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Key to diagnosis of HTN
Making sure that there is not an underlying disease that is causing it.
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DIURETICS- K SPARING
- *Prevent Hypokalemia by preserving k loss.
- *Aldosterone antagonists- modulate vascular tone often used an additive to other drugs though must use caution because of potential for hyperkalemia.
- 1. Spiranolactone-
- Aldosterone antagonise, increases potassium, may cause gynecomastia.
- 2. Eplernone-
- caution with dereased creatinine clearance- watch kidney function, increases potassium, NO gynecomastia.
- 3. Triamterene-
- Conserves K in late distal tubule of kidney, minimal diuresis.
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DIURETICS- LOOP
- MOA- Decrease blood volume, watch for dehydration.
- *Reserved for pts. with poor renal function.
- 1. Lasix- most common, more potent and should be considered in elderly with decreased renal function GFR 30 or less.
- S/E- ototoxicity, volume depletion, decreased potassium, increased uric acid (watch for pts with gout), increased glucose (watch diabetics).
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BETA BLOCKERS
- *Decrease HR and contractility- which decreases CO.
- *Beneficial for patients with pre-existing heart disease, Tachycardia, MI, CHF, and DM, prevents sudden death.
- *MOA- not known. May be decrease CL and renin and outflow from CNS.
- *Can be a first line med.
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Beta 1 receptors-
- *located in heart and kidney
- *regulates HR, renin release, cardiac contractility.
- *blocking decrease renin and decrease stimulation of renin.
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Beta 2 receptors-
- *regulates bronchodilation and vasodilation.
- *blocking causes vasoconstriction.
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Alpha receptors-
*located in veins
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BETA BLOCKER CHARACTERISTICS
- 1. Noncardioselective
- - Affects beta 1 and beta 2
- S/E- bronchoconstriction, hypoglycemia, slow recovery from hypoglycemia, and absent s/s of hypoglycemia.
- -Inderal, carvedolol, and coreg
- 2. Cardioselective-
- -Affects beta 1
- -Atenolol, Tenormin, betaxolol, Kerlone, Metoprolol-Lopressor.
- -Less s/s than noncardioselective.
- 3. Intrinis sympathomimetic activity (ISA)-
- -partial agonists at beta 1 and beta 2- decrease BP by stimulating eta 2 wich decreases vascular resistance.
- -Pindolol, Visken.
- 4. Blockade of both alpha and beta receptors-
- -Labetolol, Coreg
- -all lipid soluble drugs- may take several weeks to be eliminated from a pts system.
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BETA BLOCKER SIDE EFFECTS
- *CHF
- *Heart block (decreases HR even more)
- *CNS- fatigue, insomnia, hallucinations, hypotension.
- *Impotence, decreased libido.
- *Broncoconstriction (watch with COPD and astma)
- *Bradycardia
- *Increased triglycerides and decreased HDL
- *GI effects
- *Depression *** may have to d/c
- *Mask signs of hypoglycemia and slow recovery time.
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DISCONTINUATION OF BETA BLOCKERS
- If done abruptly may cause ischemic syndromes such as unstable angina, MI, and DEATH! Rebound effect.
- Taper dose over 14 days to d/c
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ACE INHIBITORS
- *MOA- blocks conversion of angiotensin 1 to angiotensin 2
- *Degrades bradykinins, stimulates synthesis of PGE-2 and prostacyclin which causes vasoldilation and decreases BP
- *Enalapril, vasotec, captopril, capoten, fosinopril, and lisinopril
- *SE- cough, increased K, taste disturbances, hypotension, angineurotic edema(swelling of the tongue and lips...D/C)
- *CONTRAINDICATED IN PREGNANCY- CAN CAUSE FETAL DEATH- PROBLEM FOR FEMALE PATIENTS.
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ACE INHIBITORS ARE BENEFICIAL FOR THESE DISEASES-
- 1. DM
- 2. CHF
- 3. Post MI
- 4. CKD
- 5. STROKE PREVENTION
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ANGIOTENSIS 2 ANTAGONISTS-
- *MOA- angiotensin 2 receptor effects are blocked (receptor for angiotensin 2) vasoconstriction, aldosterone release, CNS medicated sympathetic activity, epinephrine release from adrenal gland.
- *Increased benefit with CHF, used with ACE's are not tolerated, higher cost.
- *CONTRAINDICATED IN PREGNANCY
- *Losartan (cozaar), valsartan (Diovan).
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CALCIUM CHANNEL BLOCKERS-
- *MOA- reflex sympathetic activation due to blockage of CA entering cardiac and smooth muscle cells. Blocks CA and it can't get into heart muscles.
- *Decreased contraction of myocardial and smooth muscle and depression of conduction velocity.
