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Pharmacology (Fall) > Drugs for Hypertension - Part 1 & 2 > Flashcards

Drugs for Hypertension - Part 1 & 2 Flashcards

1
Q

What are the 3 main takeaways from the Prevalence of Hypertension trends?

A
  1. There is a sex difference (as we age & woman enter post menopause it becomes more similar of m/f)
  2. Age difference (rates increase with age for both m/f)
  3. Race & ethnicity factor (ex: increase rates for non-hispanic black people)
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2
Q

What long-term health risks are associated with hypertension?

A

➢ Cardiovascular disease
➢ Retinopathy
➢ Cerebrovascular disease ➢ Dementia
➢ Ischemic heart disease
➢ Left ventricular hypertrophy
➢ Atrial fibrillation
➢ Heart failure
➢ Chronic kidney disease
➢ Peripheral vascular disease

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3
Q

What is hypertension often referred to as?

A

“silent killer” - often gets undiagnosed & then long-term health risks dev.

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4
Q

List Modifiable Risk Factors common in patients with hypertension

A
  • Current cigarette smoking, secondhand smoking
  • Diabetes mellitus
  • Dyslipidemia/ hypercholesterolemia
  • Overweight/obesity
  • Physical inactivity/low fitness
  • Unhealthy diet

(Factors that can be changed and, if changed, may reduce CVD risk)

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5
Q

List Relatively Fixed Risk Factors

A
  • Chronic Kidney Disease
  • Family history
  • Increased age
  • Low socioeconomic/educational
    status
  • Male sex
  • Obstructive sleep apnea
  • Psychosocial stress

(Factors that are difficult to change (CKD, low socioeconomic/educational status, obstructive sleep apnea, cannot be changed (family history, increased age, male sex), or, if changed through the use of current intervention techniques, may not reduce CVD risk (psychosocial stress).
CKD indicates chronic kidney disease; and CVD, cardiovascular disease.)

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6
Q

What is blood pressure?

A

BP = CO x TPR

  • Cardiac output (CO)
  • Total peripheral resistance (TPR)
  • Chronic increases in BP are normally due to increased arterial resistance (TPR)
  • As arteries constrict resistance increases
  • Smooth muscle constriction and arterial elasticity
  • Subject to a balance of vasoconstriction and vasodilatory signals
    – Sympathetic activity constricts peripheral arteries – Nitric oxide synthesis dilates arteries
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7
Q

Sympathetic activity ____ peripheral arteries

A

constricts

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8
Q

Nitric oxide synthesis ____ arteries

A

dilates

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9
Q

Decrease BP:

___ renin

___ Ang-II
___ aldosterone release

___ SNA
___ retention

A

increase

increase
increase

increase

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10
Q

Three (3) major compensatory responses to a decrease in BP regardless of cause may be:

A
  • physiologically useful (dehydration, hemorrhage, early heart failure,
  • pathophysiologically harmful (renal artery stenosis, decompensated heart failure).
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11
Q

What is normal BP in adults?

A

s: <120 mm Hg
d: <80 mm Hg

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12
Q

What is elevated BP in adults?

A

s: 120-139 mm Hg
d: <89 mm Hg

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13
Q

What should you do if you have normal or elevated BP?

A

manage risk factors

lifestyle modification (promote) for normal

nonpharmacologic therapy for elevated

reassess in 1 y for normal

reassess in 3-6 mo for elevated

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14
Q

What is stage 1 hypertension in adults?

A

s: 140-159 mm Hg
d: 90-99 mm Hg

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15
Q

What is stage 2 hypertension in adults?

A

s: >/ 160 mm Hg
d: >/ 100 mm Hg

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16
Q

What is emergency hypertension in adults?

A

s: >/ 180 mm Hg
d: >/ 120 mm Hg

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17
Q

What should you do if you have stage 1 or stage 2 hypertension?

A

manage with medications

lifestyle modifications

reassess in 3-6 mo or 1 mo

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18
Q

What should you do if you have emergency hypertension?

