Chs 18, 19, 20 (Cardio) Flashcards

1
Q

Where in the body is lipoprotein synthesized? (Mark all that apply.)

a. The small intestine
b. The large intestine
c. The pancreas
d. The liver

A

a (small intestine), d (liver)
There are two sites of lipoprotein synthesis: the small intestine and the liver. The chylomicrons, which are the largest of the lipoprotein molecules, are synthesized in the wall of the small intestine. The liver synthesizes and releases VLDL and HDL. The large intestine and the pancreas play no part in synthesizing lipoprotein.

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2
Q

Where in the body is lipoprotein synthesized? (Mark all that apply.)

a. The small intestine
b. The large intestine
c. The pancreas
d. The liver

A

a. (small intestine), d (liver)
There are two sites of lipoprotein synthesis: the small intestine and the liver. The chylomicrons, which are the largest of the lipoprotein molecules, are synthesized in the wall of the small intestine. The liver synthesizes and releases VLDL and HDL. The large intestine and the pancreas play no part in synthesizing lipoprotein.

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3
Q

A 35-year-old man presents to the emergency department complaining of chest pain for the last 2 hours. He describes the pain as crushing, like a huge weight is on his chest. He also states that the pain goes up into his neck and down his left arm. An acute myocardial infarction (MI) is diagnosed. When taking his history, the following things are noted:

  • Hyperlipoproteinemia for the past 7 years
  • Family history of early MI
  • Cholesterol deposits along the tendons (diagnosed 1 year ago)
  • Atherosclerosis (diagnosed 6 months ago)
  • Diabetes mellitus (type 1) diagnosed at age 16

The nurse suspects which of the following diagnoses will be made?

a. Familial hypercholesterolemia (type 2A)
b. Homozygotic cutaneous xanthoma
c. Adult-onset hypercholesterolemia (type 1A)
d. Secondary hyperlipoproteinemia

A

a. (familial hypercholesterolemia - type 2A)
Many types of primary hypercholesterolemia have a genetic basis. There may be a defective synthesis of the apoproteins, a lack of receptors, defective receptors, or defects in the handling of cholesterol in the cell that are genetically determined. For example, the LDL receptor is deficient or defective in the genetic disorder known as familial hypercholesterolemia (type 2A). This autosomal dominant type of hyperlipoproteinemia results from a mutation in the gene specifying the receptor for LDL. Although heterozygotes commonly have an elevated cholesterol level from birth, they do not develop symptoms until adult life, when they often develop xanthomas (i.e., cholesterol deposits) along the tendons and atherosclerosis appears. Myocardial infarction before 40 years of age is common. Homozygotes are much more severely affected; they have cutaneous xanthomas in childhood and may experience myocardial infarction by as early as 1-2 years of age. Homozygotic cutaneous xanthoma and adult-onset hypercholesterolemia (type 1A) are not known diseases. Causes of secondary hyperlipoproteinemia include obesity with high-calorie intake and diabetes mellitus. It does not have a genetic basis.

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4
Q

Atherosclerosis begins in an insidious manner with symptoms becoming apparent as long as 20 to 40 years after the onset of the disease. Although an exact etiology of the disease has not been identified, epidemiologic studies have shown that there are predisposing risk factors to this disease. What is the major risk factor for developing atherosclerosis?

a. Male sex
b. Hypercholesterolemia
c. Familial history of premature coronary heart disease
d. Increasing age

A

b. hypercholesterolemia
The cause or causes of atherosclerosis have not been determined with certainty. However, epidemiologic studies have identified predisposing risk factors, which include a major risk factor of hypercholesterolemia. Other risk factors include increasing age, family history of premature coronary heart disease, and male sex.

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5
Q

A group of vascular disorders called vaculitides cause inflammatory injury and necrosis of the blood vessel wall (i.e., vaculitis). These disorders are common pathways for tissue and organ involvement in many different disease conditions. What is the most common of the vasculitides?

a. Polyarteritis nodosa
b. Raynaud disease
c. Temporal arteritis
d. Varicose veins

A
c. temporal arteritis
Temporal arteritis (i.e. giant cell arteritis), the most common of the vasculitides, is a focal inflammatory condition of medium-sized and large arteries. It predominantly affects branches of arteries originating from the aortic arch, including the superficial temporal, vertebral, ophthalmic, and posterior ciliary arteries.  Neither Polyarteritis Nodosa nor Raynaud disease are the most common of the vasculitides. Varicose veins are not vasculitides.
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6
Q

