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Anti Hypertensives- pharmacology
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Anti Hypertensives- pharmacology

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pharmacology of anti hypertensive agents, contain almost all but ca channel blockers

pharmacology of anti hypertensive agents, contain almost all but ca channel blockers

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  • UPREGULATION OR SUPER SENSITIVITY OF B RECEPTORS
  • PVD; PERIPHERAL VASCULAR DISEASE

Anti Hypertensives- pharmacology Anti Hypertensives- pharmacology Presentation Transcript

  • BEENISH S. BHUTTA 315
  • CENTRALLT ACTING SYMPATHOPLEGICS  MOA REDUCE SYMPATHETIC OUTFLOW FROM VASOMOTOR CENTER BUT RETAIN OR EVEN INC SENSITIVITY TO BARORECEPTOR CONTROL Actions less dependent on posture
  • METHLY DOPA  α METHYLDOPAMINE  α METHYLNOREPINEPHERINE  ACT ON CENTRAL α ADRENOCEPTORS
  • ACTIONS  REDUCE PERIPHERAL VASCULAR RRESISTANCE  VARIABLE RED IN CARDIAC OUTPUT AND HEART RATE  DOA: 12-24HR
  • TOXICITY  Postural hypotension in vol. depleted pts  Sedation------at onset  LONG TERM USE-----persistent mental lassitude, impaired mental conc., nightmares, mental depression, extra- pyramidal signs  LACTATION—men & women.. Inhib of dopaminergic mech. in hypothalamus  POSITIVE COOMBS TEST---hemolytic anemia , hepatitis & drug fever  Discont.-----PROMPT REVERS OF ABNORMALITIES
  • DRUG INTERACTIONS  NSAIDS  SYSTEMIC CORTICOSTEROIDS
  • CLONIDINE  α ADRENOCEPTORS IN MEDULLA OF BRAIN---Sensitizes vasomotor centers to Inhib by baroreflexes  RED. SYMPATHETIC AND INC. PARASYMPATHETIC TONE  Nonadrenoceptor site----IMIDAZOLE RECEPTOR
  • ACTIONS  I/V---BRIEF INC IN BLOOD PRESSURE( PARTIAL α AGONIST) followed by MORE PROLONGED HYPOTENTION  DEC. CARDIAC RATE AND C.O  RELAXATION OF CAPACITANCE VESSELS---DEC IN PVR
  • TOXICITY  SEDATION  DRY MOUTH  MENTAL DEPRESSION----WITHDRAW  WITHDRAWAL AFTER PROTRACTED USE: LIFE THREATENING HYPOTENSIVE CRISIS  Nervousness, tachycardia, headache & sweating---omitting 1 or 2 doses of drug
  • DRUG INTERACTIONS  TCA MAY BLOCK THE ANTI HYPOTENSIVE EFFECT  NSAIDS MAY ENHANCE THE ANTIPOTENSIVE EFFECT
  • OTHERS.. GUANABENZ GUANFACINE RARELY USED….
  • GANGLION BLOCKING AGENTS  MOA  COMPETITIVELY BLOCK NICOTINIC CHOLINOCEPTORS ON POST GANGLIONIC NEURONS IN BOTH SYMPATHETIC & PARASYMPATHETIC OUTFLOW  MAY DIRECTLY BLOCK NICOTINIC Ach channel
  • TO NAME A FEW.. HEXAMETHONIUM MECAMYALINE TRIMETHAPHAN
  • ADVERSE EFFECTS  SYMPATHOPLEGIA: excessive orthostatic hypotension & sexual dysfunction  PARASYMPATHOPLEGIA: constipation, blurred vision, precipitation of glaucoma, dry mouth, urinary retention
  • ADRENERGIC NEURON BLOCKING AGENTS  MOA PREVENT NORMAL PHYSIOLOGICAL RELEASE OF NOREPINEPHRINE FROM POST GANGLIONIC SYMPATHETIC NEURONS
