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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Hypertension risk factors

A
  • Age (>50 years)
  • SBP
  • Pulse pressure
  • Alcohol/smoking
  • Diabetes
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2
Q

What is the goal of treating hypertension?

A

reduce associated morbidity and mortality from CV events

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3
Q

ACC/AHA BP guidelines: Hypertensive crisis

A

Systolic >180
and/or
Diastolic >120

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4
Q

Mean arterial pressure (MAP)

A

MAP = (SBP x 1/3) + (DBP x 2/3)

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5
Q

What is the major determinant of SBP?

A

Cardiac output

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6
Q

What is the major determinant of DBP?

A

Total peripheral resistance (TPR)

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7
Q

What are the 6 groups of antihypertensives?

A
  1. RAAS
    - ACE inhibitors
    - Angiotension II Receptor Blocker
  2. Sympathetic Antagonists/Agonists
    - Beta blockers
    - Alpha 1 blockers
    - Central alpha 2 agonists
  3. Calcium channel blockers
  4. Diuretics (thiazide)
  5. Aldosterone antagonists
  6. Direct vasodilators
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8
Q

Agents that block production or action of angiotensin: basic action

A

reduce peripheral vascular resistance

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9
Q

Sympatholytic (sympathoplegic) agents: basic action

A
  • reduce peripheral vascular resistance by inhibiting cardiac function
  • increase venous pooling in capacitance vessels
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10
Q

Calcium channel blockers: basic action

A

inhibit calcium influx leading to coronary and peripheral vasodilation

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11
Q

Diuretics: basic action

A

deplete body of sodium and reduce blood volume

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12
Q

Aldosterone antagonists: basic action

A

inibit aldosterone resulting in inhibition of sodium and water retention and inhibiting vasoconstriction

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13
Q

Direct vasodilators: basic action

A

relax vascular smooth muscle thus dilating resistance vessels and increasing capacitance

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14
Q

Where are the 4 sites diuretic agents act in the nephron?

A
  1. Proximal convoluted tubule (PCT)
  2. Thick ascending limb of loop of Henle
  3. Distal convoluted tubule
  4. Cortical collecting tubule
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15
Q

What part of the kidney is responsible for 60-70% of the total reabsorption of sodium?

A

Proximal convoluted tubule

also major site of bicarbonate reabsorption

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16
Q

Carbonic anhydrase inhibitors: subclass

A

Acetazolamide

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17
Q

Carbonic anhydrase inhibitors: clinical applications

A
  1. Glaucoma
  2. Mountain sickness
  3. Edema with alkalosis
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18
Q

Carbonic anhydrase inhibitors: Toxicities, interactions, contraindications

A
  1. metabolic acidosis
  2. Sedation
  3. Paresthesias
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19
Q

Name 3 loop diuretics

A
  • Bumetanide
  • Furosemide *
  • Torsemide
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20
Q

Name 4 thiazide diuretics

A
  • Chlorthalidone
  • Hydrochlorothiazide (HCTZ) *
  • Indapamide
  • Metolazone
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21
Q

Name 2 Potassium sparing diuretics

A
  • Amiloride (with or without HCTZ)

- Triamterene * (with or without HCTZ)

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22
Q

Name 2 Aldosterone Antagonists

A
  • Spironolctone * (with or without HCTZ)

- Eplerenone

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23
Q

Diuretics: overall mechanism

A
  • blocks reabsorption of sodium and chloride

- diuresis results in decreased plasma and stroke volume

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24
Q

What is the major site of calcium and magnesium reabsorption?

A

Thick ascending limb of the Loop of Henle

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25
Q

Loop diuretics: target

A

Na/K/Cli tri transporter

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26
Q

20-30% of sodium is reabsorbed here

A

Thick ascending limb of the loop of Henle

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27
Q

Why is furosemide given IV in ED

A

oral bioavailability goes down the more the fluid in the body

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28
Q

Loop diuretics: mechanism

A

*fluid eliminator

  • more potent diuresis
  • smaller decrease in PVR
  • less vasodilation (HCTZ more effective at lowering BP)
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29
Q

Loop diuretic: mechanism

A

blocks Na+, K+, Cl- symporter at the thick ascending loop of Henle

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30
Q

Loop diuretic: efficacy

A
  1. Diuresis > BP lowering
  2. Preferred in heart failure of severe edema
  3. Less likely to cause hyperglycemia, hyperlipidemia

