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Pharmacology 2 > Exam 1 - Hypertension > Flashcards

Exam 1 - Hypertension Flashcards

1
Q

What is the definition of hypertension for systolic and diastolic?

A

Systolic greater than 140, Diastolic greater than 90

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2
Q

What is the lifetime risk of HTN?

A

90%

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3
Q

What is the ratio of adults who have HTN?

A

1 in 3

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4
Q

What are some risk factors for developing HTN?

A

Cigarette smoking, Obesity (BMI above 30), physical inactivity, dyslipidemia, DM, renal dysfunction, men over 55 y/o, women over 65 y/o, family history of premature cardiovascular dz

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5
Q

What are the two types of Hypertension?

A

Essential Hypertension (90% of cases), Secondary Hypertension (10%)

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6
Q

What is the most common type of HTN?

A

Essential HTN

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7
Q

What is a strong component of Essential HTN?

A

Hereditary component

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8
Q

What are two common causes of Secondary HTN?

A

CKD, renovascular dz

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9
Q

Secondary HTN makes up what percentage of cases?

A

10%

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10
Q

Systolic BP represents what?

A

Cardiac contraction. Amount of blood pumped out by ventricles (cardiac output)

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11
Q

What is Cardiac Output and what number represents it?

A

Amount of blood pumped out of the ventricles. Represented by Systolic BP.

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12
Q

What does Diastolic BP represent?

A

Number that represents nadir (lowest point). Filling of heart with blood. Sum of peripheral resistance in peripheral vasculature.

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13
Q

What is happening in the heart during Diastole?

A

Filling of heart with blood

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14
Q

Sum of peripheral resistance in peripheral vasculature is represented by what measurment?

A

Diastolic BP

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15
Q

What is Total Peripheral Resistance (TPR)?

A

Sum of peripheral resistance in peripheral vasculature. Measured by Diastolic BP.

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16
Q

What guidelines are used in the treatment of HTN?

A

JNC 8

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17
Q

In a PT over 60 y/o what is the target BP?

A

150/90 or less

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18
Q

In a PT younger than 60 y/o what is the target BP?

A

140/90 or less

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19
Q

What is the target BP for any patient who has with DM or CKD?

A

140/90 or less

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20
Q

What are some non-pharmacological therapies in treating HTN?

A

Stop smoking, weight loss (biggest impact 5-10mmHg decrease per 10kg loss), increase physical activity, DASH diet, sodium restriction, limit EtOH to 2 a day or less

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21
Q

A majority of PTs will need how many medications to reach their goal?

A

2

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22
Q

What are the main four first-line options for treating HTN?

A

ACE-I, ARB, CCBs, Thiazide Diuretics

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23
Q

What two first line treatments are not used in African-Americans?

A

ACE-I, ARB

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24
Q

If PT has DM or CKD what are the two first line treatments even if they are African American?

A

ARB, ACE-I

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25
Q

Should you use ARBs and ACE-Is together?

A

No

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26
Q

What is first line treatment of HTN is PT has a cardiac history?

A

Beta Blocker

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27
Q

What is the most common treatment approach when adding a second agent and max dose?

A

Start with one agent. If not at goal add a second agent before maxing out first agent. If still not at goal then max out dose on both before adding a third agent.

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28
Q

If PT has a SBP above 160 and/or DBP above 100 how many agents do you start with?

A

Two. (But in practice you use one and then a second later, but two is the answer for exam purposes).

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29
Q

What are the three types of Diuretics?

A

Thiazide Diuretics, Loop Diuretics, and Potassium Sparing Diuretics

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30
Q

What are the three Thiazide Diuretics?

A

HCZT, chlorthalidone, metolzaone

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31
Q

What is the MOA for the three Thiadize Diuretics?

A

Inhibits sodium reabsorption in distal tubule

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32
Q

What is special about Metolazone?

A

Not used for BP management, only fluid management. Very potent, one-time use only.

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33
Q

What happens to the electrolytes in Thiazide Diuretics?

A

Down: K+ and Na+
Up: Ca++, Uric Acid, Glucose

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34
Q

What must the serum Creatine clearance be in order for HCZT to work?

A

Above 30 ml/min

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35
Q

What will a Thiazide Diuretic initially increase that is a side-effect?

