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Pharmacology II > Hypertension > Flashcards

Hypertension Flashcards

1
Q

What is the diagnosis of HTN based on?

A

Measurements not symptoms

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2
Q

What is required to make a diagnosis of HTN?

A

The average of 2 or more blood pressure readings taken at each of two or more visits after an initial screening.

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3
Q

What is the prehypertension BP classification?

A

SBP- 120-139 mmHg OR DPB- 80-89 mmHg

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4
Q

What is the stage 1 hypertension BP classification?

A

SBP- 140-159mmHg OR DBP 90-99mmHg

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5
Q

What is the stage 2 hypertension BP classification?

A

SBP- >/= 160mmHg OR DBP >/=100mmHg

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6
Q

What are the risk factors associated with the development of CV dz?

A

In those older than age 50, systolic blood pressure (SBP) of >140 mmHg is a more important cardiovascular disease (CVD) risk factor than diastolic BP (DBP)

Beginning at 115/75 mmHg, CVD risk doubles for each increment of 20/10 mmHg

Those who are normotensive at 55 years of age will have a 90 percent lifetime risk of developing hypertension

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7
Q

Every _____ mmHg increase in SBP or ______ mmHg increase DBP doubles the risk of cardiovascular dz?

A

Every 20 mmHg increase in SBP or 10 mmHg increase in DBP doubles the risk of cardiovascular disease

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8
Q

What are the benefits of antihypertensive therapy?

A

35-40% reduction in stroke
20-25% reduction in myocardial infarction
>50% reduction in heart failure

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9
Q

What are the mechanisms for controlling blood pressure?

A

Mean arterial pressure= CO x PVR
Baroreceptor/sympathetic nervous system
Renin-angiotensin-aldosterone system

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10
Q

Is baroreceptor/SNS short or long term controlled? And what receptors is is mediated by?

A

Short-term controlled
Mediated by beta1 receptors in the heart
Mediated by alpha1 receptors in arterioles

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11
Q

Is renin-angiotensin-aldosterone system short or long term control?

A

Long term control

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12
Q

What is the early function of the proximal tubules?

A

Organic solutes and sodium bicarbonate are reabsorbed.
Na+/H+ exchanger on luminal membrane
H+ combines with filtered HCO3- to make carbonic acid => Carbonic Anhydrase=> H20 and CO2 in cell

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13
Q

What is the late function of the proximal tubule?

A

Sodium chloride reabsorption
Na+/H+ exchanger continues w/o bicarbonate causing luminal pH to drop
Activates Cl-/base exchanger causing NaCl reabsorption

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14
Q

What is the function of the thin limb of the loop of henle?

A

Does not participate in NaCl reabsorption

Does participate in H20 absorption (osmotic)

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15
Q

What is the function of the thick ascending limb (diluting segment) in the loop of henle?

A

Actively reabsorbs 35% of filtered NaCl (2Cl-/Na+K+ pump)
Impermeable to water – dilutes tubular fluid
K+ increases in cell secondary to interstitial Na/K ATPase which is then luminally excreted
Resultant electrochemical gradient drives Ca2+ and Mg2+ reabsorption via intercellular pathways

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16
Q

What is the function of the distal convoluted tubule?

A
  • Actively reabsorbs 10% filtered NaCl via Na/Cl pump (pharmacologically distinct- drugs that target the first pump don’t affect this pump)
  • Impermeable to water – further dilution
  • No potassium recycling across interstitial membrane (no Ca2+ or Mg2+ exchange)
  • Active calcium reabsorption under influence of PTH
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17
Q

What is the function of the collecting tubule?

A

–2-5% NaCl reabsorption – Not active
Principal cells – separate ion channels for Na
–Major site of potassium secretion – more Na absorbed greater K excretion
Regulated by aldosterone
–Active hydrogen ion excretion via the intercalated cells
–ADH activity – regulates water permeability, therefore, volume and concentration

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18
Q

What is the major site of potassium secretion in the kidney?