  • GUANITHIDINE  MOA---transported across symp nerve ending by NET, conc. In vesicles, NE replaced….gradual depletion of NE
  • TOXICITY  SYMPTOMATIC POSTURAL HYPOTENTION OR AFTER EXERCISE  DIARREHA  DELAYED OR RETROGRADE EJACULATION
  • CONTRA-INDICATIONS  SYMPATHOMIMETIC AGENTS—cause HYPERTENSION  CAN PRODUCE HYPERTENSIVE CRISIS BY RELEASING CHATECHOLAMINES IN PTS WITH PHEOCHROMOCYTOMA  TCA ATTENUATE ANTIHYPERTENSIVE EFFECT--- SEVERE HYPERTENSION
  • THESE BLOCK NEURONAL UPTAKE OR DISPLACE AMINES FROM NERVE TERMINALS  COCAINE  AMPHETAMINE  TCA  PHENOTHIAZINES  PHENOXYBENZAMINE
  • RESERPINE  MOA  Blocks the ability of aminergic transmitter vesicles to take up and store biological amines----interfere VMAT  -> DEPLETION OF NE, DOPAMINE & SEROTININ BOTH IN CENTRAL AND PERIPHERAL NERVOUS SYSTEM  CROMAFFIN GRANULES OF AD. MEDULLA ARE ALSO DEPLETED
  • TOXICITY  LOW DOSES—LITTLE POSTURAL HYPOTENSION  HIGH DOSES– SEDATION, LASSITUDE, NIGHTMARE S, SEVERE MENTAL DEPRESSION— occasionally with low doses too  EXTRAPYRAMIDAL EFFECTS due to low dopamine in CS.  GIT MILD DIARREHA, GIT CRAMPS, INCREASED GASTRIC ACID SECRETION  CONTRAINDICATED WITH H/O PEPTIC ULCER
  • β- ADRENOCEPTOR BLOCKERS
  • PROPRANOLOL  MOA  NONSELECTIVE β- BLOCKADE  PRIMARILY DECREASE IN CARDIAC OUTPUT  INHIBITS STIMULATION OF RENIN PRODUCTION BY CATECHOLAMINES( β1)  ACTS ON PERIPHERAL PRESYNAPTIC β- ADRENOCEPTORS TO REDUCE SYMPATHETIC VASOCONSTRICTIVE ACTIVITY  IN MILD TO MODERATE HYPERTENSION SIGNIFICANT REDUCTION IB B.P WITHOUT PROMINENT POSTURAL HYPOTENSION
  • TOXICITY  BRADYCHARDIA  WORSONED ASTHAMA  FATIGUE  VIVID DREAMS  COLD HANDS  DISCONTINUATION AFTER PROLONGED REGULAR USE WITHDRAWAL SYNDROME: nervousness, tachycardia, increased intensity of angina, increased B.P
  • OTHERS  METOPROLOL & ATENOLOL  GREATER SELECTIVITY TO β1- ADRENOCEPTERS  INDICATIONS: HYPERTENSION, ARRYTHMIAS, ANGIN A, EARLY MANAGEMENT OF MI  Metoprolol thyrotoxicosis & migraine prophylaxis
  •  NADOLOL & CARTEOLOL: NONSELECTIVE β - RECPTOR ANTAGONISTS, REDUCED DOSES IN RENAL DISEASE  BETAXOLOL & BISOPROLOL:β1 BLOCKER
  • PINDOLOL, ACEBUTOLOL, P ENBUTOLOL  PARTIAL AGONISTS: β- BLOCKERS WITH SOME INTRINSIC SYMPATHOMIMETIC ACTIVITY  REDUCE VASCULAR RESISTANCE  REDUCE CARDIAC OUTPUT OR H.R LESS THAN OTHERS due to agonist activity beneficial in cases of bradyarrhythmias or PVD
  • LABETOLO, CARVEDILOL, NE BIVOLOL  β- BLOCKING AND VASODILATING ACTIVITY  LABETOLOL: 4 ISOMERS; 3:1 RATIO OF β:α BLOCKADE REDUCED SYSTEMIC VASCULAR RESISTANCE(α- BLOCKADE), COMBINED ACTIVITY PHEOCROMOCYTOMA & HYPERTENSIVE EMERGENCIES
  • CONT..  CARVEDILOL: HEART FAILURE AND HYPERTENSION  NEBIVOLOL:  D- ISOMER: β-1 SELECTIVE  L-ISOMER: NITRIC OXIDE SYNTHASE INDUCER PVR is acutely lowered, has fewer side effects
