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Pathology > Acute Inflammation > Flashcards

Acute Inflammation Flashcards

1
Q

What is acute inflammation and what is it’s aim?

A

Response of living tissue to injury in aim to minimise damage to tissue

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2
Q

5 clinical signs of acute inflammation?

A

Rubor, tumor, calor, dolor, loss of function

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3
Q

What are 5 causes of inflammation?

A 
Microbial - e.g. bacterial
Necrosis
Hypersensitivity - e.g. hives
Physical agents - e.g. heat 
Chemicals - e.g. acids
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4
Q

What is heat and redness caused by in inflammation?

A

Vasodilation

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5
Q

What are the vascular changes in inflammation (stage 1)

A

1) Transient vasoconstriction
2) Vasodilation - aim to increase b flow to bring inflame mediators
3) Increased permeability - exudate out (of protein rich fluid) - swelling also slows circulation
4) = Stasis in small blood vessels due to increased ratio of RBCs due to fluid leaving

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6
Q

What cell defines inflammation? What other cell after that?

A

Neutrophil

Macrophages

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7
Q

What happens during stage 3 of vascular changes Exudation of fluid and what effects does this have (3) ?

A

Protein rich fluid moves out of leaky capillaries into interstium. This

1) Delivers plasma proteins to the area of injury
2) Dilutes toxins
3) Increases lymphatic drainage (takes micro-organisms to phagocytes and antigens to immune system).

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8
Q

What is the hallmark of acute inflammation (2)?

A 
Exudate of (oedemal) fluid
Infiltration of inflammatory cells
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9
Q

What kind of plasma proteins are delivered to site of injury?

A

Immunoglobulins
Inflammatory mediators
Fibrinogen
(Acute phase proteins)

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10
Q

What is the definition of oedema?

A

Excess fluid in the interstitium

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11
Q

What is there a lot of in infection exudate?

A

Proteins

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12
Q

What kinds of proteins would you find in exudate?

A

Opsonins
Complement
Antibodies

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13
Q

Which chemical mediators increase blood flow (3)

A

Serotonin
Histamine
Prostaglandins

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14
Q

Which chemical mediators increase vascular permeability (4)

A

Serotonin
Histamine
Bradykinin
Leukotrienes

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15
Q

Which chemical mediators are important for neutrophil chemotaxis (3)?

A

C5a
LTB4
Bacterial peptides

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16
Q

What happens during stage 2 - Vasodilation in inflammation response vascular changes?

A

Vasodilators e.g. histamine, serotonin, prostaglandins increase blood flow, which increases the amount of fluid and leucocytes to the site of injury. Pressure in capillaries rise (increased hydrostatic pressure).

Venules become leaky

Blood stasis due to increased haematocrit with fluid beginning to move out into interstitium

17
Q

Name an opsonin for phagocytosis in acute inflammation

A

C3b

18
Q

What are the 7 stages of neutrophil migration, infiltration, and killing? What occurs in each?

A

1) Migration - to site of injury via chemotaxis - chemoattractants include c5a, LTB4, bacterial peptides
2) Activation - to a higher metabolic level
3) Margination - stasis causes neutrophils to line up at the edge of blood vessels along the endothelium (normally would be in centre of laminar flow)
4) Diapedesis through blood vessel wall
6) Recognition - attachment - recognise bacterium e.g. c3b opsonin and bind to bacterium
7) Phagocytosis
8) Killing - O2 dependent (free radicals) and O2 independent (enzymes)

19
Q

How do neutrophils roll/diapedesis?

A

1) Digestion of basement membrane
2) Relaxation of interendothelial junctions
3) Extends pseudopod through vessel wall

20
Q

Is bacterial endotoxin a chemoattractant? Is it a pyrogen?

A

Yes lipopolysaccharide is a chemoattractant

Yes a pyrogen too

21
Q

What is different about an ‘activated’ neutrophil?

A

It is stickier than normal cells

22
Q

What do neutrophils do in 4 easy steps?

A

Contact
Recognition - opsonins
Internalisation - phagolysosome
Degradation with lysosomal enzymes or free radicals

23
Q

4 local complications of inflammation?

A

1) Damage to normal tissue
2) Loss of function
3) Loss of fluid (e.g. large burns)
4) Obstruction of tubes (e.g. bile duct)/compression of vital structures (TUMOR)

24
Q

Give an example of a structure that could be compressed in inflammation? An example of a tube blocking? Loss of fluids?

A

Heart - cardiac tamponade
Tube - e.g. bile duct
Loss of fluids - e.g. burns

25
Q

What is fever caused by?

A

Endogenous pyrogens (ie cytokines and bacterial endotoxins) e.g. bradykinin, IL-1 TNF, endotoxin, prostaglandins

26
Q

What are 4 systemic effects of inflammation? What happens

A

1) Fever - caused by pyrogens e.g. IL-1, TNF, endotoxin, prostaglandins
2) Leucocytosis - increased WBC during infection
3) The Acute phase response
4) Shock - Bacterial products or inflammatory mediators get into the blood stream - can cause inflammation round the body and cause shock (rapid drop in BP can be fatal)

27
Q

What is the acute phase response? What proteins does it include?

A

Changes in the synthesis of some proteins by the liver in response to inflammation (some more some less).

E.g. albumin reduces, CRP increases

28
Q

Is CRP an opsonin

A

Yes

29
Q

What are the 4 stages of inflammation resolution?

A

1) Fibrin broken down by plasmin and other proteases
2) Neutrophils apoptose and phagocytosed by macrophages
3) Fluid is taken back up by venues or drained into lymphatics
4) Regeneration of tissue where possible

30
Q

What is the sequelae of acute inflammation (4)?

A

1) Complete resolution
2) Abcess (acute inflam with chronic inflam)
3) Fibrous (chronic inflam with fibrous repair)
4) Death

31
Q

What are the 4 types of exudate? When are they commonly seen?

A

1) Pus/abscess - gives idea it’s bacterial
2) Haemorrhagic - if vascular disruption/infiltration of malignancy
3) Serous - not infected e.g. blister, clear with plasma proteins
4) Fibrinous - fibrin deposited without blood clot e.g. in pericardial sac increases friction

32
Q

What is hereditary angio-oedema?

A

Rare condition where you get rapid oedema of the dermis, sub cut, mucosal and sub mucosal tissues. Get abdo pain too due to the oedema around intestine

33
Q

What is granulomatous disease?

A

Phagocytes unable to generate free radical superoxide due to defective NADPH oxidase.

Can engulf but can’t kill bacteria

Present with many infections in first year of life e.g. pneumonia and numerous granulomas affecting skin lymph nodes etc.

Pathology (13 decks)

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