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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
ACE-inhibitor indications
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
Angiotensin II Receptor Blockers (ARBs) | SARTAN SQUAD
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
Direct renin inhibitors: | DRI
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
Aldosterone Antagonists | ONE SQUAD
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
Dihydropyridine Calcium Channel Blockers | PINE SQUAD
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
Amlodipine | Dihydrophine Calcium Channel Blockers
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
Nifedipine | Dihydrophine Calcium Channel Blockers
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
Felodipine | Dihydrophine Calcium Channel Blockers
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
Nimodipine | Dihydrophine Calcium Channel Blockers
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
Nicardipine | Dihydrophine Calcium Channel Blockers
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
Clevidipine | Dihydrophine Calcium Channel Blockers
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
Non-Dihydrophine Calcium Channel Blockers
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
Verapamil | Non-Dihydrophine Calcium Channel Blockers
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
Diltiazem | Non-Dihydropyridine Calcium Channel Blockers
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
Classification of Hypertension (HTN)
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
HTN Management
Diagnose (primary or secondary) Evaluate for factors that increase CV risk + target organ damage Treatment goals Therapeutic management (DEET)
41
HEART FAILURE (comorbid condition)
Drugs to avoid/Use with caution VERAPAMIL DILTIAZEM
42
AV BLOCK (comorbid condition)
Drugs to avoid/Use with caution BETA-BLOCKERS VERAPAMIL DILTIAZEM
43
RENAL INSUFFICIENCY (comorbid condition)
Drugs to avoid/Use with caution K-SPARING DIURETICS K-SUPPLEMENTS
44
ASTHMA (comorbid condition)
Drugs to avoid/Use with caution | BETA-BLOCKERS
45
GOUT (comorbid condition)
Drugs to avoid/Use with caution | THIAZIDE AND LOOP DIURETICS
46
HYPERKALEMIA (comorbid condition)
``` Drugs to avoid/Use with caution K-SPARING DIURETICS ACE-INHIBITORS DIRECT RENIN INHIBITORS ANGIOTENSION RECEPTOR BLOCKERS ALDOSTERONE ANTAGONISTS ```
47
HYPOKALEMIA (comorbid condition)
Drugs to avoid/Use with caution | THIAZIDE AND LOOP DIURETICS
48
Hypertensive emergency
DBP > 120 mmHg End organ damage Need to rapidly decrease BP over one hour --Requires IV meds -Sodium nitroprusside, labetalol, clevidipine, nicardipine
49
Hypertensive urgency
DBP > 120mmHg No end organ damage Decrease BP gradually over 24 hours --Can use IV or PO meds
50
Chronic HTN in pregnancy (patho)
Existed before pregnancy or developed prior to 20 weeks gestation Discontinue all category X drugs: ACE-i ARBs DRI Preferred drugs: Labetalol Methyldopa
51
Preeclampsia and Eclampsia (patho)
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
Diuretic Classes
Loop Diuretics Thiazide diuretics Potassium-Sparing Diuretics Osmotic Diuretics
53
What is the main difference between dihydropyridine calcium channel blockers and non-dihydropyridine calcium channel blockers?
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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