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acute inflammation 1 and2 Flashcards

understand

1
Q

what is acute inflammation

A

series of protective changes occurring in living tissue as a response to injury

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2
Q

characteristics of acute inflammation

A

it is a dynamic homeostatic mechanism that occurs in higher beings with a living tissue.

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3
Q

what are the cardinal signs of inflammation

A

redness
heat
swelling
pain
loss of function

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4
Q

what are the causes of acute inflammation

A

1.microorganisms such as bacteria and fungi
2.mechanical such as trauma injury to tissue
all injury even sterile injuries such as surgery might cause injury.
3.chemical causes such as acid and alkali , bile and urine example in the peritoneum.
4.weather conditions which might cause stress on the body.These conditions include ; heat , cold, and ionising radiation.
5.hypersensitivity for example allergic reactions.
6.dead tissue which is caused by necrosis and irritates adjacent tissue.

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5
Q

what is microcirculation

A

this is capillary beds that are fed by arterioles and drained by venules.

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6
Q

extracellular compartment has fluid which is drained into the

A

lymphatic system

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7
Q

what is the dynamic balance of the microcirculation capillaries

A

hydrostatic( blood pressure ) and colloid osmotic pressure ( pressure exerted by the plasma proteins)

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8
Q

steps in acute inflammation

A

1.changes in vessel radius - flow
2.change in the permeability of the vessel wall – exudation of fluid
3.movement of neutrophils from the vessel to the extravascular space - emigration

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9
Q

results of increased diameter of the blood vessels

A

for increased flow of the blood ; there is always reduced resistance with the increased diameter.

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10
Q

triple response

A

flush , flare , wheal
flush - dilation of the local capillary that is affected.
flare - dilation of adjacent arterioles
wheal - accumulation of fluid that is oedema in the local vessels.

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11
Q

rapid local changes in the blood vessel in an acute inflammation

A

1.few moments after injury there is constriction as a protective measure .
2.there is dilation of the artery .
3.relaxation of the smooth muscle- this is the flush flare wheal.

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12
Q

benefits of endothelial permeability

A

1.movement of materials such as plasma into the extravascular space and this is known as exudation.
2. the rate of flow slows and there is a change in the flow of blood.

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13
Q

what is exude ?

A

this is fluid that is rich in protein and plasma

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14
Q

effects of exudation

A

oedema is formed and there is accumulation of fluid in the extravascular space.

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15
Q

describe the normal laminar flow

A

the erythrocytes on the periphery, the neutrophils on the innermost.

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16
Q

what changes are seen in the capillary blood flow during inflammation

A

there is neutrophil pavementation and adhesion on the endothelial lining .
the red cells aggregate in the centre.

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17
Q

phases of migration of the neutrophils

A

movement to the periphery of the vessel,
adhesion to the surface that is pavementation.
movement out of the vessel that is called emigration

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18
Q

examples of acute inflammation

A

pleural inflammation
appendicitis
acute pyelonephritis
bacterial endocarditis

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19
Q

what are the outcomes of acute inflammation

A

nciting agent isolated and destroyed​

macrophages move in from blood and phagocytose debris; ​

then they leave​

epithelial surfaces regenerate​

inflammatory exudate filters away​

vascular changes return to normal​

inflammation resolves​

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20
Q

what are the benefits of acute inflammation

A

apid response to non-specific insult​

cardinal signs and loss of function​

transient protection of inflamed area​

neutrophils destroy organisms and denature antigen for macrophages to phagocytose​

plasma proteins localise process​

resolution and return to normal​

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21
Q

what are the names of inflammation on different sites in the body

A

structure”-itis​

	peritoneal cavity 		-peritonitis ​

	meninges 			-meningitis​

	appendix 			-appendicitis​

lungs -pneumonia​

pleural cavity -pleurisy​

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22
Q

function of neutrophils

A

phagocytosis - they recognise the foreign antigen and they move to it through chemotaxis.
direct killing of the cells - there granules contain enzymes and oxidants such as sodium peroxide that cause degradation of the foreign materials.

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23
Q

what is pus

A

a collection of dead neutrophils ,bits of cells, organisms and endogenous proteins

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24
Q

what is the role of plasma proteins in inflammation

A

immune response
clotting factors that drive process of clotting

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25
Q

what are the effects of the mediators for acute response

A

vasodilation
increased permeability
adhesion of the neutrophils
chemotaxis
itch and pain

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26
Q

mediators in acute response

A

molecules on endothelial cell surface membrane​

molecules released from cells​

molecules in the plasma​

molecules inside cells​

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27
Q

molecules involved in the adhesion of neutrophils on the blood vessel

A

CAM-1 helps neutrophils to stick together with the endothelial cell.
P selectin helps to roll over the neutrophils
so that they can easily attach to the endothelial cells.