-useful when GFR <30 or serum creatinine of 2.5-3

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31
Q

Loop Diuretic: drug interactions

A

*similar to HCTZ

  • increase effect of digoxin and certain antiarrhythmics
  • increases levels of lithium
  • NSAIDS may decrease efficacy
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32
Q

Loop diuretics: side effects

A
  • hypokalemia
  • hypomagnesemia
  • hypocalcemia *

-hypovolemia

  • hyperuricemia
  • ototoxicity
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33
Q

Which diuretic has decreased absorption with edema of the bowel?

A

Loop diuretics (Furosemide, bumetanide, torsemide)

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34
Q

If a patient had too much hypercalcemia what two meds could you give?

A

furosemide and torsemide

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35
Q

What do thiazide diuretics target?

A

cotransporter (Na+ and Cl-) in the distal convoluted tubule

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36
Q

Calcium is reabsorbed in the distal convoluted tuble under control of ____________

A

parathyroid hormone

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37
Q

Thiazide Diuretics: name 4

A
  1. HCTZ*
  2. Chlorthalidone*
  3. Metolazone
  4. Indapamide
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38
Q

Thiazide diuretics: mechanism

A

blocks reabsorption of sodium and chloride in the distal convoluted tubule via NaCl Carrier: NCC

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39
Q

How do thiazide diuretics affect blood pressure?

A
  • decrease in peripheral vascular resistance

- direct smooth muscle relaxation

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40
Q

What are the clinical applications of thiazide diuretics?

A
  • hypertension

- mild heart failure

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41
Q

What are the electrolyte imbalances thiazide diuretics can precipitate?

A
  • hypokalemia
  • hyponatremia
  • hypercalcemia
  • hyperglycemia
  • hyperlipidemia
  • hyperuricemia
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42
Q

Is chlorthalidone a thiazide diuretic?

A

No, but effects are indistinguishable.

**Longer duration of action

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43
Q

Thiazides: limitations

A
  • GFR <30 for HCTZ

- Unrestricted salt intake reduces efficacy

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44
Q

What needs to be monitored with thiazides?

A
  • BUN
  • Creatinine
  • Uric acid level **
  • electrolytes (K+, Na+, Ca++, Mg+++)
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45
Q

HCTZ and Chlorthalidone: dosage

A

low dose is as effective

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46
Q

Metolazone (thiazide) dosage note

A

more effective with concurrent kidney disease

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47
Q

Indapamide (thiazide) dosage

A

does not alter serum lipid levels

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48
Q

Thiazide drug interactions: what do they increase effect/levels of?

A
  1. ACE inhibitors
  2. Carbamazepine
  3. Lithuim
  4. Oxcarbazepine
  5. Topiramate
  6. ARB
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49
Q

Thiazide drug interactions: What do they decrease levels/effectiveness of?

A

antidiabetic agents

NSAIDS

50
Q

Name the things that increase levels/effects of HCTZ

A
  1. Alcohol
  2. Opioid
  3. Barbiturates
  4. Beta-2 agonists**
  5. corticosteroids**
  6. licorice**
51
Q

Sodium reabsorption in the colecting tubule is controlled by?

A

aldosterone

52
Q

Where is ENaC located, primary site of acidification of the urine and last site of potassium excretion?

A

Collecting tubule

53
Q

Where do potassium-sparing diuretics work?

A

collecting tubule

54
Q

Potassium sparing diuretics: Spironolactone warnings:

A
  • Hyperkalemia
  • Hyponatremia
  • Gynecomastia
55
Q

Potassium sparing diuretics: amiloride cautions?

A

Hyperkalemia

56
Q

Aldosterone antagonists (spironolactone) efficacy

A
  • modest diuresis

- Monitor K+ levels

57
Q

Alternative uses of aldosterone antagonists

A
  • female acne and hirsutism
  • HTN in peds
  • Diuretic in peds
58
Q

Amiloride, triamterene are what type of medication?

A

Potassium sparing diuretics

59
Q

Amiloride, triamterene: contraindications

A
  • renal failure

- avoid in patients with ACE inhibitors

60
Q

Amiloride, triamterene: mechanism

A

blocks epithelial Na+ channel action proximal to the distal convoluted tuble = stops K+ secretion

61
Q

When should triamterene be avoided?

