Inflammation Flashcards

(67 cards)

1
Q

what vascular changes occur in acute inflammation?

A

increased flow
increased permeability

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2
Q

what cellular reactions occur in acute inflammation?

A

extravasation of leukocytes
migration of leukocytes to target area

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3
Q

what is the onset of acute inflammation?

A

rapid onset

<2 days - mins to days

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4
Q

when is acute inflammation terminated?

A

when stimulus is withdrawn and mediators die down

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5
Q

what is the prominent cell type in acute inflammation?

A

Polymorphonuclear Leukocytes

neutrophils*, eosinophils, basophils

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6
Q

what is the pattern of increased flow in acute inflammation?

A

initial transient vasoconstriction
vasodilation
slows down = stasis = oedema

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7
Q

what mediates vasodilation in acute inflammation?

A

PG12
NO

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8
Q

what are the x4 reasons of increased permeability in acute inflammation?

A

endothelial gap widening
cells damaged
increased transcytosis from endothelium
angiogenesis

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9
Q

what is endothelial gap widening in acute inflammation mediated by?

A

histamine
bradykinin
PAF (platelet activating factor)
leukotrienes
Substance P

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10
Q

what vessels are affected in endothelial gap widening?

A

ONLY VENULES

capillaries + arterioles = unaffected

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11
Q

what are x3 conditions where vascular permeability may account for oedema in?

A

acute anaphylaxis
adult respiratory distress syndrome
serum sickness

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12
Q

what are the x2 mediators of arteriolar dilatation in early stages of acute inflammation?

A

prostocyclin (PG12)
nitric oxide (NO)

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13
Q

what are the x2 direct actors which enable leukocytes to pavement/roll along periphery?

A

induced leukocyte adhesion molecules
endothelial cell adhesion molecules

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14
Q

what are examples of induced leukocyte adhesion molecules?

A

oligosaccharides
intergrins
selectins

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15
Q

what are examples of endothelial cell adhesion molecules?

A

selectins
immnoglobulins

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16
Q

name x4 key chemokines?

A

leukotrine B4
completment C5a
TNF
IL8

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17
Q

what are the x2 steps in phagocytosis?

A

attachment
endocytosis

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18
Q

what are the x3 opsonins responsible for attachment in phagocytosis?

A

IgG (sub-type 1 +3)
C3b
collectins

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19
Q

when is opsonisation most effective in endocytosis?

A

when simultaneous C3 and Fc Fibronectin binding occurs

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20
Q

what are the x3 ways bacteria is killed?

A

oxygen dependent pathway
oxygen independent pathway
acid proteases

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21
Q

what is the most powerful killing system?

A

peroxide-myeloperoxidase-halide system

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22
Q

how dos bactericidal permeability increasing protein work?

A

damages bacterial cell membrane

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23
Q

how does lactoferrin work?

A

Fe binding
deprives bacteria of Fe for metabolism

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24
Q

bacteria is killed by 3 processes but what is not guearanteed?