A

Collecting tubule

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19
Q

What is the primary therapeutic objective for HTN?

A

Reduction of blood pressure

Limit the development of subsequent organ damage

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20
Q

Reduction of blood pressure is done by drugs whose MOA do what?

A

Alter blood volume
Cardiac output (HRxSV)
Peripheral vascular resistance

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21
Q

Limiting development of subsequent organ damage includes limiting what?

A

LVH, angina, MI, heart failure, stroke, chronic kidney disease, peripheral arterial disease, retinopathy

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22
Q

What is another name for primary HTN?

A

Essential HTN

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23
Q

What causes primary HTN?

A 
Cause unknown
90% of all cases
Risk Factors:
Age
Genetic predisposition
Obesity
ETOH
Smoking
Physical inactivity
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24
Q

What causes secondary HTN?

A

Identifiable cause:
Vascular disease
Endocrine disorders- DM
Drugs – Corticosteroids, anorexiants/decongestants, thyroid hormone excess, OCPs, NSAIDs/COX-2, occassionally TCA’s and venlafaxine, excessive licorice

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25
Q

What are the signs of HTN?

A

Elevated BP often the only sign
Other signs may develop due to complications of the disease:
retinal hemorrhages, AV nicking, arteriolar narrowing
neurologic deficits
extra heart sounds
left ventricular hypertrophy

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26
Q

What are the symptoms of HTN?

A 
Often asymptomatic
Symptoms often due to complications of the disease:
cardiovascular
cerebrovascular
renal
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27
Q

What is step 1 to the step by step approach to treatment of HTN?

A

Decide whether or not drug therapy is indicated

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28
Q

What is step 2 to the step by step approach to treatment of HTN?

A

Establish a treatment goal

No diabetes, no kidney dz: goal <130/80 mmHg

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29
Q

What is step 3 to the step by step approach to treatment of HTN?

A

Promote lifestyule modification

  • Weight reduction
  • Adopt DASH eating plan
  • Dietary sodium restriction
  • Physical activity
  • Moderation of alcohol conumption
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30
Q

What is DASH?

A

Dietary Approaches to Stop Hypertension (diet rich in potassium and calcium)

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31
Q

What is step 4 to the step by step approach to treatment of HTN for stage 1?

A

(without compelling indications)
1st choice Thiazide
2nd choice ACEI, ARB, BB, CCB, or combination

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32
Q

What is step 4 to the step by step approach to treatment of HTN for stage 2?

A

(without compelling indications)
2-drug combination for most:
Thiazide + ACEI, or ARB, or BB, or CCB

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33
Q

What is the initial treatment for normal BP classification?

A

None

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34
Q

What is the initial treatment for prehypertension BP classification?

A

No comorbities: lifestyle modification

Comorbidities: drug therapy

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35
Q

What is the initial treatment for stage 1 HTN BP classification?

A

Drug therapy

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36
Q

What is the initial treatment for stage 2 HTN BP classification?

A

Drug therapy (usually two drugs required)

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37
Q

What are the treatments for heart failure?

A

1st choice: ACEI* +BB

2nd choice :Aldosterone antagonist or Amlodipine or Felodipine or Thiazide

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38
Q

What are the treatments for coronary artery disease?

A

1st choice: BB + ACEI*

2nd choice: Amlodipine or Felodipine or Thiazide

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39
Q

What are the treatments for diabetes?

A

1st choice: ACEI or ARB

2nd choice: BB or Thiazide or CCB

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40
Q

What are the treatments for chronic kidney disease?

A

1st choice : ACEI or ARB

2nd choice: BB or CCB

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41
Q

What are the treatments for recurrent stroke?

A

1st choice: ACEI + Thiazide

2nd choice: BB or ARB or CCB

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42
Q

What are the treatments for systolic hypertension?

A

1st choice : Thiazide

2nd choice: Long-acting dihydropyridine CCB

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43
Q

What can be used in patients that are unable to take ACE inhibitors?

