HYPERTENSION 3

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ssilvis
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195483
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HYPERTENSION 3
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2013-01-28 11:09:10
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HYPERTENSION
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anti-hypertensive medications
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  1. Key to diagnosis of HTN
    Making sure that there is not an underlying disease that is causing it.
  2. 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.
  3. 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).
  4. 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.
    • *
  5. Beta 1 receptors-
    • *located in heart and kidney
    • *regulates HR, renin release, cardiac contractility.
    • *blocking decrease renin and decrease stimulation of renin.
  6. Beta 2 receptors-
    • *regulates bronchodilation and vasodilation.
    • *blocking causes vasoconstriction.
  7. Alpha receptors-
    *located in veins
  8. 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.
  9. 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.
  10. 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
  11. 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.
  12. ACE INHIBITORS ARE BENEFICIAL FOR THESE DISEASES-
    • 1.  DM
    • 2.  CHF
    • 3.  Post MI
    • 4.  CKD
    • 5.  STROKE PREVENTION
  13. 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).
  14. 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.
  15. 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
  16. CALCIUM CHANNEL BLOCKERS S/E's
    Constipation, hypostension, dizziness, h/a, fatigue, PERIPHERAL EDEMA!
  17. 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.
  18. 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.
  19. 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.
  20. 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.
  21. 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.
  22. 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
  23. 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.
  24. 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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