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Pharm > Cardiopulmonary 1: HTN > Flashcards

Cardiopulmonary 1: HTN Flashcards

1
Q

benefit of olmesartan

A

can titrate very precisely - may be beneficial for petite patient

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2
Q

endocrine adverse effect of spirinolactone

A

gynecomastia

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3
Q

3 main AEs ACE inhibitors

A

angioedema
cough
teratogenicity

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4
Q

ACC/AHA Guidelines: Normal BP

A

<120 / <80

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5
Q

ACC/AHA Guidelines: Elevated BP

A

120 - 129 / <80

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6
Q

ACC/AHA Guidelines: HTN stage 1

A

130 - 139 systolic OR 80 - 89 diastolic

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7
Q

ACC/AHA Guidelines: HTN Stage 2

A

Systolic at least 140 OR diastolic at least 90

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8
Q

ACC/AHA Guidelines: threshold to start treatment for a patient with clinical cardiovascular disease or a 10 year atherosclerotic cardiovascular disease (risk greater than 10%)

A

start treatment for a pressure greater than or equal to 130/80

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9
Q

ACC/AHA Guidelines: threshold to start treatment for a patient with no clinical CVD and no 10 year atherosclerotic CVD (risk less than 10%)

A

start treatment at greater than or equal to 140/90

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10
Q

ACC/AHA Guidelines: when should you consider two anti htn agents?

A

if patient, regardless of their risk, was greater than 20/10 mmHg over goa.

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11
Q

ACC/AHA Guidelines: BP goal for ALL patients

A

< 130/80

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12
Q

blood pressure goal when someone is hospitalized

A

generally will be a little more liberal. won’t intervene until over 150 systolic. do not want to risk organ perfusion.

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13
Q

ACE inhibitor (definition)

A

angiotensin converting enzyme inhibitor

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14
Q

ARB (definition)

A

angiotensin II receptor blocker

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15
Q

DHP CCB (definition)

A

Dihydropyridine calcium channel blocker

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16
Q

DHP CCBs are more geared towards

A

pressure control rather than rhythm control

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17
Q

drug of choice categories for HTN in non-african american patients with no compelling indication (3)

A

thiazides
ACE-1/ARB
DHP CCB

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18
Q

drug of choice categories for African-American patients with no compelling indication (2)

A

Thiazides

DHP CCB

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19
Q

ACE inhibitors and ARBs in African American patients

A

inferior if given as mono-therapy for HTN

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20
Q

drugs of choice categories for non African-American diabetic patients without CKD (3)

A

Thiazides
ACE-1/ARB
DHP CCB

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21
Q

Drug of choice categories for African-American patients with diabetes but no CKD (2)

A

Thiazides

DHP CCB

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22
Q

Drug of choice category for patient of any race who has CKD

A

ACE-1

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23
Q

When a patient with HTN or diabetes starts approaching CKD, what will they be prescribed and why?

A

an ACE because they are renal protective and may slow down progression of CKD.

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24
Q

Drug of choice for patient of any age and race who is s/p MI ?
What if HF is present ?

A
  • Beta blocker + ACE-1

- Aldosterone antagonist if HF is present

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25
Q

What drug should be prescribed for a patient of any age/race who is s/p MI and also has a degree of HF present?

A

Aldosterone antagonist

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26
Q

Drug of choice for patient of any age/race who is being medicated for recurrent stroke prevention

A

Thiazide + ACE-1

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27
Q

Drugs of choice for patient with heart failure of any age/race (4)

A

Beta Blocker + ACE-1
Diuretics for fluid retention
Aldosterone antagonist
Hydralazine / ISO DN

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28
Q

Why thiazides + ACE-1 for patients at risk for recurrent stroke?

A

In setting of stroke, you may not want to have beta blocker because you don’t want to slow down heart and risk perfusion.

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29
Q

What kind of diuretic is preferred in heart failure?

A

loop

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30
Q

Beta Blockers after MI

A

May benefit the heart by supporting it/giving it a slight break

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31
Q

african american patients and hydralazine/ISO DN

A

in the setting of HF, pts do better or at least do not do worse than patients just on ace inhibitors.

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32
Q

Four major classes of anti hypertensives (first lines)

A

Thiazides
CCBs
ACE-Is`
ARBs

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33
Q

If response is not effective enough on first line therapy, what should you do next?

A

increase dose (up to max dose) of that first line drug and reevaluate prior to adding a second agent.