A

Urination, so give it in the morning

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36
Q

Thiazide diuretics can cause what to the skin?

A

Sun burns more easily

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37
Q

Thiazide Diuretics are ineffective in PT’s with what?

A

Severe renal disease

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38
Q

Thiazide Diuretics contain ____ which some Abx also contain so to ask the PT what their reaction is before giving

A

Sulfa

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39
Q

If a PT is taking ____ don’t give a Thiazide Diuretic because of possibly toxic concentrations

A

Lithium

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40
Q

What do Loop Diuretics end in?

A

“-ide”

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41
Q

What is the MOA for Loop Diuretics?

A

Inhibits active transport of Na, Cl, and K in thick ascending limb of Loop of Henle causing them to be excreted with water into collecting ducts

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42
Q

Does a Loop Diuretic work before or after a Thiazide Diuretic?

A

Before

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43
Q

Loop Diuretics are the preferred diuretic for what condition?

A

CHF

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44
Q

Loop Diuretics used in what main three conditions?

A

CHF (preferred diuretic), Edema (peripheral and pulmonary), HTN (not as potent as Thiazide)

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45
Q

What happens to electrolyes in Loop Diuretics?

A

Down: Na, K, Ca, Mg
Up:Uric Acid

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46
Q

Diuretics can complicate gout because they increase what?

A

Uric Acid

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47
Q

Loop Diuretics can easily cause dehydration because?

A

Na is excreted out, taking with it water

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48
Q

How frequent does Ototoxicity occur with Loop Diuretics?

A

Very rare. Usually only when combined with another ototoxic drug

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49
Q

What does a Loop Diuretic do to serum Cr? What must the SrCr be for a Loop Diuretic to work?

A

Increase SrCr. Above 10 ml/min to work.

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50
Q

What two things must you be take precaution in when using Loop Diuretics?

A

Sulfa allergies, nephrotoxicity

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51
Q

What are the two types of Potassium Sparing Diuretics?

A

Aldosterone Receptor Blockers, Potassium Sparing Drugs

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52
Q

What is the MOA of Aldosterone Receptor Blockers (a type of K-Sparing Diuretic)?

A

Competes with Aldosterone, prevents Na reabsorption and K excretion

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53
Q

What are the two Aldosterone Receptor Blocker drugs?

A

Spironolactone, Eplerenone

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54
Q

What is the MOA of Potassium Sparing Drugs (a type of Potassium Sparing Diuretic)?

A

Blocks Na reabsorption and K excretion. Effect is independent of aldosterone blocker.

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55
Q

What are the two Potassium Sparing Drugs (a type of Potassium Sparing Diuretic)?

A

Triamterene, Amiloride

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56
Q

Are Potassium Sparing Drugs ever used on their own to treat HTN?

A

No. Very poorly effective on their own but they are used in conjunction with others.

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57
Q

What is the MOA of Potassium Sparing Diuretics?

A

Blocks Na reabsorption and K excretion in distal tubule

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58
Q

Potassium Sparing Diuretics are often used in combination with what else? Why?

A

Thiazide Diuretic, to help balance K

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59
Q

Spironolactone is most often used for what condition

A

Class IV Heart Failure

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60
Q

What are some adverse effects of Potassium Sparing Diuretics?

A

Both Spirinolactone and Eplerenone: Hyperkalemia
Spironolactone: Gynecomastia, menstural irregularities
Eplerenone: Fewer side effects as more selective

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61
Q

What converts Angiotensin I to Angiotensin II?

A

ACE (Angiotensin Converting Enzyme)

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62
Q

What converts Angiotensinogen to Angiotensin I?

A

Renin

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63
Q

What converts Bradykinins to inactive kinins?

A

ACE

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64
Q

What is the cause of the ACE-I cough?

A

Build up of Bradykinins. Inhibition of ACE prevents the conversion of Bradykinins to inactive kinins causing the kinins to stay around longer and cause cough

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65
Q

What do ACE-Inhibitors end in?

A

“-pril”

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66
Q

What is the MOA of an ACE Inhibitor

A

Inhibits ACE to prevent conversion of Angiotensin I to Angiotensin II

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67
Q

What does ACE-I do to the kidneys?