Although the etiology of essential hypertension is mainly unknown, several risk factors have been identified. These risk factors fall under the categories of constitutional risk factors and lifestyle factors. What are the primary risk factors for hypertension? (Select all that apply.)

a. Race and excessive sodium chloride intake
b. Type 2 diabetes and obesity
c. Age and high intake of potassium
d. Race and smoking
e. Family history and excessive alcohol consumption

A

a, b, e

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7
Q

A 37-year-old woman is admitted to your unit with a differential diagnosis to rule out pheochromocytoma. What are the most common symptoms you would this patient to exhibit?

a. Nervousness and periodic severe headache
b. Variability in blood pressure and weight loss
c. Excessive sweating and pallor
d. Periodic severe headache and marked variability in blood pressure

A

d Periodic severe headache and marked variability in blood pressure

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8
Q

The extended, severe exposure of the walls of the blood vessels to the exaggerated pressures that occur in malignant hypertension cause injuries to the walls of the arterioles. Blood vessels in the renal system are particularly vulnerable to this type of drainage. Because hypertension is a chronic disease and is associated with autoregulatory changes in the blood flow to major organs, what would be the initial treatment goal for malignant hypertension?

a. Partial reduction in blood pressure to less critical values
b. Reduction to normotensive levels of blood pressure
c. Rapid decrease in blood pressure to less critical levels
d. Slow, gradual decrease in blood pressure to normotensive blood pressures

A

a Partial reduction in blood pressure to less critical values

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9
Q

A 56-year-old woman presents at the clinic complaining of the unsightliness of her varicose veins and wants to know what can be done about them. The nurse explains that the treatment for varicose veins includes which of the following interventions?

a. Surgical or fibrotherapy
b. Sclerotherapy or surgery
c. Trendelenburg therapy or sclerotherapy
d. Surgery or Trendelenburg therapy

A

b. Sclerotherapy or surgery
Sclerotherapy, which often is used in the treatment of small residual varicosities, involves the injection of a sclerosing agent into the collapsed superficial veins to produce fibrosis of the vessel lumen. Surgical treatment consists of removing the varicosities and the incompetent perforating veins, but it is limited to persons with patent deep venous channels. Sclerotherapy produces fibrosis of the vessel lumen. There is no fibrotherapy for varicose veins. There is no Trendelenburg therapy for varicose veins. There is a Trendelenburg test that is diagnostic for primary or secondary varicose veins.

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10
Q

Pregnancy-induced hypertension is a serious condition affecting between 5% and 10% of pregnant women. The most serious classification of hypertension in pregnancy is preeclampsia-eclampsia. It is a pregnancy-specific syndrome that can have both maternal and fetal manifestations. What is a life-threatening manifestation of the preeclampsia-eclampsia classification of pregnancy-induced hypertension?

a. Hepatocellular necrosis
b. Thrombocytopenia
c. HELLP syndrome
d. Decreased renal filtration rate

A

c HELLP syndrome

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11
Q

Although the etiology of essential hypertension is mainly unknown, several risk factors have been identified. These risk factors fall under the categories of constitutional risk factors and lifestyle factors. What are the primary risk factors for hypertension? (Select all that apply.)

a. Race and excessive sodium chloride intake
b. Type 2 diabetes and obesity
c. Age and high intake of potassium
d. Race and smoking
e. Family history and excessive alcohol consumption

A

a, b, e
The constitutional risk factors include a family history of hypertension, race, and age-related increases in blood pressure. Another factor that is thought to contribute to hypertension is insulin resistance and the resultant hyperinsulinemia that occurs in metabolic abnormalities such as type 2 diabetes. Lifestyle factors can contribute to the development of hypertension by interacting with other risk factors. These lifestyle factors include high salt intake, excessive calorie intake and obesity, excessive alcohol consumption, and low intake of potassium. Although stress can raise blood pressure acutely, there is less evidence linking it to chronic elevations in blood pressure. Smoking and a diet high in saturated fats and cholesterol, although not identified as primary risk factors for hypertension, are independent risk factors for coronary heart disease and should be avoided.

