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

25
how long does it take heart cells during myocardial ischemia to lose myocardial contractily
less than 2 minutes
26
how long does it take heart cells during myocardial ischemia to to have ultrastrucula changes and what are these
a few minues myofibrillar rexlation, glycogen depletion, cell and mitochonal swelling
27
how long does it take heart cells during myocardial ischemia to have yocyte necotis and what is this
distuptio of integiry of sarcolemmal memabne and leakage of intercllaru macromolues within 20-40 minues
28
how long does it take for injry to the microvasculature
greater than 1 hour
29
how to detect leackage of intracellau macromolues
blood tests
30
what does a infration look like with less than 24 hours
slight swollen mitochonai on electon micros after a few hours to 24 hours
31
what is te apperance of infracts after 24-48 hours
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
what is the apperance of infracts after 72 hours
macroscopically - pale infract, yellow white and red periphery red impact little change microscopy - chroin inflation, macrophage, granuat tissu forming, fibrois
33
what is the end result of infaracts
scare replaces are of tisue damage, shape depend o teriary of occuled fevsl reperfusion injury
34
what happen in the first 4-8 ours after an mi
early coagulation necosi, oedema, haemoarage
35
what happens 12-48 hours after an mi
ongin coagulation, necrosi, myocyte chanes, early neutrophillic infilatatio
36
what happens 1-3 days after an mi
coaguation necros, loss of nuclei and striation, brisk neutiphillic infalte
37
what happesn 3-7 days after an mi
disintegration of dead myogiber, dying neutrophils, early phagocytois
38
what happens 7-10 days fater an mi
well developed phagocytois, granuatio tissue at margin
39
what happens 10-14 days after an mi
well estabiled granulation tissue with new blood vessels and collagen deposistion
40
what happens 2-8 weeks after an mi
increased collagen deposion and decreaed celluarity
41
what happens after 2 monts afer an mi
dense collagenous scar
42
what does a tranmurla infraction effect
the whole thickenss of the myocardium
43
what does asubendocaril infatio effect,
mostly limited to the zone of myocaridum under the endocarial ling of the heart
44
what differ between a subendocaril infraction and a transmural infration
repair time
45
how is a non stemi herat attack diage
elevated troponin
46
what type of heart attack is anon stemi through to be
subendocardial
47