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Clinical Pharm Exam 2 (Jaclyn) > HTN > Flashcards

HTN Flashcards

1
Q

Correct BP technique

A
  • Automated electronic device > sphygmomanometer
  • Take 2 readings 1-2 minutes apart
  • Measure BP in both arms @ initial visit
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2
Q

__% of cases of ischemic HD & CVA are attributable for HTN

A

50

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3
Q

What is the new BP goal?

A

130/80

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4
Q

Even though some do well with a new goal of 130/80, what else do we need to consider when establishing BP goals?

A

Tailor to the PATIENT

e.g. pt. with orthostatic hypotension -> goal of <140/90 more appropriate

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5
Q

Treatment for normal BP (120/80)

A

Maintain health lifestyle habits

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6
Q

Treatment for elevated BP (120-129/<80)

A

Lifestyle changes + check for meds that can raise BP

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7
Q

Treatment for Stage 1 HTN (130-139/80-89)

A
  • Lifestyle changes alone if ASCVD risk is <10%

- BP meds for pts. with CV disease, DM, CKD, or ASCVD >10%

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8
Q

Treatment for Stage 2 HTN (>140/90)

A

Lifestyle changes + BP meds

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9
Q

Who do we suggest home BP monitoring for?

A

ALL pt. (esp. if you suspect white coat HTN, resistant HTN)

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10
Q

What do you do if you use an automatic BP monitor in the office and get a high/unusual BP read?

A

Verify with manual check (esp. before changing med!)

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11
Q

How do anti-HTN agents compare to each other?

A

They are roughly equally effective

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12
Q

Black pt. respond less to what meds?

A

ACEI, ARBs, BB

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13
Q

Preferred anti-HTN meds (combos)

A
  • ACEI or ARB + thiazide

- ACEI or ARB + DHP-CCB

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14
Q

Meds that induce HTN

A
  • OCPS
  • Stimulants
  • Transplant meds (cyclosporine)
  • EPO
  • Corticosteroids
  • NSAIDs
  • Sympathomimetics
  • Neuropsychiatrics
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15
Q

25% of pts stop anti-HTN within _____

A

6mo

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16
Q

What can cut nonadherence?

A
  • Identifying ADRs & switching therapy
  • Eval cost
  • Explain importance of mgmt
  • Get pts engaged
  • Advise pt to engage automatic refill program
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17
Q

What is chronotherapy?

A

Taking >1 BP med at night

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18
Q

In what patients should chronotherapy should be recommended?

A

Pt. w/ morning BP rise OR pt. whose BP dose NOT dip @ night like it should

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19
Q

Chronotherapy has what additional benefit?

A

Lowers CV risk

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20
Q

What is the best predictor of BP control?

A

Med adherence

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21
Q

Mannitol formulations

A

IV, urogenic solution

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22
Q

Mannitol MOA

A

Nonabsorbable polysaccharide that acts as an osmotic diuretic (“sugar that pulls water in”); inhibits Na+ and H2O reabsorption

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23
Q

Mannitol site of action

A

Proximal tubule and loop of Henle

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24
Q

Mannitol clinical indications

A
  • Decreased ICP ass. w/ cerebral edema

- GU irrigate in TURP or other transurethral procedure

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25
Q

What do we monitor in a pt. on mannitol?

A
  • Daily I&O
  • Renal fcn & electrolytes
  • Serum & urine osmolality
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26
Q

Mannitol ADRs

A
  • Fluid & electrolye imbalance

- Dehydration/hypovolemia secondary to rapid diuresis

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27
Q

Drug interactions of ALL anti-HTN meds

A

Anti-HTN & vasodilators (e.g. nitrates, PDE5 inhibitors)

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28
Q

Acetazolamide formulations

A

PO, IV

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29
Q

Acetazolamide MOA

A

Reversible inhibition of carbonic anhydrase -> ↓ H+ secretion at renal tubule & ↑ renal excretion of Na+, K+, HCO3, & H2O

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30
Q

Acetazolamide site of action

A

Proximal tubule and loop of Henle

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31
Q

Acetazolamide clinical indications

A

Acute mountain sickness (prevention or sx relief)

- ↓ blood pH stimulates extra breathing = higher blood [O2]

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32
Q

Loop diuretic drugs

A
  • Furosemide
  • Torsemide
  • Bumetanide
  • Ethacrynic acid
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33
Q

Which loop diuretic does not contain a sulfa group?

