MOD Acute Inflammation Flashcards

1
Q

Definition

A

Acute inflammation is innate, stereotyped and immediate response to tissue damage in order to limit the damage.

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2
Q

Give an outline of what happens

A

Vasodilation of arterioles (histamine, c5a, c3a)
Increased vascular permeability (histamine)
Exudation due to pressure changes
Increased lymphatic drainage.
Infiltration of neutrophils
Phagocytosis, killing, activation of immune response
Resolution

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3
Q

What causes vasodilation and increased leakage.

A

Histamine from mast cells, basophils and platelets.

Serotonin from platelets.

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4
Q

What do prostaglandins do?

A

Cause vasodilation
Induce pain and fever
PG3 causes ductus arteriosus to close

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5
Q

Describe exudation

A

Increased capillary hydrostatic pressure and increased vascular permeability allows leakage of plasma into tissue. This raises interstitial colloid oncotic pressure causing yet more exudation.
This results in oedema.

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6
Q

What is the function of oedema

A

Drains into lymphatics with microorganisms and antigens.

Presented to immune system

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7
Q

Exudate vs tea sheath

A

Exudate is a protein rich fluid lost to tissue in inflammation
Transudate is a protein poor fluid lost due to rised capillary hydrostatic pressure only.

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8
Q

What are neutrophils

A

Short life span
Phagocytosis
Release of chemical mediators

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9
Q

How to neutrophils enter the tissue

A
Chemotaxis
Activation
Margination
Rolling
Adhesion
Diapedesis
Emigration
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10
Q

Give a chemo attractant. Describe how neutrophils do chemotaxis.

A

C5a
Binds to receptor on neutrophil PM.
Directional movement down concentration gradient

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11
Q

Opsonin

A

Coat pathogens for phagocytosis

C3b

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12
Q

How do neutrophils kill

A

Oxygen dependent

Oxygen independent - enzymes

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13
Q

Function of pain and loss of function

A

Enforce rest

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14
Q

Bradykinin

A

Vasodilation, venular leakage, pain

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15
Q

Complement

A

Form a membrane attack complex which perforated cell membranes
C3a - vasodilator
C5a - chemoattractant
C3b - Opsonin

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16
Q

Local complications

A
Obstruction of tubes
Damage to normal tissue
Compression of organs
Loss of fluid
Pain and loss of function
17
Q

Systemic consequences

A
Fever
Leukocytosis
Acute phase response
Changes in plasma protein conc
Shock
18
Q

How does acute inflammation die down

A
Inflammatory mediators 
Have short half lives
Are degraded
Are diluted by exudate
Produced only in quick bursts if stimulus persists
19
Q

Describe resolution

A

Return of vascular permeability
Exudate drained
Fibrin degraded
Neutrophils undergo apoptosis

20
Q

sequelae

A

Abscess
In solid tissue, exudate pulls tissue apart. May be creamy white and filled with neutrophils

Haemorrhagic exudate
Vascular damage

Serous exudate
Few leucocytes but contains plasma proteins

21
Q

Hereditary angiooedema

A

C1 esterase complement deficience
Non itchy cutaneous angiooedema
Autosomal dominant

22
Q

Alpha 1 antitrypsin deficiency

A

Protease inhibitor that is released from neutrophils in inflammation.
In lack of, protease act unchecked in lung causing emphysema
Abnormal protein accumulates in liver causing hepatocyte damage

23
Q

Causes

A

Same as cell injury causes