A

life threatening

may lead to stroke

(hospitalized)

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19
Q

Which laboratory tests should be done in newly diagnosed cases?

A

Newly diagnosed hypertension
❑Measure hemoglobin or hematocrit, serum electrolytes, serum creatinine, serum glucose, and fasting lipid levels
❑Urinalysis with microscopic examination (access kidney function)
❑12-lead electrocardiography
(see if HTN has been undiagnosed in patient for awhile)

Tests indicated by clinical factors or anticipated treatment
❑Echocardiography (more sensitive than EKG for LVH)
❑Serum uric acid levels (if patient has gout) (esp. if older patient)
❑Microalbuminuria (if patient has diabetes)

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20
Q

Common Causes of Secondary Hypertension With Clinical Indications

A
  • Renal parenchymal disease
  • Renovascular disease
  • Primary aldosteronism
  • Obstructive sleep apnea
  • Drug or alcohol induced (may need to stop taking certain meds)
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21
Q

Uncommon Causes of Secondary Hypertension With Clinical Indications

A
  • Pheochromocytoma/paraga nglio ma
  • Cushing’s syndrome
  • Hypothyroidism
  • Hyperthyroidism
  • Aortic coarctation (undiagnosed or repaired)
  • Primary hyperparathyroidism
  • Congenital adrenal hyperplasia
  • Mineralocorticoid excess syndromes other than primary aldosteronism
  • Acromegaly
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22
Q

What is prehypertension, and what is its proper management?

A

➢Blood pressure 120/80 to 139/89 mm Hg

➢“Prehypertension” is not in evidence-based guidelines for management of adult high blood pressure

➢Drug therapy is NOT recommended for prehypertension
❑Evidence lacking on whether it decreases or prevents cardiovascular events
❑Focus on lifestyle changes for these patients

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23
Q

What are the recommended
lifestyle modifications for
treating hypertension?

A

➢Salt restriction (*1 of the best things)

➢Weight loss (to <20% above ideal weight for height)

➢Exercise (≥30 minutes aerobic exercise most days)

➢Smoking cessation

➢Alcohol intake limited to no more than 2 drinks daily

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24
Q

What are the Best Proven Nonpharmacological Interventions for Prevention and Treatment of Hypertensio?

A
  • Weight loss
  • Healthy diet
  • Reduced intake of dietary sodium
  • Enhanced intake of dietary potassium
  • Physical activity
  • Moderation in alcohol intake
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25
Q

What are the major/minor classes of drugs to treat hypertension?

A

4 Major Classes - approved as 1st line single treatment
- diuretic
- ACEi, ARB
- calcium channel blocker (CCB)
- B-adrenergic receptor antagonist

3 Minor Classes
- added on when above fail
- a1-adrenergic receptor antagonist
- a2-adrenergic receptor agonist
- vasodilators

Pulmonary Arterial Hypertension

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26
Q

List the diuretics for hypertension

A
  • hydrochlorothiazide
  • metolazone
  • furosemide
  • spironolactone
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27
Q

List the ACEi, ARB for hypertension

A
  • enalapril
  • losartan
  • valsartan
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28
Q

List the calcium channel blocker (CCB) for hypertension

A
  • verapamil
  • nifedipine
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29
Q

List the B-adrenergic receptor antagonist for hypertension

A
  • carvedilol
  • metoprolol
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30
Q

List the a1-adrenergic receptor antagonist for hypertension

A

Prazosin

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31
Q

List the a2-adrenergic receptor agonist for hypertension

A

Clonidine

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32
Q

List the vasodilators for hypertension

A
  • sodium nitroprusside
  • hydralazine
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33
Q

List the Pulmonary Arterial Hypertension for hypertension

A
  • sildenaphil
  • bosentan
  • epoprostenol
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34
Q

What are the three main physiologic mechanisms for antihypertensive drugs?