A

Ethacrynic acid

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34
Q

Loop diuretic MOA

A

Inhibit Na+/K+-ATPase

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35
Q

Loop diuretic site of action

A

Thick segment (ascending limb) of the loop of Henle

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36
Q

Loop diuretic clinical indication

A
  • Acute pulmonary edema & other edematous states

- Acute hypercalcemia

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37
Q

What do we monitor in a pt. on a loop?

A
  • BMP
  • Ca+, Mg+
  • Daily wts
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38
Q

Why are loops better than thiazides for treatment of HF?

A

Loops cause more Na+ secretion which results in a profound diuretic effect

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39
Q

Starting dose for loops

A

20-40mg qAM (titrate to lowest dose that achieves fluid balance)

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40
Q

Which do we do first for loops: increase the dose or add a second dose?

A

INCREASE the dose! (“double the dose until the urine flows”)
- Titrate to 80mg qAM; if more needed add 80mg in the afternoon

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41
Q

If additional diuresis/sx relief is needed for a pt. on a loop, what drugs can we add to the treatment regimen?

A

Aldosterone agonist - spironolactone! (esp. for HFrEF of GFR >30)
Thiazide for persistent sx

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42
Q

Loops work better than thiazides for a GFR of what

A

<30

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43
Q

Which loop causes the most ototoxicity?

A

Ethacrynic acid

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44
Q

Drug interactions w/ loops

A
  • NSAIDs (antagonize diuretic effect via Na+ retention)
  • Anti-arrhythmics (QT!)
  • Lithium toxicity
  • Antagonizes gout (urate absorption) & DM medications (hypoK+)
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45
Q

Loop ADRs

A
  • Volume depletion
  • HypoK+, hypoMg
  • HypoNa+
  • Hyperuricemia
  • SNHL (“ringing”)
  • Hyperglycemia
  • Rash (r/t sulfa cross-reactivity?)
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46
Q

Thiazide drugs

A
  • HCTZ
  • Chlorthalidone
  • Metolazone
  • Indapamide
  • Chlorothiazide
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47
Q

Which thiazide is the only available IV? (all others tablets)

A

Chlorothiazide

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48
Q

Thiazide MOA

A

Inhibit Na+/K+-ATPase

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49
Q

Thiazide site of action

A

Distal convoluted tubule

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50
Q

Chlorthalidone vs. HCTZ

A

Chlorthalidone…

  • 2x as potent
  • Longer DOA
  • 25mg more effective than 50mg of HCTZ in decreasing BP at night
  • Extensive partitioning into RBCs (creates a “depot”)
  • ADRs equivalent
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51
Q

Which do we use more: Chlorthalidone vs. HCTZ?

A

HCTZ in most fixed-dose combinations

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52
Q

Thiazide indication

A

HTN

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53
Q

When do we dose thiazides?

A

In the AM

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54
Q

What do we monitor in a patient on a thiazide?

A
  • BMP

- Ca+, Mg+

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55
Q

Every thiazide beside what drug is less effective when CrCl <30mL/min?

A

Metolazone

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56
Q

How does thiazide effect Ca++?

A 
Enhances reabsorption (improves hypercalciuria/kidney stones, may benefit osteoporosis) 
*opposite of loops
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57
Q

Thiazides have the potential to unmask what types of conditions?

A

Conditions that increase Ca+ (e.g. hyperPTH, CA, sarcoid, PHEOS)
*thaizides do not traditionally cause hypercalcemia

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58
Q

What drug can be used with loop diuretics for synergy in refractory edematous states?

