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Pharmacology > Week 10 Hypertension > Flashcards

Week 10 Hypertension Flashcards

1
Q

8 drugs that increase BP?

A 
corticosteroids
estrogens
NSAIDs
sympathomimetics
cyclosporins
danazol
erythropoietin
megestrol acetate
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2
Q

6 drugs/classes that decrease BP?

A 
anasthetics
anxiolytics
hypnotics
dopamine agonists
Tricyclic antidepressants
nitrates
antipsychotics
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3
Q

why tx HTN since it doesn’t produce sxs unless rapid & severe onset?

A

to prevent or reduce severity of disease

atherosclerosis, CAD, AA, CHF, stroke, DM, renal and retinal disease

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4
Q

examples of target organ damage from HTN?

A

cerebrovascular disease
stroke - ischemic, or transient ischemic attack
aneurysmal subarachnoid hemorrhage
hypertensive retinopathy
left ventricular dysfunction - hypertrophy (must pump against high pressure which causes muscle to thicken; restricting blood flow)
CAD - MI, angina, CHF
Renal disease - hypertensive nephropathy; albuminuria
PAD - intermittent claudication
AA/dissection

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5
Q

what are the 2 main categories of the physiological etiology behind HTN?

A

increased cardiac output
or
increased systemic vascular resistance

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6
Q

3 causes of increased cardiac output?

A

hypervolemia (renal artery stenosis, hyperaldosteronism, aortic coarctation, pregnancy)
stress (sympathetic activation)
pheochromocytoma (increased catecholamines)

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7
Q

7 causes of increased systemic vascular resistance?

A 
stress (sympathetic activation)
atherosclerosis
renal artery disease (increased angiotensin II)
pheochromocytoma
thyroid dysfunction
diabetes
cerebral ischemia
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8
Q

what are 3 mechanisms to reduce cardiac output?

A

reduce blood volume
reduce heart rate
reduce stroke volume

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9
Q

what is 1 mechanism to reduce systemic vascular resistance

A

dilate systemic vasculature

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10
Q

7 classes of anti-hypertensive drugs?

ABCDE

A

ACE inhibitors
Alpha-agonist
Angiotensin receptor blockers
Alpha-antagonist

B-adrenergic blockers

Ca-Channel blockers

Diuretics

Endothelin antagonists

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11
Q

2 demographic indications for use of diuretics?

A

african american

elderly

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12
Q

2 demographic indications for use of calcium channel blockers?

A

african american

elderly

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13
Q

3 demographic indications for use of beta blockers?

A

young & caucasian
post MI
CHF

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14
Q

5 demographic indications for use of angiotensin receptor blockers & ACE inhibitors?

A 
DM (protect KI)
CT disease (scleroderma)
CHF
post MI
young & caucasian
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15
Q

How does using 2 drugs affect dosing?

A

effect is synergistic therefore less dosage needed, therefore diminished side effects

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16
Q

cardiac output x total peripheral vascular resistance = ?

A

arterial blood pressure

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17
Q

heart rate x stroke volume = ?

A

cardiac output

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18
Q

beta blockers affect which:
cardiac output
OR
total peripheral resistance

A

cardiac output

heart rate & stroke volume

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19
Q

which 3 classes of drugs affect cardiac output?

A

b-adrenergic receptor antagonists
angiotensin receptor antagonists
diuretics

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20
Q

which 6 classes of drugs affect total peripheral resistance?

A

vasodilators
b-adrenergic receptor antagonists
a-adrenergic receptor antagonists (a-blockers)
angiotensin receptor antagonists
centrally acting sympatholytics
angiotensin-converting enzyme (ACE) inhibitors

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21
Q

name the 3 physiological mechanisms that control arterial BP

A
  1. sympathetic nervous system (incl. baroreceptors)
  2. renin-angiotensin-aldosterone
  3. tonically active endothelium-derived autocoids (NO and ET-1)
ET-1 = endothelin-1 (peptide that is a vasoconstrictor)
autocoid = local hormones (e.g. eicosanoids, angiotensin, neurotensin, kinins, NO)
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22
Q

how does a decrease in BP increase aldosterone?

A

decrease BP => decreased renal flow => increases renin => increased angiotensin II => increases aldosterone

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23
Q

how does a decrease in BP result in increasing blood volume?

A

decreased BP => decreased renal blood flow => decreased GFR => increased sodium & water retention => increased blood volume (which increases cardiac output)

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24
Q

how do baroreceptors regulate BP?

A
  • responsible for rapid moment to moment BP regulation
  • fall in BP causes pressure-sensitive neurons to send fewer impulses to CN enters in spinal cord
  • results in reflex response for increased sympathetic & decreased parasympathetic output to the heart & vasculature = vasoconstriction & increased CO
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25
Q

where are baroreceptors located?

A

aortic arch and carotid sinuses (at bifurcation of internal and external carotids)

The carotid sinus baroreceptors are innervated by the sinus nerve of Hering, which is a branch of the glossopharyngeal nerve (IX cranial nerve). The glossopharyngeal nerve synapses in the nucleus tractus solitarius (NTS) located in the medulla of the brainstem. The aortic arch baroreceptors are innervated by the aortic nerve, which then combines with the vagus nerve (X cranial nerve) traveling to the NTS. The NTS modulates the activity of sympathetic and parasympathetic (vagal) neurons in the medulla, which in turn regulate the autonomic control of the heart and blood vessels.