A

Dialates the efferent arteriole. “Protects kidneys”.

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68
Q

Which HTN drug is “kidney protective”? How?

A

ACE-I. Dialates efferent arteriole and preventing microproteinuria from becoming macroproteinuria.

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69
Q

What conditions is an ACE-I possible first line therapy for?

A

HTN, CKD

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70
Q

How often is an ACE-I dosed?

A

Most often once a day, sometimes twice.

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71
Q

What two things must be monitored in within 4 weeks of starting an ACE-I?

A

Serum K and Serum Cr.

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72
Q

What can happen to Serum Cr soon after starting an ACE-I?

A

Benign increase in Serum Cr less than 30% within 4 weeks of starting ACE-I. Will go back down to base and be normal.

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73
Q

What can an ACE-I do to serum K levels?

A

Dangerously raise them

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74
Q

What is a serious, life-threatening side-effect of an ACE-I?

A

Angioedema (swelling of face, tongue, throat). Due to allergy.

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75
Q

What causes the ACE-I cough? What percentage of PTs get it?

A

Increased bradykinins from ACE-I. Up to 20% of PTs get it.

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76
Q

Hyperkalemia when an ACE-I is used happens most commonly in what two conditions?

A

DM and CKD

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77
Q

Can an ACE-I be used in pregnancy?

A

NO

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78
Q

If a PT has had angioedema with another ACE-I can you use a different one?

A

No. Having had angioedema from an ACE-I is a contraindication to further ACE-I use.

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79
Q

Can you use an ACE-I in a PT with renal artery stenosis?

A

No

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80
Q

What three drugs classes can an ACE-I interact with?

A

Potassium supplements, Potassium Sparing Diuretic, NSAID

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81
Q

What is the only ACE-I that is available in IV?

A

Enalaprilat

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82
Q

What is the most common ACE-I and its dose?

A

Lisinipril, 10-40mg daily

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83
Q

Catopril absorption is decreased by 30-40% when taken with what?

A

Food

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84
Q

Angiotensin II Receptor Blockers end in what?

A

“-sartan”

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85
Q

What is the MOA for ARBs?

A

Inhibits angiotensin II at its receptor sites.

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86
Q

What is the effect of an ARB on bradykinin?

A

Nothing. Does not prevent the breakdown of bradykinin to its inactive forms.

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87
Q

What are two first line conditions ARBs can treat?

A

HTN, CKD

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88
Q

Is CHF treatable with ARBs and ACE-Is?

A

Yes

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89
Q

How often is an ARB dosed?

A

Usually once daily

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90
Q

Can ARBs cause potassium?

A

Yes. So can ACE-Is

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91
Q

What is a “Salt Substitute” and what medication classes can interact with it?

A

KCl for food instead of NaCl. Can raise K levels dangerously high if PT on ACE-I or ARB. (Also potassium sparing diuretic?)

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92
Q

Can an ARB be used in pregnancy?

A

NO

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93
Q

Can an ARB be used in PTs with renal artery stenosis?

A

Yes but with caution

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94
Q

Can an ARB be used in a PT who has had angioedema while taking an ACE-I?

A

Yes, but use caution?

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95
Q

What three categories of drugs can an ARB interact with?

A

Potassium supplements, Potassium Sparing Diuretics, NSAIDs

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96
Q

What is the MAO of Aliskiren?

A

Prevents conversion of Angiotensinogen to Angiotensin I. Directly inhibits renin.

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97
Q

Which new agent directly inhibits renin?

A

Aliskiren?

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98
Q

What converts Angiotensinogen to Angiotensin I?

A

Renin

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99
Q

Can Aliskiren be used in pregnancy?

A

No

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100
Q

Is the role of Aliskiren figured out and where it fits in treatment of HTN clear?

A

No. Still a new agent and role in HTN therapy is unclear.

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101
Q

Is Aliskiren a monotherapy, combo therapy, or both?

A

Both

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102
Q

What are the two categories of Calcium Channel Blockers (CCBs)?

A

Non-dihydropyridines and dihydropyridines

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103
Q

What are the two non-dihydropyridines?

A

Verapamil, Diltiazem

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104
Q

What do the dihydropyridines CCBs end in?

A

“-ipine”

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105
Q

What do the non-dihydropyridines CCBs end in?

