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Pharmacology (Fall) > Drugs for Hypertension - Part 3 & 4 > Flashcards

Drugs for Hypertension - Part 3 & 4 Flashcards

1
Q

Describe Calcium Channel Blockers (CCBs) & when they are useful

A
  • Excellent first line single therapy in uncomplicated hypertension
  • Low incidence of side effects (but expensive)
  • Neutral metabolic profile (no effect on cholesterol and glucose)
  • Useful when beta-blockers are contraindicated
  • not contraindicated in asthma, COPD, or diabetes
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2
Q

What are two classes that block L-type calcium channels?

A

– Vascular Acting (dihydropyridines): amlodipine, NIFEDIPINE
* greater affinity for vascular calcium channels

– Cardiac (non-dihydropyridines): VERAPAMIL, DILITIAZEM
* blocks calcium channels primarily in cardiac tissue

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3
Q

Describe Vascular Acting(dihydropyridines) which Block L-type calcium channels (Calcium Channel Blockers - CCBs)

A

AMLODIPINE, NIFEDIPINE
* greater affinity for vascular calcium channels (acting primarily through arterial system)
* relaxes blood vessels (arteries)
** reduce TPR WITHOUT apparent direct cardiac actions

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4
Q

When are Vascular Acting(dihydropyridines) which Block L-type calcium channels (Calcium Channel Blockers - CCBs) useful/used for?

A

– Useful for angina and hypertension treatments (chronic HTN)
– Used for hypertensive crisis
– Long acting medications are used for hypertension
– Also used to treat pulmonary hypertension
– NIFEDIPINE is safe to use for blood pressure lowering in pregnancy – diuretics may block nifedipine effects on BP

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5
Q

Describe Cardiac (non-dihydropyridines) which Block L-type calcium channels (Calcium Channel Blockers - CCBs)

A

VERAPAMIL, DILTIAZEM
– Used to treat hypertension when there is a concern about heart rate regulation in atrial fibrillation or in patients with angina

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6
Q

Verapamil:

A
  • blocks calcium channels mainly in cardiac tissue
  • Should not be combined with a beta-adrenergic receptor blocker because both drugs block AV node (therefore, decrease HR –> decrease CO even more than it is)
  • Contraindicated in heart failure

(a Cardiac (non-dihydropyridines) which Block L-type calcium channels (Calcium Channel Blockers - CCBs)

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7
Q

Diltiazem:

A
  • both vascular and cardiac effects
  • Used to treat angina and hypertension
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8
Q

What are Calcium Channel Blockers Adverse Effects?

A
  • Adverse effects related to vasodilation: (get too much vasodilation & decrease BP)
  • especially:
  • increased mortality post-MI with short acting preparations of nifedipine
  • never decrease BP rapidly, only 20mmHg at a time
    ** Combination of beta-blockers with CCBs leads to hypotension
  • Amlodipine causes carries risk of edema
  • Combination with ACEi avoids edema
  • since verapamil reduces cardiac contractility it *can’t be used in heart failure
  • published concerns about increased risk of cancer and GI bleeding appear unsubstantiated in larger studies

(quite safe to treat HTN)

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9
Q

What are Common Side effects of Calcium Channel Blockers?

A
  • Constipation
  • Vertigo
  • Headache
  • Fatigue
  • Hypotension
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10
Q

What are Metoprolol & Carvedilol?

A

B-Adrenergic Receptor Blockers

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11
Q

Describe B-Adrenergic Receptor Blockers

Metoprolol, Carvedilol

A
  • many many B-blockers but all ↓ blood pressure.
  • mechanism of BP reduction not really known.
    – obvious to think - decreased CO
    — but CO may return to normal over the long-term
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12
Q

Describe B-Adrenergic Receptor Blockers

Carvedilol

A
  • blocks B- AND a-adrenergic receptors (non-selective)
  • a-adrenergic receptor blockade helps to relax (dilate) arteries
    – the heart does not have to work as hard to eject blood
    — decreases afterload
  • B-adrenergic receptor blockade slows the heart and decreases force of contraction (↓ BP)
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13
Q

Describe B-Adrenergic Receptor Blockers

Metoprolol

A
  • similar benefits to carvedilol
  • selectively blocks B1-adrenergic receptors (↓ BP)
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14
Q

How effective are B-Adrenergic Receptor Blockers?