A

Metolazone

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59
Q

Drug interactions w/ thiazides

A
  • NSAIDs (antagonize diuretic effect via Na+ retention)
  • Anti-arrhythmics (QT!)
  • Lithium toxicity
  • Antagonizes gout (urate absorption) & DM medications (hypoK+)
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60
Q

Thiazide ADRs

A
  • Volume depletion
  • HypoK+, hypoMg (@ risk for metabolic acidosis w/ higher doses)
  • HypoNa+
  • Hyperuricemia
  • Hyperglycemia
  • Rash (r/t sulfa cross-reactivity?)
  • Hyperlipidemia
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61
Q

K+ sparing diuretic drugs

A
  • Spironolactone
  • Eplerenone
  • Amiloride
  • Triamterene
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62
Q

Spironolactone & eplerenone MOA

A

Anti-aldosterone drug

- Antagonizes mineralocorticoid receptors -> ↓ transcription of gene for Na+/K+-ATPase

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63
Q

Amiloride & triamterene MOA

A

Inhibit Na+/K+-ATPase

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64
Q

K+ sparing diuretic site of action

A

Collecting tubule

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65
Q

Which K+ sparing diuretic is the only available as a solution? (all others tablets)

A

Spironolactone

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66
Q

Spironolactone & eplerenone clinical indication

A
  • Mineral corticoid excess (primary OR secondary - CHF, cirrhosis, nephrotic syndrome)
  • Acne vulgaris
  • Hirsutism
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67
Q

Amiloride & triamterene clinical indication

A

Generally used with other diuretics to prevent or correct hypokalemia

  • Overall weak diuretic effect
  • Falling out of favor d/t addition of ACEI/ARB to diuretics
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68
Q

Do NOT use K+ sparing diuretics for K+ >____ or eGFR

A

5.5; 30

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69
Q

What do we monitor in a patient on a K+ sparing diuretic?

A

K+ & BUN/Cr (baseline, 1wk, monthly for 3mo, quarterly for 1yr, then q6mo)

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70
Q

Drug interactions with K+ sparing diuretics

A
  • K+ supplements/salt substitutes

- Drugs that retain K+ (BB, TMP-SMX, NSAIDs, ACEI/ARBs)

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71
Q

K+ sparing diuretics ADRs

A

Hyperkalemia

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72
Q

Spironolactone ADRs

A
  • TERATOGEN
  • Painful gynecomastia
  • Amenorrhea
  • ED
  • ↓ libido
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73
Q

Triamterene ADRs

A

Nephrotoxin: crystalluria & cast formation => stones or AKI

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74
Q

Use of 2 diuretic drugs acting at a different nephron sites may……

A

Have a synergistic effect

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75
Q

ACEI drugs end in “___”

A

pril

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76
Q

What drug is the only true QD ACEI?

A

Lisinopril (half life = 12hrs)

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77
Q

Which ACEI is a prodrug?

A

Enalapril

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78
Q

ACE is a kininase, if it’s inhibited what increases?

A

Bradykinin

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79
Q

What are the implications of ↑ bradykinin

A

Cough (bad)

Release of endothelial NO = vasodilation (good)

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80
Q

ACEI MOA

A

Vasodilate efferent arteriole -> ↓ glomerular pressure

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81
Q

ACEI clinical indications

A
  • HTN (esp. w/ LVH)
  • HF with systolic dysfcn
  • CKD (both DM & non-DM)
  • Post-AMI (which resulted in ↓ systolic fcn)
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82
Q

What population is less sensitive to ACEI monotherapy?

A

AA

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83
Q

ACEI have synergy with what other drug

A

Diuretics

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84
Q

Are ACEI & ARBs good or bad for the kidneys

A

Renal protectors!

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85
Q

At what GFR are ACEI not recommended

A

There is NO absolute GFR when ACEIs can’t be used

- The lower the GFR, the greater the need for neph consultation

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86
Q

What do we monitor in a patient on a ACEI?

A
  • BUN/Cr

- K+

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87
Q

Drug interactions with ACEI

A

Other meds that cause hyperkalemia (BB, TMP-SMX, NSAIDs, ACEI/ARBs)

88
Q

Precautions/contraindications w/ ACEI

A
  • Pt. w/ hereditary or idiopathic angioedema

- Bilateral RAS or stenotic lesion to solitary kidney

89
Q

ACEI ADRs

A
  • Cough
  • TERATOGEN
  • Decrease intrarenal perfusion = renal fcn decline (CHECK SCr!!! Increase of <30% acceptable)
  • Hyperkalemia
  • Angioedema
90
Q

What do we do if a pt. on an ACEI/ARB has a SCr increase of <30% and K+ <5.5?

