acute inflammation 1 and2

Question 1

what is acute inflammation

Answer 1

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

Question 2

characteristics of acute inflammation

Answer 2

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

Question 3

what are the cardinal signs of inflammation

Answer 3

redness
heat
swelling
pain
loss of function

Question 4

what are the causes of acute inflammation

Answer 4

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.

Question 5

what is microcirculation

Answer 5

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

Question 6

extracellular compartment has fluid which is drained into the

Answer 6

lymphatic system

Question 7

what is the dynamic balance of the microcirculation capillaries

Answer 7

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

Question 8

steps in acute inflammation

Answer 8

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

Question 9

results of increased diameter of the blood vessels

Answer 9

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

Question 10

triple response

Answer 10

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.

Question 11

rapid local changes in the blood vessel in an acute inflammation

Answer 11

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.

Question 12

benefits of endothelial permeability

Answer 12

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.

Question 13

what is exude ?

Answer 13

this is fluid that is rich in protein and plasma

Question 14

effects of exudation

Answer 14

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

Question 15

describe the normal laminar flow

Answer 15

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

Question 16

what changes are seen in the capillary blood flow during inflammation

Answer 16

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

Question 17

phases of migration of the neutrophils

Answer 17

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

Question 18

examples of acute inflammation

Answer 18

pleural inflammation
appendicitis
acute pyelonephritis
bacterial endocarditis

Question 19

what are the outcomes of acute inflammation

Answer 19

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​

Question 20

what are the benefits of acute inflammation

Answer 20

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​

Question 21

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

Answer 21

structure”-itis​

	peritoneal cavity 		-peritonitis ​

	meninges 			-meningitis​

	appendix 			-appendicitis​

lungs -pneumonia​

pleural cavity -pleurisy​

Question 22

function of neutrophils

Answer 22

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.

Question 23

what is pus

Answer 23

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

Question 24

what is the role of plasma proteins in inflammation

Answer 24

immune response
clotting factors that drive process of clotting

Question 25

what are the effects of the mediators for acute response

Answer 25

vasodilation increased permeability adhesion of the neutrophils chemotaxis itch and pain

Question 26

mediators in acute response

Answer 26

molecules on endothelial cell surface membrane​ molecules released from cells​ molecules in the plasma​ molecules inside cells​

Question 27

molecules involved in the adhesion of neutrophils on the blood vessel

Answer 27

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.

Question 28

molecules that are released from the cells

Answer 28

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

Question 29

intracellular inflammatory pathways

Answer 29

JAK -STAT MAPK NF-KB

Question 30

role of histamine in inflammatory response

Answer 30

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

Question 31

which cells release histamine

Answer 31

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

Question 32

results of IgE mediated reactions

Answer 32

release of histamine from mast cells

Question 33

effect of serotonin

Answer 33

causes vasoconstriction performed in platelets released when platelets degranulate in coagulation

Question 34

prostaglandins precursor

Answer 34

arachidonic acid

Question 35

cells that produce prostaglandins

Answer 35

endothelial cells and leukocytes

Question 36

thromboxane

Answer 36

thromboxane promotes aggregation and vasoconstriction and are anti-inflammatory

Question 37

properties of thromboxane that makes it a good NSAID

Answer 37

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

Question 38

what are cytokines and chemokine s

Answer 38

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

Question 39

function of cytokines

Answer 39

they stimulate intracellular pathways and signalling.

Question 40

effect of nitric oxide

Answer 40

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

Question 41

oxygen free radicals

Answer 41

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

Question 42

pattern associated molecules

Answer 42

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

Question 43

NF -kB( nuclear factor kappa B)

Answer 43

intracellular inflammatory pathway that is stimulated by a ligand

Question 44

signalling molecules for acute inflammation

Answer 44

pattern associated molecular patterns danger associated molecular patterns

Question 45

examples of intracellular inflammatory pathways

Answer 45

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)

Question 46

plasma role in inflammation

Answer 46

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.

Question 47

what are the immediate systemic effects of inflammation

Answer 47

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.

Question 48

long term effects of acute inflammation

Answer 48

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.

Question 49

pus formation

Answer 49

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

Question 50

pyogenic membrane

Answer 50

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

Question 51

a collection of pus under pressure

Answer 51

abscess

Question 52

suppuration

Answer 52

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

Question 53

what causes a multiloculated abscess

Answer 53

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

Question 54

pus in the pleural cavity

Answer 54

empyema

Question 55

outcomes of acute inflammation

Answer 55

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

Question 56

sepsis

Answer 56

spread to bloodstream - patient “septic”​ bacteraemia - bacteria in blood​ septicaemia - growth of bacteria in blood ​ toxaemia - toxic products in blood​

Question 57

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

Answer 57

sepsis

Question 58

septic shock

Answer 58

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

Question 59

effects of systemic infection

Answer 59

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

Question 60

presentations of sepsis

Answer 60

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

Question 61

pathogenesis of septic shock

Answer 61

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.

Question 62

what happens when compensation for septic shock is reduced

Answer 62

there is tissue hypoxia loss of tissue and organ failure

Question 63

Outcome of septic shock

Answer 63

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​

Question 73

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