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Therapeutics 2 Final Exam > Therapeutics of Hypertension > Flashcards

Therapeutics of Hypertension Flashcards

1
Q

What is hypertension?

A

Persistently elevated arterial blood pressure

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2
Q

What are the symptoms of hypertension?

A

Majority of patients are asymptomatic

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3
Q

What is the most significant risk factor for cardiovascular disease?

A

Hypertension

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4
Q

By 2030, what percent of Americans are expected to have hypertension?

A

40%

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5
Q

What is essential hypertension?

A

Elevated arterial blood pressure with an unknown cause

(hypertension is the main or “essential” disease state)

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6
Q

What is secondary hypertension?

A

Elevated arterial blood pressure due to an identifiable cause
(such as concurrent medical conditions or medications)

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7
Q

What is isolated systolic hypertension?

A

Systolic BP values are elevated but diastolic BP values are not

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8
Q

What patients is systolic hypertension more common in and why?

A

Older patients
-vasculature is not as flexible

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9
Q

What are the criteria for diagnosis of resistant hypertension?

A

Fail to attain goal BP while adherent to regimen of at least 3 agents at max dose (must include a diuretic)

OR

When 4 or more agents are needed

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10
Q

What are the criteria for diagnosis of orthostatic hypotension?

A

Systolic blood pressure decrease of > 20 mmHg

OR

Diastolic blood pressure decrease of > 10 mmHg within 3 minutes of positional change

OR

Increase in heart rate > 20 bpm

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11
Q

What is the equation for blood pressure?

A

BP= CO x TPR

CO= cardiac output
TPR=total peripheral resistance

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12
Q

What is the equation for cardiac output?

A

CO=SV x HR

SV= strove volume
HR= heart rate

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13
Q

What two factors determine blood pressure?

A

Cardiac output

Total peripheral resistance

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14
Q

What two factors determine cardiac output?

A

Stroke volume

Heart rate

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15
Q

What are the modifiable hyprtension risk factors?

A

-High sodium intake
-Obesity
-Low potassium intake
-Excess alcohol intake

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16
Q

What is considered excess alcohol intake?

A

Men: > 2 drinks per day

Women: > 1 drink per day

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17
Q

What are the non-modifiable hypertension risk factors?

A

-Age
-Ethnicity
-Genetic predisposition
-Gender

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18
Q

What gender is more likely to develop hypertension?

A

Age < 55: Male

Age 55-64: Female

Age > 64: Female

*menopause plays a role in this

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19
Q

What substances increase BP?

A

-Illicit drugs (cocaine, ecstasy)
-Caffeine
-Nicotine
-Decongestants (pseudoephedrine, phenylephrine)
-Amphetamines (methylphenidate, dextroamphetamine)
-Antidepressants (MAOIs, SNRIs, TCAs)
-Atypical antipsychotics (clozapine, olanzapine)
-Immunosuppressants (cyclosporine)
-Oral contraceptives
-NSAIDs (ibuprofen, naproxen, etc)
-Systemic steroids (methylprednisolone, prednisone, prednisolone, dexamethasone)
-Oncology agents (angiogenesis inhibitors, tyrosine kinase inhibitors)

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20
Q

What is the in-office blood pressure measurement technique?

A

-Two readings 5 mins apart
-Sitting in chair
-Confirm elevated reading in opposite arm

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21
Q

When would ambulatory BP monitoring (ABPM) be indicated?

A

Evaluation of:

white-coat hypertension
masked hypertension
nighttime BP dipping

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22
Q

When would home BP monitoring (HBPM) be indicated?

A

Evaluation of:

white-coat hypertension
masked hypertension
response to therapy
*may improve adherence

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23
Q

What is masked hypertension?

A

Hypertension not detected in office but detected at home

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24
Q

What is the classification of normal blood pressure?

A

Systolic: <120
AND
Diastolic: <80

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25
Q

What is the classification of elevated blood pressure?

A

Systolic: 120-129
AND
Diastolic: <80

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26
Q

What is the classification of Stage 1 hypertension?

A

Systolic: 130-139
OR
Diastolic: 80-89

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27
Q

What is the classification of Stage 2 hypertension?

A

Systolic: > or = 140
OR
Diastolic: > or = 90

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28
Q

What is the classification of a hypertensive crisis?