A

Repeat lab in 2-3 weeks

91
Q

What do we do if a pt. on an ACEI/ARB has a SCr increase 30% to <50% and K+ <5.5?

A

Cut dose in half and recheck every 5-7 days until stable

- D/C if persists after 4 weeks

92
Q

Why is there less of a chance of angioedema with ARBs c/t ACEI?

A

ARBs don’t directly inhibit bradykinin

93
Q

Can we use an ARB if a pt. has MILD angioedema (tongue & face swelling) with an ACEI?

A

Yes

94
Q

Can we use an ARB if a pt. has SEVERE angioedema (airway obstruction, respiratory sx) with an ACEI?

A

Consider another treatment

95
Q

How long should we wait after stopping an ACEI and starting an ARB for a pt. that experienced angioedema?

A

> 4 wks

96
Q

ARB drugs end in “___”

A

sartan

97
Q

The generic products of which ARB drug are possibly carcinogenic?

A

Valsartan

- CA risk is low, but some are being pulled from the market

98
Q

ARB MOA

A

Impairs binding of angiotensin II to AT1 receptors -> interferes with RAAS

99
Q

ARB clinical indications

A

GENERALLY THE SAME AS ACEI

  • HTN (esp. w/ LVH)
  • HF with systolic dysfcn
  • CKD (both DM & non-DM)
  • Post-AMI (which resulted in ↓ systolic fcn)
100
Q

Which ARB has the best data?

A

Losartan

101
Q

Losartan has what additional clinical indication

A

Used for gout prevention d/t uricosuric activity

102
Q

What do we monitor in a patient on a ARB?

A
  • BUN/Cr

- K+

103
Q

Losartan is a substrate of CYP____ & ____

A

2C9, 3A4 (however, minimally metabolized)

104
Q

What other drugs do we want to avoid with ARBs?

A

Drugs that retain K+

105
Q

ARB ADRs

A
  • TERATOGEN
  • Decrease intrarenal perfusion = renal fcn decline (CHECK SCr!!! Increase of <30% acceptable)
  • Hyperkalemia
  • Angioedema (less risk c/t ACEI)
106
Q

Which ARB is associated with sprue-like enteropathy?

A

Olmesartan (don’t use anyway, limited data)

107
Q

Which drug is a renin inhibitor?

A

Aliskiren

108
Q

Aliskiren MOA

A

Binds catalytic site of renin -> inhibits entire RAAS system

109
Q

Do we use aliskiren?

A

No

110
Q

Does it ever make sense to combine an ACEI with an ARB OR aliskiren with an ACEI or ARB?

A

Rarely

111
Q

Alpha-adrenergic antagonists (alpha blockers) end in “___”

A

zosin

112
Q

Which alpha blockers are long acting (QD)?

A

Terazosin, doxazosin

113
Q

Which alpha blockers are short acting (BID-TID)?

A

Prazosin

114
Q

Alpha blocker MOA

A

Highly selective a1 receptor antagonist -> decrease arterial psi by dilating vessels

115
Q

Why is it important to combine an alpha blocker with a diuretic

A

Alpha blockers commonly cause fluid retention

116
Q

Clinical indications of alpha blockers

A
  • HTN
  • BPH
  • “Medical expulsive therapy” for ureteral stones
  • PTSD, distressing dreams (prazosin)
117
Q

Are alpha blockers more likely to cause tachycardia or frequent postural hypotension?

A

Postural hypotension

118
Q

Doxazosin is a substrate of CYP___

A

3A4

119
Q

Although this is an interaction with ALL HTN drugs, the combination of alpha blockers and ________ is CONTRAINDICATED

A

Vasodilators (e.g. nitrates, PDE5 inhibitors)

120
Q

What other drug type should we avoid using concomitantly with alpha blockers and what are the implications of this interaction?