A
  • effective (?) treatment but now controversy - not metabolically neutral
    – increased TG, reduced HDLs
    (may be why they’re)— increased incidence of type 2 diabetes
    – lower blood pressure but no decrease in cardiovascular mortality (or overall mortality)?
    (ACEi lower CV mortality, so are better, BB have no effect on CV mortality)
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15
Q

When are B-Adrenergic Receptor Blockers not effective/effective?

A

Not recommended as single therapy in uncomplicated hypertension

  • effective in other situations (and therefore used)
  • preventing 2nd myocardial infarction (major)
  • improvement of heartf ailure(major)
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16
Q

What are side effects of B-Adrenergic Receptor Blockers?

A
  • Hypotension (may potentially cause large drops in BP)
  • Bradycardia (blocks B1-adrenergic receptors on the heart - normally not a problem to have a low HR)
  • Fatigue (CNS effect)
  • Insomnia (CNS effect)
  • Sexual Dysfunction (decreased libido, may cause impotence - compliance issues?)
    – decrease compliance with taking BB (don’t want to just stop taking b/c will get rebound HTN & will be higher than before taking, therefore take them off slowly)
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17
Q

When should you avoid/take B-Adrenergic Receptor Blockers?

A
  • avoid sudden withdrawal
  • good to block reflex activation of the heart by the SNS
  • avoid where β-adrenergic receptor activity needed:
  • asthma, COPD, peripheral vascular disease, insulin dependent diabetes, physically active (?)
  • good if certain other diseases present (treats both):
  • glaucoma, certain arrhythmia, myocardial infarction, angina
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18
Q

What is an example of an alpha1-Adrenergic Receptor Antagonist? Describe it

A

Prazosin
- not effective as a single agent for chronic BP lowering
- vasodilates arteries and veins

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19
Q

What are the problems with alpha1-Adrenergic Receptor Antagonist in particular Prazosin?

A
  • first dose effect: initial large ↓ BP
  • postural hypotension
    – Patients should not stand up too quickly due to poor baroreflex
  • fluid retention with long-term treatment due to Na+ retention
    – give with diuretic (to try prevent electrolyte imbalances & fluid retension)
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20
Q

What is an example of an alpha2-Adrenergic Receptor Agonist? Describe it

A

Clonidine
- acts on central vasomotor centres
- decreases SNA from the CNS
- net effect is to reduce peripheral vascular resistance - autonomic system remains intact
- given as two unequal doses
*– high dose at night: sedation (b/c makes you feel tired & than lower dose during day - b/c acting on CNS)
- typically used when patient is resistant to the use of other BP lowering medications (add on)

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21
Q

What are the problems with alpha2-Adrenergic Receptor Agonist in particular Clonidine?

A
  • rebound hypertension upon rapid cessation of drug (risk of not taking their medication)
  • dry mouth, sedation and hypotension potential adverse effects
  • not recommended to be used in pregnancy
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22
Q

What are Vasodilators NOT used for?

A

Not used for chronic blood pressure lowering (more for hospital setting - therefore less commonly used)

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23
Q

What are 2 examples of Vasodilators?

A
  1. Hydralazine
  2. Sodium nitroprusside
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24
Q

Describe Hydralazine

A

a Vasodilator
- relaxes vascular smooth muscle cells of resistance arterioles
- use in combination with a -blocker and diuretic
– stimulates SNA so may increase heart rate
– increases plasma renin so results in fluid retention (why a diuretic is also used)
*- used in pregnancy (gestational hypertension)
- safe for mother and infant and effective

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25
Q

What are the problems with Hydralazine (a vasodilator)?

A
  • risk of lupus-like syndrome with long-term treatment (inflammatory disease)
  • headache, hypotension, tachycardia, angina
  • may potentiate anti-hypertensive effects of ACEi, CCBs and diuretics (good or bad thing - could lower BP too much)
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26
Q

Describe Sodium nitroprusside

A

a Vasodilator
- both venous and arteriolar dilator
- infused intravenously
– breaks down to produce nitric oxide (NO) (a potent vasodilating molecule)
- used for acute hypertensive crisis (emergency)

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27
Q

What are problems with Sodium nitroprusside (vasodilator)?

A
  • potential for cyanide toxicity (b/c highly reactive NO molecule so potential for cyanide toxicity)
  • should not use in pregnancy
  • risk of hypotension, low heart rate
  • do not use in patients with kidney disease
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28
Q

Drug therapy for specific disease mechanisms of hypertension

What is used for Volume overload?

