Alterations Of Cardiovascular Function I Flashcards

1
Q

A diagnosis of primary hypertension is based on:

A

blood pressure readings.

A diagnosis of primary hypertension is based solely on blood pressure readings, however we generally take repeated (also known as serial) blood pressure readings.

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2
Q

How would a gene mutation leading to increased angiotensin II levels cause hypertension?

A

Vasoconstriction of systemic arteries causes an increase in systemic vascular resistance.

Angiotensin II is an important hormone that is released as part of the angiotensin-aldosterone system. Angiotensin II causes vasoconstriction of the systemic arteries (i.e., all of the main branches off of the aorta) which increases systemic vascular resistance and blood pressure.

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3
Q

Which of the following factors is thought to account for the increased incidence of hypertension and complications from hypertension among African Americans?

A

Gene mutations causing increased sodium retention

African Americans have an increase incidence of gene mutations that cause ‘salt sensitivity’. This mutation results in an increase in sodium reabsorption (i.e., retention) which results in increased water reabsorption. The increase in sodium and water reabsorption causes an increase in blood volume and blood pressure.

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4
Q

What type of changes are seen in the wall of arteries of an individual who has had primary hypertension for several years.

A

Hypertrophy and hyperplasia of smooth muscle causes a permanently constricted artery.

If a person’s hypertension goes untreated, then the smooth muscle in the wall of the arteries undergoes significant remodeling. Sustained vasoconstriction results in hypertrophy and hyperplasia of the smooth muscle, resulting in permanently vasoconstricted arteries.

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5
Q

Risk factors for primary hypertension include:

A

Drinking more than three alcoholic beverages per day
Smoking- Nicotine and other chemicals in tobacco causes vasoconstriction which can lead to hypertension.
Poorly controlled type 2 diabetes mellitus
Obesity- There are hormones released by adipose cells in our fat tissue that cause vasoconstriction. This can lead to hypertension.

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6
Q

Why can uncontrolled or untreated hypertension lead to lower limb amputation?

A

Hypertension can cause atherosclerosis in the arteries to the lower limb.

High blood pressure causes shear stress on the endothelial cells that line the cardiovascular system. This shear stress causes endothelial injury which initiates the process of atherosclerosis. Atherosclerosis in the arteries that vascularize the limbs can lead to ischemia and tissue hypoxia. If not reversed the atherosclerosis can result in necrosis and limb amputation.

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7
Q

Uncontrolled or untreated hypertension can lead to a bulging or dilation of the arteries, a condition that is called a/an:

A

aneurysm

A bulging or dilation of the arteries is called an aneurysm.

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8
Q

Why is LDL considered ‘bad’ cholesterol?

A

High LDL levels leads to the development of atherosclerosis.

When levels of LDL are elevated in the bloodstream, they can deposit in the wall of the arteries which leads to atherosclerosis.

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9
Q

A diagnosis of dyslipidemia includes high LDL and HDL levels in the blood.

A

False

A diagnosis of dyslipidemia is defined as elevated LDLs and low HDLs, as well as elevated triglycerides and total cholesterol. HDLs are consider to be ‘good’ cholesterol because they help removed cholesterol from plaques and prevent blood clotting.

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10
Q

What are the risk factors for the development of dyslipidemia?

A

Consuming trans fats in margarine and other processed foods- Transfats are found in many margarines and commercial baked goods. If consumed in high quantities they can lead to dyslipidemia.

Type 2 diabetes mellitus- Insulin resistance in type 2 diabetes mellitus leads to altered lipid metabolism resulting in dyslipidemia.

Obesity- For dietary and genetic reasons, obesity can lead to the development of dyslipidemia

Older age
Genetic predesposition
Lack of exercise

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11
Q

The fatty streak in the wall of an artery that has developed atherosclerosis is formed by:

A

phagocytosis and oxidation of LDL by macrophages.

The fatty streak forms after LDL has migrated beneath the endothelial lining and is then phagocytosed and oxidized by macrophages. The accumulation of these oxidized lipids is what forms the fatty streak, which is precursor to the atherosclerotic plaque.

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12
Q

Which lab test is the best indicator of the presence of atherosclerosis in any artery?

A

C reactive protein (CRP)

C reactive protein (CRP) is a protein released by the liver during inflammatory responses. Even small inflammatory responses will cause a rise in CRP. Since the process of atherosclerosis involves inflammation (macrophages phagocytosing LDL), CRP levels will rise, even in the early stages.

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13
Q

The process of atherosclerosis is caused by which two conditions?

A

Dyslipidemia and endothelial injury

The process of atherosclerosis starts with endothelia injury, often from smoking and/or hypertension and/or long term, uncontrolled diabetes mellitus. The endothelial injury causes an inflammatory response where macrophages eventually migrate into the wall (i.e., the tunica media) of the artery. If this individual also has dyslipidemia with elevated LDLs, the LDLs adhere to the injured endothelial cells, then are transported int the area where the macrophages are. The LDLs are phagocyosed by the macrophages and as the oxidized lipids accumulate, they develop into the fatty streak.

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14
Q

In general, coronary artery disease (CAD) leads to:

A

myocardial ischemia.