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26
Q

which baroreceptors are more sensitive?
aortic arch
OR
carotid sinus

A

carotid sinus

Maximal carotid sinus sensitivity occurs near the normal mean arterial pressure; therefore, very small changes in arterial pressure around this “set point” dramatically alters receptor firing so that autonomic control can be reset in such a way that the arterial pressure remains very near to the set point. This set point changes during exercise, hypertension, and heart failure. The changing set point explains how arterial pressure can remain elevated during exercise or chronic hypertension.

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27
Q

Baroreceptors in KI respond to reduced BP (and to sympathetic stimulation of B adrenoceptors) by releasing the enzyme ________

A

Renin

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28
Q

KI provides Long Term control of BP by altering _________

A

blood volume

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29
Q

Renin converts __________ to ________, which is then converted to _________ via ___________

A

Renin converts angiotensinogen to angiotensin I, which is converted to angiotensin II via angiotensin converting enzyme (ACE)

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30
Q

which hormone is the body’s most potent vasoconstrictor (resulting in increased BP)

A

angiotensin II

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31
Q

angiotensin II stimulates _____________ secretion

A

aldosterone

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32
Q

what are the 4 pathways that contribute to the kidney’s retention of Na+ and H2O in response to decreased BP?

A
  1. direct intrarenal hydraulic effect of reduced renal perfusion pressure
  2. release of aldosterone stimulated by renin system
  3. SNS stimulating nerves innervating renal blood vessels and tubules
  4. release of vasopressin (ADH) from pituitary stimulated by baroreceptor
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33
Q

Persistently raised arterial pressure leads to hypertrophy of which ventricle?

A

left

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34
Q

Persistently raised arterial pressure leads to narrowing of which, veins or arteries?

A

arteries

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35
Q

what are the 3 clinical variables that affect BP measurement?

A

cuff diameter
patient positioning
Kortokoff sounds

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36
Q

6 lab assessments that help in dx HTN

A 
electrolytes, creatinine level
fasting blood glucose
CBC
lipid profile
urinalysis
electrocardiography
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37
Q

Drug treatment is recommended if the diastolic BP is greater than ____ mmHg with other risk factors

A

85 mmHg

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38
Q

Drug treatment is recommended if the diastolic BP is ___ mmHg diastolic (and ___ mmHg systolic) without other risk factors

A

90 mmHg diastolic (and 140 mmHg systolic) without other risk factors

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39
Q

what is considered stage 1 hypertension?

systolic and diastolic

A

140-159 mmHg / 90-99 mmHg

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40
Q

what is considered stage 2 hypertension?

systolic and diastolic

A

> 160 mmHg / 100 mmHg

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41
Q

what is the BP tx goal in a HTN patient with diabetes/renal disease

A

less than 130/80 mmHg

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42
Q

what is the BP tx goal in a HTN patient?

A

less than 140/90mmHg

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43
Q

what is the tx protocol for stage 1 HTN

A
  • lifestyle modification
  • thiazide diuretic
  • consider ACE(-), ARB, BB, CCB

drug combo if no achieve target BP

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44
Q

what is tx protocol for stage 2 HTN

A
  • lifestyle modification
  • drug combos:
    thiazide diuretic
    PLUS
    ACE(-)
    ARB
    BB
    CCB

always starts with 2 drugs at this stage

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45
Q

which 3 drug classes are vasodilators?

A 
ACE inhibitors
direct dilators (less so)
Calcium channel blockers
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46
Q

which drug class tends to end in “-pril”

A

ACE inhibitors

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47
Q

which antihypertensive drug is preferred as first line tx in DM, CHF, CT disease

A

ACE inhibitors

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48
Q

where is the highest activity of angiotensin converting enzyme in the body?

A

endothelium of pulmonary vasculature

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49
Q

how do ACE inhibitors produce vasodilation?

A

inhibit formation of angiotensin II

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50
Q

ACE breaks down which vasodilator substance which, when inhibited by ACE inhibitors, is responsible for creating a dry cough?

A

bradykinin

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51
Q

which enzyme converts angiotensinogen to angiotensin I?

A

renin

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52
Q

angiotensin II stimulates secretion of which hormone?

A

aldosterone

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53
Q

what effect does aldosterone secretion have on blood pressure & why?

A

increases renal sodium absorption and increased blood volume, thereby increased BP

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54
Q

ACE inhibitors lower BP by reducing peripheral vascular resistance without reflexively increasing __________, _______, or ________.

A

cardiac output
heart rate
contractility

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55
Q

ACE inhibitors:
Vasodilation of both arterioles and veins occurs as a result of decreased vasoconstriction from diminished levels of _________.
Vasodilation also occurs directly from increased levels of ________ because it is not being broken down.

A

angiotensin II

bradykinin

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56
Q

route of administration of ACE inhibitors?

A

orally

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57
Q

how long is the onset of action?
for captopril?
enalapril (prodrug)

A

rapid

captopril: minutes (does not need to be transformed to more active form)
enalapril: hours

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58
Q

which 2 ACE inhibitors do not need to undergo hepatic conversion to active metabolites? (and therefore may be preferred in patients with severe hepatic impairment)

A

captopril

lisinopril

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59
Q

which demographic are ACE inhibitors most effective in?

A

young, caucasian (under 55 yoa)

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60
Q

ACE inhibitors are as effective in african americans as caucasians when combined with which other class of antihypertensives?

