Handout Packet Ischemic and Valvular Heart Diseases Flashcards
Media what layer is this and is it the thickest
Thickest layer of artery made of smooth muscle in a matrix of collagen, elastin, and proteoglycans
middle layer right after the internal elastic lamina
Atheroscleroiss what is this
The inner layer of the artery becomes ardended because of fatty deposis and fibrous tissueand and frequentyl involves the coronary and cerebral areteries
Adventitia whatr layer is this and what is it made of and whats another name for it
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
Tunica intima what layer is this and what does it house and what is it made of????
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
things disrupt the intergrity of the artery and make it hard
fatty streak, fiborous plaque, complicated lesions
Fatty streak.. is it earliest visible lesion does it pertrude into the lamina??? what else are they called??
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
Where do most artery changes occur where are foam cells derived from and what do they contain
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?
fibrous plaque - is it this more serious than the foam cells or the fatty streak if so why??
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
how does a hemmorrhage come about within a firbrous plaque and what does this cause
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
What is the role of the Endothethial wall and what antitrhombotic surface molecules play a role in the maintainece of the anit-clotting police
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
Two types of lesions tell me each type
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
Modified Respones to injury of Hypothesis
What intially causes the secrement of smooth muscle cells
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
Dyslipidemias what is this about
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.
Dyslipidemias what is this about
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.
injury to the endothethial cells what happens when the endo layer is injuried couple of things
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.
injury to the endothethial cells what happens when the endo layer is injuried couple of things
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.
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
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
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
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
Realitive risk for Smokers to get heart disease is ???
- 35 - 2.5 in studies of all smokers
1. 43 - 3.5 in heavy smokers
Realitive risk for Smokers to get heart disease is ???
- 35 - 2.5 in studies of all smokers
1. 43 - 3.5 in heavy smokers
why is HTN a primary risk factor heart disease
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.
why is HTN a primary risk factor heart disease
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.
Hypertension values stage 1 stage 2 stage 3 stage 4
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
Reasons for HTN
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
Why is Diabetes associated with Hypertension
It is postulated that that the increased risk is realted to the glycoslyation of lipoproteins in diabetics or to the increased platelet adhesivenss present.
minor modifiable CRFS
Obesity, sedentary lifestyle, stress
Sedentary Lifestyle (don’t know why this slide is called this
How does Exercise help decrease HTN
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
Major NON-modifiable characteristics
Age over 65
Genetics Females 65, Males 55
Male gender
Obesity
Above what percent is an ideal risk for diabettes
What is this condition typically associated with
above 20 percent of the ideal body weight
Practicular central obesity
associated with HTN, DM, and Sedentary lifestyle
Stress why is this linked to HTN
Cause of the release of platelets and increased levels of catachoalmines (ephinerphine and norepi)
Especially people under going emotional stress
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
Males
Yes
Etiology and Pathophysiology of Angia Pectoris
Whats the most common sign of Ischemic heart disease
Angina “strangling in the chest”
Unstable Angia what is this and what happens if not treated
Pattern of increased frequency of chest pain and duration
may occur at rest
high frequency of progression to MI if untreated
What is homocystnemia
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
stable angia how does this come about and how does it stop what does the EKG look like during these times
elevation of the ST segement chronic chest pain usally brought on by exercise, emotional stress, or eating, relieved by rest.
Variant Angia what is this and how does it come about and what does the ST segement look like
ST - segment brought on by rest but more of a vasospasm in the coronary arteries than increased oxygen demand by the myocardial tissue
Major determinants of myocaridal oxygen supply and demmand
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
If the vessel is “stenosed” more than what percent is oxygen supplementation not enough
What may happen in some individuals with these issues
90 percent and may develop collateral circulation but, not everyone develops colalteral circulation
At what percent of stenosis does the blood vessel need to be vasodialted to fulls potential
70 percent
What happens in Endothethilal dysfunction
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
Why does Platelet Aggregation occur???
Due to the lack of prostacyin secretion and endothelial relaxing factor
the aggregation of platelets stimulates pro congualates and other vasoconstricters
Myocardial infractions describe
Condition of irreversible necrosis of the heart muscle that results from prolonged blockage of an artery aka ischemia
Other causes of heart issues
decreased aortic prefusion pressure, severe decreased in blood oxygen carrying capacity
increased mark in wall stress
Syndrome X
Typical symptoms of Angina but, no signs of chest pain
Some show evidence of CAD only on ETT
vessels may not dilate properly
Transmural vs Subendocaridal MI’s describe each
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
Q wave vs non Qwave myocardial infraction in realtion to a EKG who dies faster
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)
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????
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.