A

Nothing. Just two of them and need to memorize them (Verapamil, Diltiazem)

106
Q

What is the role of a calcium channel?

A

When open allows for influx of calcium into smooth muscle (cardiac smooth muscle and vascular smooth muscle) leading activation of intracellular calcium leading to muscle contraction

107
Q

What is the MOA of CCBs in general?

A

Inhibit influx of calcium into cells to prevent muscle contraction

108
Q

What is the action of Non-Dihydropyridine CCBs on cardiac smooth muscle?

A

Decreases inotropy (force of contractions) and decreases chronotropy (rate of contractions) by inhibiting the smooth muscle

109
Q

What is the action of Dihydropyridine CCBs on vascular smooth muscle?

A

Vasodilation by inhibiting the vascular smooth muscle. Dihydropyridine.

110
Q

Do Dihydropyridine CCBs work on vascular or cardiac smooth muscle?

A

Vascular Smooth Muscle

111
Q

Do Non-Dihydropyridine CCBs work on vascular or cardiac smooth muscle?

A

Cardiac Smooth Muscle

112
Q

What do Dihydropyridine CCBs inhibit and what is the result?

A

Inhibits the flow of calcium into vascular smooth muscle, results in peripheral vasodilation

113
Q

What are four Dihydropyridine CCBs?

A

Amlodipine, felodipine, isradipine, nifedipine (AFIN)

114
Q

What do Non-Dihydropyridine CCBs inhibit and what is the effect?

A

Inhibit calcium influx into cardiac smooth muscle, resulting is decreased rate and force of contractions

115
Q

What are the two Non-Dihydropyridine CCBs?

A

Verapamil, Diltiazem (VD…venereal disease)

116
Q

Where do Non-Dihydropyridine CCBs manly work?

A

In the heart. Reduce force and speed of cardiac contractions.

117
Q

What are other conditions of Non-Dihydropyridine CCBs can treat?

A

SVT, AFib

118
Q

Verapamil is used as prophylaxis for what?

A

Migraines

119
Q

What is a common adverse effect of all CCBs?

A

Hypotension

120
Q

What are 5 possible adverse reactions in Non-Dihydropyridine?

A

Constipation (Verapamil), Exacerbation of CHF, bradycardia, heart block, gingival hyperplasia

121
Q

Which Non-Dihydropyridine can cause constipation?

A

Verapamil

122
Q

Can Non-Dihydropyridines be used to treat CHF/heart failure?

A

NO! Will exacerbate and make much worse.

123
Q

What are four possible adverse effects of Dihydropyridines?

A

Peripheral Edema (worse w/Nifedipine), reflex tachycardia, flushing, headache

124
Q

Can Dihydropyridine CCBs be used for CHF?

A

Yes; especially Amlodipine, Felodipine, and Isradipine

125
Q

Peripheral edema occurs with which type of CCBs?

A

Dihydropyridine CCBs. Worst with Nifedipine.

126
Q

Which CCB causes the worst peripheral edema?

A

Nifedipine

127
Q

Peripheral edema from Dihydropyridine CCBs is dependent on what?

A

Dose dependent.

128
Q

Reflex tachycardia can happen with which CCBs?

A

Dihydropyridine CCBs

129
Q

Should you ever use sublingual Nifedipine?

A

NO! Causes severe hypotension and increased risk of MI.

130
Q

Dihydropyridine CCBs are useful for patients with what? What age group?

A

Isolated systolic hypertension, especially elderly.

131
Q

What is is the most common and second most common Dihydropyridine CCBs?

A

Amlodipine (Norvasc), Felodipine (Plendil)

132
Q

What allergy contraindicates Clevidipine via IV?

A

Soy or egg allergy

133
Q

Which cytochrome system metabolizes Verapamil?

A

P450 3A4

134
Q

Which cytochrome system can Verapamil inhibit?

A

P450 3A4 (same system that metabolizes it)

135
Q

What is BP goal for 45 y/o caucasian male who has a BP of 160/84? What classes are used first to treat?

A

Less than 140/90 due to age under 60. ACE-I, ARB, CCB, or Thiazide Diuretic.

136
Q

Furosemide is what type of diuretic?

