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Pharmacology > Hypertension > Flashcards

Hypertension Flashcards

1
Q

Furosemide

LOOP DIURETICS

A

Route: Oral/IV

Onset:

  • oral: 60 minutes
  • IV: 5 minutes

Adverse effects:

  • dehydration
  • electrolyte abnormalities
  • hypotension
  • ototoxicity
  • hyperuricemia
Considerations:
Avoid taking before bedtime
Monitor urine output
Watch for signs of dehydration
Give IV doses SLOWLY to avoid ototoxicity
Caution in patients with a sulfa allergy
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2
Q

Toresemide

LOOP DIURETICS

A

Route: Oral/IV

Onset:

  • oral: 60 minutes
  • IV: 5 minutes

Adverse effects:

  • dehydration
  • electrolyte abnormalities
  • hypotension
  • ototoxicity
  • hyperuricemia
Considerations:
Avoid taking before bedtime
Monitor urine output
Watch for signs of dehydration
Give IV doses SLOWLY to avoid ototoxicity
Caution in patients with a sulfa allergy
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3
Q

Bumetanide

LOOP DIURETICS

A

Route: Oral/IV

Onset:

  • oral: 60 minutes
  • IV: 5 minutes

Adverse effects:

  • dehydration
  • electrolyte abnormalities
  • hypotension
  • ototoxicity
  • hyperuricemia
Considerations:
Avoid taking before bedtime
Monitor urine output
Watch for signs of dehydration
Give IV doses SLOWLY to avoid ototoxicity
Caution in patients with a sulfa allergy
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4
Q

Ethacrynic acid

LOOP DIURETICS

A

Route: Oral/IV

Onset:

  • oral: 60 minutes
  • IV: 5 minutes

Adverse effects:

  • dehydration
  • electrolyte abnormalities
  • hypotension
  • ototoxicity
  • hyperuricemia

Considerations:
Monitor urine output
Can be given safely to patients with a sulfa allergy

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5
Q

Hydrochlorothiazide

THIAZIDE DIURETICS

A

Route: Oral

Onset:
1-2 hours

Adverse effects:
Dehydration
Electrolyte abnormalities
Hyperglycemia 
Hyperuricemia 
Considerations:
Avoid dosing before bedtime 
All agents equally effective 
Monitor for ADEs especially related to electrolyte abnormalities 
Caution in patients with a sulfa allergy
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6
Q

Chlorothiazide

THIAZIDE DIURETICS

A

Route: Oral/IV

Onset:
1-2 hours

Adverse effects:
Dehydration
Electrolyte abnormalities
Hyperglycemia 
Hyperuricemia 
Considerations:
Avoid dosing before bedtime 
All agents equally effective 
Monitor for ADEs especially related to electrolyte abnormalities 
Caution in patients with a sulfa allergy
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7
Q

Chlorthalidone

THIAZIDE DIURETICS

A

Route:Oral

Onset:
1-2 hours

Adverse effects:
Dehydration
Electrolyte abnormalities
Hyperglycemia 
Hyperuricemia 
Considerations:
Avoid dosing before bedtime 
All agents equally effective 
Monitor for ADEs especially related to electrolyte abnormalities 
Caution in patients with a sulfa allergy
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8
Q

Metolazone

THIAZIDE DIURETICS

A

Route: Oral

Onset:
1-2 hours

Adverse effects:
Dehydration
Electrolyte abnormalities
Hyperglycemia 
Hyperuricemia 
Considerations:
Avoid dosing before bedtime 
All agents equally effective 
Monitor for ADEs especially related to electrolyte abnormalities 
Caution in patients with a sulfa allergy
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9
Q

Loop Diuretics

A

Most effective class of diuretics

Mechanism of action:

  • block sodium and chloride reabsorption in the ascending Loop of Henle
  • 20% of Na and Cl typically reabsorbed here, inhibition leads to profound diuresis
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10
Q

Loop Diuretics

A 
Indications:
Congestive heart failure
Pulmonary edema
Peripheral edema
Hypertension
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11
Q

Thiazide diuretics

A

-Lesser diuretic effect than loop diuretics

Hydrochlorathiazide (PO)
Cholorothiazide (PO or IV)
Chlorthalidone (PO)
Metolazone (PO)

▷Mechanism of action:
○Block reabsorption of Na+ and Cl- at the early segment of the distal convoluted tubule (DCT)
○10% of Na and Cl reabsorbed from DCT; inhibition leads to diuresis