A

Systolic: >180
AND/OR
Diastolic: >120

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29
Q

What is the ACC/AHA strategy for Normal BP (<120/80)

A

Promote healthy lifestyle
Reassess in 1 year

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30
Q

What is the ACC/AHA strategy for Elevated BP (120-129/<80)?

A

Non-pharmacological treatment
Reassess in 3-6 months

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31
Q

What is the ACC/AHA strategy for Stage 1 HTN (130-139/80-90)?

A

1st: Assess if ASCVD risk >10% OR does the patient have a specific comorbidity?

If yes: Non-pharmacological treatment AND medication
Reassess in 1 month

If no: Non-pharmacological treatment
Reassess in 3-6 months

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32
Q

What is the ACC/AHA strategy for Stage 2 HTN (> or = 140/90)?

A

Non-pharmacological treatment
+ 2 medications!
Reassess in 1 month

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33
Q

How often should hypertension patients at goal have their follow-up appointments?

A

every 3-6 months

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34
Q

What is the standard process we follow when scheduling follow-up appointments for hypertension patients?

A

No high BP: 1 year
Life style modification only: 3-6 months
Medication change: 1 month

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35
Q

What is the goal blood pressure for most comorbidities and clinical conditions?

A

Less than 130/80

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36
Q

In what three instances would a patient have a goal blood pressure of 140/90?

A

No clinical CVD and 10 year ASCVD risk <10%

Secondary stroke prevention

Elderly/frail patients with high comorbidity burden + limited life expectancy

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37
Q

What are the specific comorbidities that should be taken into consideration when establishing HTN treatment?

A

-Diabetes mellitus
-Chronic Kidney Disease
-Heart Failure
-Stable ischemic heart disease
-Secondary stroke prevention
-Peripheral artery disease

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38
Q

What is the blood pressure goal for elderly/frail patients with high comorbidity burden and short lifespan?

A

<140/90

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39
Q

What is the blood pressure goal for the majority of people?

A

<130/80

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40
Q

What is the KDIGO systolic blood pressure goal for adults with elevated BP and CKD?

A

<120

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41
Q

What was the SPRINT trial investigating and what were the result?

A

Intensive (<120) vs Standard (<140) BP goals
in patients without diabetes

-Primary composite outcome of cardiovascular issues/ death was reduced in the intensive group

-Intensive goal is difficult to maintain and the trial group did not reach the goal. Also 2.8 medications needed for intensive goal

-Intensive group was at higher risk of kidney injury, hypotension, and electrolyte abnormalities

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42
Q

What was the ACCORD trial investigating and what were the results?

A

Intensive (<120) vs Standard (130-140) BP treatment
in patients with type 2 diabetes

Lowering blood pressure under 140/90 has major benefits!

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43
Q

If a low blood pressure is shown to be beneficial in the SPRINT and ACCORD trials, why is the blood pressure goal for most people <130/80 and not 120?

A

Having a stricter goal but not 120 makes it easier for patients to adhere to and achieve the goal

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44
Q

By how much should sodium be reduced to decrease blood pressure?

A

<1500 mg/day OR 1000 mg reduction per day

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45
Q

By how much should potassium intake be increased to decrease blood pressure?

A

3500-5000 mg/day

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46
Q

Which intervention has the largest impact on lowering blood pressure?

A

DASH diet
(-11 mmHg)

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47
Q

What foods should be limited in a DASH diet?

A

-High in saturated fats
-Sugar-sweetened beverages and sweets

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48
Q

What are the first-line agent for hypertension?

A

-Thiazide diuretics
-CCBs (calcium channel blockers)
-ACE inhibitors
-ARBs

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49
Q

What is considered the overall first-line hypertension treatment?

A

Thiazide diuretics

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50
Q

What did the ALLHAT trial examine and what are the takeaways?

A

-Accessed antihypertensive and lipid-lowering treatment to prevent heart attacks

Takeaways:
-Thiazide diuretics should be first-line
-For patients who cannot take a diuretic: calcium channel blocker or ACEi
-Most high BP patients need more than one drug

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51
Q

If a patient needs to start 2 antihypertensive agents, are all first-line medication combinations acceptable?

A

NO

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52
Q

What are the 4 preferred combination therapies?

A

ACEi/CCB
ARB/CCB
ACEi/diuretic
ARB/diuretic

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53
Q

What is an acceptable but not preferred combination therapy?

A

CCB/diuretic

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54
Q

What is not an acceptable combination therapy?

A

ACEi/ARB

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55
Q

What is the hypertension treatment for Stable Ischemic Heart Disease?