A

ARB (angiotensin receptor blockers)

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44
Q

Can mild HTN be controlled by a single drug?

A

Yes and frequently

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45
Q

What does drug choice for treatment of HTN depend on?

A

Race, ace, concurrent illnesses

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46
Q

What are 50% of failures of tx of HTN due to?

A

Noncompliance

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47
Q

What is step 5 to the step by step approach to treatment of HTN?

A

Follow up and monitoring
Should occur monthly until BP is reached.
SrCr should be drawn 1-2x yearly
Once BP is at goal and stable, follow up can occur every 3-6 months; more frequently if the patient has other co-morbidities.

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48
Q

What is the failure to reach goal BP in patients who are adhering to full doses of a 3 drug regiment that includes a diuretic?

A

Resistant hypertension

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49
Q

What should be done for resistant HTN?

A

Work up for underlying medical conditions

Some patients may require 6-7 drugs in this situation.

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50
Q

Target tissues for anti-hypertensive agents include?

A
  • -The sympathetic nerves which release the vasoconstrictor NE
  • -The kidney which regulates blood volume
  • -The heart which generates CO
  • -The arterioles which determine PVR
  • -Endothelial cells which regulate circulation levels of the endogenous hypertensive and hypotensive agents such as angiotensin II and NO, respectively
  • -The CNS, which senses the BP and controls set point by regulating some of the systems involved.
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51
Q

What are drugs affecting body sodium balance?

A

Diuretic and dietary manipulation of sodium balance

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52
Q

What are the mechanisms that increase vascular resistance due to excessive body sodium?

A

increased vessel rigidity
increased fluid retention
increased release of norepinephrine and epinephrine from sympathetic terminals and adrenal medulla

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53
Q

How does dietary sodium restriction help HTN?

A
  • -The restriction of dietary sodium alone can significantly decrease arterial pressure although to varying degrees in patients with essential hypertension.
  • -Obese subjects have a more pronounced decrease in arterial pressure with sodium restriction.
  • -The restriction of dietary sodium can markedly improve the efficacy of antihypertensive drugs.
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54
Q

What is recommended as first line therapy for uncomplicated HTN (monotherapy or adjunctive)?

A

Diuretics

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55
Q

What are diuretics proven to do?

A

Decrease sick of stroke, MI, CHF, and total mortality

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56
Q

Does antihypertensive action correlate with diuretic activity?

A

No

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57
Q

Hydrochlorothiazide (HCTZ)-MOA

A

Thiazide diuretic
Inhibit luminal NaCl transport in distal tubule
Changes in urine ionic content –> increase loss of Na+, K+, water
Short-term - sodium & water excretion = decreases plasma volume
Long-term - decrease peripheral vascular resistance

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58
Q

Hydrochlorothiazide (HCTZ)- therapeutic uses

A
  • -HTN - thiazide diuretics lose efficacy as renal function declines and are generally not used if creatinine clearance is < 30 mL/min
  • -CHF- thiazide diuretic + loop diuretic = synergistic diuretic effect
  • -Nephrogenic diabetes insipidus
  • -Prevent kidney stones due to hypercalciuria
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59
Q

Hydrochlorothiazide (HCTZ)- Adverse Effects

A

Hypokalemia, hyperuricemia, hypomagnesemia
Impaired carbohydrate tolerance, hyperglycemia
Hyperlipidemia
Hyponatremia - can be severe
Allergies – rare but potentially serious (sulfa)
Weakness, fatigue, paresthesias
Impotence
Photosensitivity

60
Q

What is the most significant adverse effect to be aware of with HCTZ?

A

Hypokalemia

61
Q

Are thiazide first line for DM patients?

A

No due to hyperglycemia as side effect

62
Q

Metalazone (Zaroxolyn)-Uses

A

Thiazide analogue
Often used in combination with loop diuretics when patients are refractory to loop diuretics alone
Metolazone given 30 minutes before lasix
Combination can mobilize fluids in patients refractory to both

63
Q

What should be closely monitored in Metalazone (Zaroxolyn)?