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12
Q

Potassium sparing diuretics

A

Therapeutic effects:
○Small amount of diuresis
○Decrease potassium excretion
○Reduce cardiac remodeling

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13
Q

Renal physiology

PATHO

A

Filtration
•Occurs at the glomerulus
•All small molecules get filtered

Reabsorption
•99% of water, electrolytes and nutrients undergo reabsorption via active transport

Active tubular secretion
•Located in proximal convoluted tubule
•Excrete products into lumen of nephron

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14
Q

Amiloride and Triamterene

A

Administration: Oral

NON-ALDOSTERONE POTASSIUM SPARING DIURETICS

Mechanism of action:
•Direct inhibitor of the Na/K ion exchange transporter
•Increased excretion of sodium and retention of potassium

Indications:
•Hypertension
•Edema

Adverse effects
•Hyperkalemia

DDI:
•Thiazide and loop diuretics
•Agents that raise potassium

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15
Q

Spironolactone

A

Administration: Oral

Mechanism of action
•blocks aldosterone in the DCT
•aldosterone typically causes sodium retention and potassium excretion
•Increased excretion of sodium and retention of potassium

Indications:
•Hypertension and edema
•Heart failure
•Acne
•Polycystic ovarian syndrome

Adverse effects
•Hyperkalemia
•Endocrine effects

DDI:
•Thiazide and loop diuretics
•Agents that raise potassium

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16
Q

Renal physiology (patho)

A

Three basic functions:

Cleansing of extracellular fluid (ECF) and maintenance of ECF volume and composition
Maintenance of acid-base balance
Excretion of metabolic wastes (drugs/toxins

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17
Q

Mannitol

A

Osmotic diuretic made of a 6-carbon sugar

Route: IV

  • *Inspect product prior to administration**
  • Mannitol can crystalize
  • Must be administered through 0.22 micron filter to remove microcrystals

Mechanism of action:

  • Filtered by the glomerulus
  • Does NOT undergo reabsorption and remains in the lumen
  • Increased osmotic pressure keeps water from being reabsorbed

Indications:
-Reduce elevated intracranial and intraocular pressures

Adverse effects:
Edema
Electrolyte imbalances

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18
Q

Renin-Angiotensin-Aldosterone-System (RAAS)

patho

A

The RAAS system plays critical role in regulating blood pressure, blood volume and fluids and electrolytes

Related drug classes:
Angiotensin converting enzyme inhibitors (ACE-i)
Angiotensin II receptor blockers (ARB)
Direct renin inhibitors (DRI)
Aldosterone antagonists
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19
Q

RAAS KEY COMPOUNDS

A

Angiotensin
Aldosterone
Renin

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20
Q

Angiotensin

A RAAS

A

Three subtypes

Angiotensin I: inactive; converted into angiotensin II by angiotensin-converting enzyme (ACE)

Angiotensin II: 
Powerful vasoconstrictor (increases blood pressure)
Stimulates release of aldosterone (increases blood pressure)
Causes remodeling and hypertrophy of the myocardium

Angiotensin III: effects incompletely understood

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21
Q

Aldosterone

RAAS

A

Stimulates Na+ retention and K+ excretion in the distal convoluted tubule

Na+ retention leads to water retention which increases blood pressure

Causes pathologic remodeling and hypertrophy of the myocardium

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22
Q

Renin

RAAS

A

Enzyme that starts the whole RAAS pathway

Produced by the kidney in response to:

Low blood pressure
Low blood volume
Low blood sodium content

Renin release is SUPPRESSED when the above factors return to normal

23
Q

Angiotensin Converting Enzyme Inhibitors (ACE-I)

A 
LISINOPRIL
ENALAPRIL
ENALAPRILAT
CAPTOPRIL
BENAZEPRIL

Very effective for treating
Hypertension
Heart failure
Diabetic nephropathy

Generally well-tolerated

All agents are equally efficacious

24
Q

ACE-inhibitors

-pril meds

A

Pharmacokinetics:

  • All administered orally, EXCEPT enalaprilat is IV
  • Long half-lives EXCEPT captopril
  • Renally excreted