A

1st Line:
-Beta blocker
-ACEi/ARB

Reduce BP < 130/80

If 1st line agent added and BP goal not met + patient develops angina:
-Add dihydropyridine CCB

If 1st line agent added and BP goal not met but the patient does not develop angina:
-Add dihydropyridine CCB, thiazide, and/or MRA

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56
Q

What are the benefits of using beta blockers?

A

Reduce CV events and anginal symptoms

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57
Q

What are the benefits of using ACEi/ARBs?

A

Reduce:
-MI
-Stroke
-CVD

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58
Q

What is the hypertension treatment for heart failure?

A

Reduced ejection fraction:
-Follow most recent guidelines
-AVOID non-dihydropyridine CCB (no benefit/worse outcomes)

Preserved ejection fraction:
–Use any of the following:
Diuretic (fluid overload) Loop
ACEi/ARB (elevated BP)
Beta blocker (elevated heart rate)

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59
Q

In heart failure, when would you choose to treat hypertension with a diuretic?

A

Fluid overload

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60
Q

In heart failure, when would you choose to treat hypertension with an ACEi/ARB?

A

Elevated BP

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61
Q

In heart failure, when would you choose to treat hypertension with a beta blocker?

A

Elevated heart rate

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62
Q

What is the hypertension treatment for Chronic Kidney Disease?

A

Stage 1 or 2 WITH albuminuria:
ACEi (or ARB if not tolerated)

Stage 1 or 2, NO albuminuria:
Normal first-line options

Stage 3 or higher:
ACEi (or ARB if not tolerated)

Post kidney transplant:
Dihydropyridine CCB
(improved GFR and kidney survival)

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63
Q

What are the GFR ranges for the different stages of kidney disease?

A

Stage 1: >90%
Stage 2: 60-89%
Stage 3: 30-59%
Stage 4: 15-29%
Stage 5: <15%

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64
Q

What is the hypertension treatment in cerebrovascular disease?

A

Secondary stroke prevention:
1st: thiazide
2nd: ACEi/ARB
*combination of both

BP Goal: <140/90 (usefulness of lower goal is unknown)

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65
Q

What is the hypertension treatment in diabetes?

A

No Albuminuria:
All first-line classes are useful
(thiazide or CCB)
*ACE/ARB used in combination therapy if needed

Albuminuria:
ACEi or ARB

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66
Q

What is the definition of albuminuria?

A

> 300 mg/day
OR
300 mg/g albumin-to-creatinine ratio

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67
Q

What are the preferred agents in pregnancy?

A

Methyldopa (central alpha-2 agonist)
Nifedipine (dihydropyridine CCB)
Labetalol (beta blocker)

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68
Q

What drugs are contraindicated in pregnancy?

A

ACEi
ARBs
Direct renin inhibitors

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69
Q

In black adults with no HF or CKD, what is the initial antihypertension treatment?

A

Thiazide diuretic or CCB

*this includes black patients with diabetes

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70
Q

What are the 4 thiazide diuretics?

A

-Chlorthalidone
-Hydrochlorothiazide
-Indapamide
-Metolazone

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71
Q

What are the 4 loop diuretics?

A

-Furosemide
-Torsemide
-Bumetanide
-Ethacrynic acid*

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72
Q

What are the 2 aldosterone antagonists?

A

-Spironolactone
-Eplerenone

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73
Q

What are the 2 potassium-sparing diuretics?

A

-Amiloride
-Triamterene

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74
Q

What 2 types of diuretics INCREASE potassium levels?

A

-Aldosterone antagonists
-Potassium-sparing diuretics

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75
Q

What 2 types of diuretics DECREASE potassium levels?

A

-Thiazide
-Loop

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76
Q

What are the initial effects of anti-hypertensive agents?

A

Diuresis -> Reduced Stroke Volume -> Increase in Peripheral Vascular Resistance (PVR)

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77
Q

What are the chronic effects of anti-hypertensive agents?

A

Stroke volume returns to normal -> Decrease in Peripheral Vascular Resistance (PVR) (to below pre-treatment levels)

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78
Q

What is the most potent thiazide diuretic?

A

Chlorthalidone
(1-2 x more potent than HCTZ)

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79
Q

At what CrCl are thiazide diuretics more effective than loop diuretics?

A

CrCl > 30 mL/min

(thiazide diuretics work in the kidneys and so must have at least some kidney function to work)

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80
Q

What time of day should diuretics be taken?

