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30 Cards in this Set
- Front
- Back
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Decreasing Body Weight (Non-Drug)
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- Obese pts have increased insulin secretion causing increase Na+ reabsorption (water
follows), so blood volume increases = increased BP - Obese pts have increased SNS activity |
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Restricting Sodium Intake (Non-Drug)
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- When levels are too high it causes excess water to be reabsorbed by kidneys
- Increased blood volume = increased BP - Limiting salt intake to 5g/day decrease BP 12/6 |
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Physical Exercise (Non-Drug)
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- Regular exercise decreases BP by 10mmHg
- Decreased fluid volume |
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Potassium Supplementation (Non-Drug)
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- Increased K+ causes...
- Decreased BP - Increased sodium excretion - Decreased renin release - Pts taking ACE inhibitors should not be on a high potassium diet |
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Smoking Cessation (Non-Drug)
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- Just quit.
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Alcohol Restriction (Non-Drug)
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- Excessive alcohol increases BP
- Can decrease response to antihypertensive drugs |
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Main Classes of Diuretics (3) and Mechanism of Action (General)
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- Loop, Thiazide, and Potassium Sparing diuretics
- Block Na+ and Cl- ion reabsorption from the nephron - This prevents water reabsorption - Decreases blood volume = decreased BP |
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Loop Diuretics
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- Most effective diuretic
- Block Na+ and Cl- ion reabsorption in ascending Limb of Henle - Usually reserved for: - Edema, severe renal failure, and severe hypertension that didn't respond to mild drugs |
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Adverse Effects of Loop Diuretics
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- Hypokalemia (decreased K+ in blood)
- may cause cardiac dysrhythmias - Hyponatremia (decreased (Na+ in blood) - Dehydration - Hypotension |
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Thiazide Diuretics
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- Most commonly used
- Block Na+ and Cl- reabsorption in distal tubule |
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Adverse Effects of Thiazide Diuretics
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- Hypokalemia (decreased K+ in blood)
- may cause cardiac dysrhythmias - Dehydration - Hyponatremia (decreased Na+ in blood) |
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Potassium Sparing Diuretics
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- Minimal lowering of BP
- Inhibit aldosterone receptors in collecting duct - Causes increased Na+ excretion and K+ retention - Should not be used with ACE inhibitors or ARBs |
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Beta Blockers (affect on cardiac beta 1 receptors)
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- Bind of catecholamines (i.e. epinephrine) to these receptors causes increased CO
- Beta blockers block beta receptors causing decreased CO - suffix "olo" (e.g. propanolol) |
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Beta Blockers (affect on juxtaglomerular cells)
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- These cells release renin which activates RAAS
- Beta blockers block beta receptors causing decreased RAAS activity - suffix "olo" (e.g. propanolol) |
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Classes of Beta Blockers
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1st Generation Beta Blockers
- Produce non-selective blockade - Could inhibit beta 2 (in the lung) receptors 2nd Generation Beta Blockers - Produce selective blockade |
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Adverse Effects of Beta Blockers
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- Bradycardia
- Decreased CO - Heart failure (rare) - Rebound hypertension when withdrawn abruptly - Bronchospasm (Non-selective beta blockers) - Glycogenolysis inhibition (Non-selective) |
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Angiotensin Converting Enzyme (ACE) Inhibitors
(mechanisms of action) |
Decreases angiotensin II production causing:
- Vasodilation - Decrease total blood volume Inhibit bradykinin breakdown causing: - Vasodilation - suffix "pril" (e.g. captopril) |
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Adverse Effects of ACE Inhibitors
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- Hyperkalemia (increased K+ in blood)
- Persistent cough - Angioedema - Certain NSAIDs may decrease ACE Inhibitor effect |
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Angiotensin Receptor Blockers (ARBs)
(mechanism of action) |
-Blocks binding of angiotensin II to its receptor causing:
- Causes vasodilation - Increases Na+ and water secretion - suffix "sartan" (e.g. valsartan) |
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Direct Renin Inhibitors (DRIs)
(mechanism of action) |
- Binds to renin inhibiting conversion of
angiotensinogen ot angiotensin I |
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Adverse Effects of DRIs
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- Hyperkalemia (increased K+ in blood)
- Diarrhea |
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Calcium Channel Blockers (mechanism of action and sub classes)
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- Blocks entry of calcium into heart and smooth muscle cells decreasing contraction
Subclasses - Dyhydropyridine calcium channel blockers - Non-dyhydropyridine calcium channel blockers |
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Dyhydropyridine Calcium Channel Blockers
(mechanism of action) |
- Decrease arteriolar smooth muscle calcium influx resulting in vasodilation
- suffix "dipine" (e.g. nifedipine) |
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Adverse Effects of Dyhydropyridine Calcium Channel Blockers
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- Flushing
- Dizziness - Headache - Peripheral Edema - Reflex tachycardia - Rash |
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Non-Dyhydropyridine Calcium Channel Blockers
(mechanism of action) |
- Block calcium channels in both the heart and vessels
- Decrease CO |
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Adverse Effects of Non-Dyhydropyridine Calcium Channel Blockers
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- Constipation
- Dizziness - Flushing - Headache - Edema - May compromise cardiac function |
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Centrally Acting Alpha 2 Receptor Agonists
(mechanism of action) |
- Bind to and activate alpha 2 receptors in brainstem decreasing sympathetic outflow to heart and vessels
- Causes decreased CO and peripheral resistance |
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Adverse Effects of Centrally Acting Alpha 2
Receptor Agonists |
- Drowsiness
- Dry mouth - Rebound hypertension if withdrawn abruptly |
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Treatment Algorithm - Hypertension Only
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Treatment Algorithm - Diabetes and Renal
Disease |
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