4 - Acute inflammation Flashcards

1
Q

Acute inflammation response

A

Basic pathological process
Non-specific initial reaction to tissue damage
Stereotyped irrespective of aetiology

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2
Q

Three options following acute inflammation

A

Cells can regrow
Cells cannot regrow
Damaging agent persists and so damage continues

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3
Q

Cells can regrow

A

Healing by regeneration

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4
Q

Cells cannot regrow

A

Healing by repair

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5
Q

Damage agent persists

A

Chronic inflammation

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6
Q

Why do we have acute inflammation?

A

Clear away dead tissues
Locally protect from infection
Allow access of immune system components

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7
Q

Calor

A

Heat

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8
Q

Rubor

A

Redness

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9
Q

Dolor

A

Pain

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10
Q

Tumour

A

Swelling

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11
Q

Serous inflammation

A

Copious non-viscous serous fluid release w/o WBCs and so is clear.

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12
Q

Fibrinous inflammation

A

Occurs when extensive leakage of fluid - fibrinogen coagulates forming fibrin

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13
Q

Purulent (pseudomembranous) inflammation

A

Made in response to powerful necrotising toxin, characterised by false membrane (of fibrin, necrotic epithelium and leucocytes) formation

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14
Q

Components of the acute inflammatory response

A

Vascular -> exudative -> cellular

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15
Q

Vascular reaction

A

Dilatation (=rubor), changes in flow

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16
Q

Exudative reaction

A

Formation of inflammatory exudate (=tumour)

17
Q

Cellular reaction

A

Migration of inflammatory cells out of vessels

18
Q

Pyrexia definition

A

Raised body temperature

19
Q

Acute phase reaction definition

A

Summary of complex metabolic/neurological/immunological/inflammatory changes that occur after quick onset of injury/infection

20
Q

Vascular reaction process

A

Microvascular dilatation
Initially flow up then down
Increased permeability

21
Q

Mediated vascular reaction hormones

A
Histamine
Bradykinin
NO
Leukotriene B4
Complement components
22
Q

Non-mediated vascular reaction hormones

A

Direct damage to endothelium e.g. toxins, physical agents

23
Q

Composition of acute inflammatory exudate

A

Protein rich -> immunoglobulins, fibrinogen

Constantly turning over of loads of agents

24
Q

Cellular reaction process

A

Accumulation of neutrophils in extracellular space

In severe cases, accumulation of neutrophils, cellular debris and bacteria forms pus

25
Q

How neutrophils get through the walls

A

Axial stream of neutrophils -> margination -> rolling - adhesion (pavementing) -> migration (RBC diapedesis) -> chemotaxis

26
Q

Mediators of acute inflammation types

A

Cell derived and plasma derived

27
Q

Types of cell derived mediators

A

Stored (histamine)

Synthesised (prostaglandins, leukotrienes, PAF, cytokines, NO, chemokines)

28
Q

Plasma derived

A

Kinin system
Clotting pathway
Thrombolytic pathway
Complement pathway

29
Q

Mediators for vascular dilatation

A
Histamine
PGE2/I2
VIP
NO 
PAF
30
Q

Mediators for increasing permeability

A
Histamine
Bradykinin
NO
C5a
LTB4
PAF
31
Q

Mediators for neutrophil adhesion

A
IL-8
C5a
LTB4
PAF
IL-1
TNF
32
Q

Mediators for neutrophil chemotaxis

A

LTB4
IL-8
Chemokines

33
Q

Systemic inflammatory response syndrome (SIRS)

A

Response to immune system for infection but whole body - related to sepsis

34
Q

Acute (adult) respiratory distress syndrome (ARDS)

A

Severe, life-threatening inflammation of whole lungs. Triggered by trauma or sepsis.

35
Q

Chronic granulomatous disease of childhood

A

Certain compounds in the immune system have problems forming the oxidative compounds needed for the immune response

36
Q

Hereditary angio-oedema (HAE)

A

Rare, autosomal dominantly inherited blood disorder causes episodic attacks which swell the face, extremities, genitals, GI tract and upper airways

37
Q

Amyloidosis

A

Rare condition where amyloid is deposited in tissues and organs