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Pharmacology > Unit 4 &10--CV AND ENDOCRINE > Flashcards

Unit 4 &10--CV AND ENDOCRINE Flashcards

1
Q

How does the central nervous system affect BP?

A

beta receptors stimulate release of norepinephrine producing vasodilation and decreased bp

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2
Q

How does the peripheral nervous system affect BP?

A

Receptors located on effector cells-Alpha 1 and Beta 1 and Beta 2

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3
Q

what do Alpha 1 receptors on venues and arterioles cause?

A

vasoconstriction

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4
Q

Where are beta 1 receptors and what do they do?

A

heart and kidneys-regulate heart rate and contractility, as well as renin release thus affecting cardiac output.

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5
Q

where are beta 2 receptors and what do they do?

A

Located in lungs, liver, pancreas and arteriolar smooth muscle.. Regulate bronchodilation and vasodilation.

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6
Q

Where are baroreceptors located?

A

large arteries such as aorta and carotids

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7
Q

Describe the RAAS.

A

Renin is released in response to change in BP. Renin catalyzes conversion of angiotensinogin to angiotensin I which is converted to potent vasoconstrictor angiotensin II by ACE. Angiotensin II stimulates release of aldosterone from adrenals resulting in Na and H2O retention.

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8
Q

what is considered normal blood pressure?

A

<120/80-encourage pt

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9
Q

what is considered prehypertension? is this treated?

A

120-139/80-89-no treatment unless compelling indications

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10
Q

what is considered Stage I hypertension? What are first line choices?

A

140-159/90-99. Thiazide diuretics, may consider aces, arbs, bb, ccb or combo

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11
Q

What is considered stage II hypertension? What is first line treatment?

A

> 160/100. Two drug combo or thiazide and either ace, arb, bb, or ccb

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12
Q

What is the goal of therapy for htn?

A

decreasing CV and renal morbidity and mortality.

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13
Q

In which patients are thiazide diuretics contraindicated?

A

anuric patients or those with known sensitivity to thiazides and/or sulfonamides

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14
Q

What are side effects of spironolactone?

A

gynecomastia, hirsutism, menstrual irregularities

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15
Q

which beta blockers are cardioselective (i.e. Beta 1 receptor blockers) and are better choices for patients with asthma or copd?

A

atenolol, metoprolol, bisoprolol

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16
Q

What class of antihypertensives is first line therapy in hypertensive diabetic patients w/ proteinuria?

A

ACE inhibitors

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17
Q

what are nondihydropyridine CCBs? In whom should they be avoided?

A

verapamil and diltiazem. Patients with cardiac dysfunction-can accelerate HF.

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18
Q

What can occur with hydrazine? What meds should be given with it to prevent this?

A

May cause fluid retention and reflex tachy. Given w/ diuretics and beta blocker or other heart-slowing agent

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19
Q

What is the first choice for hypertension in patients with stable angina?

A

beta blockers and long acting CCBs

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20
Q

What is first line therapy for patients w/ hypertension and HF?

A

BB and ACE inhibitors.

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21
Q

What makes up metabolic syndrome

A

abdominal obesity, glucose intolerance, bp of at least 130/85, trigs of over 150, HDL <40 or 50 for men and women respectively

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22
Q

What is the best choice of antihypertensives for african americans?

A

chlorthalidone and amlodipine

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23
Q

what constitutes malignant hypertension?

A

DBP over 120

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24
Q

how do antioxidants improve cholesterol?

A

They block conversion of LDL to modified LDL in the vascular endothelium. Modified LDL may be more atherogenic so slowing its production could decrease atherogenic process.

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25
Q

How is LDL calculated?

A

Total Chol-HDL-VLDL (VLDL=trigs/5)

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26
Q

what is first line treatment for newly diagnosed hyperlipidemia (most patients)

A

lifestyle modification for 6-12 weeks

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27
Q

what is main goal of drug therapy in hyperlipidemia?

A

reduce CV risk without affecting quality of life

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28
Q

what meds can affect metabolism of statins?

A

CYP450-cyclosporine, emycin, azole antifungals

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29
Q

when should hepatic function labs be drawn on patients after starting statin therapy?

A

baseline, 6-12 weeks, and periodically thereafter.

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30
Q

what meds interact with bile acid resins?

A

abx and thyroid

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31
Q

what are major side effects of bile acid resins?

A

GI symptoms

32
Q

what is niacin useful for treating?

A

low hdl, high trigs, ldl to some extent

33
Q

what are cholesterol absorption inhibitors?

A

zetia, fibrin acid derivatives, gemfibrizol

34
Q

After statins, what is the next line of treatment in hlp?

A

niacin, bile acid resins

35
Q

how do CCBs treat angina?

A

act as vasodilators

36
Q

what are some dihydropyridines?

A

nifedipine, felodipine, amlodipine

37
Q

What antianginal medication can interfere with CYP3A4 inhibitors?

A

Ranexa

38
Q

what is thought to be first line therapy for acute anginal episodes?

A

beta blockers

39
Q

What is second line therapy for acute anginal episodes?

A

Combo with beta blocker and CCB or long-acting nitrate

40
Q

what are symptoms of right sided heart failure?

A

pitting edema, abdominal pain, anorexia, N/V, JVD, ascites

41
Q

what are symptoms of left sided heart failure?

