonic acid

25
Q

What is leukocytosis?

Which mediators cause it to occur?

A

Accelerated release of cells from bone marrow

1l-1 and TNFa

26
Q

Which proteins are acutely affected by AI in the serum

A

CRP, a1-antitrypsin, fibrinogen, amyloid A protein

27
Q

How are mediators inactivated? (5)

A

Short half lives

Enzymes eg heparinase

Inhibitors may bind eg antiproteases

Specific inhibitors eg lipoxins and endothelin (peptides which constrict blood vessels)

Diluted by the exudate

28
Q

Bacterial meningitis:

What causes it?

Symptoms?

How does it cause death?

A

Infection of the meninges - protective layers of the spinal cord and brain

Stiff neck, non-blanching rash, fever

Inflammation causes vascular thrombosis and reduced cerebral perfusion

29
Q

4 stages of lobar pneumonia:

A

1) Congestion - fluid build up, heavy lungs
2) Red hepatisation
3) Grey hepatisation
4) Resolution

30
Q

Skin blisters:

What causes them?

Why is the exudate clear?

What happens after?

A

Heat, sunlight or chemicals - fluid strips away epithelium

Few inflammatory cells

Resolvable or scars over

31
Q

Describe what is in an abscess

A

Inflammatory exudate forces tissues apart with liquefactive necrosis in the centre

Causes high pressure and pain

32
Q

3 types of exudate into serous cavities

A

Ascites (abdomen)

Pleural effusion

Pericardial effusion

33
Q

Other inherited disorders:

A

Angio-oedema

Complement deficiencies

Chronic granulomatous disease

34
Q

How are prostaglandins made and what do they do?

A

Made from cell membrane phospholipids and causes vasodilation, fever and increased pain sensitivity

35
Q

Fresh blood isn’t chemotactic - why is clotted blood?

A

Breakdown products of thrombin and fibrin and chemotactic

36
Q

How do cells respond to chemotaxins?

A

Chemotaxin binds to cell receptor

Ca and Na rush into cell

Cell swells and reorganises its cytoskeleton

Cell assumes a triangular shape pointing in the direction of the chemotactic stimulus - sending out pseudopod

37
Q

What is the difference between rolling and adhesion?

A

Rolling - neutrophils bind to selectins

Adhesion - neutrophils bind to intergrins

38
Q

Which chemical mediators causes chemotaxis (5)

A

Leukotriene b4

C5a

C3a

Chemokines

Endotoxins

39
Q

What is shock?

What causes it?

A

Dramatic drop in BP due to widespread vasodilation and increased vascular permeability

Bacterial products or inflammatory mediators spreading around the body

40
Q

Sequelae to AI (4)

A

Pus/ abscess (purulent exudate)

Haemorrhagic exudate

Serous exudate

Fibrinous exudate

41
Q

What is purulent exudate?

A

Cream/white exudate rich in neutrophils

42
Q

What is a haemorrhagic exudate?

A

Red bloody exudate because of RBCs released from ruptured blood vessels

Seen in destructive infections and malignant tumours

43
Q

What is a serous exudate?

What protein doesn’t it contain?

A

Clear exudate with plasma proteins but few leucocytes so infection unlikely

Seen in blisters

Fibrinogen

44
Q

What is a seroma?

A

A tissue space filled with clear, sterile fluid

Seen as a post-operative complication

45
Q

What is a fibrinogen exudate?

A

Exudate with significant deposition of fibrin

46
Q

Hereditary angio-oedema:

What causes it?

Symptoms

A

C1-esterase inhibitor deficiency

Itchy cutaneous angio-oedema
Recurrent abdominal pain due to intestinal oedema

47
Q

Complications of pneumonia: (5)

A

Bacteraemia leading to meningitis, arthritis or endocarditis

Lung abscesses

Empyema

Pleural effusion

Lung fibrosis

Pathological Processes (5 decks)

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