A

Volume depletion and hypokalemia

64
Q

Furosemide (Lasix)- MOA

A

Loop Diuretic
–Act on the ascending loop of Henle at chloride pump (potentially 25-30% reduction in Na content of urine)
–Most potent diuretics – work on pts with renal insufficiency and those that have failed thiazide diuretics
Often required as CrCl becomes < 30-40ml/min
–May increase renal blood flow
–Relieve pulmonary congestion, and decrease LV filling pressures before diuresis occurs
–Changes in urine ionic content –> increase loss of Na+, K+, water, and calcium

65
Q

Furosemide (Lasix)- therapeutic uses

A

Edema (pulmonary or peripheral ie., acute pulmonary edema, CHF)
Heart Failure-reduce fluid retention, neutral effects on mortality
Hypercalcemia
Hyperkalemia
Acute renal failure

66
Q

Furosemide (Lasix)- adverse effects

A 
Hyperuricemia 
Hyperglycemia
Hypovolemia, hypotension
Potassium and magnesium depletion
ALLERGIC  REACTIONS- SKIN RASH, EOSINOPHILIA AND RARELY INTERSTITIAL NEPHRITIS
OTOTOXICITY
67
Q

What are the potassium-sparing diuretics?

A

Spironolactone (Aldactone)

Triamterene (Dyrenium)

68
Q

Spironolactone (Aldactone)-MOA

A

Potassium-sparing diuretic
Synthetic steroid antagonist of aldosterone (intracellular receptor) (Aldo ANT)
Inhibits Na+ reabsorption and K+ secretion in collecting tubules

69
Q

Spironolactone (Aldactone)- Uses

A
  • -Effective antihypertensive but limited use due to hyperkalemia
  • -Primary aldosteronism, Secondary aldosteronism
  • -Blunt K+ wasting tendencies of other diuretics
70
Q

Spironolactone (Aldactone)- adverse effects

A

GYNECOMASTIA
MENSTRUAL IRREGULARITIES
Hyperkalemia – d/c K supplements before starting
Hyperchloremic metabolic acidosis

71
Q

Triamterene (Dyrenium)- MOA

A

Directly inhibits the sodium flux through the ion channels of the collecting tubule

72
Q

Triamterene (Dyrenium)- Uses

A

Blunt K+ wasting tendencies of other diuretics
HTN
Weak diuretic alone–Usually combined with thiazides

73
Q

Triamterene (Dyrenium)- Adverse effects

A
  • -Hyperkalemia – d/c K supplements before starting
  • -Hyperchloremic metabolic acidosis
  • -Kidney stones
74
Q

What NSAIDs have drug interactions with diuretics?

A

All of them

Decreased diuretic activity

75
Q

What are the drug interactions of loop diuretics?

A

Cholestyramine and sucralfate – decrease absorption of furosemide (Lasix)

76
Q

What are the drug interactions of loop and thiazide diuretics?

A
  • ACE inhibitors - exaggerated hypotension
  • Digoxin – increased risk of arrhythmias
  • Diabetic meds – decreased glucose tolerance
77
Q

What are the drug interactions of potassium sparing diuretics?

A

ACE inhibitors – exaggerated hyperkalemia

78
Q

Angiotensin II contributes to the development and/or maintenance of hypertension in patients with?

A

(i) renal artery stenosis or disease
(ii) malignant hypertension in which tissue ACE activity may be high
(iii) in patients with essential hypertension
(iv) patients receiving diuretics, vasodilators or on a sodium restricted diet

79
Q

What are the ACE inhibitors (ACEI)?