A

Loop Diuretic

137
Q

Hypercalemia occurs with which type of diuretic?

A

Occurs with Thiazide Diuretics, not Loop Diuretics

138
Q

Aliskerin directly inhibits what?

A

Renin

139
Q

If a PT is taking Lisinipril (ACE-I) what dietary substitute should they avoid?

A

Avoid “salt substitute”

140
Q

Where do Thiazide Diuretics work?

A

In Distal Tubule (not in Loop of Henle) by inhibiting Na+ reabsorption leading to Na+ and H2O excretion

141
Q

Where do Loop Diuretics work?

A

in Thick Ascending Limb of Loop of Henle by inhibiting Na+, K+, and Cl- reabsorption leading to Na+ and H2O excretion

142
Q

Where do Potassium Sparing Diuretics work?

A

In Distal Tubule before Collecting Ducts (not in Loop of Henle) by either competing with Aldosterone or another non-Aldosterone mechanism leading to inhibiting of Na+ reabsorption and Na+ and H2O excretion

143
Q

Where do CCBs work?

A

In vascular and cardiac smooth muscle by inhibiting influx of serum Ca++ into smooth muscle preventing muscular contraction and leading to vasodilation

144
Q

Where do diuretics work?

A

In Nephron of kidney

145
Q

What is the preferred diuretic class for CHF?

A

Loop Diuretics

146
Q

Which class of diuretics is most potent?

A

Thiazides

147
Q

What are two gender side effects of Spirinolactone?

A

Gynecomastia, menstural irregularities

148
Q

What are the three most common ß-blockers?

A

Atenolol, Metoprolol Succinate, Metoprolol Tartrate

149
Q

How often are the three most ß-blockers dosed?

A

Atenolol: 1/day
Metoprolol Succinate: 1/day
Metoprolol Tartrate: 2/day

150
Q

What is the place in line of ß-blockers in HTN treatment?

A

Not first in line. Used only in PTs with heart or kidney disease.

151
Q

What is a ß-blocker used first in line for?

A

Heart failure, post-MI, high CAD, CKD

152
Q

ß-blockers are reserved for PTs who have significant histories of what two conditions?

A

Significant heart disease or kidney disease

153
Q

What is the MOA for ß-blockers?

A

Block Beta-1 receptors which decreases BP and HR by decreasing effects of epinepherine and norepineperhine.

154
Q

Beta 1 receptors are specific to which organ?

A

Heart. (We have 1 heart.)

155
Q

Beta 2 receptors are specific to which organ?

A

Lungs. (We have 2 lungs.)

156
Q

Beta 1 receptors are located in the ____, Beta 2 receptors are located in the ____

A

Beta 1=heart
Beta 2=lungs
(1 heart, 2 lungs)

157
Q

What do ß-blockers end in?

A

“-lol”

158
Q

ß-blockers that effect only Beta-1 receptors are known as what?

A

Cardioselective

159
Q

Which are the cardioselective ß-blockers?

A

Atenolol, Metopolol, Esmolol, Bioprolol, Betaxalol, Acebutol. (AMEBBA)

160
Q

Cardioselective ß-blockers are dependent on what?

A

Dose

161
Q

What are the two mixed alpha and beta blockers?

A

Carvedilol and Labetolol (CL)

162
Q

What are the four ISA ß-blockers?

A

Carteolol, Acebutolol, Pentbutolol, Pindolol (CAPP)

163
Q

How often are the ISA ß-blockers used?

A

Rarely, if at all

164
Q

Which receptors do the Non-Specific ß-blockers hit?

A

Beta 1 and Beta 2

165
Q

What are the three non-specific ß-blockers?

A

Nadolol, Propanolol, Timolol (NPT)

166
Q

Other than HTN what two other conditions is Propanolol used for?

A

Migraines and Hyperthyroidism (dose up to 4x/day to help with hyperthyroid symptoms)

167
Q

What is the major initial ß-blocker side effect?

A

“Beta Blocker Blues”: tired, fatigued, depressed, and a “funny” feeling in chest from heart beating slower. Will eventually go away within 1 month.

168
Q

What is a ß-blocker side effect that won’t go away after a month?

A

Sexual dysfunction

169
Q

What can happen if a ß-blocker is suddenly discontinued?