A

BP = CO x TPR

  1. Decrease blood volume–decrease CO
  2. Relax blood vessels (mainly arterial) – decrease TPR
  3. Decrease stimulation of the heart – decrease in CO
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35
Q

Which antihypertensive drugs “Decrease blood volume–decrease CO”?

A
  • diuretics (hydrochlorothiazide, furosemide)
  • interrupt renin angiotensin aldosterone system (spironolactone)
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36
Q

Which antihypertensive drugs “Relax blood vessels (mainly arterial) – decrease TPR”?

A
  • interrupt renin ANGIOTENSION aldosterone system
  • ACEIs (enalapril)
  • ARB (losartan)
  • CCB (nifedipine)
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37
Q

Which antihypertensive drugs “Decrease stimulation of the heart –decrease in CO”?

A
  • B-adrenergic receptor antagonist (carvedilol, metoprolol)
  • CCB (verapamil)
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38
Q

What is diuresis?

A
  • Increased production of urine by the kidneys
  • Drinking water produces mild diuresis to maintain fluid- electrolyte balance (increase water, remove excess water from body)
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39
Q

What are diuretics?

A
  • Substance that increases the production of urine
  • patients with heart failure and kidney failure need diuretic medications to help the kidney deal with fluid overload of edema
  • Treat hypertension by decreasing blood volume (if you can decrease BV by diuretics, you can decrease BP)
  • Treat electrolyte imbalances
40
Q

What are clinical uses of diuretics?

A

used for EDEMA forming conditions and ARTERIAL HYPERTENSION

  1. Hypertension
  2. Tissue Edema
  3. Hepatic cirrhosis
  4. Cardiac failure
41
Q

How are diuretics used for hypertension?

A
  • 1st line single therapy (thiazide diuretic)
  • but possible ↑ LDL, ↑ plasma glucose (not metabolically neutral)
  • good as second medication to treat sodium and water retention (may not be good for someone with hyperedemia or diabetes)
  • common side effect of other anti-hypertensives (can help restore electrolyte balance)
42
Q

How are diuretics used for tissue edema?

A
  • fluid shift into the extra cellular space has exceeded 3 to 4L
  • due to salt and water retention
  • Loop diuretic (FUROSEMIDE) preferred, if no response to the Loop diuretic, add a thiazide – normally metolazone
  • fluid excreted in urine is taken from the “vascular space” (bloodstream), allow time for this to be replaced by the interstitial (edematous) fluid
  • otherwise cardiovascular collapse
43
Q

How are diuretics used for hepatic cirrhosis?

A
  • sodium/water accumulates in the abdomen and/or tissue
  • abdominal fluid movement into vascular space may be a concern
  • slower than fluid movement from interstitial to vascular space
  • aggressive treatment will remove fluid faster from the vascular space than can be replaced by the abdominal fluid
44
Q

How are diuretics used for cardiac failure?

A
  • fluid retention increases vascular volume
  • helps to increase preload and stimulate the heart - as failure continues so does fluid retention
  • preload increases to levels causing edema
  • diuretics decrease vascular volume
  • successful treatment of heart failure requires adequate control of vascular volume
45
Q

Describe Kidney Reabsorption

A

PROXIMAL TUBULE reabsorbs almost all glucose and amino acids and about 60% of Na+ (back into bloodstream)
* Na+ is reabsorbed through a Na+/K+ ATPase
* Cl- exchanged for formate or oxalate anions
* Water follows passively to maintain osmolarity

ASCENDING LOOP of Henle is IMpermeable to water
* Na+/K+/2 Cl- co-transporter reabsorbs 30% of these ions

DISTAL CONVULATED TUBULE is IMpermeable to water
* Na+/Cl- reabsorbed and Ca2+ excreted

COLLECTING TUBULE AND DUCT reabsorb Na+ and water from the urine and excrete K+
* Na+/K+ ATPase performs this function

46
Q

Where ___ goes, water will follow

A

Na+

47
Q

What is the definition of diuretics?

A

agents which increase urine flow

48
Q

What is the clinic use of diuretics?

