Handout Packet Ischemic and Valvular Heart Diseases Flashcards

1
Q

Media what layer is this and is it the thickest

A

Thickest layer of artery made of smooth muscle in a matrix of collagen, elastin, and proteoglycans

middle layer right after the internal elastic lamina

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2
Q

Atheroscleroiss what is this

A

The inner layer of the artery becomes ardended because of fatty deposis and fibrous tissueand and frequentyl involves the coronary and cerebral areteries

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3
Q

Adventitia whatr layer is this and what is it made of and whats another name for it

A

made up of fibroblasts and collagen contains the blood vessels nerves and lymphatics that serve the artery. External Elastic Lamina secrond to outermost layer tunica externa outermost layer

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4
Q

Tunica intima what layer is this and what does it house and what is it made of????

A

composed of a single layer of endothelium that rests on a bed of connective tissue housese the circulating blood within the lumen of the artery serves many metabolic signaling functions that help maintain the intergrity of the wall

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5
Q

things disrupt the intergrity of the artery and make it hard

A

fatty streak, fiborous plaque, complicated lesions

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6
Q

Fatty streak.. is it earliest visible lesion does it pertrude into the lamina??? what else are they called??

A

Fatty streak also called foam cells… they dont disturb the blood flow usally made of lipids from marcophages they dont pertrude into the lumen of the artery its like the beginning stages of the block

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7
Q

Where do most artery changes occur where are foam cells derived from and what do they contain

A

most changes appear in the intimall layer fo am cells derived from smooth muscle

often contain debris, of nercotic other dead cells and cholestrol crystals which are seperated from the aterial lumer by a fibrous cap?

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8
Q

fibrous plaque - is it this more serious than the foam cells or the fatty streak if so why??

A

This is a more serious form of clot it develops from fatty streaks and its a fibrous plaque an elevated lesion that projects into the lumen and can cause reduced blood flow

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9
Q

how does a hemmorrhage come about within a firbrous plaque and what does this cause

A

The fibrous plaque may burst or the caps that vascularize the plaque may result in a hemoattoma that may block the cell wall. and this bursting may form an embolism that may result in a MI , PE, or stroke very serious issue

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10
Q

What is the role of the Endothethial wall and what antitrhombotic surface molecules play a role in the maintainece of the anit-clotting police

A

the wall forms a barrier that contains cirulating blood within the lumen. some clot busters are herapen sulfate, thrombomodulin, plasomingen activators, prostacyclin, endothelium-derived relaxing factor

secretes vasoactive substance that directly modulates the contraction of smooth muscle in the medial layer on the other side of the wall

inhibits smooth muscle cell migration and proliferation

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11
Q

Two types of lesions tell me each type

A

Calcification - of a fibrous plaque that results in pipelike rigidity of the vessel wall. This increaes the its fragility

Ruputure of a fiborous plaque- exposes thrombogenic material throughout the body. and weaking of the walls may result in an aneurysm

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12
Q

Modified Respones to injury of Hypothesis

What intially causes the secrement of smooth muscle cells

A

it is then the endothethilial cells become injured or dysfunctional that atheroscelerosis occurs

what intially attracts the cells into the intimia is the release of platelet growth factor and secretion of chemotactic factors that attract other cells

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13
Q

Dyslipidemias what is this about

A

abnormal amount of circulating lipid levels are a major risk factor for heart disease

countries with low sat fat counts have less risk for heart disease go figure.

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13
Q

Dyslipidemias what is this about

A

abnormal amount of circulating lipid levels are a major risk factor for heart disease

countries with low sat fat counts have less risk for heart disease go figure.

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14
Q

injury to the endothethial cells what happens when the endo layer is injuried couple of things

A

increased premability therefore the smooth muscles can get into the intimia layer and into the blood faster

decreased antithrombitcs properties probadly can’t cant signal for them as fast.

reduced secretion of vasodilators impairing smooth muscle relaxation of the medial layer.