A

diuretics

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61
Q

ACE inhibitors are particularly useful for tx HTN associated with other risk factors, such as? (4)

A

post-MI
diabetes
Kidney disease
stroke

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62
Q

ACE inhibitors are effective in the management of chronic CHF, unlike which other class?

A

beta blockers

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63
Q

why are ACE inhibitors effective in patients post-MI?

A

help reduce deleterious remodeling that occurs post-infarction (dilatation, hypertrophy, and the formation of a discrete collagen scar; Hypertrophy is an adaptive response during postinfarction remodeling that offsets increased load, attenuates progressive dilatation, and stabilizes contractile function)

Thrombolysis is of proven value in the acute infarction, in which the primary objectives are limiting infarct size and salvaging ischemic myocardium. Once infarct evolution has occurred, pharmacological intervention may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.

The mechanism of improvement with ACE inhibition is related in part to peripheral vasodilatation, ventricular unloading, and the attenuation of ventricular dilatation.

It is recommended that patients with left ventricular dysfunction or heart failure be treated with ACE inhibitors without delay after infarction. Alternatively, all patients should be treated with ACE inhibitors initially, with a review of the need for continuation later on the basis of left ventricular function assessment.

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64
Q

Adverse effects of ACE inhibitors (8)

A
  • persistent dry cough (10-30% of patients;d/t elevation of - bradykinin)
  • rashes
  • altered/loss of taste
  • hypotension
  • hyperkalemia (K+ levels must be monitored & supplements used cautiously)
  • reversible acute renal failure (CI in severe renal artery stenosis)
  • swelling of mucus membranes - angioedema (rare but life-threatening)
  • fetal malformation - SHOULD NOT BE USED BY PREGNANT WOMEN
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65
Q

ACE (-) herbal interactions (6)

A
  • cayenne (predispose to cough)
  • ephedra (antagonise hypotensive effect)
  • rhubarb (improves Captopril effect on decreasing progression of chronic KI failure)
  • antacids significantly decrease absorption of ACE (-)
  • Lithium increases toxic concentrations of ACE inhibitors
  • theoretically: anything that lowers BP, e.g. theanine, CoQ10, olive, liquorice, reishi, stinging nettle, fish oil, garlic black cohosh.
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66
Q

ACE (-) nutrient interactions (2)

A

potassium (accentuates hyperkalemia)

zinc (ACE (-) deplete body of zinc)

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67
Q

What class of antihypertensives ends in “-sartans”

A

Angiotensin receptor blockers

e.g. losartan, valsartan

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68
Q

ARBs are receptor antagonists that block _________ receptors on bloods vessels and other tissues such as the heart.

A

type 1 angiotensin II (AT1)

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69
Q

Why do ARBs not cause an increase in bradykinin?

A

ARBs do not inhibit ACE

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70
Q

Why do ARBs not have the side effects of dry cough & angioedema?

A

ARBs do not increase bradykinin levels

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71
Q

Why should ACE (-) and ARBs not be combined for the tx of HTN?

A
  • similar mechanisms and adverse effects
  • no real BP benefit & increase side effects when taken together

this combo is reserved for very ill patients: advanced HF, proteinuric nephropathy

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72
Q

How do Centrally Acting Adrenergic Drugs work?

A

These drugs decrease the BP by reducing the firing rate of sympathetic nerves [decrease in sympathetic tone, decrease CO]
This action is mediated by activation of α2-adrenergic receptors in the CNS to inhibit sympathetic vasomotor centers [MOSTLY CENTRAL!]

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73
Q

describe adrenergic receptors

A 
The adrenergic receptors (or adrenoceptors) are a class of G protein-coupled receptors that are targets of the catecholamines, especially norepinephrine (noradrenaline) and epinephrine (adrenaline).
Many cells possess these receptors, and the binding of a catecholamine to the receptor will generally stimulate the sympathetic nervous system.
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74
Q

What are the 2 Centrally Acting Adrenergic Drugs that we learn in class?

A

Clonidine

Methyldopa

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75
Q

What is clonidine indicated for?

A

mild/moderate HTN not responding to diuretics

also opioid withdrawal

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76
Q

Are clonidine and methyldopa a2 adrenergic agonists or antagonists?

A

a2 adrenergic agonists

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77
Q

what are the 3 mild adverse effects of clonidine?

A

sedation
drying of nasal mucosa
edema

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78
Q

who is methyldopa indicated for?

A
  • patients with renal insufficiency

- pregnancy

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79
Q

3 most common adverse effects of methyldopa?

A

sedation
impotence
rare hepatic necrosis (life-threatening)

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80
Q

How do a-adrenoceptor blocking agents decrease peripheral vascular resistance & lower arterial BP?

A

cause relaxation of both arterial and venous smooth muscle

81
Q

b1 receptors are found where?

A

myocardium

82
Q

b2 receptors are found where?

A

smooth muscle and most other sites

83
Q

how does prazosin/doxazosin work?

A

blocks a1 receptors in arterioles and veins => fall in peripheral vascular resistance and in venous return to the heart

84
Q

why does prazosin/doxazosin not increase cardiac output and rate?

A

because it decreases cardiac preload

85
Q

the first dose of prazosin/doxazosin often causes what?

A

fainting (orthostatic hypotension)

therefore 1st dose should be given at bedtime; eventually self-regulates

86
Q

which disease process of the male genitalia is prazosin/doxazosin also used for?