A

Decongestants

- Acute urinary retention (d/t increased tone in bladder neck)

121
Q

Alpha blocker ADRs

A
  • Postural hypotension (COMMON)
  • Drowsiness/fatigue
  • Nasal congestion/rhinitis
  • Retrograde ejaculation
  • Floppy-iris syndrome
122
Q

How do we mitigate the postural hypotension/dizziness that is commonly experienced with the first few doses of alpha blockers?

A

Give 1st few doses @ bedtime

123
Q

Beta blockers end in “___”

A

lol

124
Q

Non-selective beta blocker (B1) drugs

A
  • Propranolol
  • Nadolol
  • Timolol
125
Q

Selective beta blocker (B1) drugs

A
  • Metoprolol
126
Q

Are non-selective BB or selective BB more associated with bronchospasm? And are, therefore, use more cautiously in pt. with what conditions?

A

Non-selective!

- Caution in pt. w/ asthma, COPD, raynaud’s

127
Q

What BB has the best clinical data in treating pt. post-AMI, w/ HF, w/ Afib?

A

Metoprolol

128
Q

What is metoprolol tartrate

A

IR product (dosed BID-TID)

129
Q

What is metoprolol succinate

A

ER product (dose QD)

130
Q

Examples of BB with vasodilatory effects (CHF > HTN)

A
  • Non-selective: carvedilol, labetalol

- Selective: nebivolol

131
Q

Examples of BB with intrinsic sympathomimetic activity (ISA)

A
  • Non-selective: pindolol

- Selective: acebutolol

132
Q

What is the physiologic significance of drugs with intrinsic sympathomimetic activity (ISA)

A

These agents have partial agonist activity = decrease BP w/ less decrease in HR

133
Q

BB MOA

A

Competitive inhibitors of catecholamines at beta receptors

134
Q

Where are B1 receptors located?

A

Heart muscle (increase HR, contractility, AV conduction)

135
Q

Where are B2 receptors located?

A

Heart muscle, but more prominent in bronchial & peripheral vascular smooth muscle (vasodilation, bronchodilation)

136
Q

Clinical use of BB

A
  • HTN (esp. if additional indication (below))
  • Stable/unstable angina
  • Post-AMI
  • Systolic HF/HFrEF
  • Certain arrhythmias (Afib)
  • Perioperative
137
Q

Other clinical indications for BB

A
  • Proliferating infantile hemangiomas (propranolol)
  • Migraines
  • Essential tremors
  • Symptomatic mgmt of pheos/hyperthyroid
138
Q

What population is less sensitive to BB monotherapy?

A

AA

139
Q

What must we do when d/c BB therapy?

A

TAPER (1-3wks)

- Could lead to accelerated angina, AMI, death

140
Q

What pt. population should we avoid giving BB? Clue: adolescent w/ CP in the ED

A

Cocaine-induced CP or AMI

141
Q

Are BB more or less effective in preventing CV events, such as CVA, c/t ACEI, ARBs, CCB?

A

Less

142
Q

What are some positive implications of long-term use of BB in pt. w/ HF?

A
  • Reduce hospital admission
  • Improve sx
  • Improve QOL
  • Improve survival
143
Q

What BB do pt. w/ HF get?

A

Carvedilol

144
Q

If a pt. w/ HF has symptomatic hypotension or ventricular arrhythmias, what BB should they be on instead of carvedilol?

A

Metoprolol succinate

145
Q

In what populations do we avoid use of BB?

A
  • Asthma, COPD?
  • Pt. w/ 2nd or 3rd degree heart block
  • Pt. w/ SSS
  • Pt. w/ bradycardia (<50bpm)
146
Q

Which 3 beta blockers are CYP2D6 substrates?

A

Metoprolol, propanolol, carvedilol

147
Q

BB blunt the effects of what neurotransmitter

A

Epinephrine

148
Q

BB are used cautiously with other drugs that depress myocardial fcn or pacemaker activity, such as…..

