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Cardiovascular > IPathophysioloyg of ischaemia and infraction > Flashcards

IPathophysioloyg of ischaemia and infraction Flashcards

1
Q

Ischaemia

A

lack of blood supply to tissue/ organ leading to inadequate 02 supply to meet needs of tissue/organ

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2
Q

what are the types of hypoxia

A

hypoxic, aneami, stagnet, cytotoixc, histologic

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3
Q

hypoxic hypoxia

A

lack of inspiroed o2 , or low pa02 with normal inspired o2

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4
Q

what is stagnet hypoxia

A

normal inspired o2 but abnoral deliver e.g. occlusion of a vessel or systemic

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5
Q

what is cytotoxic hypoxia

A

nrma inspbired oxygen but abnormal at tissue level

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6
Q

what are hte 6 factors effecting oxygen supply

A

inspired o2, pulmonary function, blood consituents, blood flow, integrity of vasculature, tissue mechanism

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7
Q

what factors affect o2 demand

A

tissue its self - ie differt tisuse have differ oxygen demands
activity of tissue above baseline value

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8
Q

what suppply issues can lead to ischeamic heart disease

A

cornary artey atheroma, cardiac failure, pulmonar funtio , pulmary odema , lvf, anaemiak, previous mi

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9
Q

what demand issues can lead to ischeamic heart diese

A

heart havign high intrinsic demand, exertion and stress

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10
Q

what type of angina is seen if tehr is an esatbliced atheroma in a coronary artery

A

stable

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11
Q

what type of angina is seen is there is a complicated atheroma in a coronary atrery

A

unstable

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12
Q

what is the effect of an atheromatous on blood flow and pressure of radis decrasing by half

A

increaed blodo pressure by factor of 16

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13
Q

what are the differt types of ischeame

A

acutre, chronic, acute on chronic

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14
Q

what are the biochemical effects of ischaemia

A

ther is an increae in lactate produced by anerobic metablis, this increase pyruvate, leading to increase acetyl coa + co2 +nadh, there is insufficient energy and cell death ocras

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15
Q

which die quicker cells with high or low metabolic rate when starved of 02

A

high

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16
Q

what are the 3 clincal effect oischameia

A

pain, dysfuoin and physicall damage

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17
Q

what are the outcome for iscame

A

no clinal effect
resoluoin
infration

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18
Q

infraction

A

the occuloin of arteri supply or venou drainge, resultin in iscaheami necrosis

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19
Q

what are examples of cessation of blood flow leading to infraction

A

thrombosis, embolism, strangulation e.g gut, trauma

20
Q

what factors effect the scale of damage of ischemai

A

time
tissue /organ
pattern of blood supply
previous disease

21
Q

what is coagulative necrosis and where does it occur

A

anywher except the brain, wher blood flow is stoped or slowed down as a result of iscehmai

22
Q

what is colliquitive necorsis and wher does it occur

A

it is when the dies cells die and perfuation into the blood stream, thus stoping the blood flow to other cells, can happen anywhere including the brain

23
Q

what cells die in a mi

A

myocyte death

24
Q

how long does it take heart cells during myocardial ischemia to atp deplte

A

secondas

25
Q

how long does it take heart cells during myocardial ischemia to lose myocardial contractily

A

less than 2 minutes

26
Q

how long does it take heart cells during myocardial ischemia to to have ultrastrucula changes and what are these

A

a few minues
myofibrillar rexlation, glycogen depletion, cell and mitochonal swelling

27
Q

how long does it take heart cells during myocardial ischemia to have yocyte necotis and what is this

A

distuptio of integiry of sarcolemmal memabne and leakage of intercllaru macromolues
within 20-40 minues

28
Q

how long does it take for injry to the microvasculature

A

greater than 1 hour

29
Q

how to detect leackage of intracellau macromolues

A

blood tests

30
Q

what does a infration look like with less than 24 hours

A

slight swollen mitochonai on electon micros after a few hours to 24 hours

31
Q

what is te apperance of infracts after 24-48 hours

A

pale infraction - myocarium, spleen, knidys
red inflact, lung , liver
loose tissues,
microsoppy acute inflation initial at the edge of the infract, loss of speicl cell features

32
Q

what is the apperance of infracts after 72 hours

A

macroscopically - pale infract, yellow white and red periphery
red impact little change
microscopy - chroin inflation, macrophage, granuat tissu forming, fibrois

33
Q

what is the end result of infaracts

A

scare replaces are of tisue damage, shape depend o teriary of occuled fevsl
reperfusion injury

34
Q

what happen in the first 4-8 ours after an mi

A

early coagulation necosi, oedema, haemoarage

35
Q

what happens 12-48 hours after an mi

A

ongin coagulation, necrosi, myocyte chanes, early neutrophillic infilatatio

36
Q

what happens 1-3 days after an mi

A

coaguation necros, loss of nuclei and striation, brisk neutiphillic infalte

37
Q

what happesn 3-7 days after an mi

A

disintegration of dead myogiber, dying neutrophils, early phagocytois

38
Q

what happens 7-10 days fater an mi

A

well developed phagocytois, granuatio tissue at margin

39
Q

what happens 10-14 days after an mi

A

well estabiled granulation tissue with new blood vessels and collagen deposistion

40
Q

what happens 2-8 weeks after an mi

A

increased collagen deposion and decreaed celluarity

41
Q

what happens after 2 monts afer an mi

A

dense collagenous scar

42
Q

what does a tranmurla infraction effect

A

the whole thickenss of the myocardium

43
Q

what does asubendocaril infatio effect,

A

mostly limited to the zone of myocaridum under the endocarial ling of the heart

44
Q

what differ between a subendocaril infraction and a transmural infration

A

repair time

45
Q

how is a non stemi herat attack diage

A

elevated troponin

46
Q

what type of heart attack is anon stemi through to be

A

subendocardial

47
Q
A

Cardiovascular (37 decks)

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