A

BPH

87
Q

prazosin/doxazosin is CI in whom?

A

adults >55 yoa

88
Q

which class of antihypertensives typically end in “-olol”?

A

b-blockers

89
Q

what is the prototype drug of b-blockers?

A

propranolol

90
Q

which class of antihypertensives relieves nightmares?

A

a1-antagonists

91
Q

propanolol has equal affinity for which receptors?

A

b1 and b2 adrenergic receptors

thus it is nonselective

92
Q

b-blockers reduce BP primarily by decreasing _______.

A

cardiac output

93
Q

which b-blockers are selective for b1 subtype?

A

atenolol

metoprolol

94
Q

Propanolol readily penetrates into the CNS. Which 2 b-blockers do not?

A

sotalol

atenolol

95
Q

what kind of agonist is pindolol at b1 and b2?

A

partial agonist
therefore small reductions in resting HR and BP.
may be preferred as antiHTN in pxs w/diminished cardiac reserve or bradycardia

96
Q

which 2 b-blockers are also antagonists at a1 adrenergic receptors?

A

labetalol

carvedilol

97
Q

Common to all BB is the ability to competitively antagonize the effects of norepinephrine and epinephrine on _________ in the heart and inhibit the_____-secreting cells of the KI

A

B1 adrenergic receptors in the heart
inhibit renin

Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.

98
Q

what does ‘chronotropic’ mean?

A

changes heart rate

b-blockers are negative chronotropes

99
Q

what does ‘inotropic’ mean?

A

alters force or energy of muscular contractions

100
Q

how do b-blockers affect calcium?

A

block calcium entry into vascular smooth muscle => vasodilation

101
Q

4 CIs to BB use?

A
  • severe chronic obstructive lung disease
  • chronic CHF; angina
  • severe symptomatic occlusive peripheral vascular disease (more w/elderly & diabetics)
  • asthmatics
102
Q

if someone cannot use propranolol d/t a CI, what other BB can they use?

A

trick question - they can’t

103
Q

what are the cardiac effects of BB?

A

decrease contractility (-ve inotropy)
decrease relaxation rate
decrease HR (-ve chronotropy)
decrease conduction velocity

104
Q

which demographic are BB most effective for?

A

young caucasians

vs elderly & african-american

105
Q

the primary therapeutic benefits of b-blockers are seen in patients with which conditions?

A

HTN w/concomitant:
heart disease, e.g. supra ventricular tachyarrhythmia (AF), previous MI, angina pectoris, chronic heart failure, migraines

106
Q

therapeutic uses of propranolol

A 
HTN
glaucoma (chronic)
migraine
hyperthyroidism
angina pectoris
MI
107
Q

therapeutic uses of atenolol/metoprolol

A

HTN
(asthmatics/smokers/DM)
b/c selective for B1 class

108
Q

therapeutic uses of pindolol/acebutolol

A

HTN (athletes)

also a partial agonist, weaker effect on CO so stamina is not substantially reduced

109
Q

therapeutic uses of labetalol

A

chronic and ER HTN

no lipid/sugar effects

110
Q

therapeutic uses of carvedilol

A

CHF (antioxidant properties)

protects vasculature from free radical damage

111
Q

explain metabolism of BB

A

extensively metabolized by LV

except atenolol

112
Q

which side effect of BB limits the dose, otherwise it becomes too dangerous?

A

bradycardia

b/c dangerous if slow down too much

113
Q

3 CV side effects of BB?

A

bradycardia
hypotension
CHF

114
Q

5 CNS side effects of BB?

A 
depression
fatigue
lethargy
insomnia
hallucinations
115
Q

Why does bronchoconstriction occur when nonselective b-blockers administered to asthmatic patients?

A

Because sympathetic nerves innervating bronchioles normally activate b2 receptors that promote bronchodilation.

116
Q

Why can hypoglycaemia occur with beta blockade?

A

b2 adrenoreceptors normally stimulate hepatic glycogen breakdown (glycogenolysis) & pancreatic release of glucagon (which increase plasma glucose)

on BB, tachycardia which serves as a warning sign for insulin-induced hypoglycaemia may be masked, therefore use cautiously in diabetics.

117
Q

aside from CV and CNS side effects, what other side effects do we see with BB?

A

bronchoconstriction - at high doses
disturb lipid metabolism - decrease HDL,increase plasma TG - which increases risk of CVD, precisely what we are trying to prevent!
abrupt cessation of BB may = tachycardia, angina pectoris, MI (rare)

118
Q

7 herbal interactions w/BB

A
  • ginkgo seed & leaf (atenolol lowers seizure threshold)
  • yohimbe (BB protect against yohimbe toxicity)
  • valerian, wild lettuce, hops (additive sedation?)
  • caffeine, cola, mate, tea, guarantee (opposing effects)
  • ephedra (= severe hypertension)
  • theoretically: anything that decreases sympathetic tone: CoQ10, theanine, reishi, fish oil, garlic goldenseal, stinging nettle
  • CYT P450 sensitive (St.John’s wort, goldenseal, ginseng, echinacea, milk thistle)
119
Q

Ca2+ channel blockers can be classified into DHP and non-DHP. What does DHP stand for?

A

dihydropyridine

120
Q

DHP CCBs end in which suffix?