A

Prototype: Enalapril (Vasotec)
Prodrug – active form available as an IV
captopril, enalapril, lisinopril, ramipril, benazapril, quinapril, fosinopril,

80
Q

Ace inhibitor (ACEI)(Prototype: Enalapril (Vasotec)
Prodrug – active form available as an IV
captopril, enalapril, lisinopril, ramipril, benazapril, quinapril, fosinopril)- MOA

A

Block conversion of angiotensin I => angiotensin II
Vasodilation of vascular smooth muscle
Reduce PVR, without reflexive increase in CO, HR or contractility
Stimulate synthesis of vasodilatory prostaglandins
Decrease aldosterone & Na/H2O retention
Inhibit breakdown of bradykininincreased NO and prostacycline

81
Q

What is the “Ace escape”?

A

AIAII via non-ACE enzymes

A way to make aldosterone without going through angiotension 1 and 2.

82
Q

Ace inhibitor (ACEI)(Prototype: Enalapril (Vasotec)
Prodrug – active form available as an IV
captopril, enalapril, lisinopril, ramipril, benazapril, quinapril, fosinopril)- Contraindications

A

Pregnancy-DO NOT USE, Renovascular hypertension

83
Q

Ace inhibitor (ACEI)(Prototype: Enalapril (Vasotec)
Prodrug – active form available as an IV
captopril, enalapril, lisinopril, ramipril, benazapril, quinapril, fosinopril)- Adverse effects

A
  • -Dry cough, altered taste, rashes, fever
  • -Hyperkalemia – must be monitored, hold potassium supplementation and K-sparing diuretics when started
  • -Elevations in SrCr and BUN
  • -Hypotension and first-dose syncope – greatest risk if hypovolemic or on diuretics
  • -Angioedema – facial, neck and laryngeal swelling (very serious)- rare rxn
84
Q

What are the angiotensin II antagonists (ARBs)?

A

Losartan (Cozaar)-prototype

Valsartan, Candesartan, Irbesartan, Olmesartan

85
Q

Angiotensin II antagonists (ARBs)(Losartan (Cozaar)-prototype
Valsartan, Candesartan, Irbesartan, Olmesartan)- MOA

A

Block the angiotensin II receptors competitively inhibiting angiotensin II binding to AT1 receptors. Blocks pressor and aldosterone-releasing effects causing vasodilation and decreased PVR
Inhibit angiotensin II generated from all pathways
Unlike ACEI do not stimulate synthesis of vasodilatory compounds

86
Q

Are ARB’s as effects in decreasing blood pressure as ACEI?

87
Q

Angiotensin II antagonists (ARBs)(Losartan (Cozaar)-prototype
Valsartan, Candesartan, Irbesartan, Olmesartan)- Indications

A 
HTN, CHF
Renal protective (reducing proteinuria) in patients w/DM can be 1ST LINE.
88
Q

Angiotensin II antagonists (ARBs)(Losartan (Cozaar)-prototype
Valsartan, Candesartan, Irbesartan, Olmesartan)- Contraindications

A

Pregnancy- DO NOT USE, renal artery stenosis

89
Q

Angiotensin II antagonists (ARBs)(Losartan (Cozaar)-prototype
Valsartan, Candesartan, Irbesartan, Olmesartan)- ADR’s

A 
Rashes
Altered taste
Hyperkalemia- pootassium sparring 
Elevations SrCr, BUN
DO NOT CAUSE COUGH
Losartan reduces uric acid
90
Q

Beta blocking agents- effects

A
  • -Reduction in HR
  • -Reduction in contractility (which will decrease cardiac output and therefore decreasing arterial output)
  • -Reduction in BP
  • -Suppression sympathetic nervous system activity
91
Q

Beta blocking agents- therapeutic uses

A

Ischemic Heart Disease
Heart Failure
Dysrhythmias
Hypertension

92
Q

Do beta blockers have a high first pass?

