Chs 18, 19, 20 (Cardio) Flashcards
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 (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.
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. (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.
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. (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.
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
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.
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
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.
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, b, e
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
d Periodic severe headache and marked variability in blood pressure
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 Partial reduction in blood pressure to less critical values
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
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.
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
c HELLP syndrome
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, 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.
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
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.
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. 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.
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
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.
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
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.
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
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.
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. 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.
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
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.
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
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.