4 - Acute inflammation Flashcards

(37 cards)

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
How neutrophils get through the walls
Axial stream of neutrophils -> margination -> rolling - adhesion (pavementing) -> migration (RBC diapedesis) -> chemotaxis
26
Mediators of acute inflammation types
Cell derived and plasma derived
27
Types of cell derived mediators
Stored (histamine) | Synthesised (prostaglandins, leukotrienes, PAF, cytokines, NO, chemokines)
28
Plasma derived
Kinin system Clotting pathway Thrombolytic pathway Complement pathway
29
Mediators for vascular dilatation
``` Histamine PGE2/I2 VIP NO PAF ```
30
Mediators for increasing permeability
``` Histamine Bradykinin NO C5a LTB4 PAF ```
31
Mediators for neutrophil adhesion
``` IL-8 C5a LTB4 PAF IL-1 TNF ```
32
Mediators for neutrophil chemotaxis
LTB4 IL-8 Chemokines
33
Systemic inflammatory response syndrome (SIRS)
Response to immune system for infection but whole body - related to sepsis
34
Acute (adult) respiratory distress syndrome (ARDS)
Severe, life-threatening inflammation of whole lungs. Triggered by trauma or sepsis.
35
Chronic granulomatous disease of childhood
Certain compounds in the immune system have problems forming the oxidative compounds needed for the immune response
36
Hereditary angio-oedema (HAE)
Rare, autosomal dominantly inherited blood disorder causes episodic attacks which swell the face, extremities, genitals, GI tract and upper airways
37
Amyloidosis
Rare condition where amyloid is deposited in tissues and organs