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12
Q

A 37-year-old woman is admitted to your unit with a differential diagnosis to rule out pheochromocytoma. What are the most common symptoms you would this patient to exhibit?

a. Nervousness and periodic severe headache
b. Variability in blood pressure and weight loss
c. Excessive sweating and pallor
d. Periodic severe headache and marked variability in blood pressure

A

d. Periodic severe headache and marked variability in blood pressure
Like adrenal medullary cells, the tumor cells of a pheochromocytoma produce and secret the catecholamines epinephrine and norepinephrine. The hypertension that develops is a result of the massive release of these catecholamines. Their release may be paroxysmal rather than continuous, causing periodic episodes of headache, excessive sweating, and palpitations. Headache is the most common symptom and can be quite severe. Nervousness, tremor, facial pallor, weakness, fatigue, and weight loss occur less frequently. Marked variability in blood pressure between episodes is typical.

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13
Q

The extended, severe exposure of the walls of the blood vessels to the exaggerated pressures that occur in malignant hypertension cause injuries to the walls of the arterioles. Blood vessels in the renal system are particularly vulnerable to this type of drainage. Because hypertension is a chronic disease and is associated with autoregulatory changes in the blood flow to major organs, what would be the initial treatment goal for malignant hypertension?

a. Partial reduction in blood pressure to less critical values
b. Reduction to normotensive levels of blood pressure
c. Rapid decrease in blood pressure to less critical levels
d. Slow, gradual decrease in blood pressure to normotensive blood pressures

A

a. Partial reduction in blood pressure to less critical values
Because chronic hypertension is associated with autoregulatory changes in coronary artery, cerebral artery, and kidney blood flow, care should be taken to avoid excessively rapid decreases in blood pressure, which can lead to hypoperfusion and ischemic injury. Therefore, the goal of initial treatment measures should be to obtain a partial reduction in blood pressure to a safer, less critical level, rather than a normotensive levels.

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14
Q

A client with malignant hypertension is at risk for hypertensive crisis, including the cerebral vascular system often causing cerebral edema. As the nurse caring for this patient, what are the signs and symptoms you would assess for?

a. Papilledema and lethargy
b. Headache and confusion
c. Restlessness and nervousness
d. Stupor and hyperreflexia

A

b. Headache and confusion
Cerebral vasoconstriction probably is an exaggerated homeostatic response designed to protect the brain from excesses of blood pressure and flow. The regulatory mechanisms often are insufficient to protect the capillaries, and cerebral edema frequently develops. As it advances, papilledema (i.e., swelling of the optic nerve at its point of entrance into the eye) ensues, giving evidence of the effects of pressure on the optic nerve and retinal vessels. The patient may have headache, restlessness, confusion, stupor, motor and sensory deficits, and visual disturbances. In severe cases, convulsions and coma follow. Lethargy, nervousness, and hyperreflexia are not signs or symptoms of cerebral edema in malignant hypertension.

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15
Q

Pregnancy-induced hypertension is a serious condition affecting between 5% and 10% of pregnant women. The most serious classification of hypertension in pregnancy is preeclampsia-eclampsia. It is a pregnancy-specific syndrome that can have both maternal and fetal manifestations. What is a life-threatening manifestation of the preeclampsia-eclampsia classification of pregnancy-induced hypertension?

a. Hepatocellular necrosis
b. Thrombocytopenia
c. HELLP syndrome
d. Decreased renal filtration rate

A

c. HELLP syndrome
Liver damage, when it occurs, may range from mild hepatocellular necrosis with elevation of liver enzymes to the more ominous hemolysis, elevated liver function tests, and low platelet count (HELLP) syndrome that is associated with significant maternal mortality.

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16
Q

In infants and children, secondary hypertension is the most common form of hypertension. What is the most common cause of hypertension in an infant?

a. Cerebral vascular bleed
b. Coarctation of the aorta
c. Pheochromocytoma
d. Renal artery thrombosis

A

d. Renal artery thrombosis
Hypertension in infants is associated most commonly with high umbilical catheterization and renal artery obstruction casued by thrombosis. Cerebral vascular bleeds, coarctation of the aorta, and the pheochromocytoma all can raise blood pressure; they are not the most common cause of hypertension in an infant.

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17
Q

Hypertension in the elderly is a common finding. This is because of the age-related rise in systolic blood pressure. Among the aging processes, what is a contributor to hypertension?

a. Baroreceptor sensitivity
b. Aortic softening
c. Decreased peripheral vascular resistance
d. Increased renal blood flow

A

a. Baroreceptor sensitivity
Among the aging processes that contribute to an increase in blood pressure are a stiffening of the large arteries, particularly the aorta; decreased baroreceptor sensitivity; increased peripheral vascular resistance; and decreased renal blood flow.