A

“-dipine”

121
Q

All dihydropyridines have a much greater affinity for calcium channels in:
the heart
or
the vasculature

A

VASCULAR calcium channels

  • therefore particularly beneficial in tx HTN
  • little interaction w/other CV drugs e.g. warfarin, digoxin
    (often used concomitantly)
122
Q

describe normal Ca2+ channel modulation

A
  • resting membrane is impermeable to Calcium (Ca++ channels closed)
  • when membrane depolarizes, channels open = Ca2+ influx
  • slowly L-type Ca++ channels inactivated & must transition to resting conformation before can open again
  • L-type Ca++ channels play important role in pacemaker currents and phase 0 of action potentials; therefore by blocking => muscle relaxation (vasodilation), negative inotropy, negative chronotropy & decreased conduction velocity particularly at AV node
123
Q

Which drug shows more frequency-dependence? (binding affinity proportional to depolarization rate)
nifedipine or verapamil

A

verapamil

124
Q

Where is the primary site of action of non-DHP CCBs?

A

myocardial cells

125
Q

what is MOA of CCB (non-DHP) on myocardial cells?

A

inhibit Ca++ ion influx into CV smooth mm cells = cardiac depression; rate/contractility

more marked negative inotropic effects than DHP (vascular)

126
Q

3 cardiac effects of CCBs?

A 
decrease contractility (negative isotropy)
decrease HR (negative chronotropy)
decrease conduction velocity
127
Q

3 therapeutic indications for CCBs?

A

HTN (systemic & pulmonary)
angina
arrhythmias

128
Q

CCBs are first choice tx in which demographics?

A

> 55 yoa

african american

129
Q

what is the implication of the short half life of CCBs on dosing?

A

3x daily or sustained release formula

130
Q

CCBs are useful in the treatment of HTN patients who also have asthma, diabetes and/or PVD because unlike _________ they do not have the potential to adversely affect these conditions.

A

b-blockers

131
Q

How do CCBs have a therapeutic effect on angina?

A

vasodilator & cardiodepressant actions
Systemic vasodilation reduces arterial pressure which reduces ventricular after load (wall stress) thereby decreasing oxygen demand.

esp. verapamil & diltiazem

132
Q

how do CCBs help arrhythmias?

A

Decrease firing rate of aberrant pacemaker sites within the heart.
Decrease conduction velocity & prolongs re-polarization, esp. at AV node.

133
Q

describe natriuresis

A

Natriuresis is the process of excretion of sodium in the urine via action of the kidneys. Natriuresis is promoted (more sodium is excreted) by Ventricular and Atrial natriuretic peptides as well as calcitonin, and it is inhibited (sodium is conserved) by chemicals such as aldosterone. Natriuresis lowers the concentration of sodium in the blood and also tends to lower blood volume because osmotic forces make water follow sodium out of the body’s blood circulation and into the urine. Many diuretic drugs take advantage of this mechanism to treat medical conditions like hypernatremia and hypertension.

134
Q

why do you not need to use diuretics with CCBs concurrently?

A

Ca++ have a natriuretic effect (excretes sodium in the urine)

135
Q 
A 45 year old man was just started on therapy for a HTN and developed a persistent, dry cough. Which is most likely responsible for this side effect?
Enalapril
Losartan
Nifedipine
Prazosin
Propranolol
A

Enalapril

ACE inhibitor

Losartan is an ARB w same beneficial effects as ACE(-) but less likely to produce cough.
Nifedipine, prazosin, propranolol do not cause this side effect.

136
Q 
Which may cause reflex tachycardia and/or postural hypotension on initial administration?
Atenolol
Hydrochlorothiazide
Metoprolol
Prazosin
Verapamil
A

Prazosin.

produces first-dose hypotension by blocking a-receptors

137
Q 
Which can precipitate a hypertensive crisis following abrupt cessation of therapy?
Clonidine
Diltiazem
Enalapril
Losartan
Hydrochlorothiazide
A

Clonidine

Increased SNS activity occurs if clonidine therapy abruptly stopped after prolonged administration. Uncontrolled elevation in BP can occur. Patients should be slowly weaned.

138
Q 
A 48-year old hypertensive patient has been successfully treated with a thiazide diuretic for the last 5 years. Over the last 3 months, his diastolic pressure has steadily increased and he was started on an additional antihypertensive agent. He complains of several instances of being unable to achieve an erection and not being able to complete three sets of tennis as he once did. Which is the likely second antihypertensive medication?
Captopril
Losartan
Metoprolol
Minoxidil
Nifedipine
A

Metoprolol

b-blocker

side effect of interference with sexual performance and decreased exercise tolerance

139
Q 
A 40-year old male has recently been diagnosed with HTN d/t pressure readings of 163/102 and 165/100 mmHg. He also has diabetes that is well controlled with oral hypoglycaemic medications. Which is the best initial treatment regimen for treatment of HTN in this patient?
Felodipine
Furosemide
Lisinopril
Lisinopril and hydrochlorothiazide
Metoprolol
A

Lisinopril and hydrochlorothiazide

systolic BP is more than 20 mmHg above goal, tx with two different medications if preferred.

b/c patient is diabetic, he also has a compelling indication for an ACE inhibitor or ARB.

140
Q 
A 60-year old white female has not reached her BP goal after 1 month of treatment with a low dose of lisinopril. All of the following would be appropriate next steps in the treatment of her HTN except:
increase dose of lisinopril
add a diuretic medication
add on a CCB medication
add on an ARB medication
A

add on an ARB medication

ARBs have similar mechanism of action of ACE inhibitors and combination therapy may increase the risk of adverse effects.