A

Clinically: interest is in renal solute excretion (sodium and water)
- block sodium absorption → water will follow later

49
Q

What is the aim of therapy for diuretics?

A
  • only need to decrease sodium reabsorption a few % - change of 5% has a great effect

99.6% of Na reabsorbed (goes back into bloodstream)

50
Q

Main point: if Na reabsorption decreases only by 5%…

A
  • then 1250 mmol/day of Na is excreted
  • this would represent 9 liters of extracellular fluid loss
  • potential for severe cardiovascular problems
51
Q

Which drugs are used on the proximal tubule?

A

-mannitol

  • acetazolamide
  • dapagliflozin
52
Q

Which drugs are used on the loop of henle?

A

loop diuretics

53
Q

Which drugs are used on the distal tubules?

A

thiazide diuretics

54
Q

Which drugs are used on the collecting tubule?

A

potassium sparing

55
Q

Which drugs are used on the collecting duct?

A

tolvaptan

56
Q

Which drugs are the Loop Diuretics?

A
  • FUROSEMIDE
  • bumetanide
  • ethacrynic acid (non-sulfonamide)
57
Q

What do Loop Diuretics do?

A
  • inhibit the Na+/K+/2 Cl- co-transporter in the ascending loop of Henle
  • very potent and efficacious - high ceiling diuretics
  • up to 20% of filtered load excreted (dangerous!!)
    (if we dose it too high it can cause CV problems)
  • Increases prostaglandin production (vasodilation?)
    (separate function)
  • increases Na, Cl, K, Mg, Ca2+ excretion (note Ca effect)
58
Q

What effects do Loop Diuretics have?

A

INCREASED urinary excretion
- Na+
- K+
- Ca2+
- Volume of urine

59
Q

Loop diuretics have a much _____ effect on urine volume and sodium excretion than ____ diuretics.

A

GREATER

THIAZIDE

60
Q

Loop diuretics effect on calcium is ______ of what thiazide diuretics do to calcium.

A

opposite
- by increasing its urinary excretion

61
Q

What are problems with Loop diuretics?

A

(in addition to electrolyte imbalances)
- deafness and kidney damage- never combine with aminoglycoside antibiotics (e.g.- kanamycin/streptomycin)
- interaction with the anti-arrhythmic agent amiodarone leads to a more irregular heartbeat

62
Q

What are uses of Loop diuretics?

A
  • preferred in renal insufficiency
  • glomerular filtration rate < 30 ml/min
  • Heart failure
  • Edema (pulmonary)
  • Hypertension
  • NOT as first-line hypertension treatment (more for an add-on medication)
  • NOT as sole medication
  • Electrolyte imbalances
  • hypercalcemia (opposite to thiazides diuretics)
63
Q

Which drugs are the Thiazide Diuretics?

A
  • METOLAZONE
  • HYDROCHLOROTHIAZIDE
  • similar mechanism(s), parallel dose response curves
    (1st line treatment)
64
Q

What do Thiazide Diuretics do?

A

similar mechanism(s), parallel dose response curves

distal tubule is primary site of action
- inhibit Na /Cl transporter
- ↓ Na/Cl reabsorption (↑ Na+ excretion )
- ↑ Ca2+ reabsorption (↓ Ca2+ excretion )

Secondary site of action at the proximal tubule
- Additional diuretic effect when combined with loop
diuretic
- Not usually important because of compensation in loop of Henle

+-
- inhibit Na /Cl transporter
-  Na/Cl reabsorption ( Na+ excretion ) -  Ca2+ reabsorption ( Ca2+ excretion )
Secondary site of action at the proximal tubule
- Additional diuretic effect when combined with loop
diuretic
- Not usually important because of compensation in loop
of Henle

** may decrease blood pressure without perceivable volume loss - low dose may be effective
(also decreased toxicity)

65
Q

If refractory to a Loop diuretic add a _____ (proximal tubule effect may help)

A

thiazide

66
Q

Where is hydrochlorothiazide’s site of action?

