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MoD > L7 - Acute Inflammation > Flashcards

L7 - Acute Inflammation Flashcards

1
Q

what causes the formation of fluid exudate?

A
  • chemical mediators; histamine, NO, leukotriene
  • direct vascular injury (trauma)
  • endothelial injury (bacteria and toxins)
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2
Q

what are the 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
  • high turnover
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3
Q

how is cellular exudate formed?

A
  • loss of fluid into tissues and increased calibre of vessels = slower blood flow and increased viscosity of blood (stasis).
  • Neutrophils line up along vascular endothelium and migrate through vessel wall into tissues
  1. margination of neutrophils
  2. pavementing of neutrophils (adhere)
  3. diapedesis/transmigration
  4. migration into adventitia.
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4
Q

what is acute inflammation?

A
  • initial tissue reaction to injury
  • lasts minutes-days
  • characteristic cell: neutrophil
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5
Q

Physical characteristics of acute inflammation?

A

RCTDF

Rubor (redness)
Calor (heat)
Tumour (swelling)
Dolor (pain)
Functio laesa (loss of function)
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6
Q

causes of acute inflammation?

A

physical agents

infection

hypersensitivity reactions

chemicals

tissue necrosis

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7
Q

what chemically mediates acute inflammation?

A
  • vasodilation
  • migration of neutrophils
  • chemotaxis
  • increased vascular permeability
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8
Q

general effects of acute inflammation?

A
  • pyrexia (fever)
  • lymph node enlargement
  • nausea, malaise, anorexia
  • leukocytosis
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9
Q

harmful effects of acute inflammation?

A
  • digestion of normal tissues e.g abscess cavities
  • swelling e.g epiglottis
  • inappropriate inflammatory response e.g hayfever
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10
Q

what changes in vessel calibre occur in acute inflammation?

A

Vasodilation ([after] initial transient vasoconstriction)

  • Early change (15 mins to several hours)
  • Increases blood flow (<10x) - Heat and redness
  • Mediated by histamine and NO on vascular smooth muscle
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11
Q

characteristics of neutrophils.

A
  • produced in bone marrow
  • most common WBC
  • increased in acute inflammation
  • motile/amaeboid, can move into tissues
  • directional chemotaxis
  • short lifespan (hours)
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12
Q

major components/features of acute inflammation?

A
  1. changes in vessel calibre
  2. increased vascular permeability
  3. fluid ad cell exudate
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13
Q

what is exudate?

A

Implies inflammation

extravascular fluid with high protein concentration, containing cellular debris.

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14
Q

what is transudate?

A

low protein, little or no cellular component

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15
Q

what is oedema?

A

excess fluid in interstitial tissue / serous cavities – exudate or transudate

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16
Q

what is pus?

A

inflammatory exudate rich in neutrophils, dead cell debris and microbes

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17
Q

what affect does histamine have on the CNS?

A

NONE

[Different tissues have different susceptibility e.g. CNS is insensitive to
histamine but skin, conjunctiva & bronchial mucosa are sensitive →
hayfever]

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18
Q

how is fluid exudate formed?

A

Increased permeability of microvasculature results in escape of protein rich fluid into tissue

  • hydrostatic pressure
19
Q

list cell derived mediators of acute inflammation

A
  • histamine
  • prostaglandins
  • lysosomal componenents
  • leukotrienes
  • cytokines
20
Q

list plasma derived mediators of acute inflammation

A
  • complement system
  • kinin system
  • coagulation system
  • fibrinolytic system
21
Q

what does phospholipase do in the Arachidonic acid, prostaglandins and leukotriene pathway?

A

converts cell membrane phospholipid into arachidonic acid

22
Q

what do steroids inhibit? what physiological effect does this have?

A

phospholipase

prevent vasodilation

23
Q

what does cycloxygenase do in the Arachidonic acid, prostaglandins and leukotriene pathway?

A

converts arachidonic acid to prostaglandins

24
Q

what physiological effect do prostaglandins have?

A

vasodilation

oedema

25
Q

what inhibits cycloygenase? what physiological effect does this have?

A

Aspirin & indomethacin inhibit cyclooxygenase

reduces the inflammation

26
Q

what does 5-Ilpoxygenase do in the Arachidonic acid, prostaglandins and leukotriene pathway?

A

converts arachidonic acid to leukotrienes

27
Q

what physiological effect do leukotrienes have?

A

vasoconstriction

bronchospasm

increased vessel permeability

28
Q

what are the general effects of acute inflammation?

A

➢Pyrexia
➢Lymph node enlargement
➢Nausea, malaise, anorexia
➢Leukocytosis

29
Q

what are the harmful effects of acute inflammation?

A
  • digestion of normal tissues e.g abscess cavities
  • swelling eg epiglottis
  • inappropiate inflammatory response eg swelling of lips
30
Q

what happens if acute inflammation is not resolved?

A
  • excessive exudate (suppuration and formation of pus)
  • excessive necrosis (repair or fibrosis)
  • chronic inflammation
31
Q

what effect do Anti-inflammatory glucocorticoid steroids have?

A

stabilize membranes and prevent phospholipid

hydrolysis thereby inhibiting both prostaglandins and leukotriene pathway

32
Q

what effect do Aspirin and other NSAIDs have on the prostaglandins and leukotriene pathway?

A

inhibit cyclooxygenase

but not lipoxygenase

33
Q

what effect do Leukotriene receptor antagonists (LTRAs) have on the prostaglandins and leukotriene pathway?

A

inhibit the bronchoconstrictive and

inflammatory mechanisms of leukotrienes

34
Q

what would you see on a blood test (full blood count) if inflammation was apparent?

A

Full blood count – significant increase in lymphocyte levels

higher erythrocyte sedimentation rate (increases with the higher the level of inflammation)

increase in C-reactive Protein (CRP)

35
Q

What are the possible complications of pneumonia (inflammation of the lungs)

A

Bacteria in the bloodstream (bacteremia)

Difficulty breathing.

Fluid accumulation around the lungs (pleural effusion)

Lung abscess.

36
Q

what is systemic inflammatory response syndrome?

A

systemic inflammation, organ dysfunction/failure

Abnormal regulation of various cytokines (cytokine storm)

37
Q

What is Acute (adult) respiratory distress syndrome?

A

wide spread inflammation of the lungs

triggered by various pathologies such as pneumonia and sepsis

38
Q

what is chronic granulomatous disease of childhood?

A

hereditary disease

phagocytes cannot form reactive oxygen compounds (required to kill infections)

= long term (chronic) and repeated infections

39
Q

what is Hereditary angio-oedema?

A

rare, autosomal dominant
Inherited blood disorder

causes episodic attacks of swelling

40
Q

what is Amyloidosis?

A

Amyloidosis is when an abnormal protein called amyloid builds up in your tissues and organs. When it does, it affects their shape and how they work.

Caused by accumulation of amyloid fibrils (abnormal insoluble proteins) within extracellular space of tissues

Can be local or systemic = inflammation

41
Q

how would acute inflammation present under a microscope?

A

[Neutrophils are seen and some necrotic and dead cells and sometimes microbial agents]

42
Q

how is fluid exudate formed?

A

Increased permeability of microvasculature results in escape of protein rich fluid into tissue

43
Q

what are some chemical mediators of acute inflammation?

A

➢ Vasodilatation
➢ Migration of neutrophils
➢ Chemotaxis
➢ Increased vascular permeability

44
Q

what are the outcomes of acute inflammation?

A
  • resolution (body goes back to normal)

OR:

● Excessive exudate
● Excessive necrosis
● Persistent causal agent → Chronic inflammation

MoD (19 decks)

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