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14
Q

injury to the endothethial cells what happens when the endo layer is injuried couple of things

A

increased premability therefore the smooth muscles can get into the intimia layer and into the blood faster

decreased antithrombitcs properties probadly can’t cant signal for them as fast.

reduced secretion of vasodilators impairing smooth muscle relaxation of the medial layer.

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15
Q

Cardiac risk factors major modfiable

At individual at what cholestrol level will be at risk for cardiac disease twice the risk with someone at what level

What do you want your HDL, Total, and LDL cholestrol levels to be

A

Tobbacco smoking, DM, HTN, and Dyslipidemas (high cholestrol essentially because this is what help form the “foam cells” in the first place and eventually into the fibrous plaques.

240 mg/dl places someone at twice the risk verse if they were say at 200 mg/dl

total you want 200 mg Dl

LDL normal 130

people with caridac issues less than 100

HDL greater or equal to 35

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15
Q

Cardiac risk factors major modfiable

At individual at what cholestrol level will be at risk for cardiac disease twice the risk with someone at what level

What do you want your HDL, Total, and LDL cholestrol levels to be

A

Tobbacco smoking, DM, HTN, and Dyslipidemas (high cholestrol essentially because this is what help form the “foam cells” in the first place and eventually into the fibrous plaques.

240 mg/dl places someone at twice the risk verse if they were say at 200 mg/dl

total you want 200 mg Dl

LDL normal 130

people with caridac issues less than 100

HDL greater or equal to 35

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16
Q

Realitive risk for Smokers to get heart disease is ???

A
  1. 35 - 2.5 in studies of all smokers

1. 43 - 3.5 in heavy smokers

16
Q

Realitive risk for Smokers to get heart disease is ???

A
  1. 35 - 2.5 in studies of all smokers

1. 43 - 3.5 in heavy smokers

17
Q

why is HTN a primary risk factor heart disease

A

realitively unkown but in animal studies it shows that the high pressure against the artierial walls causes injuries and increases the premability so lipoproteins can get in.

17
Q

why is HTN a primary risk factor heart disease

A

realitively unkown but in animal studies it shows that the high pressure against the artierial walls causes injuries and increases the premability so lipoproteins can get in.

18
Q

Hypertension values stage 1 stage 2 stage 3 stage 4

A

stage 1 SBP 140-159 DBP 90-99

stage 2 SBP 160-179 DBP 100-109

stage 3 SBP 180-200 DBP 110-114

stage 4- SBP anything over 200 DBP anything over 115

19
Q

Reasons for HTN

A

Low HDL

inappropiate stimulation of SNS aka red bull or caffine

Displacement of Oxygen from hemoglobin due to carbon monoxide

increase platetlet adhesions.- the blockage causes the blood to work harder to get through the vessel

Endothethial dysfunction due to components of cigarette smoking

20
Q

Why is Diabetes associated with Hypertension

A

It is postulated that that the increased risk is realted to the glycoslyation of lipoproteins in diabetics or to the increased platelet adhesivenss present.

21
Q

minor modifiable CRFS

A

Obesity, sedentary lifestyle, stress

22
Q

Sedentary Lifestyle (don’t know why this slide is called this

How does Exercise help decrease HTN

A

well number one exercise increases HDL counts whi

Can decrease BP in those with HTN
ch can reduce the chance of HTN
Helps to normalize blood gluclose

increased fibrinolysis

decreased platelet aggregability

23
Q

Major NON-modifiable characteristics

A

Age over 65
Genetics Females 65, Males 55
Male gender

24
Q

Obesity

Above what percent is an ideal risk for diabettes

What is this condition typically associated with

A

above 20 percent of the ideal body weight

Practicular central obesity

associated with HTN, DM, and Sedentary lifestyle

25
Q

Stress why is this linked to HTN

A

Cause of the release of platelets and increased levels of catachoalmines (ephinerphine and norepi)

