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EMS MOD > acute inflammation > Flashcards

acute inflammation Flashcards

1
Q

what is acute inflammation?

A

it is a common , non-specific response to injury
protective response to injury - essential to survival
it aims to rid the body of the initial cause of injury and the consequences of the injury

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2
Q

what is it under?

A

it is under complex biochemical control

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3
Q

what is an example of acute inflammation?

A

pneumonia

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4
Q

what is the duration of acute inflammation?

A

minutes, hours or days

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5
Q

what is the characteristic cell and describe it?

A

neutrophil polymorph - it has a multilobed nucleus - around 3

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6
Q

what is the basis of AI?

A

it delivers white cells or plasma proteins to the site of infection or injury

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7
Q

what are the five characteristics of AI?

A

dolor, calor, rubor, tumor and loss of function

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8
Q

what are the three major causes of AI?

A

infections, physical and chemical agents

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9
Q

what is a hypersensitivity reaction?

A

when the normally protective immune system damages the individual’s own tissues. They tend to be persistent and difficult to cure.

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10
Q

why does tissue necrosis occur?

A

when the extent of damage is too severe for cells to regenerate so they repair using fibrosis

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11
Q

what is meningitis?

A

it is inflammation of the meningeal lining of the brain - it is pus collecting made of neutrophil polymorphs and dead or dying tissue

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12
Q

what happens in acute cholecystitis?

A

fibrinogen leaks out of the blood vessels and makes contact with the tissues meaning that fibrin is formed in the fibrinous reaction. this is because gall stones block the exit from the gall bladder and therefore there is fat collection. The condition shows cardinal signs of inflammation.

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13
Q

why would the peritoneal cavity appear red and inflamed?

A

peritonitis. If the peritoneal cavity is filled with exudate (fluid with a lot of protein) then there is serious inflammation. This is from thin fluid from mesothelial or plasma cell secretions. Accumulation can result in effusion.

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14
Q

what are the three major components of AI?

A

cellular exudate formation, increased vascular permeability and fluid exudate formation and changes in vessel calibre

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15
Q

how are vessels adapted in AI?

A

they undergo changes to maximise the movement of plasma proteins and cells to the site of injury

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16
Q

what is exudate?

A

it is extravascular fluid with a high protein concentration containing cellular debris. it implies inflammation.

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17
Q

what is transudate?

A

it is a fluid with low protein and little or no cellular component

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18
Q

what is oedema?

A

when there is excess fluid in the interstital fluid or serous cavities - it can be exudate or transudate and can result from heart failure - pulmonary or peripheral

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19
Q

what is pus?

A

it is inflammatory exudate that is rich in neutrophils, dead cell debris and microbes

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20
Q

what are the changes in vessel calibre?

A

there is initial transient vasoconstriction. Then there is vasodilation that is from around 15 minutes to several hours, this is an early change. It increases blood flow by up to ten times, and produces redness and heat from vessels and capillaries close to the surface of the skin. It is mediated by histamine and NO on vascular smooth muscle.

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21
Q

what do skin lesions show?

A

they show the cardinal signs of inflammation - tumor, dolor, rubor, calor

22
Q

how is fluid exudate formed?

A

the increased permeability of microvasculature results in the escape of fluid rich fluid into the tissue. It is caused by chemical mediators (histamine, leukotrienes and NO). injury to vasculature from trauma and injury to endothelium from bacteria and toxins.

23
Q

what is an example of the difference in susceptibility of different body parts to chemical mediators?

A

the CNS is insensitive to histamine, but skin, conjunctiva and bronchial mucosa are sensitive to this

24
Q

why is exudation increased in AI and what is the result?

A

the hydrostatic pressure of the venous end of the capillaries is higher and therefore fluid is not absorbed. Therefore once plasma proteins escape into extravascular space increasing the colloid osmotic pressure so more fluid follows

25
Q

what are the effects of fluid exudate?