A

Yes both IV/PO

93
Q

Beta blockers- cardioselectivity

A
  • -Beta-1 selectivity limits adverse effects with concomitant diseases (asthma, copd)
  • -Beta -1 selective: Atenolol, Metoprolol, Acebutolol, Bisoprolol
  • -Beta- 1 and- 2: Propranolol, Sotolol, Timolol, Nadalol, Pindolol, Carvidelol, Labetaolol
94
Q

Beta blockers- intrinsinsic sympathomimetic activity (ISA)

A

Partial agonist activity, less reduction in resting HR, CO, and BP (may be detrimental)
Acebutolol, Pindolol, Carteolol

95
Q

Beta blockers- alpha 1 blocking activity

A

Added vasodilatory properties

Carvidelol, Labetaolol

96
Q

Beta blockers- contraindications

A

Severe asthma

Severe bradycardia, heart block, overt HF

97
Q

Beta blockers- Caution

A

Asthma/COPD
Peripheral vascular disease
Diabetes
Dyslipidemia

98
Q

Beta blockers- adverse effects

A 
Fatigue, lethargy, insomnia, depression
Bronchoconstriction, cold extremities
Sexual dysfunction- decreased libido & impotence
Decrease HDL, increase LDL
Bradycardia
Abrupt withdrawal may precipitate MI
99
Q

Beta blocking agents- Monitor

A

BP
HR
Symptoms of HF, difficulty breathing
CNS disturbances

100
Q

Calcium channel blockers- MOA

A

Calcium enters myocytes through voltage sensitive calcium channels and triggers Ca2+ release from SR
Maintains tone of smooth muscle- Contraction of myocardium
MOA: CCBs block the inward movement of Ca2+ by binding to L-type calcium channels
Smooth muscle relaxation – arteriolar dilation

101
Q

Calcium channel blockers- pharmacologic effects

A

Coronary Vasodilation
Peripheral Vasodilation
Negative inotropic and chronotropic effects
Alleviate coronary vasospasm

102
Q

Calcium channel blockers- therapeutic uses

A

Hypertension
Ischemic Heart Disease
Dysrhthmias (non-dihydropyrididines only)

103
Q

What are calcium channel blockers usually used for?

A

Patients with unstable angina and MI

104
Q

What are the non-dihydropyridine calcium channel blockers?

A

Verapamil (Calan)

Diltiazem (Cardizem)

105
Q

What are the dihydropyridines calcium channel blockers?

A

Nifedipine (Procardia)-prototype, Felodipine, Amlodipine, Isradapine

106
Q

Verapamil (Calan)- MOA and indications

A

Non-Dihydropyridines
Effects both cardiac and vascular smooth muscle.
Indications: angina, HTN, supraventricular tachyarrhythmias, and migraines

107
Q

Diltiazem (Cardizem)- MOA

A

Non-Dihydropyridines
Effects both cardiac and vascular smooth muscle but less negative inotropic effect on the heart therefore fewer side effects

108
Q

Nifedipine (Procardia)-prototype, Felodipine, Amlodipine, Isradapine- MOA

A

Dihydropyridines

  • -Much greater affinity for vascular cells in the periphery and does not effect cardiac contractility.
  • -Beneficial for decrease PVR through greater peripheral vasodilation. May induce reflex tachycardia
  • -Second generation agents very effective antihypertensives and very widely used–such as amlodipine and felodipine.
109
Q

Calcium channel blockers dihydropyrodines- Adverse effects

A

Hypotension
Dizziness
Peripheral Edema-through precapillary dilation
No effect on blood sugar or lipids

110
Q

Calcium channel blockers Non- dihydropyrodines- Adverse effects

A 
Hypotension
Dizziness
Constipation (esp verapamil)
Bradycardia
Exacerbation of HF
No effect on blood sugar or lipids
111
Q

What type of patients are calcium channel blockers good options for?

A

Patients w/ DM or hyperlipidemia due to no effects on sugars or lipids

112
Q

Calcium channel blockers dihydropyrodines- contranindications

A

Hypotension

Avoid immediate-release for cardiovascular indications in adult patients due to potential cardiac ischemia

113
Q

Calcium channel blockers Non- dihydropyrodines- contraindications

A

Severe bradycardia, hypotension, heart block, overt HF
Should be given with caution in susceptible patients taking beta blockers because of the possibility of AV block or heart failure.

