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96 Cards in this Set

  • Front
  • Back
Serious MIs usually result from a plug in the _______________.
The L anterior descending artery
The _____ coronary artery profuses the RV & RA
Right Coronary Artery
L and R coronary arteries arise from the:
root of the aorta
Venous blood returns via the:
coronary sinus
The coronary sinus drains into the:
Right atrium
Each coronary artery branches into major vessels, including the ___________ and __________.
Septal and marginal
The circumflex is going to be profusing the ________ and the _______
The walls of the of LA and LV
the R coronary artery profuses the:
Posterior IVA and the Marginal Artery
the IVA profuses the:
ventricular walls
The marginal artery sends blood to the:
walls of the RA and the RV
The L Coronary Artery sends blood to the:
Circumflex artery and the anterior interventricular artery
the Circumflex artery sends blood to the:
walls of the LA and LV
the AIV artery sends blood to the:
ventricular walls
Ventricular walls receive blood from the:
Posterior Interventricular Artery and the Anterior Interventricular Artery
The ____________ are the smallest cardiac veins that pass through the endocardium and drain blood into the heart chambers.
Thebesian veins
Which heart chamber has the most thebesian veins?
The RA
What do the thebesian veins allow?
They allow blood to percolate directly from the arterial side to the chamber without getting recycled and without going through venous circulation.
Blood flow in the LV is dependent on what?
the heart being in diastole due to the compression on the subendocardial arteries
This is the area most prone to MI. Why is this the case?
LV because of blood flow compromise/lack of diastole; during systole the vessels shut
the Coronary arteries have 2 types of receptors. What are they?
What is the effect of α-Adrenergic stimulation
β-adrenergic stimulation
generally, sympathetic stimulation of the coronary arterioles leads to:
when the systemic BP falls, reflex increases in sympathetic tone. This results in the __________ that is due to locally released mediators.
Aortic stenosis results in ________________________ to eject blood.
increased ventricular pressure and increased work
aortic stenosis causes the valve to have a _________________ and an incompletely closed valve which leads to _____________.
decreased diameter; regurgitation
Aortic stenosis increases the likelihood of what?
Myocardial ischemia
The heart takes ___________% of the oxygen in the blood supplied to it
To increase consumption you need ________________.
increased blood flow
What is angina pectoris?
pain arising from insufficient perfusion/oxygenation in the myocardium; it usually occurs during exertion
When does angina pectoris usually present?
During exertion
Symptoms of angina pectors include:
pain going down the arm
Diaphoresis (sweating)
When does CAD lead to other conditions with significant morbidity and mortality?
When the person goes from CAD --> MI
CAD is largely a _________ disease.
Risk factors/lifestyle choices for the primary cause of atherosclerosis:
type 2 DM
hypcholesterolemia (not always, though, because some people have a genetic predisposition)
Primary risk factors for CAD
family history of atherosclerosis
What does the 'congenital' cause of CAD entail?
people that have tortuous arteries due to natural variation have a higher incidence of turbulent blood flow that contributes to atheroma formation and clots
What is the most common problem that can lead to CAD?
Where are plaques most likely to form?
areas of high shear stress/locations of turbulent blood flow/bifurcation points
What is the primary goal for treating atheromas?
Reduce the risk factors (obestity, HTN, smoking, etc) so that the lesions may resolve on their own
When are surgical interventions considered for atheroma formation?
They're considered when the lesions compromise the blood flow
What types of surgical interventions are commonly offered to deal with atheroma formation?
Coronary bypass surgery

stent placement (interventional radiology)
Define Myocardial Infarction
interruption of the blood supply to a part of the heart; this leads to myocardial cell death.
What are the major causes of MI?
arrhythmias (major cause)


Diabetes (most for the CAD associated with it)

Idiopathic hypertrophic subaortic stenosis
Why is IHSS a risk factor for MI?
the heart has to beat more vigorously so there is less diastole = less perfusion of the heart muscles and the blood flow is more turbulent. This leads to an increased risk for microemboli formation.
Define transmural MI
infarct through the entire muscle wall. Typically seen in atherosclerosis of the major coronary blood vessels
Define subendocardial MI
infarction involves a small area of the subendocardium of the LV, ventricle septa or the papillary muscles. This is a more focal kind of necrosis.
Why is the subendocardium of the LV, ventricle septa, and the papillary muscles more susceptible to damage?
because they are areas at the end of the blood supply path.
Classic symptoms of MI
Men-chest pain down the L arm
women--feeling of indigestion
nausea & vomiting
Symptoms of silent MI
general feeling of malaise
What does lipid handling refer to?
how lipids are handled in the blood
based off of dietary lipid; generated in the intestinal tract so when cholesterol is absorbed from the diet the lipid is packaged and sent out into the blood stream. Can come from the portal system.