A

low creatinine clearance (<10ml/min)

62
Q

Potassium sparing diuretics: amiloride, triamterene- Drug interactions

A

-decrease cardiac glycoside, quinidine (antiarrhythmics)

63
Q

Important actions of ACE inhibitors

A
  • Reduces direct stimulation by angiotensin II on myocardial cells to help prevent or regress LVH
  • Reduces angiotensin II mediated vasoconstriction and aldosterone secretion
  • Bradykinin accumulated= vasodilation by releasing nitric oxide
64
Q

ACE and ARB adverse effects

A
  • Hyperkalemia
  • taste disturbances
  • increase in serum creatinine (modest ~35%)
65
Q

ACE inhibitor adverse effects

A
  • cough

- angioedema

66
Q

What type of patient are ACE and ARB most effective in?

A
  • *young white patient
  • Diabetes mellitus patients

(less effective in blacks and older patients)

67
Q

What should you monitor in a patient on ACE or ARB?

A
  • serum creatinine*
  • K+ (so it doesn’t get too high)
  • BUN
  • CBC with differential in collagen vascular disease and/or renal impairment
68
Q

What effect does PDE55 medication have on ACE and ARB?

A

PDE5 (ex. Cialis) may increase levels of ACE and ARB

69
Q

When is ARB and ACE contraindicated?

70
Q

Aliskiren

A

renin inhibitor

71
Q

What type of patient should ACE, ARB, and renin inhibitors be avoided?

A
  • Hyperkalemia
  • Pulmonary (cough)
  • Chronic Kidney disease
  • Pregnancy
72
Q

Where are alpha 1 receptors located?

A

peripherally

arterioles and venules

73
Q

Where are alpha 2 receptors located?

A
  • centrally located

- regulates alpha 1

74
Q

Beta 1 receptors

A
  • sympathetic
  • adrenergic
  • increase HR
  • increase contractility
  • Renin release (heart and kidney)
75
Q

Beta 2 receptors

A
  • sympathetic
  • adrenergic
  • vasodilation of arterioles and venules
  • bronchodilation
  • gluconeogenesis
76
Q

Parasympathetic nervous system has what type of receptors

A

muscarinic

77
Q

Name the 5 locations of muscarinic receptors

A
  1. CNS
  2. Heart
  3. Smooth muscle
  4. Peripheral nerves
  5. Glands
78
Q

Which beta blocker is non-selective (B1 and B2)

A

Propranolol

79
Q

Which beta blocker is selective for B1

A

Metoprolol

80
Q

Mechanism of action: Beta blockers

A

-negative chronotropic
-negative inotropic
decreased CO

-inhibit release of renin

81
Q

Beta blockers: side effects

A
  • bradycardia
  • AV conduction abnormalities
  • development of acute heart failure
  • Bronchospasm (Asthma,COPD)
  • Transient increase in blood glucose and serum cholesterol
  • Increase in TG and decrease in HDL

*AVOID abrupt cessation ( taper over 1-2 weeks)

82
Q

Which beta blockers are cardioselective?

A
  • atenolol

- metoprolol

83
Q

Which beta blockers ISA?

A
  • acebutolol
  • pindolol

(increase risk post MI- rarely used)

84
Q

Which beta blockers have a membrane stabilizing effect?

A

all of them

85
Q

Name 2 important things to monitor with beta blockers?

A
  1. CHF (edema, new cough, dyspnea, weight gain, unresolved fatigue)
  2. Blood sugar in diabetes
86
Q

Do you need to adjust beta blocker dose in renal impairment?

A

no, but may need to lower dose in hepatic impairment

87
Q

Propranolol and metoprolol undergo extensive _____________

A

first pass effect

88
Q

Name 2 drugs that are both beta 1 blockers and alpha 1 blockers and do no raise TG or lower HDL?