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34
Q

disadvantage of adding second agent

A

unsure of where potential side effect may be coming from

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35
Q

what to consider before putting patient on a single tablet combination drug? (ie: an ACE/thiazide) Why?

A

try the patient on the two separate tablets first before putting them on a combo tablet. evaluate their response. it is easier to titrate individual agents separately. combo drug doses are fixed. once patient is solid for a month or two, then consider combo pill.

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36
Q

Advantages of combo drugs

A

less pill burden

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37
Q

disadvantage of combo drug

A

cannot titrate

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38
Q

once established that max dose of first line is not effective enough for pt’s HTN, what is the appropriate next step?

A

start the pt on a second agent as an individual pill. do not start the pt on second agent as a combo pill.

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39
Q

later line alternatives “A” list (5)

and why are they later line?

A
  • alpha 1/beta blockers
  • direct vasodilators
  • central alpha2-adrenergic agonists
  • beta-blockers
  • loop diuretics
  • too powerful as a first line treatment
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40
Q

example: direct vasodilator

A list

A

hydralazine

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41
Q

example: beta-blocker

A list

A

metoprolol

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42
Q

example: loop diuretic

A list

A

furosemide

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43
Q

which beta blocker is recommended to pregnant women with htn?

A

labetalol

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44
Q

other use for labetalol, carvedilol, or hydralazine

A

hypertensive urgency

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45
Q

you’ll more often see furosemide prescribed for

A

heart failure rather than htn

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46
Q

later-line alternatives “B” list (3) for htn

A
  • aldosterone antagonists
  • alpha-1 blocker
  • vasodilating beta-blocker
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47
Q

example: aldosterone antagonist

B list

A

spirinolactone

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48
Q

Example: vasodilating beta blocker

B list

A

nebivolol

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49
Q

nebivolol FYI

A

not a popular medication

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50
Q

Mechanism of action: thiazide

A

inhibit active exchange of Na and Cl (in equal amounts) in the distal convoluted tubule (last step of tubule)
*most often used

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51
Q

mechanism of action: loop diuretics

A

inhibit exchange of Na/Cl/K on thick segment of ascending loop of henle (where a lot of concentration takes place)
*HF

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52
Q

mechanism of action: K sparing diuretics and main function

A

inhibits reabsorption of Na in distal convoluted tubule and collecting duct. The main function is antagonizing aldosterone (while sparing potassium). Allows you to pee out sodium and hold on to K.

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53
Q

you may often see K sparing diuretics prescribed with _____ and why?

A

thiazides, which waste a lot of K. adding a K sparing diuretic may help prevent hypokalemia.

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54
Q

aldosterone is released when body perceives

A

that you need fluid

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55
Q

what does it mean when it is said that K sparing diuretics antagonize aldosterone?

A

that they bind to receptor and prevent aldosterone from being released and retaining fluid. They allow your body to excrete the fluid instead.

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56
Q

Therapeutic indications of thiazides (2)

A

hypertension

edema

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57
Q

3 thiazide drugs used for HTN

A

chlorothiazide
hydrochlorothiazide
chlorthalidone

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58
Q

which thiazide do you see in pediatric htn

A

chlorothiazide

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59
Q

which thiazide do you see more in adult htn?

A

hydrochlorothiazide

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60
Q

chlorthalidone vs hctz

A

old thiazide drug used for htn which has a longer duration of action

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61
Q

thiazide drug used for edema

A

metalozone

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62
Q

metolazone may be seen when a patient is already prescribed

A

a loop diuretic. it provides an extra push.

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63
Q

drug interactions involving thiazide involve

A

electrolytes

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64
Q

thiazide and digoxin

A

k wasting drug predisposes pt to hypokalemia, putting them at risk for digoxin toxicity. requires tighter monitoring.

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65
Q

thiazide and lithium

A

thiazide wastes sodium. lithium resembles sodium to the kidney. if you are wasting a lot of sodium, the lithium will be retained by the kidney and can accumulate, resulting in lithium toxicity.
requires tighter monitoring.

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66
Q

thiazide and electrolyte supplements

A

the electrolyte supplement may not be as effective

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67
Q

thiazide and ototoxicity

A

no risk, unlike other diuretics

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68
Q

thiazide and sulfonamide allergy

A

there is a sulfa-like compound in thiazide, proceed with caution. understand what the allergy actually is before proceeding.