A
  • CCB

- Antiarrhythmics

149
Q

BB ADRs

A
  • Bradycardia
  • HyperK+
  • Fatigue/exercise intolerance
  • ED
  • Floppy-iris syndrome
  • Bronchospasm (non-selectives >)
  • Mask/delay recovery from hypoglycemia (non-selectives >)
150
Q

CCB end in “_____”

A

dipine

151
Q

Short-acting DHP-CCBs

A

Nifedipine

152
Q

Longer-acting DHP-CCBs

A

Felodipine, isradipine, nicardipine, nisoldipine

153
Q

Long-acting DHP-CCBs

A

Amlodipine

154
Q

Non-DHP-CCBs

A

Verapamil, diltiazem

155
Q

CCB MOA

A

Inhibit L-type Ca+ channels -> no intracellular influx of Ca+

156
Q

DHP-CCBs affects what MOST: vasodilation OR cardiac contractility/conduction?

A

Vasodilation

157
Q

Non- DHP-CCBs affects what MOST: vasodilation OR cardiac contractility/conduction?

A

Cardiac contractility/conduction ( - ionotropic effect by suppressing sinus node activity & AV conduction)

158
Q

DHP-CCBs clinical indications

A
  • HTN
  • Angina
  • Raynaud’s
159
Q

Non-DHP-CCBs

A
  • Cardiac arrhythmias (SVT, Afib)

- Cluster HA prophylaxis (verapamil)

160
Q

The IR formulation of what drug has increase CV mortality, esp. in CAD pts.?

A

Nifedipine

161
Q

Precautions/contraindications to use of CCB

A
  • Pt. w/ 2nd & 3rd degree AV block
  • Pt. w/ SSS
  • Pt. w/ bradycardia (<50bpm)
  • HF pt.
162
Q

Which 4 drugs are substrates of CYP3A4?

A

Nifedipine, amlodipine, diltiazem, verapamil

163
Q

Interaction between amlodipine and what ABX may lead to hypotension, edema, bradycardia, AKI (d/t reduced perfusion)

A

Clarithromycin

164
Q

What if we NEED clarithromycin and a pt. is on amplodipine?

A

Hold amlodipine or lower dose

165
Q

Use non-DHP-CCBs cautiously with what other drugs?

A

BB and digoxin

166
Q

DHP-CCBs class ADRs

A
  • HA, dizziness, flushing, peripheral edema, reflex tachycardia
  • Dyspepsia
167
Q

Non-DHP-CCBs class ADRs

A

HA, dizziness, flushing, peripheral edema

168
Q

Special ADR: nifedipine > amlodipine

A

Gingival hyperplasia

169
Q

Special ADR: verapamil

A

Constipation

170
Q

Central acting alpha-adrenergic agonists

A

Clonidine & methyldopa

171
Q

What formulation is clonidine available in

A

Transdermal

172
Q

Alpha agonist MOA

A

Stimulate a2 receptors in brainstem -> decrease sympathetic outflow from CNS -> decrease PVR, renal vascular resistance, HR, BP

173
Q

Alpha agonist clinical indications

A

HTN

174
Q

Clonidine ADRs (mostly PO)

A
  • Dry mouth, sedation

- Abrupt withdrawal (nervousness, tachy, HA, sweating) may lead to HTN crisis

175
Q

How do we decrease incidence of HTN crisis r/t clonidine?

A

TAPER (1-2 wks)

176
Q

Methyldopa ADR

A
  • Overt sedation
  • Lactation (both M&F)
    • Coomb/s test
177
Q

Direct vasodilator drugs

A

Hydralazine

Minoxidil

178
Q

Direct vasodilator MOA

A

Exact mech NOT well understood: relaxes arterial smooth muscle -> decrease PVR

  • Hydralazine alters Ca+ metabolism
  • Minoxidil opens ADP-sensitive K+ channels
179
Q

Hydralazine clinical indications

A
  • HTN
  • Preeclampsia/eclampsia
  • HF (blacks; add isosorbide dinitrate)
180
Q

Minoxidil clinical indications

A
  • HTN

- Alopecia

181
Q

Direct vasodilators are given with what two drug classes to minimize reflex tachycadia/CO

A

BB or central acting

182
Q

Direct vasodilators are given with what drug class to avoid Na+ & H2O retention

A

Diuretic

183
Q

Hydralazine ADR

A

Lupus-like rxn

184
Q

What drugs should we use in a hypertensive pt. of child-bearing age?