A

Rebound HTN

170
Q

Can a PT with asthma or COPD take a ß-blocker?

A

Yes, but cannot be a non-selective ß-blocker. Must be a cardioselective ß-blocker!

171
Q

What type of ß-blocker must an asthma or CPOD patient take and which to definitely avoid?

A

Take Cardioselective only. Definitely not “mixed” due to Beta-2 blocking.

172
Q

What condition can ß-blockers mask?

A

Hypoglycemia. PT may only be sweating but not other symptoms. Tell them to check BGL if sweating.

173
Q

If a PT is on a ß-blocker and is sweating what condition might they have?

A

Hypoglycemia

174
Q

ß-blockers are first line treatment for what heart condition? What do they prevent? Which three ß-blockers?

A

Heart failure, but only early stages by preventing heart remodeling. Metoprolol Succinate, Carvedilol, and Bisoprolol.

175
Q

What pregnancy category are ß-blockers in?

A

C

176
Q

Sotalol is a ß-blocker used for what condition?

A

Class III anti-arrhythmic. Most often used as anti-arrhythmic agent.

177
Q

Class III heart failure is treated by which medication?

A

Sotolol

178
Q

What class of heart failure does Solotol treat?

A

Class III

179
Q

What are the two types of Alpha blockers/agonists? Where in the body and which receptors do they work on?
(eg what receptors?)

A

Alpha 1 blockers cause vasodilation in periphery

Alpha 2 agonists cause vasodilation in brain “central”

180
Q

Where do Alpha 1 blockers work?

A

In periphery, cause vasodilation

181
Q

Where do Alpha 2 Agonists work?

A

In brain, cause vasodilation

182
Q

What do Alpha blockers end in?

A

“-zosin”

183
Q

What will Alpha 1 receptors normally do to vessels? Where are Alpha 1 receptors?

A

Alpha 1 causes constriction, found in periphery.

184
Q

What will Alpha 2 receptors normally do to vessels? Where are they found?

A

Alpha 2 normally causes dilation, found in brain

185
Q

Are Alpha blockers used as monotherapy or add-on?

A

Add-on

186
Q

What condition is an Alpha blocker used for as monotherapy?

A

Benign Prostatic Hypertrophy (BPH)

187
Q

What is the MOA for Alpha Blockers? Which receptor does it work on?

A

Completely inhibits Alpha-1 receptors in the periphery which causes vasodilation

188
Q

Who are Alpha blockers especially used in?

A

Males

189
Q

What two conditions are Alpha blockers used in?

A

HTN, BPH

190
Q

Which two Alpha blockers are used for BPH?

A

Tamsulosin (Flomax), Alfuzosin (Uroxatral)

191
Q

What is the Alpha blocker “first dose effect”?

A

Significant hypotension with first dose and subsequent dose titrations

192
Q

What type of “reflex” might happen in Alpha Blockers, especially in early therapy? When does it not happen?

A

Reflex Tachycardia. Doesn’t happen if also taking Beta-blocker.

193
Q

When does Reflex Tachycardia not happen with an Alpha blocker?

A

When PT is also on Beta-blocker

194
Q

What needs to happen to dose of an Alpha blocker in order to minimize side effects?

A

Slowly titrate up

195
Q

What are the daily frequency of Doxazosin, Terazosin, and Prazosin?

A

Doxazosin=1/day
Terazosin=1-2/day
Prazosin=2-3/day

196
Q

What is the MOA of an Alpha 2 Agonist?

A

Stimulates Alpha-2 receptors in brain which reduces sympathetic outflow from brain, which produces decrease in BP and peripheral vascular resistance

197
Q

What are the two Alpha 2 Agonists?

A

Methyldopa, Clonidine

198
Q

What class is Methyldopa?

A

Alpha 2 Agonist

199
Q

What is Methyldopa used for?

A

Limited use, but good in preggers (Category B)

200
Q

What is the pregnancy category for Methyldopa?

A

Category B.

201
Q

What drug class in Clonidine?

A

Alpha 2 Agonist

202
Q

What is Clonidine majorly used for?

A

Resistant HTN

Also for opiate substance withdrawal, adjunct in pain management, ADHD in kids

203
Q

What are some adverse effects of Alpha 2 Agonists?