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18
Q

A 75-year-old man presents at the clinic for a routine physical check-up. He is found to be hypertensive. While taking his blood pressure in the sitting, standing, lying positions, the nurse notes that the brachial artery is pulseless at a high cuff pressure, but she can still feel it. What condition would the nurse suspect?

a. Essential hypertension
b. Pseudohypertension
c. Orthostatic hypertension
d. Secondary hypertension

A

b. Pseudohypertension
Pseudohypertension should be suspected in older persons with hypertension in whom radial or brachial artery remains palpaple but pulseless at higher cuff pressures. The presenting parameters of the patient are not compatible with essential, orthostatic, or secondary hypertension.

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19
Q

The rennin-angiotensin-aldosterone system is a negative feedback system that plays a central role in blood pressure regulation. How does that end result of this feedback loop regulate blood pressure in the body?

a. Vasodilates blood vessels to decrease blood pressure
b. Vasoconstricts blood vessels to increase blood pressure
c. Increases salt and water retention by the kidney
d. Decreases salt and water retention by the kidney

A

c. Increases salt and water retention by the kidney
The renin-angiotensin-aldosterone system plays a central role in blood pressure regulation. Angiotension II has two major functions in the rennin-angiotensin-aldosterone system and acts as both a short- and long-term regulation of blood pressure. It is a strong vasoconstrictor, especially the arterioles regulating blood pressure in the short term. However, its second major action, the stimulation of aldosterone secretion from the adrenal gland, is the end of the rennin-angiotensin-aldosterone loop. The aldosterone that is secreted notifies the kidneys to stop production of renin (the negative feedback in the loop) and contributes to the long-term regulation of blood pressure by increasing salt and water retention by the kidney.

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20
Q

Nearly everyone with paricarditis has chest pain. With acute pericarditis the pain is abrupt in onset, sharp, and radiates to the neck, back, abdomen, or sides. What can be done to ease the pain of acute pericarditis?

a. Have patient sit up and lean forward
b. Have patient change positions to unaffected side
c. Have patient breathe slowly
d. Have patient swallow slowly and frequently

A

a. Have patient sit up and lean forward
The pain typically is worse with deep breathing, coughing, swallowing, and positional changes because of changes in venous return and cardiac filling. All other answers make the pain worse.

21
Q

Cardiac tamponade is a serious life-threatening condition that can arise from a number of other conditions. What is a key diagnostic finding in cardiac tamponade?

a. Increase in stroke volume
b. Pulsus paradoxus
c. Narrowed pulse pressure
d. Rise in systolic blood pressure

A

b. Pulsus paradoxus
A key diagnostic finding is pulsus paradoxus or an exaggeration of the normal variation in the systemic arterial pulse volume with respiration. None of the other answers occur in cardiac tamponade.

22
Q

The scar tissue that occurs between the layers of the pericardium becomes rigid and constrictive from scar tissue in constrictive pericarditis. What is a physiologic sign of constrictive pericarditis?

a. Kussmaul breathing
b. Pulsus peradoxus
c. Kussmaul sign
d. Widening pulse pressure

A

c. Kussmaul sign
Kussmaul sign is an inspiratory distension of the jugular veins caused by the inability of the right atrium, encased in its rigid pericardium, to accomodate the increase in venous return that occurs with inspiration. None of the other physiologic signs occur in constrictive pericarditis.

23
Q

Unstable plaque, a condition of atherosclerotic heart disease, occurs in unstable angina and myocardial infarction. Unstable plaque can rupture, causing platelet aggregation and thrombus formation. What are the major determinants of the vulnerability of plaque to rupture? (Mark all that apply.)

a. Size of lipid-rich core
b. Preponderance of smooth muscle cells
c. Presence of inflammation
d. Decrease in blood pressure and coronary blood flow
e. Thickness of fibrous cap

A

a, c, e - Size of lipid-rich core, presence of inflammation, thickness of fibrous cap
The major determinants of plaque vulnerability to disruption include the size of the lipid-rich core, the stability and thickness of its fibrous cap, the presence of inflammation, and lack of smooth muscle cells. A decrease in blood pressure and coronary blood flow are not determinants of plaque vulnerability to rupture.