A

In the morning (avoid nocturnal diuresis)

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81
Q

How frequently are ALL thiazide diuretics dosed?

A

Once daily

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82
Q

True or False: MAX doses of diuretics are more effective than lower doses at lowering BP

A

FALSE
-MAX doses tend not to be more effective at lowering blood pressure and produce more side effects
-MAX doses are rarely used for lowering blood pressure

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83
Q

True or False: Thiazide diuretics can cause hyperglycemia and therefore should not be used in diabetic patients

A

FALSE
-thiazide diuretics CAN cause hyperglycemia, however, this does not prevent us from starting them in patients with diabetes since benefits outweigh risks

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84
Q

What are the drug interactions that occur with thiazide diuretics?

A

Lithium toxicity with concurrent use

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85
Q

What are the contraindications of thiazide diuretics?

A

Sulfa allergy

-Anuria (not producing urine)

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86
Q

When are loop diuretics preferred for HTN?

A

-Heart failure for symptom management
-CrCl < 30 mL/min

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87
Q

When would the loop diuretic ethacrynic acid be used?

A

Only in patients with a sulfa allergy

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88
Q

Loop diuretics exhibit a high-ceiling dose response curve, what does this mean?

A

-May need higher doses with severely reduced renal function or fluid overload

-Switching to a different loop diuretic or from PO to IV may help

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89
Q

Which loop diuretics have a dosing frequency of 1 or 2?

A

Furosemide
Bumetanide

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90
Q

Which loop diuretic is only dosed once daily?

A

Torsemide

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91
Q

What are the contraindications of loop diuretics?

A

Sulfa allergy

-except ethacrynic acid

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92
Q

What is the preferred aldosterone antagonist?

A

Spironolactone

93
Q

When would we use eplerenone instead of spironolactone?

A

Switch patient to eplerenone if they develop gynecomastia

94
Q

When are aldosterone antagonists (spironolactone) the preferred treatment option for hypertension?

A

Resistant hypertension

95
Q

What is one of the most important side effects to know for spironolactone?

A

Gynecomastia (develops in 10% of patients)

96
Q

At what potassium levels should aldosterone antagonists NOT be initiated?

A

> 5 mEq/L

97
Q

Are aldosterone antagonists diuretics?

A

YES
-make sure to dose in morning

98
Q

What is the dosing frequency of BOTH aldosterone antagonists?
(spironolactone and eplerenone)

A

Once or Twice daily
(1 or 2)

99
Q

In what circumstances would we consider holding or reducing the aldosterone antagonist dose?

A

Potassium > 5.5 mEq/L

SCr increases >25%

100
Q

What are the drug interactions associated with aldosterone antagonists?

A

ACEi
ARBs
Renin inhibitors
NSAIDs

(all increase risk of hyperkalemia)

101
Q

What are the contraindications associated with aldosterone antagonists?

A

Eplerenone:
-Impaired renal function
CrCl <50 or SCr >2 (male) or SCr > 1.8 (female)

-Type 2 Diabetes with Proteinuria

Both:
-Concomitant use of potassium sparing diuretics

102
Q

When are potassium-sparing diuretics used?

A

-Minimal BP effects
-Use in combination with thiazide to minimize hypokalemia

103
Q

Who should potassium-sparing diuretics be used with caution in?

A

Patients with diabetes or CKD (GFR < 45)

Patients with uncontrolled gout

104
Q

What is the dosing frequency for all potassium-sparing diuretics?

A

Once or twice daily
(1 or 2)

105
Q

When should electrolytes + renal function be monitored with diuretics?

A

Baseline
1-2 weeks after initiation
3-4 weeks after initiation (loop and aldosterone only)
Every 6-12 months

106
Q

When is spironolactone a first-line option?

A

Resistant HTN

107
Q

Can potassium-sparing diuretics be used as monotherapy for hypertension?

A

No

108
Q

What is the mechanism of action of ACEi?

A

Inhibit conversion for angiotensin I to angiotensin II

109
Q

What is the mechanism of action of ARBs?

A

Block effects of angiotensin II by binding to target receptors

110
Q

What is the mechanism of action of renin inhibitors?

A

Inhibit conversion of angiotensinogen to angiotensin I

111
Q

What patients populations may have increased benefits from taking ACEi?

A

-Diabetes w/ proteinuria
-Heart Failure
-Post MI
-Chronic kidney disease

112
Q

What is an additional benefit of using ACEi or ARBs regarding time-of-day dosing?