Especially people under going emotional stress

26
Q

Gender

Who is more likely to have an MI

Is CAD the second leading cause of Death in womenn younger than 45

Once a MI occurs women of all age groups have a higher mortality rate compared to men

A

Males

Yes

27
Q

Etiology and Pathophysiology of Angia Pectoris

Whats the most common sign of Ischemic heart disease

A

Angina “strangling in the chest”

28
Q

Unstable Angia what is this and what happens if not treated

A

Pattern of increased frequency of chest pain and duration

may occur at rest

high frequency of progression to MI if untreated

29
Q

What is homocystnemia

A

homocysteine are believed to be linked to dead endothethlial cells and be an increased for CAD

and folic acid and B vitamins can decrease the chances of the these levels

30
Q

stable angia how does this come about and how does it stop what does the EKG look like during these times

A

elevation of the ST segement chronic chest pain usally brought on by exercise, emotional stress, or eating, relieved by rest.

31
Q

Variant Angia what is this and how does it come about and what does the ST segement look like

A

ST - segment brought on by rest but more of a vasospasm in the coronary arteries than increased oxygen demand by the myocardial tissue

32
Q

Major determinants of myocaridal oxygen supply and demmand

A

Myocardial oxygen Supply depends on:

Diastolic preffusion pressure Coronary vasucular resistance: these sources include (external pressure from the pericardial sac, intrinsic regulation, local metabolites, endothelial, neural intervention
Oxygen carrying capacity of the hemoglobin

Demmand: Why it needs more oxygen: Heart rate increases, Contractility increases, Wall tension

33
Q

If the vessel is “stenosed” more than what percent is oxygen supplementation not enough

What may happen in some individuals with these issues

A

90 percent and may develop collateral circulation but, not everyone develops colalteral circulation

34
Q

At what percent of stenosis does the blood vessel need to be vasodialted to fulls potential

A

70 percent

35
Q

What happens in Endothethilal dysfunction

A

The coronary arteries are imparied because the something is blocking the release of the vasodilators

leaves the direct catecholamines effect unoppsed so that realitive vasoconstriction occurs

36
Q

Why does Platelet Aggregation occur???

A

Due to the lack of prostacyin secretion and endothelial relaxing factor

the aggregation of platelets stimulates pro congualates and other vasoconstricters

37
Q

Myocardial infractions describe

A

Condition of irreversible necrosis of the heart muscle that results from prolonged blockage of an artery aka ischemia

38
Q

Other causes of heart issues

A

decreased aortic prefusion pressure, severe decreased in blood oxygen carrying capacity
increased mark in wall stress

39
Q

Syndrome X

A

Typical symptoms of Angina but, no signs of chest pain
Some show evidence of CAD only on ETT

vessels may not dilate properly

40
Q

Transmural vs Subendocaridal MI’s describe each

A

Transmural- span of thickness of the myocardium and result from prolonged occulsion

Subendocardial: exclusively involve in the innermost layers of the myocardium recall that the greatest area for ischemia as wall tension increases since the blood supply has to transcend so many layers

41
Q

Q wave vs non Qwave myocardial infraction in realtion to a EKG who dies faster

A

Q wave MI- widened QRS complex inital hospital mortatlity is higher (T wave first elevates, R elevation, inverts, weeks later normalizes

Non q wave - doesn’t demonstrate signifcant Q waves these patients have to multivessel diease (T wave inversion or ST depression)

42
Q

Can CK-MB be normalized in 48-72 hours

What can be detected in the first 3 hours if an MI is suspected???

What level is the CK-MB above is usally indication that a MI has occured

When does CK levels peak

Lactate Dehydrogenase (LDH)

Serum levels of LDH peak at what time frame important why????

A

Yes and has be caught early on and is a indication of a breakdown of the myocaridal tissue,

Troponin can be expected within the first 3 hours

above 2.5 percent

CK levels peak at 24 hours

LDH peaks about 3-5 days post MI and is important to look for these levels because the Creatine Kinase Myocardial bands probadly already have normalized by then.