141
Q 
A patient returns to her health care provider for routine monitoring 3 months after her HTN regimen was modified. Labs reveal elevated serum potassium. Which is likely responsible for this hyperkalemia?
Chlorthalidone
Clonidine
Furosemide
Losartan
Nifedipine
A

Losartan

ARB - can cause increase in serum K+ similar to ACE(-).

Furosemide & chlorthalidone can cause decrease in serum K+. Nifedipine and clonidine do not affect K+ levels.

142
Q 
a 58-year old female reports that she recently stopped taking her BP medications because of swelling in her feet that began shortly after she started treatment. Which is most likely to cause peripheral edema?
Atenolol
Clonidine
Felodipine
Hydralazine
Prazosin
A

Felodipine

peripheral edema is one of the most common side effects of CCBs.

None of the other agents commonly cause peripheral edema.

143
Q 
Which is an appropriate choice for HTN treatment during pregnancy?
Aliskiren
Fosinopril
Hydralazine
Valsartan
A

Hydralazine

ACE(-), ARBs, and the direct renin inhibitor, alizarine, are all CI in pregnancy d/t teratogenicity.

144
Q 
DD is a 50-year old male with a newly diagnosed HTN. His comorbidities include diabetes and chronic hepatitis C infection with moderate liver impairment. He requires two drugs for initial treatment of his HTN. Which should be prescribed in combination with a thiazide diuretic?
Lisinopril
Spironolactone
Fosinopril
Furosemide
Hydralazine
A

Lisinopril

Diabetes = compelling indication for an ACE inhibitor or ARB for tx of HTN & prevention of diabetic nephropathy. However, most ACE(-) undergo hepatic conversation to active metabolites, so his hepatitis is a concern.
Lisinopril is one of 2 ACE inhibitors that does not undergo hepatic conversion to active metabolites, it is the best choice.

Fosinopril is the only ACE(-) that is not eliminated primarily by the kidneys but does undergo hepatic conversion.

An additional diuretic (spironolactone/furosemide is not indicated).

No compelling indications for hydralazine.

145
Q

Verapamil has a high or low affinity?

Why?

A

Low - extensive first pass effect

146
Q

DHP or non DHP?

nifedipine

A

DHP

147
Q

DHP or non DHP?

diltiazem

A

non-DHP

148
Q

DHP or non DHP?

verapamil

A

non-DHP

149
Q

DHP or non DHP?

amlodipine

A

DHP

150
Q

Which of the following has the shortest half life? Which has the longest?
diltiazem
verapamil
nifedipine

A

shortest: nifedipine = 2 hrs
longest: verapamil = 5 hrs

diltiazem = 3.5 hrs

151
Q

Which class of CCBs are most selective for smooth muscle?

A

dihydropyridines (DHP)

152
Q

Why are all DHPs CI in angina patients?

A
  • cause reflex tachycardia
  • they are a powerful systemic vasodilator & their pressure-lowering effects can lead to reflex cardiac stimulation (tachycardia & increased inotropy) => dramatically increase myocardial oxygen demand
153
Q

bioavailability % of nifedipine?

A

60-70%

154
Q

Diltiazem affects both cardiac and vascular smooth muscle cells, but it has a less pronounced negative inotropic effect on _________ compared to that of verapamil.

A

the heart

Diltiazem causes little or no change to heart rate

155
Q

Verapamil is CI in patients with ________

A

CHF

Verapamil has a negative inotropic effect, which in most patients is compensated by a simultaneous reduction in afterload (i.e. decreased systemic vascular resistance) without a net impairment of ventricular performance. However, congestive heart failure or pulmonary edema have developed in approximately 2% of patients treated with verapamil. Mild symptoms of cardiac failure should be under control, if possible, prior to initiating verapamil therapy.

The use of verapamil is contraindicated in patients with severe left ventricular dysfunction (e.g., ejection fraction < 30%) or moderate to severe symptoms of cardiac failure and in patients with any degree of ventricular dysfunction if they are receiving a beta-adrenergic blocker. Likewise, verapamil should not be given to patients with acute myocardial infarction and pulmonary congestion documented by X-ray on admission, since associated heart failure may be acutely worsened.

156
Q

With CCBs, sudden withdrawal of high dose may lead to _____________ and precipitate angina.

A

coronary vasoconstriction

157
Q

Which 2 CCBs that we learn about possess negative inotropic activity (bradycardia, myocardial depression):

verapamil
diltiazem
nifedipine
amlodipine

A

verapamil
diltiazem

Therefore should be avoided in patients w/HF or AV block.

DHPs (-ipines) have much greater affinity for vascular calcium channels than Ca++ channels in the heart.

158
Q

verapamil & diltiazem are inhibitors of P450 ___

A

P450 3A4

159
Q

what impact does the inhibition of P450 3A4 by verapamil & diltiazem have on other meds?