A

– Thiazide; loop diuretic; aldosterone antagonist

(underline edema)

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29
Q

Drug therapy for specific disease mechanisms of hypertension

What is used for Sympathetic overactivity?

A

– B-blocker (use to counteract reflex tachycardia from vasodilators or in heart failure)

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30
Q

Drug therapy for specific disease mechanisms of hypertension

What is used for Increased vascular resistance?

A

– ACE inhibitor or ARB (use in heart failure)

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31
Q

Drug therapy for specific disease mechanisms of hypertension

What is used for Smooth-muscle contraction?

A

– Dihydropyridine CCBs; B-blocker; hydralazine (vasodilator)

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32
Q

How often should patients with hypertension be seen?

If they have Stable, well-controlled hypertension?

A

Recheck at 6- to 12-month intervals

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33
Q

How often should patients with hypertension be seen?

If their Blood pressure 140/90 to 159/99mmHg?

A

Recheck at 2 months intervals (stage 1)

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34
Q

How often should patients with hypertension be seen?

If their Blood pressure ≥160/100mmHg?

A

Recheck at ≤1 month intervals (stage 2)

35
Q

After adjusting medications:

A

allow 2-4 weeks for blood pressure to stabilize

36
Q

Lab testing:

A

intervals depend on number and type of medications and medical comorbidity (electrolyte imbalances should be checked)

37
Q

Pulmonary Arterial Hypertension

What is Essential hypertension?

A

increase in blood pressure through WHOLE body

38
Q

Pulmonary Arterial Hypertension

What is Pulmonary hypertension?

A

hypertension LIMITED to the pulmonary vasculature

39
Q

What is the incidence of Pulmonary Arterial Hypertension?

A
  • In the US ~1000 new cases each year
  • Women more affected than men
  • Onset typically between 20 and 60 years of age (younger than essential HTN)
  • Mortality is 32%, 52% and 66% at 1, 3, 5yr diagnosis (*mortality rates are higher)
40
Q

What are the risk factors for Pulmonary Arterial Hypertension?

A
  • Overweight
  • Family History of PAH (genetic component)
  • Living at High Altitude
  • Sleep apnea
  • Drug Abuse
  • HIV infection

(but not much known)

41
Q

What are the symptoms for Pulmonary Arterial Hypertension?

A

*onset is typically gradual so symptoms may not be apparent until disease is advanced (therefore diagnosis can be late –> why mortality rates are high)
* Shortness of breath
- Initially only during exercise
- Later also at rest
* Fatigue
* Dizziness
* Chest pressure/pain
* Edema in ankles/legs
* Bluish colour of lips/skin
* Cardiac palpitations

42
Q

Symptoms of Pulmonary Arterial Hypertension

A
  • Tiredness, dizziness or fainting
  • Swelling of the abdomen
  • Swelling of the legs & ankles
  • SOB during normal activity, chest pain, fast heartbeat
  • Blue tint to lips or skin
43
Q

What are the complications of Pulmonary Arterial Hypertension?

A
  • Right ventricular hypertrophy/heart failure
  • Blood clots (in pulmonary circulation)
  • Cardiac arrhythmias
  • Blood in the lungs
44
Q

What is Pulmonary hypertension mainly due to?

A

mainly due to the tiny blood vessels in the lung becoming thickened, narrowed or blocked thereby increasing pulmonary vascular resistance
* Cells that line the pulmonary arteries become stiff and thick as well as inflamed and tight

45
Q

What are the many potential causes of the increased resistance seen in Pulmonary hypertension?

A
  • Congenital heart disease
  • Heart failure
  • Emphysema
  • Blood clots (pulmonary embolism)
  • Lung tumours
  • Drugs (e.g. methamphetamines)
  • Unknown causes (don’t notice until more adv. stages)
46
Q

What does the increased resistance to flow to the right ventricle, lung capillaries, & left atria cause in pulmonary hypertension?

A
  • increased resistance to flow through lungs
  • right ventricle must work harder – enlarges
  • may not be able to pump effectively
  • Increased preload on right side of heart
    – venous pressure increases - edema (in peripheral circulation)
47
Q

In healthy pulmonary blood vessels constriction and relaxation are balanced. How?

A
  • constrictors - endothelin
  • relaxers - nitric oxide (NO), prostacyclin
48
Q

In pulmonary hypertension there is an imbalance. How?

A
  • too much constriction - endothelin (overactive)
  • not enough relaxation - NO and prostacyclin
49
Q

What does Nitric oxide do on the system?

