REVIEW AND ASSESSMENT NOTES

Question 1

The 2013 ACC/AHA cholesterol guidelines recommend moderate- or high-intensity statin therapy for primary prevention of CV disease for individuals with an estimated 10-year risk of?

Answer 1

≥7.5%.

Question 2

simvastatin is metabolized primarily by cytochrome P450 CYP3A4, which if inhibited by other medications leads to an augmented serum simvastatin level and the potential for increased toxicity, including myositis and rhabdomyolysis

Answer 2

The FDA advises that gemfibrozil not be prescribed concurrently with simvastatin, and that the dosage of simvastatin should not exceed 10 mg daily for patients who also take verapamil, diltiazem, or amiodarone

Question 3

moderate intensity regimens recommended by the 2013 ACC/AHA guidelines include

Answer 3

atorvastatin 10-20 mg daily or rosuvastatin 5-10 mg daily.

Question 4

Optional high-intensity r mens include

Answer 4

atorvastatin 40-80 mg daily or rosuvastatin 20-40 mg daily.

Question 5

Reduction of dietary sodium intake to <100 mmol/d (2.4 g of sodium or 6 g sodium chloride) decreases systolic BP approximately

Answer 5

2 to 8 mm Hg

Question 6

Adoption of the DASH (Dietary Approaches to Stop Hypertension) eating planrich in fruits, vegetables, and low-fat dairy products and low in total and saturated fat—has been shown to reduce BP by .

Answer 6

11.4/5.5 mm Hg

Question 7

Ethanol consumption of no more than——–
(24 oz beer, 10 oz wine, 3 oz 80-proof liquor for a normal-size man and less for a woman) is associated with decreased cardiac mortality, but excessive alcohol intake exerts a pressor effect, so that alcohol abuse is actually a cause of reversible hypertension.

Answer 7

1 oz/d

Question 8

Fibromuscular renovascular disease arises primarily in women aged 20-60

Answer 8

aged 20-60

The second, and less common, form of renal artery stenosis is fibromuscular dysplasia,

nvolves mainly the distal two thirds of the main renal artery,

involvement of the media is most common.

Question 9

Renovascular disease is one of the most common causes of secondary hypertension and has two main etiologies. The most common cause (80% to 90% of cases) is athero sclerotic disease affecting the——– of the main renal artery, typically seen in older men

Answer 9

proximal third

Question 10

A renovascular etiology of hypertension should be suspected in patients who develop high blood pressure ———- with the abrupt onset of severe and resistant hypertension

Answer 10

before age 30, or after age 50

Question 11

Renal parenchymal disease is the most common cause of secondary hypertension

Answer 11

t

Question 12

Essential hypertension accounts for approximately 90% of patients with elevated blood pressure. 1 Renal parenchymal disease is the second most common cause, responsible for approximately 5%

Answer 12

T

Question 13

Grouped together, coarctation of the aorta, Cushing disease, and pheochromocytoma contribute to <1%.

Answer 13

t

Question 14

. Primary aldosteronism accounts for ~1% of h tension in the general population but a higher percentage (~11%) in patients with resistant hypertension

Answer 14

the

Question 15

Pure “white coat” hypertension, in which blood pressures taken in the office are persistently elevated but outof-office readings are not, is found in—– of patients.

Answer 15

20% to 30%

Question 16

Most patients with white coat hypertension are found to be free of target organ damage and have an excellent 10-year prognosis with respect to cardiovascular disease.

Answer 16

T

Question 17

The cuff bladder should encircle and cover —— of the length of the arm

Answer 17

two thirds

Question 18

WHAT IS THE LIFE TRIAL?

Answer 18

However, in the LIFE trial, the ARB losartan was compared with the beta-blocker atenolol in high-risk hypertensive patients with electrocardiographic LVH, the majority of whom were also treated with a diuretic. Despite a similar reduction in blood pressure, the individuals who received losartan demonstrated reduced cardiovascular morbidity and mortality compared with those who received the beta-blocker. 2

Question 19

The use of oral contraceptives (OCs) is a cause of secondary hypertension in young women. The likelihood of such patients developing hypertension is increased by

Answer 19

alcohol consumption
age >35 years
Obesity
probably related to the estrogen content of the agent.

Question 20

Because estro gen increases the hepatic production of angiotensinogen, a probable mechanism for hypertension induced by oral contraceptives is activation of the

Answer 20

renin-angiotensin system with subsequent sodium retention and volume expansion.