A

Good options for PM dosing

-ensure “BP dipping” overnight

113
Q

How do ACEi and ARBs affect hypertension?

A

Vasodilation
Reduced pulmonary vascular resistance (PVR)
Increased diuresis

114
Q

Do ACEi need to be titrated?

A

Need to start at low dose and increase SLOWLY
Never start on a max dose

115
Q

What is the only ACEi that does not have once daily dosing?

A

Captopril
(2 or 3)

116
Q

What are 4 side effects of ACEi?

A

-Angioedema

-Cough (up to 20%) (due to excess bradykinin, dry and hacky)

-Hyperkalemia

-Acute renal failure w/ severe bilateral renal artery stenosis

117
Q

What are the contraindications associated with ACEi?

A

-History of angioedema while on an ACEi
-Concomitant use of aliskiren in patients with DM
-Pregnancy/breastfeeding

118
Q

True or False: If a patient has adverse effects on one ACEi we can try starting them on a different one

A

FALSE, do not try another ACEi
*especially if angioedema

119
Q

Why do ARBs not cause cough like ACEi do?

A

Do not block bradykinin breakdown

120
Q

True or False: All ARBs offer once daily dosing?

A

True

121
Q

Which two ARBs have both once daily and BID dosing?

A

Eprosartan

Losartan

122
Q

What time of day are ARBs given?

A

Prefer to give at bedtime but can be ok to take in the morning

123
Q

What are the adverse effects of ARBs?

A

-Angioedema
-Hyperkalemia
-Acute renal failure w/ severe bilateral renal artery stenosis

same as ACEi except for cough

124
Q

True or False: ARBs can still be used with history or angioedema due to ACEi

A

TRUE

-even though angioedema is a side effect of ARBs, they can still be used to replace ACEi in patients with ACEi-related angioedema

125
Q

What contraindications are associated with ARBs?

A

-History of angioedema on an ARB
-Concomitant use of aliskiren in patients with DM
-Pregnancy/breastfeeding

*basically same as ACEi

126
Q

What two things need to be monitored with ACEi/ARB use?

A

Potassium

Renal Function

127
Q

In what two scenarios would we consider holding or reducing an ACEi or ARB dose?

A

Potassium > 5.5 mEq/L

SCr increase > 30%

128
Q

What agent is the only direct renin inhibitor?

A

aliskiren

129
Q

Why are direct renin inhibitors not first-line agents?

A

Very expensive and are no better than ACEi/ARBs

130
Q

What are the contraindications for aliskiren?

A

Pregnancy

Concomitant use with an ACEi or ARB in patients with diabetes

131
Q

What is a down-side to dosing of aliskiren?

A

Not a lot of dose titration available

132
Q

How frequently is aliskiren dosed?

A

Once daily

133
Q

What is monitored with aliskiren use?

A

Potassium
BUN
SCr

134
Q

What broad category do ACEi, ARBs, and Renin inhibitors fall into?

A

Angiotensin Inhibitors

135
Q

What affect do all angiotensin inhibitors have on potassium levels?

A

Increase potassium
(hyperkalemia is a risk)

136
Q

Can angiotensin inhibitor drug classes be combined?

A

NO
Do not combine ACEi, ARBs, or Renin inhibitors

-increased risk of adverse effects

137
Q

What is an important thing to remember about angiotensin inhibitors and women of childbearing age?

A

Need to discuss contraceptive methods with these women

*If a patient is wanting to become pregnant, do not use these drugs!

138
Q

What is the mechanism of action of calcium channel blockers (CCBs)?

A

Inhibit influx of calcium across cardiac and smooth muscle cell membranes

-Leads to coronary and peripheral vasodilation

139
Q

What are the 2 subclasses of calcium channel blockers (CCBs)?

A

Dihydropyridines
Nondihydropyridines

*both have similar effect on BP

140
Q

Which subclass of CCB’s is preferred?

A

Dihydropyridines cause more vasodilation so are preferred

-Nondihydropyridines can cause more negative inotropic effects

141
Q

What patient populations may have added benefits from dihydropyridine calcium channel blockers?

A

Reynaud’s syndrome

Elderly patients w/ isolated systolic HTN (due to vascular stiffness)

*this is because of CCB’s ability to cause vasodilation

142
Q

Which subclass of calcium channel blockers causes more vasodilation?

A

Dihydropyridine CCBs

143
Q

What effect can CCBs have on heart rate?