Adverse effects

  • First-dose hypotension
  • Dry cough
  • hyperkalemia (high potassium levels)
  • Renal failure in patients with bilateral renal artery stenosis
  • Fetal injury
  • Angioedema
DDI:
Diuretics 
Antihypertensive agents
Drugs that raise potassium
Lithium
NSAIDs
25
Q

ACE-inhibitor indications

A

Hypertension: reduce the risk of cardiovascular mortality
Heart failure: Inhibits aldosterone release decreases pathologic remodeling on the heart

Myocardial Infarction: decrease mortality

Diabetic nephropathy: delay renal injury, decrease pressure in thenglomerulus

Prevention of MI, stroke and death in patients at high risk for CV disease

26
Q

Angiotensin II Receptor Blockers (ARBs)

SARTAN SQUAD

A

Route: Oral

Mechanism of action:
Block angiotensin II from binding to its receptor

Physiologic effects:
Vasodilation
Decrease production of aldosterone
Reduce cardiac remodeling
Dilation of renal blood vessels
Therapeutic uses:
Hypertension
Heart failure
Diabetic neuropathy
M.I
Prevention of MI, stroke, and death in high-risk patients

Adverse effects:
Angioedema
Fetal harm
❤️ failure

DDI:
Diuretics
Anti hypertensives
Drugs that raise potassium (K)

Drugs in this group (SARTAN SQUAD):
Losartan
Valsartan
Telmisartan
Olmesartan
27
Q

Direct renin inhibitors:

DRI

A

Route: Oral

Mechanism of action:
binds to renin and prevents it from cleaving angiotensinogen from angiotensin I

Physiologic actions:
Vasodilation
Decrease production of aldosterone
Reduce cardiac remodeling
Dilation of renal blood vessels

Indication:
Hypertension

Adverse effects:
Angioedema
Dry cough
Diarrhea
Hyperkalemia
Fetal injury

Drug: Aliskiren

28
Q

Aldosterone Antagonists

ONE SQUAD

A

Route: Oral

Mechanism of action:
Blocks aldosterone from binding to receptors in kidney

Physiologic effects:
Decrease Na+ reabsorption and Increase reabsorption of potassium
Decrease BP and blood volume
Reduce pathological remodeling of the heart

Indications:
Hypertension
Heart failure

Adverse effects:
Hyperkalemia
Diarrhea
Gynecomastia

Drugs in this group (ONE SQUAD):
Eplerenone—selective for aldosterone receptors
Spironolactone—NON-selective

29
Q

Dihydropyridine Calcium Channel Blockers

PINE SQUAD

A

Mechanism of action:
Block calcium channels in the vascular smooth muscle
MINIMAL effects on the heart

Hemodynamic effects:
Vasodilation of the arteries and arterioles—> decreases BP
Vasodilation of the cardiac vasculature—> increases myocardial perfusion
Reflex tachycardia

Indications:
Angina pectoris
Hypertension

Drugs in this group (PINE SQUAD): 
Amlodipine
Nifedipine
Felodipine 
Nimodipine 
Nicardipine 
Clevidipine
30
Q

Amlodipine

Dihydrophine Calcium Channel Blockers

A

Route: Oral

Onset: 12-24 hours

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium

31
Q

Nifedipine

Dihydrophine Calcium Channel Blockers

A

Route: Oral

Onset: 12-24 hours

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium

32
Q

Felodipine

Dihydrophine Calcium Channel Blockers

A

Route: Oral

Onset: 12-24 hours

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium

33
Q

Nimodipine

Dihydrophine Calcium Channel Blockers

A

Route: Oral

Onset: 12-24 hours

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium
ONLY indicated for SAH

34
Q

Nicardipine

Dihydrophine Calcium Channel Blockers

A

Route: IV

Onset: 5-10 minutes

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium
With Clevidipine, it is a first-line IV medication for hypertension

35
Q

Clevidipine

Dihydrophine Calcium Channel Blockers

A

Route: IV

Onset: 5-10 minutes

Adverse effects: 
Flushing
Dizziness
Headache
Peripheral edema
Reflex Tachycardia

Considerations:
DDI with beta blockers
Toxic doses can affect myocardium
With Nicardipine, it is a first-line IV medication for hypertension

36
Q

Non-Dihydrophine Calcium Channel Blockers

A

Mechanism of action:
Block of calcium channels in the vascular smooth muscle AND heart