114
Q

Verapamil- drug interactions

A

Verapamil increases plasma digoxin levels.

115
Q

What are the less commonly used antihypertensives?

A

Alpha-1 Receptor Antagonists
Alpha-2 agonists and other centrally acting drugs
Direct Vasodilators
Direct Renin Inhibitors

116
Q

What are the alpha1 blocking agents?

A

Prazosin (Minipress), Doxazosin (Cardura), Terazosin (Hytrin)

117
Q

Alpha1 blocking agents- Prazosin (Minipress), Doxazosin (Cardura), Terazosin (Hytrin)- MOA

A
  • -Competitively block alpha1 receptor
  • -Lowers MAP by causing relaxation of both arterial and venous smooth muscle
  • -Minimal changes in CO, renal blood flow and GFR
118
Q

Alpha1 blocking agents- Prazosin (Minipress), Doxazosin (Cardura), Terazosin (Hytrin)- therapeutic use

A
  • -Primary use for reducing symptoms of benign prostatic hyperplasia
  • -Not used much for hypertension : High incidence of postural hypotension and 1st dose syncope
  • -Proven inferior to diuretics
119
Q

Alpha1 blocking agents- Prazosin (Minipress), Doxazosin (Cardura), Terazosin (Hytrin)- Comorbid conditions “caution”

A

Poorly controlled angina w/o beta blocker, incontinence

120
Q

Alpha1 blocking agents- Prazosin (Minipress), Doxazosin (Cardura), Terazosin (Hytrin)-Adverse effects

A

First dose syncope

Dizziness, HA, fatigue, Postural hypotension, weakness, nausea, palpitations.

121
Q

What are the centrally acting adrenergic drugs?

A

Clonidine (Catapres)

Methyldopa (Aldomet)

122
Q

Clonidine (Catapres)- MOA

A

Centrally acting adrenergic

  • -α2-adrenergic agonist which activate presynaptic α2-adrenoceptors causing inhibition of NE release causing vasodilation. They also reduce the activity of the vasomotor center in the brain, causing reduced sympathetic activity and subsequent vasodilation.
  • -Long-term antihypertensive effects of this drug involve a reduction in cardiac output due to a decrease in heart rate and relaxation of capacitance vessels.
  • -Does not decrease renal blood flow or GFR and is an agent of choice of patients with chronic renal disease
123
Q

Clonidine (Catapres)- Indications

A

HTN, drug w/drawal, side effects associated w/neuroleptics

124
Q

Clonidine (Catapres)- ADR’s

A

dry mouth, sedation, depression, hypotension, sexual dysfunction, urinary retention, constipation, dizziness
**Abrupt discontinuance may cause severe hypertension

125
Q

Methyldopa (Aldomet)- MOA

A

Centrally acting adrenergic drug

  • -Analogue of L-Dopa, converted to methylnorepinephrine centrally decreases adrenergic outflow from the CNS
  • -MNE is stored and released by the same processes which release NE.
  • -Acts as alpha2 agonistacts to decrease sympathetic outflow from the CNS
  • -Body compensates by retaining Na+/H20
  • -Does not decrease renal blood flow
126
Q

Methyldopa (Aldomet)- uses

A

Is an agent of choice of patients with chronic renal disease and pregnancy

127
Q

Methyldopa (Aldomet)- adverse effects

A

Sedation, depression, dry mouth, hyperprolactinemia, nightmares, inability to concentrate

128
Q

What is the peripherally acting vasodilators?

A

Hydralazine

129
Q

Hydralazine-MOA

A

Peripherally acting vasodilator

  • -Directly act on vascular smooth muscle, primarily arterioles, to decrease tone
  • -Appears to involve a decrease in both calcium entry and mobilization of intracellular stores of calcium.
  • -Reflex increase in HR – therefore increase myocardial O2 demand
  • -Body compensates for the low blood pressure by increasing Na+/H20 reabsorption
  • -Used for moderate to severe hypertension – needs to be given with diuretic and sympatholytic drug
130
Q

Hydralazine- Adverse effects

A
  • -Headache, nausea, anorexia, palpitations.
  • -Angina or ischemic arrhythmias in patients with ischemic heart disease as a result of reflex tachycardia.
  • -Higher doses produce a high incidence of symptoms that resemble lupus erythematosus
131
Q

What are the renin inhibitors?