24
Q

A patient with a suspected MI is brought to the emergency department by ambulance. As the nurse caring for this patient, what laboratory work would you expect to receive an order for, to confirm a diagnosis of MI?

a. Creatine kinase marker
b. Complete blood components
c. Calcium level
d. Troponin level

A

d. Troponin level
The troponin assays have high specificity for myocardial tissue and have become the primary biomarker for the diagnosis of myocardial infarction (MI). The troponin complex, which is part of the actin filament, consists of three subunits (i.e., TnC, TnT, and TnI) that regulate calcium-mediated actin-myosin contractile process in striated muscle (see Chapter 1, Fig. 1-19). TnI and TnT, which are present in cardiac muscle, begin to rise within 3 hours after the onset of MI and may remain elevated for 7 to 10 days after the event. This is especially adventitious in the late diagnosis of MI. The other blood work may be ordered, but not to confirm the diagnosis of MI.

25
Q

Unstable angina (UA)/non-ST-segment elevation myocardial infarction (NSTEMI) is a clinical syndrome that ranges in severity between stable angina to MI. It is classified according to its risk of causing an acute MI and is diagnosed based on what? (Mark all that apply.)

a. Severity of pain and abruptness of onset
b. Serum biomarkers
c. Coexisting chronic conditions
d. ECG pattern
e. Blood-flow angiography

A

b, d - Serum biomarkers, ECG pattern
UA/NSTEMI is classified as either low or intermediate risk of acute MI, the diagnosis of which is based on the clinical history, ECG pattern, and serum biomarkers. The other answers are not diagnostic of UA/NSTEMI.

26
Q

When an acute MI occurs, many physiologic changes occur very rapidly. What causes the loss of contractile function of the heart within seconds of the onset of an MI?

a. Conversion from aerobic to anaerobic metabolism
b. Overproduction of energy capable of sustaining normal myocardial function
c. Conversion from anaerobic to aerobic metabolism
d. Inadequate production of glycogen with mitochondrial shrinkage

A

a. Conversion from aerobic to anaerobic metabolism
The principal biochemical consequence of MI is the conversion from aerobic to anaerobic metabolism with inadequate production of energy to sustain normal myocardial function. As a result, a striking loss of contractile function occurs within 60 seconds of onset. None of the other answers occur.

27
Q

ST-elevated myocardial infarction is accompanied by severe, crushing pain. Morphine is the drug of choice used to treat the pain of STEMI when the pain cannot be relieved with oxygen and nitrates. Why is morphine considered the drug of choice in STEMI?

a. Action increases autonomic nervous system activity
b. Action decreases metabolic demands of the heart
c. Action increases anxiety increasing matabolic demands of heart
d. Action relieves pain and gives sense of depression

A

b. Action decreases metabolic demands of the heart
Although a number of analgesic agents have been used to treat the pain of STEMI, morphine is usually the drug of choice. It usually is indicated if chest pain is unrelieved with oxygen and nitrates. The reduction in anxiety that accompanies the administration of morphine contributes to a decrease in restlessness and autonomic nervous system activity, with a subsequent decrease in the metabolic demands of the heart. Morphine does not cause a feeling of depression to the client.

28
Q

During an acute MI there is ischemic damage to the heart muscle. The location and extent of the ischemic damage is the major predictor of complications, ranging from cardiac insufficiency to death, following an MI. What is the “window of opportunity” in restoring blood flow to the affected area so as to diminish the ischemic damage to the heart and maintain the viability of the cells?

a. 10 to 20 minutes
b. 30 to 40 minutes
c. 20 to 40 minutes
d. 10 to 30 minutes

A

c. 20 to 40 minutes
If blood flow can be restored within the 20- to 40-minute time frame, loss of cell viability does not occur or is minimal.

29
Q

What are the signs and symptoms of heart failure? (Mark all that apply.)

a. Fluid retention
b. Ruddy complexion
c. Fatigue
d. Bradycardia
e. Chronic productive cough

A

a, c (fluid retention, fatigue)
The signs and symptoms of heart failure include shortness of breath and other respiratory manifestations, fatigue and limited exercise tolerance, fluid retention and edema, cachexia and malnutrition, and cyanosis. Persons with severe heart failure may exhibit diaphoresis and tachycardia. A ruddy complexion, bradycardia, and a chronic productive cough are not signs or symptoms of heart failure.