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69
Q

thiazide use in anuric renal failure

A

if you have an impaired GFR (<10ml/min) or CrCl (<30), thiazide will not be effective.

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70
Q

normal creatinine clearance is usually

A

> 100ml/min

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71
Q

Adverse effects of thiazides:

what will it decrease? (5)

A

Mainly sodium, potassium, chloride

also phosphorus and magnesium

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72
Q

adverse effects of thiazides:

what will it increase?

A

calcium, uric acid

potentially glucose and lipids

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73
Q

adverse effect of thiazide, unrelated to electrolytes

A

photosensitivity and propensity to burn

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74
Q

Most powerful diuretics are

A

loop diuretics

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75
Q

aside from HF, what are two other indication for loop diuretics re: edema?

A

hepatic cirrhosis and renal disease (CrCl <30ml/min)

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76
Q

if a patient has a CrCl < 30 mL/min, which diuretic would be appropriate?

A

Loop diuretic

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77
Q

4 Examples of loop diuretics

A

Lasix
Bumetanide
Ethacrynic acid
Torsemide

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78
Q

Most potent loop diuretic

A

bumetanide (bumex)

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79
Q

How many doses per day may you need of lasix?

A

2-3

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80
Q

If patient has a true sulfa allergy, which loop diuretic is safest? and what are two downsides of this drug?

A

ethacrynic acid

  • PO is extremely expensive
  • ototoxic
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81
Q

Torsemide tends to be used when

A

lasix is in shortage

82
Q

Duration of onset for lasix

A

~6 hours

Lasix “lasts six”

83
Q

what time should you avoid giving lasix?

84
Q

Which lytes are decreased in loop diuretic use? (5)

A

sodium, potassium, chloride, magnesium, calcium

85
Q

What rate should loops be given IV and why?

A

No faster than 10mg/min, ototoxicity

86
Q

Which metabolic alterations might you see in loop diuretic

A

increased glucose, uric acid, lipids

87
Q

ototoxicity risk increases with

A

higher doses of loop diuretics

88
Q

furosemide IV to oral conversions

89
Q

Bumex IV to PO conversion

90
Q

Bumex potency to lasix IV

A

1mg bumex: 40mg lasix

91
Q

Which loop diuretic is most useful in refractory response to diuretics?

A

bumetanide

92
Q

Loop diuretic drug interaction: digoxin

A

hypokalemia -> dig toxicity

93
Q

loop diuretic drug interaction -> lithium

A

Na wasting, kidney retains lithium as it resembles Na. -> lithium toxicity

94
Q

Loop diuretic drug interactions with other ototoxic drugs

A

ototoxicity - watch with k sparing diuretics

95
Q

loop diuretics and sulfa allergy

A

proceed with caution

96
Q

K sparing diuretic mech of action

A

block aldosterone in the distal convoluted tubule and collecting duct

97
Q

K sparing diuretics are typically

A

used in combo with other agents as they have a modest diuretic effect

98
Q

most common k sparing diuretic

A

spirinolactone

99
Q

mechanism of action of triamterene and amiloride

A

acts on sodium-potassium exchange in the distal nephron

100
Q

the diuretic effect of triamterene and amiloride is

A

modest. acts quicker than spirinolactone

101
Q

caution with dyazide (triamterene/hctz)

A

order frequent bmps. this comvo drug can, over a long period of time, cause hyperkalemia.

102
Q

best diuretic group in the setting of htn

103
Q

long term implication with K sparing diuretic

A

watch for hyperkalemia

104
Q

what is a possible explanation for ACE inhibitor induced cough?

A

degradation of bradykinin

105
Q

ACE inhibitor mechanism of action

A

blocks conversion of angiotensin I to angiotensin II, halting vasoconstriction

106
Q

in cases when renal afferent arteriolar pressure is increased, what is an intervention?

A

ACE inhibitors act as a renal protectant, lowering afferent and efferent pressure. * does not help in already low afferent pressures

107
Q

ace inhibitors as a renal protectant in already low afferent pressures

A

does not help

108
Q

best diuretic group in HF

A

loop diuretic

109
Q

ACE inhibitors vs ARBs

A

they are not used together. Similar but not the same. people on ARBs probably did not benefit from ACEs.

110
Q

degradation of bradykinin

A

The enzyme ACE (angiotensin converting enzyme) is the enzyme converting angio I to angio II. ACE is in the lungs. Bradykinin is usually released in response to ACE. When that conversion isn’t able to happen, bradykinin (inflammatory mediator) has nowhere to really go and cannot be broken down. This causes a cough (or the very serious adverse effect - angioedemia)

111
Q

ACE inhibitor which you’ll most likely see dry cough

112
Q

how to fix ACE inhibitor dry cough?

