02 - Acute inflammation Flashcards

(33 cards)

1
Q

characteristic cell of acute inflammation

A

neutrophil polymorph

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2
Q

What is a rapid host response

A

delivers white cells and plasma proteins/ such as antibodies

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3
Q

Physical characteristics inflammation

A
REDNESS (rubor)
HEAT (calor)
SWELLING (tumour)
PLAIN (dolor)
LOSS OF FUNCTION (function laesa)
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4
Q

Causes acute inflammation

A

physical agents + Infections + hypersensitivity reactions + chemicals + Tissue necrosis

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5
Q

Serous inflammation

A

thin fluid from plasma or mesothelial secretions

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6
Q

major components of acute inflammation

A
  1. changes vessel calibre
  2. increased vascular permeability + fluid exudate formation
  3. Cellular exudate formation
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7
Q

Exudate

A

extravascular fluid with high prot. conc. containing cellular debris

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8
Q

transudate

A

low protein, little or no cellular component

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9
Q

oedema

A

excessive fluid in interstitial tissue / serous cavities

Exudate or transudate

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10
Q

Pus

A

inflammatory exudate rich in neutrophils, dead cell debris and microbes

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11
Q

what mediates vasodilation

A

histamine + NO

on vascular smooth muscle

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12
Q

how does formation of fluid exudate affect microvasculature

A

increases permeability to allow escape of exudate into tissue

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13
Q

What increases permeability of microvasculature

A

chemical mediators = histamine, NO, leukotriene
Direct vascular injury = trauma
Endothelial injury = bacteria and toxins

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14
Q

susceptibility to histamine

A

CNS –> insensitive

skin, conjuctiva, bronchial mucosa –> sensitive

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15
Q

How does acute inflammation affect hydrostatic pressure

A

increased

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16
Q

what effect does plasma proteins escaping into the extravascular space have?

A

increases colloid osmotic pressure

More fluid leaves vessels –> exudation

17
Q

effects of fluid exudate

A

dilution of toxins

entry of antibodies

transport of drugs

fibrin formation

delivery of nutrients and oxygen

stimulation of immune response

18
Q

How does exudate leaving cells effect the blood

A

slows blood flow

increases viscosity –> stasis

19
Q

neutrophils move towards vessels

20
Q

neutrophils adhere + stick to vessels

21
Q

neutrophil polymorphs move through vessel wall

22
Q

Where neutrophils produced

23
Q

movement of neutrophils

A

directional chemotaxis

24
Q

chemical mediators of vasodilation

A

migration of neutrophils

25
histamine affect acute inflammation
increase vascular dilation Permeability
26
prostaglandins affect acute inflammation
inflammation + oedema
27
origins of prostaglandins
it is a long chain fatty acid from arachnoid acid
28
leukotrienes affect acute inflammation
vasoactive properties
29
origins of leukotrienes
from arachnoid acid
30
Plasma derived mediators of acute inflammation
complement system kinin system coagulation system Fibrinolytic system
31
how do cycloxygenase inhibitors affect vasodilation pathways
inhibit pathway, reducing levels of prostaglandins these are drugs which can be used to limit the inflammatory process
32
general effects of inflammation
pyrexia lymph node enlargement nausea, malaise, anorexia leukocytosis
33
harmful effects inflammation
digestion normal tissue e.g abscess cavities Swelling e.g acute epiglottis inappropriate inflammatory response e.g hay fever