A

primary - NaCl transporter on distal tubule (blocking Na+ retention/reabsorb so you get more excreted)

secondary - Na transporter on proximal tubule

67
Q

Where is furosemide site of action?

A

ascending loop of henle

(isn’t as effective so we add the hydrochlorothiazide)

68
Q

Which are the Thiazide Diuretics?

A
  • HYDROCHLOROTHIAZIDE
  • METOLAZONE
69
Q

Where do the Thiazide Diuretics act?

A
  • distal tubule (primary site of action)
  • inhibit Na+/Cl- transporter
70
Q

What do Thiazide Diuretics do?

A

↓ peripheral resistance & ↓ sodium, water retension which ↓ BV & ↓CO

both ↓BP

71
Q

At higher doses of Thiazide Diuretics, patients…

A

at higher doses - patient perceives need to urinate - “pee pill”

72
Q

At lower does of Thiazide Diuretics, patients…

A

seen at lower doses - may not perceivably increase urine flow - but takes time to be effective (months)

73
Q

What effects do Thiazide Diuretics have?

A

INCREASED URINARY EXCRETION:
- Na+
- K+
- Volume of urine

DECREASED URINARY EXCRETION:
- Ca2+

74
Q

Thiazide Diuretics effect on calcium is ____ of what loop diuretics do to calcium.

A

opposite
- decreasing excretion of Ca2+

75
Q

What are problems with Thiazide Diuretics?

A
  • hypokalemia – increased Na+ in urine at distal tubule causes more K+ to be exchanged for Na+ causing loss of K+ from body
  • hyperglycemia - problem for type 2 diabetes
  • (↓ insulin release; ↓ tissue utilization)
  • ↑ LDL levels (bad cholesterol - must monitor)
  • less effective than RAS blockers in reducing CVD events
  • decrease GFR so less effective in CKD patients
  • interaction with the anti-arrhythmic agent amiodarone can lead to a more irregular heartbeat
76
Q

What are the uses of Thiazide Diuretics?

A
  • edema, hypertension
77
Q

What are the advantages of Thiazide Diuretics?

A
  • orally active
  • no postural hypotension, low toxicity
  • potentiate other anti-hypertensive medications (good to use in combo with others)
78
Q

What drugs are Potassium Sparing Diuretics?

A

SPIRONOLACTONE (less common –> often used in combo with other diuretics b/c they are weak diuretics)

79
Q

What do Potassium Sparing Diuretics (i.e. Spironolactone) do?

A

aldosterone receptor antagonist

prevents aldosterone from binding to receptor
- decreases sodium reabsorption
- decreases potassium excretion

80
Q

Potassium Sparing Diuretics are…

A

weak diuretics

81
Q

What are Potassium Sparing Diuretics used in?

A
  • Used in treatment of heart failure, resistant hypertension, hyperaldosteronism, hypokalemia
  • give with other diuretics to decrease potassium loss
  • may cause hyperkalemia
    • never combine with K+ supplements* (b/c of the 2 points above)
82
Q

What effects do Potassium Sparing Diuretics have?

A

INCREASED URINARY EXCRETION:
- Na+
- Volume of urine

DECREASED URINARY EXCRETION:
- K+

83
Q

Potassium Sparing Diuretics have a ___ effect on sodium excretion and urine volume.

A

weaker

84
Q

Potassium Sparing Diuretics _____ potassium excretion (_____ to loop and thiazide diuretics).

A

decreases

opposite

(why its called K+ sparing diuretics)

85
Q

Describe Electrolyte Disturbances – loop and thiazide diuretics

A

Potassium depletion due to thiazide and/or loop diuretics - not a problem in “healthy patients”
- more a problem if low potassium already a problem in for eg. heart failure, cirrhosis, etc

86
Q

What are two major causes of Electrolyte Disturbances – loop and thiazide diuretics?