Hemodynamic effects:
Vasodilation of the arteries and arterioles—>decrease BP
Vasodilation of the cardiac vasculature —> increases myocardial perfusion
Blockade of the SA and AV node —> decreases HR
Decreased force of myocardial contraction

Indications:
Angina pectoris
Hypertension
Cardiac dysrhythmias

Drugs in this class:
Verapamil
Diltiazem

37
Q

Verapamil

Non-Dihydrophine Calcium Channel Blockers

A

Route: Oral, IV

Onset:
Oral: 1-2 hours
IV: 5 minutes

Adverse effects: 
Constipation
Dizziness
Flushing
Headache
Bradycardia
AV nodal block
Peripheral edema
Considerations:
DDI with digoxin and beta blockers
***Possible interaction with grapefruit juice***(main difference to diltiazem)
Monitor BP, ECG, and HR
Do NOT CRUSH or CHEW ER products
38
Q

Diltiazem

Non-Dihydropyridine Calcium Channel Blockers

A

Route: Oral, IV

Onset:
Oral: 1-2 hours
IV: 5 minutes

Adverse effects:
Dizziness
Flushing
Headache
Bradycardia
AV nodal block
Peripheral edema

Considerations:
DDI with digoxin and beta-blockers
Monitor BP, ECG, and HR
DO NOT CRUSH OR CHEW ER PRODUCTS

39
Q

Classification of Hypertension (HTN)

A

Diagnosis requires one of the following:

  • Minimum of 2 elevated BP readings at different office visits
  • Separate BP measurements at the same visit by 5 minutes
40
Q

HTN Management

A

Diagnose (primary or secondary)
Evaluate for factors that increase CV risk + target organ damage
Treatment goals
Therapeutic management

(DEET)

41
Q

HEART FAILURE (comorbid condition)

A

Drugs to avoid/Use with caution
VERAPAMIL
DILTIAZEM

42
Q

AV BLOCK (comorbid condition)

A

Drugs to avoid/Use with caution
BETA-BLOCKERS
VERAPAMIL
DILTIAZEM

43
Q

RENAL INSUFFICIENCY (comorbid condition)

A

Drugs to avoid/Use with caution
K-SPARING DIURETICS
K-SUPPLEMENTS

44
Q

ASTHMA (comorbid condition)

A

Drugs to avoid/Use with caution

BETA-BLOCKERS

45
Q

GOUT (comorbid condition)

A

Drugs to avoid/Use with caution

THIAZIDE AND LOOP DIURETICS

46
Q

HYPERKALEMIA (comorbid condition)

A 
Drugs to avoid/Use with caution
K-SPARING DIURETICS
ACE-INHIBITORS
DIRECT RENIN INHIBITORS
ANGIOTENSION RECEPTOR BLOCKERS
ALDOSTERONE ANTAGONISTS
47
Q

HYPOKALEMIA (comorbid condition)

A

Drugs to avoid/Use with caution

THIAZIDE AND LOOP DIURETICS

48
Q

Hypertensive emergency

A

DBP > 120 mmHg
End organ damage
Need to rapidly decrease BP over one hour
–Requires IV meds
-Sodium nitroprusside, labetalol, clevidipine, nicardipine

49
Q

Hypertensive urgency

A

DBP > 120mmHg
No end organ damage
Decrease BP gradually over 24 hours
–Can use IV or PO meds

50
Q

Chronic HTN in pregnancy (patho)

A

Existed before pregnancy or developed prior to 20 weeks gestation

Discontinue all category X drugs:
ACE-i
ARBs
DRI

Preferred drugs:
Labetalol
Methyldopa

51
Q

Preeclampsia and Eclampsia (patho)

A

Disorder characterized by HTN and proteinuria (increased levels of protein in urine) after 20w gestation
-Presence of seizures=eclampsia

Serious risks to the mother and fetus

Treatment:
Labetalol
Magnesium (anticonvulsant)
Delivery baby (if possible and safe)

52
Q

Diuretic Classes

A

Loop Diuretics
Thiazide diuretics
Potassium-Sparing Diuretics
Osmotic Diuretics

53
Q

What is the main difference between dihydropyridine calcium channel blockers and non-dihydropyridine calcium channel blockers?

A

Dihydropyridines work on vascular smooth muscle, but non-dihydropyridines work on the heart AND vascular smooth muscle.

Therefore, non-dihydropyridines may treat cardiac arrythmias

Pharmacology (5 decks)

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