Question 21

BP normalizes within 6 months of initiating OC therapy in approximately 50% of patients.

Answer 21

t

Question 22

Most pheochromocytomas arise in the adrenal medulla, where —— are bilateral and —– are malignant.

Answer 22

10%

Question 23

Approximately —— of pheochromocytomas are extra-adrenal (paragangliomas).

Answer 23

15%

Question 24

The most reliable screening test for pheochromocytoma is the——- , the catecholamine metabolite least affected by interfering substances.

Answer 24

24-hour urine assay for metanephrines

Question 25

Approximately 10% of pheochromocytomas are familial, and may be inherited alone or in combination with other abnormalities, most commonly multiple endocrine neoplasia (MEN) type 2A or 2B.

Answer 25

TRUE

Question 26

The most common side effect is an annoying dry cough that occurs in in 5-20% of patients taking ACE inhibitors, likely related to increased

Answer 26

bradykinin.

Question 27

The cough from ACE-I may persist for —— after discontinuation of the medication

Answer 27

more than 3 weeks

Question 28

Calcium channel blockers vasodilate and lower blood pressure by interacting with plasma membrane L-type calcium channels in vascular smooth muscle and cardiac myocytes. A common side effect is ankle edema (———why?— Less common adverse effects include ——

Answer 28

which arises because of arterial > venous vasodilation).

headache, flushing, and gingival hyperplasia.

Question 29

Hydralazine is a direct vasodilator with potential adverse effects that include

These side effects can be prevented, and the antihypertensive effect increased, by co-administration of a beta-blocker.

Answer 29

tachycardia, flushing, and headaches.

Question 30

Verapamil and diltiazem can also impair —-

Answer 30

cardiac conduction and cause bradycardia.

Question 31

Minoxidil is a direct vasodilator that is occasionally used in patients with renal failure and severe hypertension. Its side effects include

Answer 31

reflex increase in cardiac output
fluid retention
hirsutism.

Question 32

Minoxidil is a direct vasodilator that is occasionally used in patients with renal failure and severe hypertension. Its side effects include

Answer 32

reflex increase in cardiac output
fluid retention
hirsutism

Question 33

EFFECTS OF THIAZIDES

LOWERS THE FF

Answer 33

HYPOKALEMIA
HYPOMAGNESEMIA
HYPONATREMIA

Question 34

EFFECTS OF THIAZIDES

INCREASES THE FF

Answer 34

HYPERCALCEMIA
HYPERURICEMIA
higher dosages (≥50 mg daily) may increase the total blood cholesterol, LDL, and triglyceride levels

Question 35

statins increase the cell surface expression of LDL

Answer 35

By reducing the i lular cholesterol concentration, the expression of cellsurface low-density lipoprotein (LDL) receptors is increased (resulting in enhanced removal of LDL particles from the circulation) and the hepatic production of very-lowdensity lipoprotein (VLDL), the precursor of LDL choles terol, is reduced.

Question 36

Myonecrosis, consisting of muscle aching or weakness in association with a serum creatine kinase level >10 times normal occurs in <0.5% of patients. This adverse effect should prompt immediate discontinuation of the statin. The risk of myopathy is increased when there is concurrent therapy with other drugs that interfere with cytochrome P-450 metabolism of many of the statins. Examples of such drugs include

Answer 36

erythromycin, cyclosporine, and antifungal agents.

Question 37

P450 INHIBITORS

Answer 37

SICKFACES.COM 
Sodium valproate 
Isoniazid 
Cimetidine 
Ketoconazole 
Fluconazole 
Alcohol..binge drinking 
Chloramphenicol 
Erythromycin 
Sulfonamides 
Ciprofloxacin 
Omeprazole 
Metronidazole
Grapefruit juice

Question 38

P450 Inducers

CRAP GPS induces me to madness!!

Answer 38

Carbemazepines
Rifampicin
Alcohol (chronic)
Phenytoin

Griseofulvin
Phenobarbitone
Sulphonylureas

Question 39

Effect of Drugs on Lipid Profile

Beta-blockers, particularly non–beta 1 -selective agents, . Thiazides
Hormonal replacement therapy with estrogen
Protease inhibitors, for patients with human immunode ficiency virus infection,

Answer 39

BB: increase triglyceride levels and lower high-density lipoprotein (HDL) levels
t: tend to increase triglyceride levels
E: increases both HDL and triglyceride levels.
P: dyslipidemic syndrome characterized by elevated triglyceride and total cholesterol levels with decreased HDL levels

Question 40

.is an autosomal co-dominant disorder that results from defects in the LDL receptor gene.