30
Q

When an acute event occurs and the circulatory system can no longer provide the body with adequate perfusion of its tissues and organs, cellular hypoxia occurs and the body goes into shock. What are the causes of shock in the human body?

a. Maldistribution of blood flow
b. Hypovolemia
c. Excessive vasoconstriction
d. Obstruction of blood flow
e. Hypervolemia

A

a, b, d, e (Maldistribution of blood flow, hypovolemia, obstruction of blood flow, hypervolemia)
Shock is not a specific disease but a syndrome that can occur in the course of many life-threatening traumatic conditions or disease states. It can be caused by an alteration in cardiac function (cardiogenic shock), a decrease in blood volume (hypovolemic shock), excessive vasodilation with maldistribution of blood flow (distributive shock) or obstruction of blood flow through the circulatory system (obstructive shock). Excessive vasoconstriction and hypervolemia are not causes of shock.

31
Q

What are the physiologic signs and symptoms of cardiogenic shock? (Mark all that apply.)

a. Decrease in mean arterial blood pressures
b. Increase urine output related to increased renal perfusion
c. Rise in central venous pressure (CVP)
d. Hypercapnic lips and nail beds
e. Increased extraction of O2 from hemoglobin

A

a, c, e (Decrease in mean arterial blood pressures, rise in central venous pressure CVP, increase extraction of O2 from hemoglobin)
Signs and symptoms of cardiogenic shock include indications of hypoperfusion with hypotension, although a preshock state of hypoperfusion may occur with a normal blood pressure. The lips, nail beds, and skin may become cyanotic because of stagnation of blood flow and increased extraction of oxygen from the hemoglobin as it passes through the capillary bed. Mean arterial and systolic blood pressures decrease due to poor stroke volume, and there is a narrow pulse pressure and near-normal diastolic blood pressure due to arterial vasoconstriction. Urine output decreases due to low renal perfusion pressures and the increased release of aldosterone. Elevation of preload is reflected in a rise in CVP and pulmonary capillary wedge pressure. Neurologic changes, such as alterations in cognition or consciousness, may occur due to low cardiac output and poor cerebral perfusion. The other physiologic occurrences are not signs or symptoms of shock.

32
Q

In hypovolemia shock the main purpose of treatment is correcting or controlling the underlying cause of the hypovolemia and inproving the perfusion of the tissues and organs of the body. Which of the following treatments is not a primary form of therapy for hypovolemic shock?

a. Surgery
b. Administration of intravenous fluids and blood
c. Vasoconstrictive drugs
d. Infusion of blood and blood products

A

c. Vasoconstrictive drugs
The treatment of hypovolemic shock is directed toward correcting or controlling the underlying cause and improving tissue perfusion. Ongoing loss of blood must be corrected, such as in surgery. Oxygen is administered to increase oxygen delivery to the tissues. Medications usually are administered intravenously. In hypovolemic shock, the goal of treatment is to restore vascular volume. This can be accomplished through intravenous administration of fluids and blood. The crystalloids (e.g., isotonic saline and Ringer’s lactate) are readily available and effective, at least temporarily. Plasma volume expanders (e.g., pentastarch and colloidal albumin) have a high molecular weight, do not necessitate blood typing, and remain in the vascular space for longer periods than the crystalloids, such as dextrose and saline. Blood or blood products (packed or frozen red cells) are administered based on hematocrit and hemodynamic findings. Fluids and blood are best administered based on volume indicators such as CVP and urine output. Vasoactive medications are agents capable of constricting or dilating blood vessels. Considerable controversy exists about the advantages or disadvantages related to the use of these drugs. As a general rule, vasoconstrictor agents are not used as a primary form of therapy in hypovolemic shock and may be detrimental. These agents are given only when volume deficits have been corrected but hypotension exists.

33
Q

Neurogenic shock, or spinal shock, is a phenomenon caused by the inability of the vasomotor center in the brain stem to control blood vessel tone through the sympathetic outflow to the blood vessels. In neurogenic shock, what happens to the heart rate and skin?

a. Heart rate slower than normal; skin warm and dry
b. Heart rate faster than normal; skin cool and moist
c. Heart rate slower than normal; skin cool and moist
d. Heart rate faster than normal; skin warm and dry

A

a. Heart rate slower than normal; skin warm and dry
In contract to other shock states due to the loss of blood volume or impaired cardiac function, the heart rate in neurogenic shock often is slower than normal, and the skin is dry and warm. This type of distributive shock is rare and usually transitory. The other answers are not correct.