A
  • Vasorelaxation
  • Anti-proliferation
  • Anti-fibrosis
  • Anti-inflammation
  • Anti-thrombosis
50
Q

What does Endothelian-1 do on the system?

A
  • Vasoconstriction
  • Proliferation
  • Fibrosis
  • Inflammation
  • Release of vasodilators & vasoconstrictors
  • Endothelial clearance
51
Q

What does Prostacyclin do on the system?

A
  • Vasorelaxation
  • Anti-profileration
  • Anti-fibrosis
  • Anti-inflammation
  • Anti-thrombosis
52
Q

What are Pulmonary Arterial Hypertension Treatments?

A

Calcium channel blockers - NIFEDIPINE (long acting)
- arterial vessel relaxation
- absence of randomized trials
- some evidence for prolonged survival, function improvement
- evidence of effectiveness in only 5% of patients that are vasoreactive

Endothelin receptor antagonist - BOSENTAN

Prostacyclin
derivative - EPOPROSTENOL

Activator of soluble guanylate cyclase - SILDENAFIL

53
Q

What is the mechanism for Bosentan which is a Endothelin Receptor Antagonists for treatment of Pulmonary Arterial Hypertension?

A

Mechanism: antagonist of both Endothelin Receptors (use it earlier on)
* ET-A and ET-B
* Used to treat moderate pulmonary arterial hypertension
* decreases endothelin-mediated arterial constriction
* improves symptoms, six minute walk test, and survival (won’t feel fatigue)

54
Q

What is the adverse effects of Bosentan which is a Endothelin Receptor Antagonists for treatment of Pulmonary Arterial Hypertension?

A
  • hepatotoxicity a major problem
    ** Liver damage due to adverse drug interaction in patients prescribed
    glyburide (glucose-lowering) medication
  • may cause peripheral edema, nasal congestion
  • Causes birth defects in pregnant women
55
Q

What is the mechanism for Epoprostenol which is a Prostacyclin Derivatives for treatment of Pulmonary Arterial Hypertension?

A

Mechanism: activates a G-protein coupled Prostacyclin Receptor
* Synthetic prostacyclin
* Raises cellular cAMP levels and activated protein kinase A
* Net effect leads to arterial smooth muscle relaxation and vasodilation
* Considered most effective treatment for pulmonary arterial
hypertension
* improves exercise performance and survival

56
Q

What are the problems with Epoprostenol which is a Prostacyclin Derivatives for treatment of Pulmonary Arterial Hypertension?

A

prostacyclines are unstable (half-life 3-5min)
* must be continuously infused intravenously - nuisance

(effective but has shorter half-life)

57
Q

What are the adverse effects of Epoprostenol which is a Prostacyclin Derivatives for treatment of Pulmonary Arterial Hypertension?

A
  • Flushing
  • Headaches
  • hypotension
58
Q

What is the mechanism of Sildenafil which is an Inhibitor of soluble guanylate cyclase?

A

Mechanism: inhibits cGMP phosphodiesterase 5 (PDE5)
* prolongs effects of nitric oxide - prevents cGMP breakdown
* phosphodiesterase type 5 inhibitors increase arterial relaxation
* improved exercise performance
* not clear if it alters survival

(Viagra)

59
Q

What are the adverse effects of Sildenafil which is an Inhibitor of soluble guanylate cyclase?

A
  • Flushing
  • Headaches
  • Nausea
  • Diarrhea
    ** Should not be used with other medications containing nitric oxide
    donors
60
Q

How can you manage hypertension in the elderly (over 65)?

A
  • Aging reduces vascular compliance due to stiffening of the arteries that raises TPR and BP
  • Aging reduces the efficiency of sodium excretion resulting in increased blood volume and BP
  • BP goal: SBP< 150mmHg DBP< 90mmHg
  • BP should be lowered gradually to avoid complications
  • Start with low dose thiazide diuretic
  • Add on ACEi (decrease mortality) or CCB
  • B-blockers used if other CV conditions apparent in elderly patient (ex: heart failure)
61
Q

Managing Hypertension at Different Ages (No Diabetes or CKD)

Adult with hypertension aged 18-60years

A

BP goal < 140/90mmHg

  1. Implement lifestyle interventions
  2. ACEi (or ARB) monotherapy
  3. Maximize first medication before adding second
62
Q

Managing Hypertension at Different Ages (No Diabetes or CKD)

Adult with hypertension aged > 60years

A

BP goal < 150/90mmHg

  1. Salt Restriction
  2. Low Dose Thiazide Diuretic
  3. add on ACEi (or ARB) or CCB then B-blocker
63
Q

How can you manage hypertension in diabetes?