  • ESMOLOL  β1- SELECTIVE BLOCKER  RAPIDLY METABOLISED BY RBC ESTERASES  INDICATIONS: INTRA & POST OP HYPERTENSION, HYPERTENSIV E EMERGENCIES PARTICULARLY WHEN HYPERTENSION IS ASSOCATED WITH TACHYCARDIA
  • PRAZOSIN & OTHER α1 BLOCKERS  SELECTIVE BLOCKAGE OF α1 RECEPTORS IN ARTERIOLES & VENULES  LESS REFLEX TACHYCARDIA THAN WITH NON SELECTIVE α BLOCKERS EG PHENTOLAMINE  DLATION OF RESISTANCE & CAPACITANCE VESSELS  B.P more in UPRIGHT position  More effective with β blockers & a diuretic
  • TAMSULOSIN INDICATED IN BENIGN PROSTATIC HYPERPLASIA & HYPERTENSION
  • TOXICITY  FIRST DOSE SYNCOPE: PRECIPITOUS DROP IN STANDING B.P AFTER 1ST DOSE 1ST DOSE ADMINISTERRED AT BEDTIME; Occurs in salt & vol. depleted pts  DIZZINESS  PALPITATIONS  LASSITUDE  HEADACHE  +VE TEST FOR ANTI NUCLEAR FACTOR BUT NO ASSOC. WITH R.A
  • NONSELECTIVE α BLOCKERS  PHENTOLAMINE +PROPRANOLOLCLONIDINE WITHDRAWAL SYNDROME  PHENTOLAMINE & PHENOXYBENZAMINE: PHEOCHROMOCYTOMA
  • VASODILATORS ORAL PARENTRAL Ca BLOCKERS
  • HYDRALIZINE  RELEASE OF N2O  ARTERIOLAR DILATION  TACHYPHYLAXIS TO ANTI-HTN EFFECTS DEVELOPED RAPIDLY  Low bioavailability ; first pass metabolism by acetylation
  • TOXICITY  Headache  Nausea  Palpitation  Sweating  Flushing  Anorexia  May provoke ANGINA or ISCHEMIC ARRHYTHMIAS  LUPUS-LIKE SYNDROME arthralgia, myalgia, skin rashes, fever  Peripheral neuropathy and drug fever…RARE
  • MINOXIDIL  SULPHATE DERIVATIVE OPENS POTASSIUM CHANNELS IN SMOOTH MUSCLESHYPERPOLARIZATION ARTIRIOLAR DILATION  INDICATIONS: HTN, HEART FAILURE, BALDNESS(local action)
  • TOXICITY  TACHYCARDIA, PALPITATIONS, ANG INA, EDEMA WITHOUT β- BLOCKER & DIURETIC  HEADACHE, SWEATING, HYPERTRIC HOSIS…RELATIVELY COMMON
  • SODIUM NITROPRUSSIDE  INDICATIONS; HYPERTENSIVE EMERGENCIES & HEART FAILURE  MOA: ACTIVATION OF GUANYLYL CYCLASE( VIA N2O OR DIRECT) INC. INTRA CELLULAR cGMP RELAXES VASCULAR SMOOTH MUSCLE ARTERIAL & VENODILATION  In pts with heart failure & low cardiac output..output inc owing to afterload reduction
  • DIAZOXIDE  EFFECTIVE & LONG ACTING  ARTERIOLAR DIATOR  RAPID FALL IN SYSTEMIC VASCULAR RESISTANCE  OPENING OF POTASSIUM CHANNELS  HYPOTENSION ACHIEVED WITH SMALLER DOSES IN CHRONIC RENAL FAILURE  Hypoglycemia secondary to insulinoma
  • TOXICITY CAN PROVOKE  ANGINA  ECG EVIDENCE OF ISCHEMIA  CARDIAC FAILURE, In pts with ischemic heart disease  HYPERGLYCEMIA , particularly in pts with RENAL INSUFFISIENCY
  • FENDOLOPAM  PERIPHERAL ARTERIOLAR DILATOR  HYPERTENSIVE EMERGENCIES & POST-OPERATIVE HYPERTENSION  AGONIST OF D1 RECEPTORS: PERIPHERAL ARTERIAL DILATION & NATRIURESIS.  Metabolized by conjugation
  • TOXICITY  REFLEX TACHYCARDIA  HEADACHE  FLUSHING  INCREASES INTRAOCULAR PRESSURE…CONTRAINDIC ATED IN GLAUCOMA