Major source of lipid in skeletal muscle cells.
Hepatocytes release VLDL. VLDL is a source of:
source of cholesterol for other cells
Cells need to have _____________ in order to effectively utilize VLDL
protein lipase
VLDLs --> _________ --> ________
VLDL --> IDL --> LDL
_______ is the good cholesterol
_______ is the bad cholesterol
chylomicrons are formed from:
dietary lipids
Where are chylomicrons metabolized?
capillary luminal side of tissues. This is where lipoprotein lipase is found.
What are chylomicrons removed by?
__________ converts VLDLs to IDL and then LDL
lipoprotein lipase
Put these in order of descending size:
chylomicron > VLDL > IDL > LDL > HDL
What does the skeletal muscle do in terms of lipid handling?
SM extracts the lipid, but the hepatocytes pull the lipid remnants out of circulation to break down the particle so that it can be utilized
What is LCAT?
lecithin cholesteroyl acyl transferase

it's the enzyme that packages cholesterol into HDL
What is LCAT's relationship to a good lipid profile?
increased HDL and LCAT = increased goodness of lipid profile
What is HDL?
HDL is the vehicle for removing cholesterol from the periphery and bringing it back to the liver
Enzymes that produce free radicals:
* xanthine dismutase
* NADPH oxidase
* Monoamine oxidase
* glucose oxidase
* P450 enzymes
Enzymes that reduce free radicals:
* glutathione peroxidase
* catalase
* super oxide dismutase
What does LDL bind to?
Platelet derived growth factor receptor
What does binding to the PDGF trigger?
proliferation, ECM synthesis, CT deposition
What is the relationship btw homocysteine and coronary heart disease?
positive association of elevated serum levels and risk for coronary heart disease, though the mechanism is not known.
What is the agent of reperfusion injuries?
xanthine dehydrogenase --> XANTHINE OXIDASE; it can produce ROS that can reactivate the cascade and re-occlude the previously blocked vessel.
Myocardial Infarctions are largely due to _______________
coronary artery blockage
what is HTN?
a syndrome representing that most common CV disease;

sustained resting adult blood pressure of more than 140/90 mmHg
Who is at risk for complications with HTN?
Those with a BP of more than 120/80 have an increased risk
What is the problem with HTN?
It's what the increased pressures do to the system and the blood compartment because it can lead to a blow out.
What is a normal BP?
less than 120/less than 80
What is pre-HTN?
What is HTN stage 1?
What is HTN stage 2?
What is isolated systolic HTN?
age = 60+
S is elevated but D is not.

140-160/less than 90
What is a HTN crisis?
_________ is predictive of CV risk
systolic pressure
Why does Systolic pressure increase more proportionally?
due to atherosclerotic stiffening of the vessels

systolic is proportional to compliance
What are the main direct causes of HTN?
increased vascular resistance
increased cardiac output
increased blood volume
increased blood viscosity
Which direct cause of HTN is least likely?
Increase in blood viscosity--cannot change much and it takes a large change to impact blood pressure.
How does HTN normally start?
with an increase in CO with normal total peripheral resistance.

Over time, CO normalizes but TPR increases.
What do the HTN hypotheses have in common?
changes in Na+ handling
What is an aortic coarctation?
a congenital narrow of the aorta that is generally below the subclavian artery
what does an aortic coarctation result in?
increased vascular resistance (afterload)

higher BP above the coarctation, lower below

increased renin secretion due to low BP in the kidneys
What is unique about an aortic coarctation?
It's congenital and can be surgically treated.
What is Liddle's syndrome?
Na+ retention = expanded EC water volume = HTN without an increase in mineralocorticoid secretion
What causes Liddle's Syndrome?
constitutive opening of the amiloride-sensitive epithelial sodium channels.
How is Liddle's different?
You see LESS secretion, not more because a lot of the channels are open.

Aldosterone will also probably be low.
What gene leads to aldosterone aldosterone expression
17, 21 Hydroxylase --> _________
glucocorticoids (cortisol, deoxycortisol)