A

Nifedipine or labetalol

185
Q

How do we define gestational hypertension (GHTN)

A

Women with normal prior BP that has a BP of >140/90 after 20 wks gestation

186
Q

Fetal complications of GHTN

A

IUGR, preterm, LBW, NICU stay, death

187
Q

Maternal complications of GHTN

A

Preeclampsia/eclampsia, AKI, pulmonary edema, C-section, placental abruption, CVA, death

188
Q

How do we monitor a pt. with GHTN?

A

Weekly in-office checks & labs

189
Q

S/sx of preeclampsia

A

Vision changes, severe HA, abd pain, worsening edema

190
Q

What is preeclampsia

A

BP >140/90 + proteinuria

191
Q

What does the data say about treating mild-moderate GHTN?

A

No evidence that it improves outcomes

192
Q

If we were to treat GHTN, what drugs would be used?

A
  • Labetalol (C)
  • Nifedipine (C)
  • Methyldopa (B) -> last resort!
193
Q

Screening for HTN in peds pt.

A

Annually for kids ≥3
OR
At each visit for kids @ high risk (obesity, DM, taking meds that may increase BP)

194
Q

What is a reasonable goal you can set for a peds pt. regarding weight loss

A

5-10% wt. loss per year OR not gaining wt. as they grow

195
Q

Drugs for pediatric HTN

A

ACEI or ARB (esp. w/ kidney dz or DM) or DHP-CCB (esp. young girls)

196
Q

Define resistant HTN

A

Uncontrolled HTN with ≥3 BP meds (including diuretic)

- Many pt. fit this definition, but are poorly adherent or have inadequate tx regimens

197
Q

How do we manage resistant HTN

A
  1. Assess for pseudoresistance
  2. Assess for factors that could contribute (meds, increase Na+ intake)
  3. Optimize PB med (#1 chlorthalidone)
  4. Screen for secondary causes of HTN (OSA, pheo, hyperthyroid)
198
Q

Define HTN urgency

A

> 180/>110 WITHOUT end organ damage

199
Q

S/sx of HTN urgency

A
  • Severe HA
  • SOB
  • Epistaxis
  • Severe anxiety
200
Q

How do we manage HTN urgency

A

FOCUS ON THE PT, NOT THE SPECIFIC BP LEVEL

  • Immediate tx may cause harm!!!
  • If asymptomatic -> urgent f/u & gradual reduction
201
Q

Define HTN emergency

A

> 180/>120 WITH end organ damage

202
Q

S/sx of HTN emergency

A

Stroke, LOC/memory loss, ocular & renal dysfcn, aortic dissection, angina/MI, pulmonary edema

203
Q

How do we manage HTN emergency

A

Admit to ICU (IV BP meds given)

204
Q

Treatment of choice: nonblack <60

A

ACE or ARB

205
Q

Treatment of choice: nonblack >60

A

ACE or ARB, CCB, thiazide

206
Q

Treatment of choice: black pt.

A

CCB or thiazide

207
Q

Treatment of choice: black pt. w/ CKD

A

ACE or ARB

208
Q

Treatment of choice: nonblack pt. w/ CKD

A

ACE or ARB

209
Q

Treatment of choice: black pt. w/ DM

A

CCB or thiazide

210
Q

Treatment of choice: nonblack pt. w/ DM

A

ACE or ARB

211
Q

Treatment of choice: pt. w/ CAD

A

ACE or ARB + BB

212
Q

Treatment of choice: pt. w/ HF

A

ACE or ARB + BB + spironolactone

213
Q

Treatment of choice: pt. w/ CVA hx

A

ACE or ARB

214
Q

When baseline BP is >___/___ above goal, adding a 2nd drug to tx regimen is recommended

A

> 20/10

215
Q

Which is generally more effective? Adding a 2nd drug with a different mechanism OR increasing the dose of the 1st drug?

A

Adding 2nd drug w/ diff MOA

Clinical Pharm Exam 2 (Jaclyn) (2 decks)

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