A

by giving an ARB

113
Q

renal afferent arteriole

A

bringing blood to the kidney

114
Q

renal efferent arteriole

A

brings blood away from kidney

115
Q

as creatinine goes up,

A

creatinine clearance goes down

116
Q

when we start someone on an ace inhibitor, you’re going to see

A

a bump in creatinine by about .2

117
Q

if a patient recently started on an ace inhibitor has a bump in creatinine of about .5 or more

A

dc the ace inhibitor

118
Q

indications for ace inhibitors (3)

A

htn, hf, post mi

119
Q

ace inhibitors and heart rate

A

causes no change in heart rate

120
Q

preload

A

force of blood coming into heart

121
Q

afterload

A

what is ejected to the vessels and periphery

122
Q

in the setting of heart failure, we want to see what in preload and afterload?

A

reduction.

123
Q

potassium in ace inhibitors

A

because they decrease Na, K is retained

124
Q

what population is at highest risk for angioedema in ace inhibitors?

A

african american women

125
Q

drugs that ace inhibitors have interactions with (3)

A

K supplements
diuretics
asa

126
Q

ace inhibitors and k supplements

A

decreased excretion of K

127
Q

ace inhibitors and diuretics

A

hypotension - monitor

128
Q

ace inhibitors and asa interaction

A

kidney function

129
Q

3 contraindications for ace inhibitors

A
  • renal artery stenosis
  • pregnancy
  • previous angioedema
130
Q

renal artery stenosis and ace inhibitors

A

if the artery isn’t able to dilate and contract, they won’t be able as effective

131
Q

pregnancy and ace inhibitors

A

category x teratogenicity

132
Q

ace inhibitors and previous angioedema

A

do not administer.

133
Q

when can ace inhibitor induced angioedema happen?

A

any time. first or hundredth dose.

also can be if patient is under more stress or taking med at unusual time.

134
Q

suffix for ace inhibitors

135
Q

Angiotensin II Receptor antagonists (ARBs) mechanism of action

A

block angiotensin II receptors on cell membranes

136
Q

suffix for ARBs

137
Q

therapeutic indications for ARBs

A

hypertension, chf

138
Q

ARBs are often seen in patients who

A

have failed ACE inhibitors

139
Q

adverse effects of ARBs (4)

and how they compare to ACEs

A
  • teratogenicity
  • cough (< ace)
  • hyperkalemia (< ace)
  • angioedema (< ace)
140
Q

contraindication for ARBs

A

renal artery stenosis

141
Q

drugs which ARBs interact with

A
  • k sparing diuretics
  • k supplements
  • nsaids * renal damage
142
Q

ACEs and ARBs: summary

A

ACEs stop the conversion of angio I to angio II, decreases aldosterone and vasocon, cant breakdown bradykinin (cough)

ARBs let that conversion happen, but they block the receptors. less cough, less hyperkalemia, less renal insufficiency.

drug interactions are very similar.

143
Q

Calcium Channel Blockers mechanism of action

A

block inward movement of calcium into muscle by binding to calcium channels in the heart and SM of the coronary and peripheral vasculature.

144
Q

2 subgroups of CCBs

A

non-dihydropyridines

dihydropyridines

145
Q

non-dihydropyridines are

A

CCBs used primarily for conduction disorders

146
Q

dihydropyridines are

A

CCBs used for dilator properties (in htn and hf)

147
Q

indications for CCBs (4)

A

hypertension
angina
arrhythmias
heart failure

148
Q

examples of 2 non-dihydropyridine CCBs

A

diltiazem

verapamil

149
Q

examples of dihydropyridines end in

150
Q

why has verapamil lost popularity

A

a lot of side effects, especially constipation

151
Q

digoxin and verapamil

A

synergistic in a bad way - slows heart too much and can lead to heart block

152
Q

verapamil and beta blockers drug interaction

A

bradycardia

153
Q

if a patient in hf or heart block absolutely needs a CCB

A

give them a dihydropyridine, not a non.

154
Q

diltiazem vs verapamil

A

just alike except without constipation

155
Q

therapeutic effects of dihydropyridine CCBs

A

vasodilation on smooth muscle

156
Q

dihydropyridine CCBs are very helpful in the setting of

A

hypertension and prinzmetal’s (and variant) angina

157
Q

types of angina CCBs treat

A

not activity induced. angina that is induced by overactive calcium channels.