34
Q

Anaphylactic shock is the most severe form of systemic allergic reaction. Immunologically medicated substances are released into the blood, causing vasodilation and an increase in capillary permeability. What physiologic response often accompany the vascular response in anaphylaxis?

a. Uterine smooth muscle reaction
b. Laryngeal edema
c. Broncodilation
d. Gastrointestinal relaxation

A

b. Laryngeal edema
Anaphylaxis is a clinical syndrome that represents the most severe form of systemic allergic reaction. Anaphylactic shock results from an immunologically mediated reaction in which vasodilator substances such as histamine are released into the blood. The vascular response in anaphylaxis is often accompanied by life-threatening laryngeal edema and bronchospasm, circulatory collapse, contraction of gastrointestinal and uterine smooth muscle, and urticaria (hives) or angioedema.

35
Q

Sepsis is growing in incidence in the United States. Its pathogenesis includes neutrophil activation, which kills microorganisms. Neutrophils also injure the endothelium, releasing mediators that increase vascular permeability. What else do neutrophils do in sepsis?

a. Releases nitric oxide
b. Vasoconstricts the capillary bed
c. Causes bradycardia
d. Activates erythopoiesis

A

a. Releases nitric oxide
Although activated neutrophils kill microorganisms, they also injure the endothelium by releasing mediators that increase vascular permeability. In addition, activated endothelial cells release nitric oxide, a potent vasodilator that acts as a key mediator of septic shock.

36
Q

What is the primary physiologic result of obstructive shock?

a. Left ventricular hypertrophy
b. Elevated right heart pressure
c. Right atrial hypertrophy
d. Decreased right heart pressure

A

b. Elevated right heart pressure
The primary physiologic result of obstructive shock is elevated right heart blood pressure due to impaired right ventricular function. The other answers are not correct.

37
Q

An important factor in the mortality of severe shock is acute renal failure. What is the degree of renal damage related to in shock?

a. Loss of perfusion and duration of shock
b. Loss of perfusion and degree of immune-mediated response
c. Severity and duration of shock
d. Severity of shock and degree of immune-mediated response

A

c. Severity and duration of shock
The degree of renal damage in shock is related to the severity and duration of shock. None of the other answers related to the damage to the renal system in shock.

38
Q

The pathogenesis of multiorgan dysfunction syndrome (MODS) is not clearly understood at this time. Supportive management is currently the focus of treatment in this disorder. What is not a major risk factor in MODS?

a. Advanced age
b. Alcohol abuse
c. Respiratory dysfunction
d. Infarcted bowel

A

c. Respiratory dysfunction
Major risk factors for the development of MODS are severe trauma, sepsis, prolonged periods of hypotension, hepatic dysfunction, infarcted bowel, advanced age, and alcohol use. Respiratory dysfunction is not a major risk factor in MODS.

39
Q

What is the primary cause of heart failure in infants and children?

a. Idiopathic heart disease
b. Structural heart defects
c. Hyperkalemia
d. Reactions to medications

A

b. Structural heart defects
Structural (congenital) heart defects are the most common cause of heart failure in children. The other answers are not correct.

40
Q

Angina pectoris is a chronic ischemic CAD that is characterized by a symptomatic paroxysmal chest pain or pressure sensation associated with transient myocardial ischemia. What precipitates an attack of angina pectoris?

a. Exposure to heat
b. Sedentary lifestyle
c. Abrupt change in position
d. Emotional stress

A

d. Emotional stress
Angina pectoris usually is precipitated by situations that increase the work demands of the heart, such as physical exertion, exposure to cold, and emotional stress. The pain typically is described as a constricting, squeezing, or suffocating sensation. It usually is steady, increasing in intensity only at the onset and end of the attack. Changing positions abruptly does not cause an attack of angina pectoris.

41
Q

The diagnosis of chronic stable angina is based on a detailed pain history, the presence of risk factors, invasive and noninvasive studies, and laboratory studies. What test is not used in the diagnosis of angina?

a. Serum biochemical markers
b. Cardiac catheterization
c. Echocardiogram
d. Nuclear imaging studies

A

a. Serum biochemical markers
Serum biochemical markers for MI are normal in patients with chronic stable angina. All other answers are tests used in the diagnosis of angina.