Corneal arcus, tendinous xanthomas, and xanthelasmas are common.

Answer 40

Familial hypercholesterolemia

Question 41

is one of the most common familial lipoprotein disorders. It is a polygenic condition with abnormalities that include elevations of LDL and/or triglycerides, a reduction in HDL, and ele vated apo B levels.

Patients with FCH have an increased risk of coronary artery disease (CAD)

Physical findings such as corneal arcus or xanthomas are rare.

Answer 41

Familial combined hyperlipidemia (FCH)

Question 42

is also a polygenic disorder and is characterized by elevated triglycerides with normal or low LDL levels and reduced HDL. Patients do not develop xanthomas or xanthelasmas, and the relationship with CAD is not as strong or consistent as with FCH.

Answer 42

Familial hypertriglyceridemia (type IV hyperlipoproteinemia)

Question 43

encodes a protease that binds to the LDL recep tor and targets it for lysosomal degradation. Gain-of-function mutations in this gene decrease the availability of the LDL receptor, which causes higher plasma LDL cho lesterol levels and an increased risk of ischemic heart disease. 3 Loss-of-function mutations in this gene result in lower LDL-cholesterol and coronary event rates.

Answer 43

The proprotein convertase subtilisin/kexin type 9 gene (PCSK9)

Question 44

Niacin (nicotinic acid) is a B vitamin with lipid-lowering effects when taken at pharmacologic doses. Its primary action is to

decreases the release of free fatty acids from adipocytes (which are used by the liver for triglyceride synthesis), thus reducing triglyceride levels.

Answer 44

reduce very low-density lipoprotein secretion from the liver, which causes a subsequent reduction in intermediate-density lipoprotein and low-density lipopro tein (LDL) levels.

Question 45

reduces LDL cholesterol by 10% to 25% and triglycerides by 20% to 50%, and increases high-density lipoprotein (HDL) cholesterol by 15% to 35%.

Answer 45

NIACIN

Question 46

NIACIN Despite these effects on the lipid profile, its widespread use has been limited historically because of side effects, including

Answer 46

flushing, hepatotoxicity, hyperuricemia, hyperglycemia, and gastritis.

Question 47

owever, in more recent trials of patients treated aggressively with statin therapy (AIM-HIGH 2 , HPS2-THRIVE 3 ), the addition of niacin did not further lower cardiovascular risk compared to the statin alone.

Answer 47

(AIM-HIGH 2 , HPS2-THRIVE 3

Question 48

Niacin also reduces c lating levels of lipoprotein (a

Answer 48

T

Question 49

In the ACCORD trial, type 2 diabetic patients already treated with simvastatin achieved a marked reduction in triglycerides with the addition of fenofibrate. However, compared with placebo, clinical outcomes (fatal cardiovascular events, nonfatal myocardial infarction, or stroke) were not reduced by the addition of fenofibrate. 3

Answer 49

ACCORD trial

Question 50

is the major protein in high-density lipoprotein (HDL) and its concentration is inversely correlated with angiographic evidence of coronary disease

Answer 50

Apo AI

Question 51

two forms of apoprotein B arise from a single gene that displays a unique editing mechanism that allows for synthesis of both proteins.

Answer 51

(apo B48 and apo B100)

Question 52

is the primary apoprotein of low-density lipoprotein (LDL), allowing recognition of the particle by the LDL receptor on cell surfaces.

Answer 52

Apo B100

Question 53

is found in very-low-density lipoproteins (VLDL) particles as well as in chylomicrons, in intermediatedensity lipoprotein (IDL) particles, and, to a small extent, in HDL.

Answer 53

Apoprotein E

Question 54

(also termed dysbetalipoproteinemia or broad beta disease) are homozygous for the apoprotein E2/2 genotype.

Answer 54

type III hyperlipoproteinemia

Question 55

one of the few interventions that can significantly reduce Lp(a); statin drugs do not. However, no study yet has shown that targeted pharmacologic reduction of Lp(a) improves cardiovascular outcomes.

Answer 55

Niacin