A
  1. secondary hyperaldosteronism (due to plasma volume depletion) - ↑ renin → ↑ Ang-II → ↑ aldosterone
    - Na reabsorption at expense of K (and H) loss
  2. increased distal delivery
    - ↑ distal delivery - due to inhibition of Na reabsorption in loop and distal tubule
    - collecting tubules therefore increase Na reabsorption
    - to conserve sodium
87
Q

What is the Potassium Depletion Treatment (for electrolyte disturbances)?

A
  1. dietary intake - apricots, bananas, etc
  2. potassium chloride tablets-chloride salt - dilute solution 3. slow-potassium tablets -ulceration
  3. emergencies
    - iv KCl - 40 mEq - repeat cautiously until potassium rises 5. potassium sparing diuretics - SPIRONOLACTONE
    - weak diuretics
    - give with other diuretics to decrease K loss - may cause hyperkalemia
    - * never combine with K supplements*
88
Q

What is the Extracellular Volume Depletion (for Electrolyte Disturbances)?

A
  • loop diuretics - kidney unable to concentrate or dilute
  • excrete an isotonic urine (not excreting the electrolytes you should be)
  • inability to concentrate urine
  • drink more water to excrete solutes
  • inability to dilute urine
  • excess water consumption is excreted as an isotonic urine
  • ingest hypotonic solution - excrete isotonic urine (drink water that doesn’t have a lot of electrolytes in it)
  • net loss of electrolytes including plasma sodium
  • chronic dilutional hyponatremia
89
Q

Describe the calcium & volume depletion and increased proximal tubule reabsorption for electrolyte disturbances?

A

Calcium
- thiazides ↓ calcium excretion
- good for hypocalciuria
- furosemide ↑ calcium excretion
- good for hypercalcemia

Volume depletion and increased proximal tubule reabsorption
- uric acid excretion (b/c diuretics cause more urinary secretion of solutes)
– initially increased
- decreased with chronic administration (gout?)
- lithium - increased proximal tubule reabsorption
- toxicity

90
Q

What are ACE Inhibitors?

A

Inhibits the Angiotensin Converting Enzyme (ACE)
- treat HTN

91
Q

Why decrease formation of angiotensin II?

A
  • Hypertension involves activation of the renin-angiotensin-
    aldosterone system (RAAS)
  • RAAS induces vasoconstriction and blood volume retention
  • ACE inhibitors (eg. ENALAPRIL)
    -decreased constriction in arteries and veins
  • decreased aldosterone by decreased angiotensin II
  • decreased blood volume (and decreased venous return)
92
Q

What are ACEi (ex: ENALAPRIL)?

A

-decreased constriction in arteries and veins
- decreased aldosterone by decreased angiotensin II
- decreased blood volume (and decreased venous return)

93
Q

What are the uses of ACEi?

A

hypertension, heart failure, kidney disease with albuminuria

94
Q

ACEis or ARBs…

A

would decrease preload and afterload

95
Q

Angiotensin Receptor Blockers (ARBs)

A

LOSARTAN

VALSARTAN

  • both of heart & BVs
96
Q

Angiotensin Receptor Blockers (ARBs):

A
  • Blocks binding of Angiotensin-II to its receptor
  • decreased constriction in arteries and veins
  • decreased aldosterone by decreased angiotensin II
  • Ultimate action is similar to ACEi but without increasing bradykinin
  • No cough
  • Similar complications to those seen with ACEi
  • Originally marketed as ACEi without the cough
97
Q

Angiotensin Converting Enzyme Inhibitors

Angiotensin Receptor Blockers – Side Effects and contraindications

A

use with caution if plasma Ang-II levels elevated -renal artery stenosis, volume depletion, diuretic use

ACEis produce non productive (dry) cough - less with ARBs

decreased aldosterone - decreased K excretion – do not use with potassium sparing diuretics –> hyperglycemia

only certain ACEIs

may decrease BP too much!! - use in combination with diuretics with caution

Both ACEIs and ARBs contraindicated in pregnancy and lactation - birth defects

(dry cough, hyperkalemia, skin rash, hypotension, fever)

Pharmacology (Fall) (28 decks)

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