A
  • Insulin has vasodilatory properties
  • Insulin stimulates SNA without raising BP
  • Insulin resistance (as in T2D) hyperinsulinemia raises BP via SNA and insulin resistance negates the vasodilatory properties of insulin
  • BP goal: SBP< 130mmHg DBP< 90mmHg (not as aggressive in the elderly)
    ** Aggressive management of weight/salt intake recommended
  • ACEi are first line prescription then add on a diuretic
  • Beta-blockers not recommended due to metabolic effects (esp. as 1st line)
  • Dihydropyridine CCBs associated with higher risk of heart failure in diabetic patients
    ** Not uncommon for these patients to need 3 or more medications to achieve BP goals
64
Q

Managing Hypertension in Diabetic Patients (No CKD)

Adult with hypertension aged 18-60years

A

BP goal < 130/80mmHg

  1. Weight loss/salt restriction
  2. ACEi or diuretic monotherapy
  3. Maximize first medication before adding second (dihydropyridine CCB)

Combination therapy with additional classes of medications likely needed to achieve BP goal

65
Q

Managing Hypertension in Diabetic Patients (No CKD)

Adult with hypertension aged > 60years

A

BP goal < 140/90mmHg

  1. Weight loss/salt restriction
  2. ACEi or diuretic monotherapy
  3. Maximize first medication before adding second (dihydropyridine CCB)

Combination therapy with additional classes of medications likely needed to achieve BP goal

66
Q

How can you manage hypertension in Chronic Kidney Disease?

A

** Decline in kidney function associated with elevated BP
* Sustained high BP hastens reduced kidney function
* Impaired salt excretion in CKD raises BP via increased blood volume…salt intake worsens conditions
* BP goal: SBP< 120mmHg DBP< 80mmHg
* Salt restriction recommended….enhances effects of anti- hypertensive agents
** ACEi (or ARB) are first line prescription then add on a diuretic
* Thiazide diuretic recommended for most patients but use loop diuretic in combination in patients with advanced CKD (when disease progresses & kidney function decreases)
* Not uncommon for these patients to need 3 or more medications to achieve BP goals

67
Q

Managing Hypertension in CKD (no diabetes)

low proteinuria

A

BP goal < 120/80mmHg

  1. Salt restriction
    Monitor K levels
  2. ACEi monotherapy
  3. Add on Thiazide Diuretic

Combination therapy with additional classes of medications likely needed to achieve BP goal

68
Q

Managing Hypertension in CKD (no diabetes)

with proteinuria > 500mg/24h

A

BP goal < 140/90mmHg

  1. Salt restriction
    Monitor K levels
  2. ACEi/ARB mono or combination therapy
  3. Add on Thiazide Or Loop Diuretic

Combination therapy with additional classes of medications likely needed to achieve BP goal

69
Q

How do you manage hypertension in post-Myocardial Infarction?

A
  • Use sodium nitroprusside in patients presenting with acute myocardial infarction and severe hypertension
  • Long-term treatment is usually aimed at relieving symptoms, protecting ischemic tissue and preventing another CV event
  • In longer term BP goal: SBP< 160mmHg DBP< 110mmHg
    ** ACEi are first line prescription (or ARB if not tolerated) - b/c most effective in preventing mortality
  • Titrate the addition of a Beta-blocker to reduce SNA and strain on heart (benefit of 2nd MI)
70
Q

Managing Hypertension Following Myocardial Infarction

Acute and Severe Hypertension

A

BP goal<160/110mmHg

Gradually reduce BP over 24-48h

Sodium nitroprusside

71
Q

Managing Hypertension Following Myocardial Infarction

Chronic

A

BP goal<160/110mmHg

ACEi (or ARB) and beta-blocker therapy

Add on Cardiac Acting CCB (Diltiazem) (so they don’t get a 2nd MI)

72
Q

How do you manage hypertension in Pregnancy?

A
  • Reducing gestational hypertension is important to reduce maternal, fetal and infant complications, preterm birth, low birth weight and pregnancy loss
  • BP goal: SBP< 140mmHg DBP< 90mmHg
  • Nifedipine or beta-blockers (metoprolol) are first-line treatments
  • Hydralazine and thiazide diuretics are second-line medications
    ** ACEi and ARBs should NOT be used since they cause acute kidney damage to the fetus (1 situation where they aren’t safe)
73
Q

When should ACEi and ARBs not be used?