42
Q

Cardiomyopathies are classified as either primary or secondary. The primary cardiomyopathies are further classified as genetic, mixed, or acquired. Identify whether the following conditions are classified as genetic, acquired, or mixed.

a. Hypertropic cardiomypathy
b. Left ventricular noncompaction
c. Myocarditis
d. Dilated cardiomyopathy
e. Peripartum cardiomyopathy

A

a. Hypertropic cardiomypathy - genetic
b. Left ventricular noncompaction - genetic
c. Myocarditis - acquired
d. Dilated cardiomyopathy - mixed
e. Peripartum cardiomyopathy - acquired

43
Q

It is known that over 100 distinct myocardial diseases can demonstrate clinical features associated with dilated cardiomyopathy (DCM). What is the most common identifiable cause of DCM in the United States?

a. Hepatic cardiomyopathy
b. Alcoholic cardiomyopathy
c. Cardiotoxic cardiomyopathy
d. Exercise induced cardiomyopathy

A

b. Alcoholic cardiomyopathy
Alcoholic cardiomyopathy is the single most common identifiable cause of DCM in the United States and Europe. The other answers are incorrect.

44
Q

In infective endocarditis vegetative lesions grow on the valves of the heart. These vegetative lesions consist of a collection of infectious organisms and cellular debris enmeshed in fibrin strands of clotted blood. What are the possible systemic effects of these vegetative lesions?

a. They can block the heart valves from closing completely
b. They can keep the heart valves from opening
c. They can fragment and cause cerebral emboli
d. They can fragment and make the lesions larger

A

c. They can fragment and cause cerebral emboli
The intracardiac vegetative lesions also have local and distant systemic effects. The loose organization of these lesions permits the organisms and fragments of the lesions form emboli and travel in the bloodstream, causing cerebral, systemic, or pulmonary emboli. Preventing the valves of the heart from either opening or closing completely is not a systemic effect of the lesions. Fragmentation of the lesions does not make them larger.

45
Q

Antibodies directed against the M protein of certain strains of streptococcal bacteria seem to cross-react with glycoprotein antigens in the heart, joint, and other tissues to produce an autoimmune response resulting in rheumatic fever and rheumatic heart disease. This occurs through what phenomenon?

a. The Aschoff reaction
b. The Syndenham reaction
c. C-reactive mimicry
d. Molecular mimicry

A

d. Molecular mimicry
It is thought that antibodies directed against the M protein of certain strains of streptococci cross-react with glycoprotein antigens in the heart, joint, and other tissues to produce an autoimmune response through a phenomenon called molecular mimicry. None of the other answers are correct.

46
Q

Mitral valve prolapse occurs frequently in the population at large. Its treatment is aimed at relieving the symptoms and preventing complications of the disorder. What drug is used in the treatment of mitral valve prolapse to relieve symptoms and aid in preventing complications?

a. B-Adrenergic-blocking drugs
b. Calcium channel blocking drugs
c. Antianxiety drugs
d. Broad-spectrum antibiotic drugs

A

a. B-Adrenergic-blocking drugs
Persons with palpitations and mild tachyarrhythmias or increased adrenergic symptoms and those with chest discomfort, anxiety, and fatigue often respond to therapy with the other B-adrenergic-blocking drugs. None of the other types of drugs are used in the treatment of mitral valve prolapse to relieve symptoms or prevent complications.

47
Q

Heart failure in an infant usually manifests itself as tachypnea or dyspnea, both at rest and on exertion. When does this most commonly occur with an infant?

a. During bathing
b. During feeding
c. During burping
d. During sleep

A

b. During feeding
Heart failure manifests itself as tachypnea or dyspnea at rest or on exertion. For the infant, this most commonly occurs during feeding. The other answers are incorrect.

48
Q

Tetralogy of Fallot is a congenital condition of the heart that manifests in four distinct anomalies of the infant heart. It is considered a cyanotic heart defect because of the right-to-left shunting of the blood through the ventricular septal defect. A hallmark of this condition is the “tets spells” that occur in these children. What is a tet spell?

a. A stressful period right after birth that occurs without evidence of cyanosis
b. A hyperoxygenated period when the infant is at rest
c. A hypercyanotic attack brought on by periods of stress
d. A hyperpneic attack in which the infant loses consciousness

A

c. A hypercyanotic attack brought on by periods of stress
The degree of obstruction may be dynamic and can increase during periods of stress causing hypercyanotic attacks (“tet spells”). None of the other answers occur in association with tetralogy of Fallot or tet spells.