A

Orthostatic hypotension, dizziness, fatigue, depression, sedation, Na+ and H2O retention, rebound tachycardia and HTN is abruptly stopped. Methyldope (liver toxicity, hemolytic anemia), Clonidine (rash with patch, anticholinergic effects like dry mouth, sedation, constipation, urinary retention)

204
Q

What are specific adverse effects of Methyldope and Clonidine?

A

Methyldope=liver toxicity, hemolytic anemia

Clonidine=rash with patch, anticholinergic effects like dry mouth, sedation, constipation, urinary retention

205
Q

How does Clonidine come and how long is it used?

A

Comes as a patch which stays on for 7 days

206
Q

How long does the Clonidine patch take to work and how long does it work after patch is removed?

A

Onset is 12-24 hours, continues to work up to 3 days after patch removed. (Alpha 2 Agonist)

207
Q

What is the MOA of Vasodilators?

A

Causes peripheral vasodilation. Direct vasodilators, especially in arteries and arterioles, leading to decreased systemic vascular resistance.

208
Q

Do Direct Vasodilators work centrally or peripherally?

A

Peripherally

209
Q

What are the two Vasodilator drugs?

A

Hydralazine, Minoxodil

210
Q

What are three common side-effects of Vasodilators?

A

Reflex Tachycardia, increased renin due to increased vasodilation causing fluid retention, headache

211
Q

How do you treat the side general side effects of Vasodilators? (Reflex tachycardia, fluid retention, headache)

A

Reflex tachycardia=Beta-blocker co-administration
Fluid Retention=Diuretic
Headache=NSAIDs

212
Q

What class is Hydralazine in?

A

Vasodilator

213
Q

What are 5 specific adverse effects of Hydralazine?

A

Lupus-like syndrome (uncommon), dermatitis, drug fever, peripheral neuropathy, hepatitis

214
Q

What class of drug is Minoxidil?

A

Vasodilator

215
Q

What is the adverse effect of Minoxidol?

A

Hirsutism (hair growth)

216
Q

Is Monoxidil used any longer for HTN?

A

No, but is used in Rogaine for hair growth

217
Q

What are the two preferred combos of HTN meds?

A

ACE-I/ARB + Thiazide

ACE-I/ARB + DihydroyrIdine CCB

218
Q

What are three acceptable combos of HTN meds?

A

CCT + Thiazide
Thiazide + Potassium Sparing Diuretic
Beta-blocker + Diuretic or Dihydropyridine CCB

219
Q

What sort of agents can induce HTN? (Lots!)

A

Corticosteroids, NSAIDs, Appetite Suppressants, Caffine, Cyclosporine, Estrogen, Pseudoephedrine, Thyroid hormone, Duloxetine, Venlafaxine, Erythropoietin?

220
Q

Why do patients stop taking their meds?

A

Think they don’t need it any longer, side-effects, cost, out of refills, confusion about what to take and when, pill burden

221
Q

44 y/o white male goes to PCP with a CC that his BP was high during health screening last month. BP last year was 158/84, advised to lose weight and exercise more.
FH: father HTN, died of MI at 54, mother DM and HTN and died from stroke at age 68.
SH: smoke 1 ppd, has job related stress
Now: 155/88, HR80, WNL labs, Scr 1.2. What is BP goal? Meds?

A

BP goal is 140/90 or less.

222
Q

Mildly overweight 55 y/o woman with a w/4-yr hx HTN and a 20 pack-year smoking. Admitted for community-acquired pneumonia. PMH: hyperlipidemia, angina, CKD (CrCl 40ml/min), and type 2 DM. FH: Father MI @ 63 years old. Meds: HCZT 25 mg/day, metoprolol tartrate 75 mg BID, Glipizide 5mg daily. Recent BP 163-167/88-108, HR 58-65. What meds? What BP goal?

A

Add ACE or ARB Losartan 50mg/day. Maintain both HCZT and Metoprolol.
BP goal: 140/90 or less

223
Q

JK 32 y/o female pregnant just diagnosed with HTN with BP 145/95. Which medication would you recommend for her?