158
Q

indications for dihydropyridine CCBs

A

htn and heart failure

159
Q

dihydropyridine CCB for hf

A

amlodipine

160
Q

if a patient is on 10 mg of a dihydropyridine CCB and has slight ankle edema,

A

decrease dose to 5mg.

161
Q

why can we use dihydro ccbs in heart failure?

A

bc they dont effect contractility as much, like non dihydros do.

162
Q

beta-adrenergic blocker mechanism of action

A

competitively inhibit beta-adrenergic agonist receptors

163
Q

two different types of beta adrenergic blockers

A

cardio selective

cardio non selective

164
Q

cardio non selective beta adrenergic receptors may be used in (3)

A

ascites
portal htn
alcohol withdrawal

165
Q

nonselective BB agents block which receptors?

A

beta 1 and beta 2

166
Q

nonselective BB agents are effective in causing

A

bronchoconstriction

167
Q

beta blocker suffix

168
Q

selective BB act on which receptor at normal doses?

169
Q

selective vs non selective BBs and glucose metabolism

A

selective - minimal effect

nonselective - may effect

170
Q

examples of selective BBs (2)

A

atenolol

metoprolol

171
Q

indications for beta blockers (4)

A

htn
angina
hf
mi

172
Q

BBs, selective or non selective, should not be used in which condition? and when would it be ok to use?

A

decompensated HF

until pt is euvolemic again

173
Q

beta blockers like propanolol and labetolol CAN cause vasoconstriction. When would you want to avoid these?

A

in patients with COPD or asthma

174
Q

true or false: propranolol is almost never used for cardiac reasons

175
Q

non selective BBs and the BBB

A

they cross the BBB.

176
Q

drug interactions: BBs

A

concurrent bp meds

oral hypoglycemics

177
Q

beta blockers and oral hypoglycemics - explain

A

they can mask hypoglycemia because the symptoms of hypoglycemia are adrenergically driven

178
Q

Alpha/Beta-Adrenergic Blockers mechanism of action

A

they block beta-1, beta-2, and alpha-1 receptors in the same preparation.

179
Q

if you have alpha-1 blockade:

A

BP is decreased

180
Q

if you have alpha-2 stimulation (like in an alpha2 agonist):

A

BP is decreased.

181
Q

alpha/beta-adrenergic blocker and lipid/carb metabolism

182
Q

Alpha-1 adrenergic blockers mechanism of action and effect

A

Competitively block alpha-1 receptors, causing relaxation of arterial and venous smooth muscle. Decrease peripheral vascular resistance.

183
Q

alpha-1 adrenergic blockers are very good at decreasing bp but

A

are so effective that it may be dangerous.

184
Q

suffix for alpha-1 adrenergic blockers

185
Q

patient education for alpha-1 adrenergic blockers

A

high likelihood of first dose postural hypotension/syncope. Stay upright for 30 min after taking med.

186
Q

centrally acting agent: alpha-2 agonist

example

187
Q

therapeutic indication of clonidine, a centrally acting alpha-2 agonist

A

hypertension

pain management

188
Q

clonidine for pain management

A

alpha2 activity can also be analgesic (IV)

189
Q

clonidine patient education

A

do not stop taking med abruptly

190
Q

caution for elderly patients and clonidine

A

cholinergic effects

191
Q

PTSD and clonidine

A

sometimes indicated for relaxation in the setting of PTSD

192
Q

HTN urgency intervention when out of other options

193
Q

alpha-2 agonist: methyldopa indication

A

useful in htn when pregnant

194
Q

pregnancy category: methyldopa

195
Q

methyldopa is

A

alpha 2 agonist

196
Q

management of the patient on methyldopa

A

monitor CBC

197
Q

Vasodilators: hydralazine

2 therapeutic effects, 1 AE

A

decreases peripheral vascular resistance
increases cardiac output

provides reflex tachycardia*

198
Q

indications of hydralazine in the htn pt

A

HTN

HTN crisis

199
Q

antihypertensive combination products typically contain

A

a diuretic

200
Q

HTN urgency

A

systolic > 180, can be treated c po meds, no end organ damage

201
Q

htn emergency

A

systolic > 200, end organ damage has taken place. need IV meds.

Pharm (31 decks)

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