A 
transport of drugs 
AB entry 
dilution of toxins 
fibrin formation - fibrinogen escape out and fibrin forms network for granulation tissue 
delivery of oxygen and nutrients 
stimulation of the immune response 
high turnover
26
Q

why does more fluid escape during AI?

A

there is stasis of blood - the blood is thicker and slower as fluid escapes meaning more time for more fluid to escape - permeability and calibre of vessels

27
Q

what is the difference between action of neutrophils normally and in AI?

A

normally neutrophils travel along centre of the vessels in axial stream, in AI the neutrophils will go along edges rolling and bouncing - margination, stick to endothelium - pavementing, and migrate into tissue through gaps - chemically mediated or due to direct trauma

28
Q

what is diapedesis?

A

how RBC move through the vessel walls - passive due to hydrostatic pressure - unlikely to happen unless penetrative direct trauma

29
Q

what chemical mediators are used for rolling and sticking of neutrophils?

A

selectins for rolling

integrins for sticking

30
Q

what is chemotaxis for?

A

to get polymorphs into the right place in tissues / area of injury

31
Q

what happens to the capillary bed in AI?

A

usually capillaries may be shut off, but in AI they are all open and used

32
Q

what are neutrophils?

A

cells that are produced in the bone marrow that are the commonest WBC and increased in inflammation.

33
Q

what are the characteristics of neutrophils?

A

the are motile, amoeboid and can move into tissues. The follow directional chemotaxis, they have a short lifespan and are raised in infection

34
Q

what are the origins of chemical mediators in AI?

A

some are cell derived and some are plasma derived

35
Q

what are cell derived chemical mediators?

A

cytokines, prostaglandins, histamine, leukotrienes and lysosomal components

36
Q

what are leukotrienes?

A

they are from arachidonic acids with vasoactive properties

37
Q

where is histamine produced?

A

released from mast cells for vascular dilation and permeability

38
Q

where do prostaglandins originate?

A

they are long chain fatty acids from arachidonic acids

39
Q

what are plasma derived chemical mediators?

A

kinin, complement, fibrin and coagulation systems

40
Q

why is aspirin good in acute inflammation?

A

it targets pain and reduced temperature

41
Q

what are the general effects of AI?

A

reaction in the hypothalamus, leukocytosis, malaise, nausea, pyrexia, anorexia and lyph node enlargement

42
Q

how can the general effects of AI be accounted for?

A

lymph node enlargement is from infection in the throat, polymorphs and macrophages produce substances that act on the hypothalamus, and malaise, nausea and anorexia are general non-specific symptoms

43
Q

what laboratory tests would be done?

A

acute phase proteins such as CRP, FBC and an erythrocyte sedimentation rate

44
Q

what is pyogenic?

A

pus forming bacteria

45
Q

how does an abscess form?

A

collection of pus will border of tissues that are infected and will then form a cavity - abscess cavities

46
Q

what are some harmful effects of AI and examples?

A

inappropriate inflammatory response - hayfever
swelling - epiglottitis
digestion of normal tissues - abscess cavities
fibrinous inflammation - restrictive pericarditis

47
Q

how does fibrin aid AI?

A

can be removed by fibrinolysis
impedes movement of the microorganism and traps them meaning phagocytosis is easier and acts as a scaffold for granulation tissue

48
Q

what is restrictive pericarditis?

A

when the heart muscle heals by fibrinous inflammation as cannot regenerate - scar therefore cannot contract properly

49
Q

what are some examples of the AI going wrong?

A

adult respiratory distress syndrome, systemic inflammatory response syndrome, chronic granulomatous disease of childhood, hereditary angio-oedema and amyloidosis

50
Q

what happens after AI?

A

if can regenerate goes back to normal
if excess exudate then suppuration - formation of pus
if persistent causal agents - chronic
if cannot resolve - repair

EMS MOD (28 decks)

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