A

Aliskiren (Tekturna)

132
Q

Aliskiren (Tekturna)- MOA

A

Renin inhibitor
Place in therapy unclear
Monotherapy or combo with diuretics or ARBS
**MOA–Inhibits generation of angiotenin I, thus preventing formation of angiotensin II and reducing activation of all AT receptors
–Unlike ACEI, protective effect on cardiac and renal function not evaluated
–Doesn’t inhibit bradykinin breakdown like ACEI

133
Q

Aliskiren (Tekturna)- Contraindications

A

Risk of fetal death or injury during pregnancy; DC as soon as possible (Cat C-1st trimester; Cat D-2,3rd trimester)

134
Q

Aliskiren (Tekturna)- ADR’s

A 
Angioedema (rare)
Diarrhea
HA
Cough (less than with ACEI’s)
Increase SrCr
135
Q

Aliskiren (Tekturna)- Drug-drug interactions

A

Competitive inhibition of CYP3A4-mediated aliskiren metabolism by atorvastatin, ketoconazole
Decreased efficacy of furosemide with concurrent administration; MOA unknown

136
Q

What is the drug of choice in pregnancy for HTN?

A

methyldopa or labetalol

  • -May require intravenous therapy if so hydralazine is preferred (in emergency situations)
  • -Delivery or abortion are indicated if ecclampsia occurs
  • -HTN can cause HELLP syndrome (Hemolysis, elevated liver enzymes, Lower platelets)
137
Q

What is considered isolated systolic hypertension?

A

SBP > 140 mm Hg with DBP < 90

Usually occurs in elderly patients

138
Q

What is the treatment goal of isolated systolic hypertension and what is the preferred treatment?

A

Treatment goal SBP< 140, but lowering BP to much to quickly may lead to hyperprofusion
Thiazide diuretics preferred

139
Q

What is hypertensive urgency?

A

Severely elevated BP without acute end organ damage

140
Q

What is a hypertensive emergency?

A
  • -Severely elevated BP associated with acute and ongoing organ damage in the kidneys, brain, heart, eyes, or vascular system
  • -Based on presence of end organ damage but usually associated with DBP > 130 mm Hg
141
Q

How do you treat hypertensive urgency?

A
  • -BP lowered over hours to days
  • -Oral agents used: Captopril, clonidine, labetolol
  • -Used because of rapid onset of action and history of safety and efficacy
142
Q

How do you treat hypertensive emergencies?

A

BP lowered over min-hr to minimize end-organ damage
IV necessary for rapid onset
Nitoprusside (SNP) agent of choice.

143
Q

Nitroprusside (SNP)- ROA and MOA

A

Administered IV
MOA- Prodrug that spontaneously decomposes to NO causing vasodilation
—SNP dilates both arteries and veins resulting in reduced TPR and venous return.
–In the absence of cardiac failure SNP decreases AP via a reduction in TPR while CO does not change much. (you can get decreased arterial pressure with an overall reduction in overall vascular resistence without causing cardia reflex, but if you have a pt with cardiac failure you induce a lot of problems with cadiac failure so iut doesn’t work and isnt a good option)

144
Q

Nitroprusside (SNP)- metabolism

A

Nitroprusside metabolism results in cyanide production, if nitroprusside has to be administered for a long duration causing cyanide toxicity, thiosulfate can be administered to produce thiocyanate a less toxic form

145
Q

Nitroprusside (SNP)- Onset of action and ADRS

A

Onset of action immediate; duration 1-2 minutes
Continuous infusion (administration)
ADRs-HA, dizziness, nausea, palpitations

Pharmacology II (23 decks)

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