A

Carvedilol (cat c in first trimester, d in 2nd and 3rd) or Methyldopa (cat b)

224
Q

75 y/o with BPH, hyperlipidemia, HTN. Meds: Metoprolol XL 100mg daily, Crestor 10mg daily. Due to his recent diagnosis of BPH which class and medication would you like to add?

A

Terazosen (Alpha 1 blocker)

225
Q

Does Acetaminophen increase BP?

A

No.

226
Q

Which lifestyle modification has greatest effect on BP?

A

Weight loss

227
Q

What is the required creatinine clearance for Metalozone and Furosemide?

A

Less than 30 mL/min

228
Q

Which of these can cause hyperkalemia? Lisinopril, Valsartan, Bisoprolol (Can be more than one.)

A

Lisinopril and Valsartan. ACE-Is and ARBs can cause hyperkalemia.

229
Q

What do you do for a patient who has developed a dry cough from taking an ACE-I?

A

Discontinue the ACE-I and start ARB.

230
Q

Which of the following is Beta-1 selective?

Bisoprolol, Carvedilol, Pindolol, Labetolol, Nadolol

A

Bisoprolol

231
Q

Can Aliskiren be combined with an ARB or ACE-I? Why?

A

No, due to K+ and kidneys issues.

232
Q

Which three drug classes are always dosed in the morning?

A

Thazides, Loop, K sparing diuretics.

233
Q

What type of ß-blocker is Propanolol?

A

Propanolol is nonselective ß blocker.

234
Q

Can you use ACE-Is and/or ARBs with renal artery stenosis?

A

Do not use ACE-I in rental art stenosis, caution with ARBs

235
Q

What classes can cause rebound HTN if suddenly discontinued?

A

Beta blocker and Alpha 2 Agonist clonidine

236
Q

What effect do ARBs have on Bradykinin?

A

ARBs do not inhibit bradykinin breakdown

237
Q

What are two good agents to use in a pregnant HTN woman?

A

Methyldopa and Levatolol

238
Q

If a PT is hyperkalemic what classes of antihypertensives should you avoid using?

A

ACE-I, ARB, K sparing diuretics

239
Q

What does an ACE-Inhibitor prevent the conversion of?

A

Conversion of Angiotensin I to Angiotensin II

240
Q

How often is metoprolol succsincate dosed?

A

Once a day

241
Q

What is Captopril’s most common side effect?

A

cough (ACE-I)

242
Q

What type of edema can happen with dihydropyridines?

A

Peripheral edema

243
Q

ARBs compete with what and cause excretion of what?

A

ARBs compete with Aldosterone which causes excretion of Na

244
Q

What HTN medications require caution is a PT has a Sulfa allergy?

A

Thazides and Loop Diuretics use caution

245
Q

How often is an ACE-I dosed?

A

1/day

246
Q

What is the #1 side-effect from Verapimil?

A

Constipation

247
Q

What is a major side-effect of ACE-Is that can possibly be fatal?

A

Angioedema-swelling of face/lips/necks in ACE-I (less commonly in ARBs)

248
Q

Which ß-blocker can prevent migraines?

A

Propranolol can prevent migraines

249
Q

HCZT causes electrolytes to go in which direction?

A

Down:Na and K
Up:Ca, Uric acid, Glucose

250
Q

How often is the Clonidine patch changed?

A

Changed every 7 days

251
Q

Which class of CCBs are avoided in CHF?

A

Non-dihydropyradine CCBs (Verapimil, Diltiazem)

252
Q

Where do Loop Diuretics work in the nephron?

A

Loop of Henle thick ascending segment

253
Q

Where do Thiazide diuretics work?

A

Distal tubule

254
Q

What are the two first-line treatments in African Americans without DM or CKD?

A

CCBs and Thiazides

255
Q

Which classes must a PT avoid “salt substitute”?

A

ACE, ARB, K sparring diuretic, Aldostone blocker

256
Q

When are Alpha 1 blockers dosed?

A

Night

257
Q

Can a pregnant PT take an ACE/ARB?

A

NO

258
Q

Can you use Propanolol in someone who has asthma?

A

NO

259
Q

Can you use a Beta Blocker in a PT who has a heart block?

A

NO

260
Q

Can you use a Beta Blocker in a PT who has a severe peripheral vascular disease?

A

No

Pharmacology 2 (17 decks)

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