A

decrease metabolism of b-blockers & other drugs

160
Q

Naturopathic interactions with CCBs?
herbal/supplemental
(7 items)

A
  • cardiac glycosides (e.g. blue cohosh; may interfere with CCB; increase the strength of heart muscle contractions, change heart rate, and increase heart blood output)
  • grapefruit juice (increases adverse effects as they are highly LR metabolized)
  • Intravenous Ca++
  • IV magnesium (causes additive effect w/CCB - increased adverse effect - severe hypotension, neuromuscular blockades)
  • ginger (synergistic effect as hypotensive & channel blocker - theoretical!)
  • theoretically: other hypotensives: black cohosh, CoQ10, fish oil, garlic, goldenseal, l-arginine, olive, theanine)
  • CYT P450: devil’s claw, echinacea, eucalyptus, garlic, siberian ginseng, kava, licorice, milk thistle, peppermint, St. John’s Wort, valerian)
161
Q

What are the 3 classes of diuretics?

A

thiazide diuretics
loop diuretics
K+ sparing diuretics

162
Q

Regardless of class, the initial mechanism of action of diuretics is based upon decreasing blood ________, which ultimately leads to decreased BP.

A

volume

163
Q

Which class of diuretic have the most widespread use?

A

thiazides

164
Q

Where in the kidney do thiazides exert their effect?

A

distal convoluted tubule

165
Q

which drug is often the 1st choice in HTN?

A

hydrochlorothiazide

166
Q

how long does it take to see an antihypertensive effect of thiazides?

A

3-4days

167
Q

What is mechanism of action of thiazide diuretics?

A

Decrease reabsorption of Na+ in distal convoluted tubule by inhibition of Na+/Cl- cotransporter on luminal membrane of tubules.
They have a lesser effect in the proximal tubule.
Thereby increase concentration of Na+ and Cl- in tubular fluid.
*Because site of action is on luminal membrane, must be excreted into tubular lumen to be effective; w/decreased renal function, diuretics lose efficacy.

168
Q

Why does serum K+ need to be monitored periodically (more frequently at the beginning of therapy) for the development of hypokalemia when using thiazide diuretics?

A

Thiazides increase Na+ in the filtrate arriving at the distal convoluted tubule, therefore more K+ is exchanged for Na+ => continual loss of K+ from the body

169
Q

How do thiazide diuretics affect Ca++?

A
  • decrease urinary Ca++ excretion
  • promote reabsorption of Ca++ in the distal convoluted tubule where parathyroid hormone regulates reabsorption
    (vs. loop diuretics, which increase Ca++ concentration in the urine)
  • may preserve bone mineral density at the hip and spine & may reduce risk of fractures!
  • used in management of nephrolithiasis (less Ca++ to make stones with)
170
Q

How do thiazide diuretics affect uric acid?

A
  • Two thirds of urate excretion occurs at the kidney, the remainder being excreted by the gut
  • thiazides increase serum uric acid by decreasing amount of acid excreted by organic acid secretory system
  • Thiazides reduce the clearance of uric acid since they compete for the same transporter
  • Diuretics reduce urate excretion by both directly and indirectly increasing urate reabsorption and decreasing urate secretion; the effect is dose dependent
  • uric acid is insoluble; deposits in the joints and may precipitate a gouty attack in predisposed individuals
  • use thiazides with caution in patients with gout or high levels of uric acid
171
Q

How do thiazide diuretics affect magnesium?

A
  • enhance excretion

- mechanism for magnesia is not understood

172
Q

How do thiazide diuretics affect potassium?

A
  • enhance excretion
  • thiazide diuretics increase Na+ in filtrate arriving at distal tubule = more K+ is also exchanged for Na+ resulting in continual loss of K+ from the body
  • hypokalemia is the most frequent problem with thiazide diuretics - can predispose patients who are taking digoxin to ventricular arrhythmias
  • thiazides decrease intravascular volume => activation of renin-angiotensin-aldosterone system; increased aldosterone contributes significantly to urinary K+ losses
  • 70% of patients experience hypokalemia (heart palpitations)
  • must be monitored in patients predisposed to arrhythmias - may increase incidence of sudden cardiac death
173
Q

How do thiazide diuretics affect sodium?

A
  • hyponatremia may develop d/t elevation of ADH as a result of hypovolemia as well as diminished diluting capacity of the kidney & increased thirst
  • increased excretion of Na+ results in the excretion of very hyperosmolar (concentrated) urine [other diuretic classes unlikely to do this]
174
Q

10% of patients on thiazides experience hyperglycemia. Why is this?

A
  • glucose intolerance possibly d/t impaired release of insulin and tissue uptake of glucose
  • new-onset diabetes has been reported more often w/thiazides than with other antiHTN agents
175
Q

5 drug interactions with thiazide diuretics?

A
  • corticosteroids (accentuate K+ loss)
  • insulin (antagonize hypoglycemic effect)
  • digoxin (increased toxicity b/c Mg, K loss)
  • lithium (decreases lithium excretion)
  • NSAIDs (increases incidence of NSAID-induced renal failure; NSAIDs inhibit production of renal PGs thereby reducing renal blood flow)
176
Q

3 important herbal interactions with thiazide diuretics?

A
  • herbal diuretics (dandelion, uva ursi, cleavers, apple cider vinegar, parsley…)
  • promoters of K+ loss (aloe, foxglove, liquorice, senna)
  • theoretically: other hyper/hypotensives: black cohosh, CoQ10, fish oil, garlic, goldenseal, theanine, reishi…)
177
Q

Which nutrients have thiazide diuretics been shown to deplete?

A 
folic acid
K+
Mg++
Zinc 
Na+
CoQ10
Vitamin B2
178
Q

Which nutrients have thiazide diuretics been shown to increase?