A

Vasodilation from CCBs can cause baroreceptor-mediated tachycardia (increased heart rate)

144
Q

What two dihydropyridines should be avoided?

A

Short-acting dihydropyridines:

-IR Nifedipine
-Nicardipine

145
Q

Which 2 dihydropyridine CCBs have BID dosing?

A

-Isradipine
-Nicardipine SR

*can also include IR nifedipine in this

**Do not use these due to tachycardia issues

146
Q

Which two dihydropyridine CCBs do not have negative inotropic effects?

A

-Amlodipine
-Felodipine

(do not affect heart rate)

147
Q

What are the side effects of dihydropyridine CCBs?

A

-Reflex tachycardia
-Flushing
-Dizziness
-Headache
-Peripheral edema (dose related)
-Gingival hyperplasia

148
Q

What warning is associated with dihydropyridine CCBs?

A

Increased risk of angina/MI in patients with obstructive coronary disease due to reflex tachycardia

149
Q

What are the drug interactions associated with dihydropyridine CCBs?

A

-Grapefruit juice
-CYP3A4 enzyme inducers/inhibitors

150
Q

What dihydropyridine CCB is preferred in patients with angina?

A

Amlodipine

151
Q

What patient populations may have additional benefit from using a nondihydropyridine CCB?

A

Supraventricular tachyarrhythmias (Afib)

Patients with angina unable to tolerate a beta blocker

152
Q

What effects do nondihydropyridine CCBs have on heart rate?

A

Slow AV node conduction

Decrease heart rate
(negative inotropic effects)

153
Q

What are the 2 nondihydropyridine CCBs?

A

Diltiazem ER

Verapamil ER

*ER forms are preferred

154
Q

What is the frequency of dosing for both diltiazem ER and verapamil ER?

A

Once or Twice daily
(1 or 2)

155
Q

What drug interactions are associated with nondihydropyridine CCBs?

A

-Concomitant use of beta blockers (increase risk of heart block)

-Grapefruit juice

-CYP3A4 inducers/inhibitors (3A4 substrates)

156
Q

What contraindications are associated with nondihydropyridine CCBs?

A

-Heart block
-Left ventricular dysfunction

157
Q

What labs should be checked with CCBs?

A

None, no routine monitoring required

158
Q

True or False: Nondihydropyridine CCB formulations can be interchanged?

A

FALSE
-not interchangeable due to differences in release mechanisms and bioavailability

159
Q

If a CCB is needed in the setting of heart failure, which one do we choose?

A

Amlodipine

160
Q

Which medication class is more likely to cause edema in an ankle? CCB, ARBs, or ACEi?

A

CCB

CCB can cause peripheral edema (usually in lower limbs) whereas ARBs and ACEi can cause angioedema (swelling of face, throat, or groin)

161
Q

What are 2 compelling indications to use a beta blocker for HTN?

A

Heart Failure

CAD

162
Q

What patient populations may have additional benefits from using a beta blocker?

A

-Tachyarrhythmias
-Tremors
-Migraines
-Thyrotoxicosis

163
Q

How do beta blockers work?

A

Decrease both heart rate and force of contraction which leads to a decrease in cardiac output (CO)

164
Q

True or False: Beta blockers need to be titrated?

A

TRUE
-Avoid abrupt cessation
-titrate off to avoid rebound increase in heart rate + BP or heart events

165
Q

What are the cardioselective beta blockers?

A

Atenolol
Betaxolol
Bisoprolol
Metoprolol tartrate
Metoprolol succinate
Nebivolol

166
Q

What is the only cardioselective beta blocker with BID dosing (not once daily)?

A

Metoprolol Tartrate

(short-acting form of metoprolol)

167
Q

What is the only beta blocker that causes nitric oxide induced vasodilation?

A

Nebivolol

168
Q

What are the 3 nonselective beta blockers?

A

Nadolol
Propranolol IR
Propranolol LA

169
Q

What is the only nonselective beta blocker with BID dosing (not once daily)?

A

Propranolol IR

170
Q

When would nonselective beta blockers be used instead of cardioselective beta blockers?

A

If we are trying to treat two conditions with one beta blocker
-Such as both blood pressure and migraine

171
Q

When should nonselective beta blockers be avoided?

A

In bronchospastic airway disease
(asthma and COPD)

172
Q

What are the 3 beta blockers with intrinsic sympathomimetic activity (ISA)?