Coronary artery disease (also known as coronary atherosclerosis) causes myocardial ischemia (decrease blood flow to the myocardium).

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15
Q

Which problem is most likely to cause a deterioration in cardiac function in individuals with coronary artery disease?

A

Low plasma hemoglobin (anemia)

Coronary artery disease results in myocardial ischemia. Anemia would result in a further decrease in oxygen delivery to the ventricles, which would cause a deterioration in cardiac function (i.e., ventricular contractility).

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16
Q

Unstable angina is a sign of:

A

impending myocardial infarction

Unstable angina, manifested by worsening episodes of chest pain, is a sign that a person’s coronary artery disease and myocardial ischemia is getting worse. This could be because the plaque is causing a more severe obstruction of the coronary arteries, or that the plaque is becoming unstable. This level of angina is associated with a greater chance that a myocardial infarction will occur.

17
Q

What is the most common cause of myocardial infarction?

A

Thrombus formation within the atherosclerotic coronary artery

The rough surface of the plaque promotes clotting and the clot can quickly instruct the entire coronary artery. The good news is that blood flow to the heart can often be restored using thrombolytic medications (generally enzymes that dissolve fibrin).

18
Q

Following a period of severe myocardial hypoxia, the reperfusion of that tissue can result in further tissue damage. What is the cause of that damage?

A

The formation of free radicals when oxygen is reintroduced.

These free radicals can cause additional damage to the infected tissue and even the tissue surrounding the infarction.

19
Q

Why is an elevated blood troponin I level an indication that a patient has had an acute myocardial infarction?

A

Hypoxic injury and cell death causes the release of intracellular troponin molecules from the myocardium

20
Q

When the sympathetic nervous system is activated, what is the physiological effect on the alpha-1 adrenergic receptors?

A

Vasoconstriction of systemic arteries

21
Q

When the renin-angiotensin-aldosterone system is activated, what is the physiological effect on the cardiovascular system?

A

Arterial vasoconstction leads in increased blood pressure.

22
Q

Which mechanism is an important underlying cause of primary hypertension?

A

Increased angiotensin II levels.

23
Q

Why is hypertension important to diagnose and treat?

A

High arterial pressures can lead to aneurysms
Left ventricular failure
Chronic renal failure
Ocular changes

24
Q

Which combination of laboratory results are consistent with a diagnosis of dyslipidemia?

A

Elevated LDL and Low HDL

25
Q

How are LDLs involved in the development of atherosclerosis?

A

LDLs migrate below the endothelium and contribute to the development of the fatty streak.

26
Q

What are the consequences of calcified plaque formation in atherosclerosis?

A

Atrophy of vascular smooth muscle cells.

27
Q

What is the clinical manifestation that describes ‘stable angina pectoris’?

A

Pain or tightness in the chest.

28
Q

What is atherosclerosis?

A

Chronic disease of the arteries characterized by abdominal thickening and hardening of the vessel wall.

29
Q

What are the clinical consequences of atherosclerosis?

A

Coronary artery disease
Peripheral artery (vascular) disease
Ischemic bowel disease/ mesenteric vascular insufficiency
Cerebral ischemia/stroke

30
Q

What is myocardial ischemia?

A

Partial blockage of 1 or more branches of the left/right coronary artery

31
Q

What are the causes of myocardial ischemia?

A

Coronary atherosclerosis (coronary artery disease) causes the vast majority of cases
Vasospasm of coronary artery
Myocardial hypoxia
Hypoxemia
Anemia
Increased myocardial demand/workload (increased heart rate and/or cardiac output)

32
Q

What are the clinical consequences of myocardial ischemia?

A

Decreased ventricular pumping (contractility)
Cardiac conduction disturbances
Ischemic chest pain- (due to the lack of oxygen)
-Stable angina pectoris- chest pain that last for a few minutes and is relieved by rest
-unstable angina pectoris- chest pain lasting 15-20 minutes not relieved by rest

33
Q

What is myocardial infraction?

A

Severe reduction of coronary artery blood flow leading to myocardial cell death

34
Q

What is the main cause of myocardial infarction?

A

Coronary atherosclerosis (coronary artery disease)

35
Q

Why does an infraction of an atherosclerotic coronary artery occurs?

A

Thrombus (blood clot) forms on the rough surface of the plaque.
Hypoxic injury- seen within 10 seconds of myocardial infarction (causing decreased ATP production & lactic acid formation)
-after 20 minutes see myocardial cell death
Reperfusion injury- causes formation of free radicals.
Repair and resolution- coagulative necrosis develops at site of infraction

36
Q

What are the clinical consequences of myocardial infarction?

A

Decreased ventricular contractility leading to heart failure
Cardiac conduction disturbances in SA/AV node leading to dysrhythmias
Ischemic chest pain
Sudden death

37
Q

What are the clinical manifestations for myocardial infarction?

A

Chest pain- pain may radiate to left jaw, neck, shoulder or arm.
Dyspnea, tachypnea, and/or increased work of breathing
Nausea and vomiting
Diaphoresis, pale/gray/cyanotic, cool and clammy skin
Loss of consciousness