A

cough, dyspnea, orthopnea, PND, cardiomegaly, S3 heart sound, rales, pulmonary edema

42
Q

what is class I heart failure?

A

symptoms of HF only at levels of activity that would produce symptoms in normal people

43
Q

what is class II heart failure?

A

symptoms with ordinary exertion

44
Q

what is class III heart failure?

A

patients have symptoms of HF on less than ordinary exertion

45
Q

what is class IV heart failure?

A

symptoms of HF at rest

46
Q

what is first line and should always be started on patients with EF <35-40%

A

ACE inhibitors

47
Q

What are class Ia Ib and Ic antiarrhythmics?

A

Sodium channel blockers. Ia: Quinidine Ib: lidocaine Ic: flecainide, propafenone

48
Q

what are class II antiarrhythmic?

A

beta blockers: atenolol, lopressor, inderal

49
Q

what are class III antiarrhythmics?

A

Potassium channel blockers: amio, tikosyn, multaq, sotalol

50
Q

what are class IV antiarrhythmics?

A

calcium channel blockers: diltiazem, verapamil.

51
Q

in whom should flecainide and propafenone (Class Ia) be avoided?

A

patients with structural heart disease including cad, LV dysfunction, valvular disease, LVH

52
Q

How does DM II affect different body shapes differently?

A

In lean people, the problem is usually with beta cells. In overweight people, problem is in target cells

53
Q

What results in Hgb A1c, FBG, and OGTT need repeat testing?

A

Hgb A1c >6.5%, FBG > 126, OGTT PG> 200

54
Q

What blood results yield diagnosis of pre-diabetes?

A

FBG 100-125 or OGTT PG 140-199

55
Q

Any random glucose over ______ indicates DM.

A

200

56
Q

What meds cause hyperglycemia?

A

glucocorticoids, furosemide, thiazides, estrogen, beta blockers, nicotinic acid

57
Q

How does the onset of DM I and DM II differ?

A

DM I is often sudden and preceded by ketoacidosis.

DM II is often gradual insidious and undiagnosed for years.

58
Q

What are the goals of drug therapy in terms of glycemic control?

A

Hbg A1c <180.

59
Q

What are common sulfonylureas? What is their mechanism of action? How is it taken?

A

glyburide, glipizide. They stimulate insulin release due to action on beta cells. once daily

60
Q

In what DM meds do patients need to be concerned with hypoglycemia?

A

sulfonylureas (glipizide, glyburide), meglitinide analogs (prandin, starlix) and pramlintide acetate as well as others IF GIVEN IN COMBINATION WITH ONE OF THE ABOVE OR INSULIN

61
Q

what are common thiazolidinediones? What is their mechanism of action? How is it taken?

A

actos and avandia They reduce insulin resistance at sites of insulin action. Taken once daily.

62
Q

what are common alpha glucosidase inhibitors? What is their mechanism of action? How is it taken?

A

glyset and precose They slow absorption of carbs from intestines, minimizing postprandial increase in blood sugar Taken tid with first bit of meal.

63
Q

what are common meglitinide analogs? What is their mechanism of action? How is it taken?

A

prandin and starlix They stimulate release of insulin from pancreas in response to a meal. with 2-4 meals daily.

64
Q

what are common dipeptidyl peptidase-4 inhibitors? What is their mechanism of action? How is it taken?

A

januvia and onglyza They block effect of against GLP1 and increase amount of circulating incretins. Taken once daily.

65
Q

What are common incretins and what is their mechanism of action?

A

Byetta. They slow gastric emptying and stimulate glucose-dependent secretion of insulin from pancreatic beta cells while suppressing release of glucagon from alpha cells Injectable only. Given 2x daily over 60 minutes or prior to largest 2 meals, at least 6 hours apart.

66
Q

How does pramlintide acetate work and how is it taken?

A

It is an injectable synthetic of pancreatic amylin which is consecrated with insulin. Delays gastric emptying, alters release of additional inappropriate glucose and increases satiety. given prior to large meals.

67
Q

What insulins are given as boluses?

A

very rapid acting-humalog

short acting-regular or “r”

68
Q

What insulins are given as basals?

A

Intermediate-NPH, lente, “n” or “l”

Long-acting-“u”, lantus

69
Q

How is daily insulin dosing divided? What is the ratio?

A

2/3 of daily dose is in the AM, 1/3 is in the PM. 2:1 ratio of intermediate to short acting before breakfast, 1:1 ratio of before dinner

70
Q

how much insulin do adults and children need daily (approximately)

A

0.5-0.6 units/kg/d

71
Q

how much insulin do adults and adolescents need during illness?

A

0.5-0.75 units/kg/d

72
Q

how much insulin do adolescents need during a growth spurt per day?

A

1.25-1.5 units/kg/day

73
Q

How much insulin to pregnant women need daily?

A

0.7 units/kg/day

74
Q

What is the “1500 rule?”

A

Divide 1500 by total daily dose of insulin. The result is how much a single unit of insulin lowers blood glucose.

75
Q

what is the Somogyi effect?

A

Rebound of hyperglycemia that occurs after early morning episode of insulin induced hypoglycemia.

76
Q

What is first line treatment for DM I? DM II?

A

DM I: Insulin
DM II: mono therapy w/ oral agent-sulfonylureas if glucose >250 et thin, biguanides et TZDs are best in metabolic syndrome.

Pharmacology (11 decks)

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