A

no guarantee that bacteria will die

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25
Mechanisms of adhesions between leukocytes and endothelium include what?
increased binding activity of integrins induction of endothelial adhesion molecules redistribution of P-selectin by histamine stimulation
26
phagocytosis of bacteria by granulocytes involves what?
phagocytic vacuole fusing with lysosomes degranulation of the granulocyte frequently requires hydrogen peroxide for destruction
27
what x2 forms of radicals are produced to kill bacteria>
superoxide radicals hydroxyl radicals
28
what are examples of free radical derivative?
hypochlorite ion hydrogen peroxide
29
what are cellular metabolic actions which prevent damage caused by activated oxygen species?
catalase reaction interaction with glutathione peroxidase
30
why does Pneumococcal pneumonia causes inflammation without significant lung necrosis?
because pneumococci induced major chemotaxis but elaborate no major toxins
31
how is Lysosome (N-aceyl muramidase) an effective antibacterial?
because lysosome enzymatically destroys specific components of bacterial cell walls
32
what is chediak-higashi syndrome?
defect in phagocytosis
33
how is inflammation and repair often defective in people with diabetes?
neutrophil reactions + chemotactic stimuli = defective impaired leukocyte-endothelial cell adhesions impaired neutrophil phagocytosis reduced inflammatory vascular reaction microvascular sclerosis
34
where do monocytes originate from and in what form do they enter interstitium?
bone marrow enter interstitium as macrophages
35
what are the mononuclear cells in acute inflammatory exudates?
mainly transformed blood monocytes
36
what do the growth factors released by macrophages do?
control fibroblast proliferation proliferation of myeloid cells, endothelial cells etc.
37
what are monocytes released as epithelioid cells adapted for?
adapted for synthesis NOT phagocytosis
38
what is an example of an epithelioid cell?
angiotensin converting enzyme
39
what are examples of monocyte/macrophages chemotactic agents?
C5a cytokines fibronectin cationic proteins fibropeptides
40
where is histamine and serotonin made?
mast cells platelets
41
what mediators are made on the spot and released?
tissue thromboplastin LTb4 IL2 No
42
what are chemicals which are activated during tissue injury but circulate as inactive plasma precursors?
C3b plasmin bradykinin
43
what is prostacyclin (PG12) an antagonist for?
antagonist of platelet aggregation
44
where is prostacyclin made?
endothelial cells
45
what does prostacyclin promote?
vasodilation
46
what is prostacyclin inhibited by?
aspirin
47
what are x2 activators which induce platelet aggregation?
thromboxane A2 thrombin
48
where is ferritin located and stored?
located in lysosomes stored in mononuclear phagocytic cells
49
what does serum ferritin levels reflect?
stores in iron EXCEPT IN ACUTE INFLAMMATION
50
when is complement activation through 'bypass' mechanism critically important?
in early defence against virulent pyogenic bacteria which has not been previously encountered before
51
what do some sub-groups of immunoglobulins not do when reacting with specific bacterial antigens?
some do not activate by 'classical' pathway
52
what is kinin activated to bradykinin?
kallikrein which in turn is activated by Factor XII
53
what is kinin metabolised by?
ACE kininase
54
what are the actions of bradykinin?
vasodilation increased permeability broncho-constriction pain
55
what do cytokines interact with?
cell surface receptors receptor specific NOT cell type specific
56
IL 1 has an important role in what?
endothelial cell activation hypothalamus mediated fever induction acute inflammation shock T-lymphocyte activation acute phase reaction
57
what are the harmful effects of TNF?
septic shock - hypotension + pyrexia DIC inflammatory symptoms of some autoimmune disease
58
what conditions result in resolution of inflammation with regeneration leading to restoration of normal structure and function?
pneumococcal pneumonia paracetamol induced hepatic necrosis acute viral hepatitis hypovolaemia acute renal tubular necrosis
59
what are some causes of chronic inflammation?
repeated acute inflammation low toxicity organisms prolonged exposure to toxic agents autoimmunity
60
what is the main PMN in chronic inflammation?
macrophages
61
what demonstrates long standing chronic colitis likely to be crohns?
marked submucosal oedema + lymphocytic infiltrate focal epithelioid cell granulomas (mucosal biopsy)
62
what is the main cell found in granulomatous inflammation?
monocytes
63
name some examples of granulomatous inflammation?
TB sarcoidosis brucellosis cat-scratch disease crohns disease, primary biliary cirrhosis
64
what is a granuloma?
focus of chronic inflammation walled off by transformed macrophages
65
what can granulomatous inflammation be composed of?
mass of macrophages + giant cells mass of epithelioid cells + giant cells
66
focal granulomatous lesions resembling those of sarcoidosis are also a characteristic of what?
berylliosis
67
classic immune (epithelioid) granulomas are characteristically seen in what?
sarcoidosis