- *VERY EFFECTIVE IN THE ELDERLY.
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CALCIUM CHANNEL BLOCKER CLASSES-
- 1. Dihydrophyridines-
- Great affinity for smooth muscles cells
- May cause reflex increase in HR or suppress cardiac contracitlity.
- *Nifedipine (Adalat; Procardia)
- *Norvasc (Amlodipine)
- 2. Nondihydropyridines-
- Effects on cardiac tissue, decrease in HR, can cause GINGIVITIS!
- *Verapamil and dilitazem
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CALCIUM CHANNEL BLOCKERS S/E's
Constipation, hypostension, dizziness, h/a, fatigue, PERIPHERAL EDEMA!
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ALPHA BLOCKERS-
- *MOA- Dilation of peripheral arteries and veins, which decreases TPR. Blocks alpha receptors.
- *Prasozin (Minipress), terazosin (Hytrin), doxazosin (Cardura).
- *S/E- FIRST DOSE SYNCOPY, short term reflex tachycardia, orthostatic hypotension, CNS effects, PRIAPISM (PAINFUL SUSTAINED ERECTION), dizziness.
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CENTRAL ALPHA 2 AGONISTS-
- *MOA- stimulation of postsynaptic alspa 2 receptors in brain (decrease sypathetic activity and increase parasympathetic activity) decrease CO nd TPR. Do not decrease renal blood flow and are useful in HTN with RENAL INSUFFICIENCY.
- *Used when HTN is resistant to other tx.
- *Methyldopa (Aldomet), clonidine (Catapres)
- *S/E- sedation, dry mouth, hepatitis, hemolytic anemia, orthostasis.
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DIRECT VASODILATORS-
- *Hydralazine (Apresoline), minoxidil (Loniten)
- *MOA- direct relaxation o f arteriolar smooth muscle by increasing cGMP. Reflex increasesin HR, CO,and renin release.
- *S/E- Increased HR, fluid retention, h/a, nausea, sweating and fluid retention, LUPUS LIKE SYNDROME.
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POSTGANGLIONIC SYMPTHETIC INHIBITORS-
- *Guanethidine (Ismelin), guanadrel (Hylorel)
- *MOA- inhibitrelease of NE from sypathetic nerve terminals. Decrease CO and TPR.
- *SE- EXPLOSIVE DIARRHEA, orhtostatic hypotenstion, IMPOTENCE, syncope, supersensitivity of postsynaptic receptors which casue a rebound effect.
- *4th or 5th line med.
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DRUG CHOICE-
- 1. Consider:
- -Coexisting disease states
- -Co-prescribed meds
- -Practical pt specific issues including cost
- -ALLHAT TRIAL
- 2. Beta blockeror diuretic-
- -1st line since proven to decrease morbidity and mortality.
- -BB- impact on morbidty and mortality
- -Other choices for 1st line are ACE's, CCB, and diuretics.
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HTN SPECIAL SITUATIONS-
- 1. Children-
- d/t sedentary lifestyle, start with lower doses, check other reasons.
- 2. Pregnancy
- Methyldopa and hydralizine can be used.
- NO ACE's or angiotesin 2 receptors!
- 3. Elderly-
- Diuretics, alpha2 angiotensin, CCB
- 4. Blacks-
- Diuretics, CCB
- 5. Asthma/COPD-
- Diuretics, CCB, NO BETA BLOCKERS
- 6. Diabetic pts with proeinuria-
- ACE's and beta blockers
- 7. Hyperlipidemia-
- Alpha blockers decrease LDL.
- 8. Left ventricular hypertrophy-
- ACES
- 9. Angina pectoris-
- BB, CCB (both decrease BP and releive angina.
- 10. CHF-
- ACE'S, diuretics, vavedilol, and losartan
- 11. Previous MI-
- BB and ACE's
- 12. Atrial tachycardia/fibrillation-
- BB
- 13. Isolated systolic HTN-
- Diuretics, ACES, and alpha blockers
- 14. Renal insufficiency-
- ACE'S, diuretics
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HYPERTENSIVE CRISIS-
- *Urgent treatment
- *oral dose of clonidine or captopril
- *Nitropursside or trimethaphan- acts on arteries and veins, reflex increase in HR.
- *Diazoxide- vasodilator on arterices ONLY- reflex increase in HR.
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4 classes of Anti-HTN meds
- 1. Diuretics-
- Reduce blood volume and CO.
- 2. Sympatholytic drugs-
- Decrease PVR
- 3. Angiotensin inhibitors-
- Reduce PVR and Aldosterone levels, have no effect on blood volue or CO.
- 4. Vasoldilators-
- Reduce PVR and provoke reflex tachycardia and fluid retention.
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