A

ACEi and ARBs should not be used since they cause acute kidney damage to the fetus

74
Q

Explain how you would manage hypertension in Pregnancy?

A

BP < 140/90mmHg
No: Normal BP Reassess at next visit
Yes: BP >160/110mmHg –> BP >160/110mmHg
Yes: Severe Hypertension
NIFEDIPINE
No: Beta-blocker (METOPROLOL) therapy Maternal/placental/fetal assessments –> DBP > 90mmHg
No: Continue Maternal/placental/fetal assessments
Yes: Increase dose of beta blocker or add on a diuretic (HYDROCHLOROTHIAZIDE)

75
Q

What is Resistance Hypertension?

A

** Blood pressure that remains above goal despite use of 3 antihypertensive medications from 3 different classes at the same time
* Cross sectional analyses suggest that anywhere from 25-50% of patients have BP controlled <130/85mmHg
* Presumably prognosis for CV events is poor

76
Q

What are the risk factors for resistance hypertension?

A

– Age>75years
– Obesity and Diabetes
– Excessive dietary salt ingestion (can reduce medication effectiveness)
– KidneyDisease
– Female Sex (high rate of undiagnosed of HTN)

77
Q

What are the drug-related causes of Resistance Hypertension?

A

– Alcohol

– Non-narcotic analgesics
* NSAIDs
* COX-2 inhibitors

– SympatheticAgents
* Decongestants
* Diet pills
* cocaine

– Oral Contraceptives

– Cyclosporine

(interact with lower BP medications)

78
Q

What are the Secondary causes of Resistance Hypertension?

A

– Obstructive sleep apnea
– Primary aldosteroidism
– Renal parenchymal disease
– Renal artery stenosis
– Uncommon:
* Cushings syndrome
* Hyperparathyroidism

(undiagnosed & contribute to HTN)

79
Q

When blood pressure is poorly controlled, how should clinicians decide among increasing dose, adding an additional agent, or switching to another drug class?

A
  • Consider ambulatory blood pressure monitoring
  • Ask about co-medication with blood pressure- increasing drugs
  • Ask about excessive alcohol or salt intake
  • Reconsider secondary causes of hypertension (maybe dev. diabetes etc.)
  • Evaluate medication adherence (not taking it, could be expensive)
  • Treat uncontrolled hypertension: use several drugs, each targeting different disease mechanism (that are underlying cause of HTN)
80
Q

When should referral to a hypertension specialist be considered?

A

➢Drug-resistant hypertension uncontrolled with ≥3 drugs

➢Uncertainty about how to evaluate or manage suspected secondary hypertension

➢Need for assistance assessing target organ damage

81
Q

Describe the flow chart of Resistance Hypertension?

A
  1. Confirm Treatment Resistance
    - Elevated BP in patient prescribed 3 or more medications at optimal doses
    Yes?
  2. Exclude Pseudoresistance
    - Obtain home or ambulatory BP measurements Is patient taking their medications?
    Yes?
  3. Reverse Contributing
    - Lifestyle Factors
    Physical inactivity, obesity, high salt intake, excessive alcohol consumption
    Yes?
  4. Discontinue Interfering Substances
    - NSAIDs, diet pills, decongestants, oral contracentives, other stimulants
    Yes?
  5. Screen for Secondary Causes
    - Sleep apnea, aldosteronism, pheochrmocytosis, chronic kidney disease, renal artery stenosis, Cushing’s syndrome, aortic coarction
    If YES refer to specialist
    No?
  6. Pharmacological Treatment
    - Maximize diuretic therapy
    Use loop diuretics in CKD patients Combine medications with different mechanisms of action
    (e.g. ACEi/diuretic/CCB)
    No?
  7. Refer to Specialist
    - If BP remains uncontrolled after 6 months of treatment refer to a hypertension specialist
82
Q

What is the management of confirmed Resistance Hypertension?

A

➢Add a fourth medication

➢Greatest BP lowering achieved with addition of
spironolactone (acting on aldosterone system –> diff. mech as others)

➢ then use alpha- or beta-adrenergic receptor antagonists

➢then use clonidine

➢Add additional medications from different classes
not already used

83
Q

CASE STUDY

A

Pharmacology (Fall) (28 decks)

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