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28
Q

molecules that are released from the cells

A

histamine
serotonin
prostaglandins
cytokines
nitric oxide
oxygen free radicals
pattern associated molecular patterns
danger associated molecular patterns

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29
Q

intracellular inflammatory pathways

A

JAK -STAT
MAPK
NF-KB

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30
Q

role of histamine in inflammatory response

A

causes vasodilation and increased permeability
acts on H1 receptors on the endothelial cells

31
Q

which cells release histamine

A

mast cells that are beside blood vessels , platelets and basophils .

32
Q

results of IgE mediated reactions

A

release of histamine from mast cells

33
Q

effect of serotonin

A

causes vasoconstriction
performed in platelets
released when platelets degranulate in coagulation

34
Q

prostaglandins precursor

A

arachidonic acid

35
Q

cells that produce prostaglandins

A

endothelial cells and leukocytes

36
Q

thromboxane

A

thromboxane promotes aggregation and vasoconstriction and are anti-inflammatory

37
Q

properties of thromboxane that makes it a good NSAID

A

thromboxane promotes vasoconstriction , aggregation of platelets and inhibits inflammatory response .

38
Q

what are cytokines and chemokine s

A

small protein molecules that are produced by macrophages , lymphocytes and endothelium in response to inflammatory stimuli

39
Q

function of cytokines

A

they stimulate intracellular pathways and signalling.

40
Q

effect of nitric oxide

A

produced by many cells
cause smooth muscle relaxation , antiplatelets , regulate leukocyte recruitment to inflammatory focus.

41
Q

oxygen free radicals

A

H2O2 , and OH-, O2 ;released by neutrophils during phagocytosis and they amplify other mediator effects.

42
Q

pattern associated molecules

A

1-these could be microbial antigen which are genetically hard wired to recognise or innate and adaptive immunity .

43
Q

NF -kB( nuclear factor kappa B)

A

intracellular inflammatory pathway that is stimulated by a ligand

44
Q

signalling molecules for acute inflammation

A

pattern associated molecular patterns
danger associated molecular patterns

45
Q

examples of intracellular inflammatory pathways

A

NF-kB ( nuclear factor kappa B)
MAPK( it is activated by surface receptors such as toll like receptors )
JAK-STAT pathway( signal transducer and activator to transcription pathway which causes direct translation of extracellular signal to molecular expression)

46
Q

plasma role in inflammation

A

1.blood coagulation pathways are activated the clotting factors present in the plasma fluid.
2.fibrinolysis the degradation of fibrin during the formation of fibrin fibres.
3.kinin system for example bradykinin which causes pain.
4.complement cascade ties inflammation with immune system and active components which stimulate increased permeability , chemotaxis ,phagocytosis and cell breakdown.

47
Q

what are the immediate systemic effects of inflammation

A

1-pyrexia which is raised temperature
feeling unwell also known as malaise ,
2-anorexia and nausea , together with abdominal pain and vomiting in children.
3-neutrophilia which is raised white cell count.; bone marrow count increases.

48
Q

long term effects of acute inflammation

A

1.lymphadenopathy which is regional
2.lymph node enlarge as a result of immune response
3.weight loss
4.anaemia - from the loss of blood.

49
Q

pus formation

A

dead tissue , dead micro - organisms , exudate , neutrophils , fibrin and red cells and debris.

50
Q

pyogenic membrane

A

capillary sprouts ,neutrophils , fibroblasts which lay off the walls off the pus.

51
Q

a collection of pus under pressure

A

abscess

52
Q

suppuration

A

an abcess that is under pressure ; the pressure comes from the growing granulation tissue

53
Q

what causes a multiloculated abscess

A

a pus that bursts through pyogenic membrane and forms new cavities.

54
Q

pus in the pleural cavity

A

empyema

55
Q

outcomes of acute inflammation

A

granulation tissue which leads to healing and repair and also leads to fibrosis and formation of a scar.

56
Q

sepsis

A

spread to bloodstream - patient “septic”​

bacteraemia - bacteria in blood​

septicaemia - growth of bacteria in blood ​

toxaemia - toxic products in blood​

57
Q

life threatening organ dysfunction caused by a dysregulated host response to infection characterised by increased organ dysfunction

A

sepsis

58
Q

septic shock

A

a subset of sepsis
profounds circulatory , cellular and metabolic abnormalities which are at a greater risk of mortality than with sepsis alone.

59
Q

effects of systemic infection

A

shock which is caused by the inability of oxygen to perfuse tissues.

60
Q

presentations of sepsis

A

peripheral vasodilation
tachycardia which is high heart rate to cater for the reduced vascular resistance.
low blood pressure
haemorrhagic skin rash

61
Q

pathogenesis of septic shock

A

release of mediators from the cells into the plasma.
the mediators cause vasodilation leading to loss of systemic vascular resistance.
there is increased catecholamine release.
increased tachycardia to maintain the flow of the cardiac output.

62
Q

what happens when compensation for septic shock is reduced

A

there is tissue hypoxia
loss of tissue and organ failure

63
Q

Outcome of septic shock

A

rapidly fatal​

tissue hypoxia - cell death​

haemorrhage​

requires urgent intervention and support​

awareness and early recognition​

ability of young people to compensate​

admit to hospital and intensive care​

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