A

Acebutolol
Penbutolol
Pindolol

173
Q

Which beta blocker with intrinsic sympathomimetic activity (ISA) is the only one with once daily dosing?

A

Penbutolol

174
Q

When should beta blockers with intrinsic sympathomimetic activity (ISA) be avoided?

A

Heart failure
Ischemic Heart Disease (IHD)

175
Q

When should beta blockers with intrinsic sympathomimetic activity (ISA) be used?

A

-Do not decrease heart rate, just prevent it from going up
-In theory, use these in patients with low heart rate
-In reality, DO NOT PUT PATIENTS ON THESE (unknown effects)

176
Q

What are the two mixed alpha/beta beta blockers?

A

Carvedilol
Labetalol

177
Q

What is the frequency of both of the mixed alpha/beta blockers?

A

BID (2)

178
Q

When would we use mixed alpha/beta blockers?

A

If blood pressure is close to goal but not quite there

179
Q

What adverse effects are associated with all beta blockers?

A

-Bronchospasm
-Bradycardia
Fatigue
-Exercise intolerance
-Depression
Masked signs of hypoglycemia

180
Q

Why can beta blockers cause fatigue?

A

Patients notice this in the first few weeks of starting the medication, occurs because heart rate is prevented from increasing which would occur normally with physical tasks

*this goes away after the patient gets used to the medication

181
Q

In patients with peripheral artery disease, which beta blocker is preferred?

A

Carvedilol

182
Q

In which groups of patients should beta blockers be used with caution?

A

-Peripheral artery disease
-Reactive airway disease

183
Q

In patients with reactive airway disease, which beta blockers are preferred?

A

Selective beta blockers

184
Q

What contraindications are associated with all beta blockers?

A

-Second or third degree heart block
-Decompensated heart failure
-Post-MI
-Severe bradycardia
-Sick sinus syndrome

185
Q

What is the last-line therapy for hypertension?

A

Direct Arterial Vasodilators

186
Q

What are the 2 direct arterial vasodilators?

A

Hydralazine

Minoxidil

187
Q

Who do we use direct arterial vasodilators in for hypertension?

A

Reserved for patients with special indications (severe CKD or hemodialysis)
OR
Very difficult to control BP

188
Q

Which direct arterial vasodilator is the most potent?

A

Minoxidil

189
Q

Can direct arterial vasodilators be used as monotherapy for HTN?

A

NO
need to be used concomitantly with a DIURETIC and BETA BLOCKER

*loop diuretic preferred

190
Q

Why do direct arterial vasodilators need to be used as a combination therapy?

A

-They cause vasodilation which increases heart rate and ultimately ends up in more fluid retention due to sodium

*need to prevent this

191
Q

Which diuretic is preferred for concomitant use with minoxidil and why?

A

Loop diuretics are preferred

-these diuretics move more fluid which is needed since minoxidil is very potent

192
Q

What is the dosing frequencies of hydralazine and minoxidil?

A

Hydralazine: 2-4

Minoxidil: 1-3

**higher dosing regimens are common, can cause adherence issues

193
Q

Why do we prefer to avoid minoxidil in women and children?

A

Can cause unwanted hair growth

194
Q

What are the adverse effects of direct arterial vasodilators?

A

-Palpitations
-Tachycardia
-Chest pain
-GI side effects
-Headache
-Hematologic dyscrasias
-Hepatotoxicity
*Fluid retention
*Lupus-like syndrome/rash (hydralazine) [joint pain, weakness, fevers]
*Hair growth (minoxidil)

195
Q

What is the boxed warning for minoxidil?

A

-May cause: pericarditis and pericardial effusion that can progress to tamponade

-Can increase oxygen demand and exacerbate angina pectoris

196
Q

Who should we use direct arterial vasodilators with caution in?

A

-CVA
-Renal impairment
-CAD
-Liver disease
-SLE

197
Q

How many other drugs need to be used before trying minoxidil?

A

Maximum therapeutic doses of a diuretic + 2 other antihypertensives

198
Q

What are the 3 alpha-1 blockers?

A

-Doxazosin
-Prazosin
-Terazosin

199
Q

True or False: Alpha-1 Blockers are never considered first-line for HTN

A

TRUE

200
Q

When do we use alpha-1 blockers for HTN?

A

Second-line for patients with concomitant benign prostatic hyperplasia (BPH)

201
Q

What is a common side effect of alpha-1 blockers? (especially in the elderly)

A

Orthostatic hypotension

202
Q

What is another use for the alpha-1 blocker prazosin?