A

Labetolol and Carvedilol

89
Q

Prazosin, terazosin, doxazosin drug class

A

Alpha 1 blockers

90
Q

Alpha 1 blockers: mechanism

A

inhibit uptake of catecholamines in smooth muscle resulting in vasodilation

-Cross the blood brain barrier

91
Q

Alpha 1 blockers: side effects

A

-First dose phenomenon: dizziness, faintness, palpitations, syncope

  • Vivid dreams
  • Priaprism
  • Sodium and water retention with higher doses (give with diuretic)
92
Q

In a male patient with BPH, what medication could be useful?

A

Alpha 1 blocker

93
Q

Alpha 1 blockers (prazosin, terazosin, doxazosin) drug interactions

A
  • decrease levels of dabigatran, linagliptin (anticoagulants)
  • vincristine (diabetes medication)
94
Q

Clonidine, methldopa drug class?

A

Central alpha 2 Agonists

95
Q

Central alpha 2 agonists: mechanism

A

-stimulate alpha 2 receptors in the brain which reduces sympathetic outflow from the vasomotor center and increases vagal tone

96
Q

Methyldopa side effects

A

sodium and water retention so give with diuretic (unless pregnant, then don’t give diuretic)

-hepatitis (transient rise in LFTs), stop if LFT persistently elevated or alk phos increases

97
Q

Clonidine side effects

A

anticholinergic effects: sedation, dry mouth, constipation, urinary retention, blurred vision

SLUDGE

-Rebound hypertension with stopping abruptly

98
Q

What is first line HTN treatment in pregnant patients?

A

methyldopa

99
Q

Central Alpha 2 Agonist drug interactions

A
  • MAO inhibitors

- Increase effect of antihypertensives, beta blockers, lithium, PDE5, SNRI, tricyclic antidepressants

100
Q

Why add thiazide diuretic to central alpha 2 agonists?

A

central alpha 2 agonists can cause sodium and water retention

101
Q

Reserpine

A

peripheral adrenergic antagonist

102
Q

How does reserpine work?

A

depletes norepinephrine from sympathetic nerve ending

103
Q

Which medications should be given with a diuretic?

A
  • Central alpha 2 agonists (clonodine, methyldopa)

- Peripheral adrenergic antagonist (reserpine)

104
Q

Side effects of reserpine (peripheral adrenergic antagonist)

A
  • sodium and water retention

- Reflex parasympathetic activity: nasal stuffiness, increased gastric acid secretion, diarrhea, and bradycardia

105
Q

Name the two classes of vasodilators

A
  1. Calcium channel blockers

2. Direct arteriole vasodilators

106
Q

Verapamil and diltiazem

A

Non-dihydropiridines

107
Q

Amlodipine, fetodipine, nicardipine, isradipine, nifedipine

A

dihydropiridines

108
Q

When would you consider using nondihydropyridine CCB (verapamil and diltiazem)?

A
  • consider using as addition to diuretic
  • elderly patient
  • Consider as first line in African americans
109
Q

Dihydropyridine CCB do they alter conduction through the AV node?

A

no (nondihydropyridines do though)

110
Q

When to use caution in CCB?

A

renal and hepatic impairment

111
Q

Calcium channel blockers: side effects

A
  • gingival hyperplasia, peripheral edema
  • Verapamil: constipation
  • caution with Beta blocker as can increase chance of heart block
  • Nifedipine metabolism inhibited by large quantities of grapefruit juice (>1 quart)
112
Q

Direct Arterial Vasodilators

A

hydralazine, minoxidil

113
Q

Why do you need to use a beta blocker or clonidine with hydralazine (direct arterial vasodilator)?

A

direct arterial vasodilators activate baroreceptors with compensatory increase in sympathetic outflow (increased HR, CO, renin)

114
Q

Which drug can give dose dependent lupus-like syndrome (slow acetylators are prone?

A

Hydralazine

115
Q

Which medication can give hypertrichosis?

116
Q

Alternative use of minoxidil??

A

male pattern baldness

117
Q

Osmotic diuretic

118
Q

How is mannitol (osmotic diuretic given?

A

IV (short duration)

119
Q

What is the major action of mannitol and where does it work?

A

Mannitol is filtered but not reabsorbed so exhibits osmotic effect.

-Used to reduce brain volume and intracranial pressure but extracting water from the tissue into the blood

120
Q

Cautions with Mannitol (osmotic diuretic)

A
  • hyponatremia followed by hypernatremia
  • headache
  • nausea
  • vomiting

Pharmacology (16 decks)

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