A

Ca++

179
Q

Which nutrients may be affected by thiazide diuretics?

A

vitamin D

phosphorus

180
Q

Where do loop diuretics have their major diuretic action?

A

ascending loop of Henle

181
Q

What is the mechanism of action of loop diuretics?

A
  • inhibit cotransport of Na+/K+/2Cl- in luminal membrane in ascending limb of loop of Henle
  • reabsorption of these ions is decreased
  • greatest diuretic effect of all the diuretic drugs since ascending limb accounts for reabsorption of 25% to 30% of filtered NaCl; downstream sites are unable to compensate for the increased Na+ load
182
Q

Which class of diuretics exhibit the most pronounced diuresis?

A

loop diuretics

  • highest efficacy in mobilizing Na+ and Cl- from the body
  • produce copious amounts of urine
  • useful for: edema of CHF, LV cirrhosis, KI disease
183
Q

loop diuretics cause depletion of which nutrients?

A

K+ , Ca++ and Mg++

  • heavy load of Na+ presented to collecting tubule results in increased exchange of tubular Na+ for K+ => possibility of hypokalemia
  • loss of K+ from cells in exchange for H+ leads to hypokalemic alkalosis
184
Q

blood glucose and uric acid are:
elevated or decreased
w/ loop diuretics?

A

elevated

  • furosemide completes with uric acid for renal secretory systems thus blocking urate secretion
185
Q

Adverse effect:

Reversible or permanent __________ loss may occur with loop diuretics.

A

hearing loss.

particularly when used in conjunction with other ototoxic drugs

ototoxicity: tinnitus, vertigo, hearing loss, ear pain

186
Q

what is the prototypical potassium-sparing diuretic?

A

spironolactone

187
Q

Which class of antihypertensive is the most powerful?

A

Direct vasodilators

188
Q

What are 2 risks in using direct vasodilators alone? (& therefore reserved for SEVERE HTN)

A

Reflex tachycardia (Produces compensatory reflex stimulation of the heart - increased myocardial contractility, heart rate, O2 consumption; Therefore can prompt angina, MI, cardiac failure)

Fluid retention (increased plasma renin concentration [Na+/H2O retention])

189
Q

How do you avoid the risks in using direct vasodilators?

A

give BB & diuretics concomitantly

190
Q

adverse effect of hydralazine?

A

lupus-like syndrome (10% patients)

191
Q

adverse effect of minoxidil?

A

hypertrichosis

192
Q

hydralazine is highly specific for which vessels?

arterial or venous?

A

arterial

193
Q 
A 75-year old woman with HTN is being treated with a thiazide.Her BP responds well and reads at 120/76mmHg. After several months on the meds, she complains of being tired and weak. An analysis of the blood indicates low values for which of the following?
Calcium
Glucose
Potassium
Sodium
Uric Acid
A

Potassium

hypokalemia is common adverse effect of thiazides & causes fatigue and lethargy in patient.

calcium, uric acid, glucose are usually elevated by thiazide diuretics. sodium loss would not weaken the patient

194
Q 
Which of the following should be avoided in a patient with a hx of severe anaphylactic reaction to sulfa medications?
Amiloride
Hydrochlorthiazide
Mannitol
Spironolactone
Triamterene
A

Hydrochlorothiazide

thiazides contain sulfa moiety

195
Q 
A male patient is placed on new meds and notes that his breasts have become enlarged and tender to the touch, Which med is he most likely taking?
Chlorthalidone
Furosemide
Hydrochlorothiazide
Spironolactone
Triamterene
A

Spironolactone

d/t effects on androgens & progesterone

196
Q 
Which is CI in a patient with hyperkalemia?
acetazolamide
chlorthalidone
chlorothiazide
ethacrynic acid
spironolactone
A

spironolactone

Acts in collecting tubule to inhibit K+ excretion & Na+ reabsorption.

The other drugs promote excretion of K+.

197
Q 
Elderly patient with hx heart disease is brought to emergency room with difficulty breathing. exam reveals that she has pulmonary edema. which tx is indicated?
acetazolamide
chlorthalidone
furosemide
hydrochlorothiazide
spironolactone
A

Furosemide

must administer diuretic that reduces fluid accumulation in lungs & thus improves oxygenation & heart function

Loop diuretics are most effective in removing large fluid volumes from the body.
The other choices are inappropriate.

198
Q 
A 55-year old male with kidney stones has been placed on a diuretic to decreased calcium excretion. After a few weeks he develops an attack of gout. Which diuretic was he taking?
Furosemide
Hydrochlorthiazide
Spironolactone
Triamterene
Urea
A

Hydrochlorothiazide - increased calcium reabsorption thus decreasing amount of calcium excreted and decreasing formation of kidney stones that contain calcium phosphate or calcium oxalate. However it can also inhibit excretion of uric acid and cause its accumulation, leading to attack of gout in some individuals.

Furosemide increases excretion of calcium. The other drugs do not have an effect.

199
Q 
Which diuretic has been shown to improve BP in resistant HTN or those already treated with 3 BP meds including thiazide or thiazide-like diuretic?
Chlorthalidone
Indapamide
Furosemide
Mannitol
Spironolactone
A

Spironolactone

“resistant HTN” = 3+ meds without reaching BP goal

Often responds well to aldosterone antagonists.

Pharmacology (5 decks)

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