A

Nightmares, especially associated with PTSD

203
Q

What are the 3 central alpha-2 agonists?

A

-Clonidine
-Methyldopa
-Guanfacine

204
Q

What drug class is considered last-line therapy for hypertension?

A

Alpha-2 Agonists

-because of adverse effects

205
Q

True or False: Central Alpha-2 Agonists need to be titrated

A

True
-avoid abrupt cessation due to rebound hypertension

206
Q

What 3 drug classes need to be titrated?

A

-ACEi (when starting)
-Beta blockers (when stopping)
-Central Alpha-2 Agonists (when stopping)

207
Q

Which central alpha-2 agonist is preferred in pregnancy?

A

methyldopa

208
Q

What two dosage forms does clonidine come in?

A

PO

Patch

209
Q

What are some reasons why we would use the patch form of clonidine and not the PO form?

A

-Lower risk of rebound hypertension with patch
-Improved adherence with patch

210
Q

How do we titrate patients off of clonidine?

A

-Slow wean (half dose every 2-3 days)
-Concomitant beta blocker prescribed
-Wean BB several days prior to clonidine wean

211
Q

When changing from oral clonidine to the patch form, how many days of overlap should there be with the oral regimen?

A

3-4 days

(takes time for patch to begin working)

212
Q

What is the titration schedule when switching from oral clonidine to the patch form?

A

Day 1: Place Patch, Give 100% of oral dose

Day 2: Give 50% of oral dose

Day 3: Give 25% of oral dose

Day 4: Patch only

213
Q

When switching from the patch form of clonidine to oral, how long after removing the patch should oral clonidine be started?

A

Do not start oral clonidine sooner than 8 hours after patch removal

After 8 hours, can start oral medication

214
Q

What parameters need to be monitored for ACEi/ARBs?

A

-BUN
-SCr
-Potassium

*Same as aldosterone antagonists

215
Q

What parameters need to be monitored for CCBs?

A

Heart rate (non-dihydropyridine)

216
Q

What parameters need to be monitored for Aldosterone Antagonists?

A

-BUN
-SCr
-Potassium

*Same as ACEi/ARB

217
Q

What parameters need to be monitored for Beta Blockers?

A

Heart rate

*same as CCB

218
Q

What should be done if a patient on antihypertensives is not at goal?

A

-Consider nighttime dosing of one antihypertensive (not diuretics)

-Assess adherence

-Educate on diet, exercise, and smoking cessation

-Rule out white coat hypertension

-Discontinue interfering substances

Patient may have resistant hypertension

219
Q

What is resistant HTN?

A

Failure to attain goal BP while:

-Adherent to at least 3 agents at max dose (including a diuretic)

OR

-When 4 or more agents are needed

220
Q

What is the estimated % of patients with resistant hypertension?

A

17%

221
Q

What does it mean by resistant HTN is a “disease of exclusion”?

A

Must rule out secondary causes of HTN (nonadherence, whitecoat HTN, etc.) before diagnosing

222
Q

What is Step 1 for resistant HTN treatment?

A

-Maximize lifestyle interventions

-Optimize 3-drug regimen (ACEi/ARB, CCB, and diuretic)

223
Q

What is Step 2 for resistant HTN treatment?

A

Substitute optimized thiazide-like diuretic

(Chlorthalidone or Indapamide)

224
Q

What is Step 3 for resistant HTN treatment?

A

Add mineralocorticoid receptor antagonist

(Spironolactone or Eplerenone)

225
Q

What is Step 4 for resistant HTN treatment?

A

Add beta blocker IF heart rate >70 bpm

If BB contraindicated or heart rate <70 bpm: use a central alpha-2 agonist (clonidine patch or guanfacine at bedtime)

*diltiazem is contraindication to BB and can be used if alpha-2 agonists not tolerated

226
Q

What is Step 5 for resistant HTN treatment?

A

Add hydralazine

227
Q

What is step 6 for resistant HTN treatment?

A

Substitute minoxidil for hydralazine

228
Q

What things should we keep in mind when de-escalating therapy (removing medications)?

A

-Presence of comorbidities that would impact drug choice

-First vs Second-line agents

-Which drug has the most potential for adverse effects

-Can we stop abruptly

-*Heart failure trumps hypertension (keep these meds on)

Therapeutics 2 Final Exam (3 decks)

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