PHARMACOLOGY OF THE AUTONOMIC NERVOUS SYSTEM

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     1  1 PHARMACOLOGY OF THE AUTONOMIC NERVOUS SYSTEM YORAM ORON, PhD PROFESSOR OF PHARMACOLOGY SACKLER FACULTY OF MEDICINE TEL AVIV UNIVERSITY
     2  2 ANATOMY OF ANS - I
     3  3 ANATOMY OF ANS ANS IS DEFINED BY TWO GROUPS OF PERIFERAL NERVES, WHICH ORIGINATE IN GANGLIA OR THE CRANIUM (CRANIAL NERVES) GANGLIA ARE RELAY PLEXI THAT TRANSMIT CNS INFORMATION VIA PRE-GANGLIONIC TO POST GANGLIONIC FIBERS
     4  4 OUTLINE OF THE ANS S P CERV THOR LUMB SACRAL VAGUS
     5  5 ANATOMY OF ANS - II TARGET TISSUES
     6  6 Responses to ANS Stimuli
     7  7 Responses to ANS Stimuli
     8  8 Responses to ANS Stimuli
     9  9 Responses to ANS Stimuli
     10  10 Responses to ANS Stimuli
     11  11 ANATOMY OF ANS - III PRE- AND POST-GANGLIONIC FIBERS
       
     13  13 ANATOMY OF ANS SYMPATHETIC NERVOUS SYSTEM POST-GANGLIONIC FIBERS EXHIBIT VARICOSITIES THAT SERVE AS PRE-SYNAPTIC ELEMENTS IN MANY LOCATIONS ALONG THE FIBRE (SYNAPSES EN PASSENT), IN ADDITION TO THE TERMINAL SYNAPSE THE ADRENAL MEDULLA SERVES AS A POST-GANGLIONIC ELEMENT, RELEASING EPINEPHRINE (EPI) AS A HORMONE INTO THE CIRCULATION
     14  14 ANATOMY OF ANS SYMPATHETIC NERVOUS SYSTEM GANGLIA ARE LOCATED CLOSE TO THE SPINAL COLUMN (SHORT PRE- AND LONG POST-GANGLIONIC FIBERS) GANGLIA ARE OFTEN INTERCONNECTED LARGE RATIO OF POST- TO PRE-GANGLIONIC FIBER NUMBER
     15  15 ANATOMY OF ANS SYMPATHETIC NERVOUS SYSTEM THE ANATOMY OF SYMPATHETIC ANS IS STRUCTURALLY DESIGNED TO PRODUCE DIFFUSE SYSTEMIC RESPONSES BY SIMULTANEOUS TARGETTING OF MULTIPLE TISSUES IN ADDITION TO THE ROUTINE HOMEOSTATIC MAINTENANCE OF VITAL FUNCTIONS, THE SYMPATHETIC NERVOUS SYTEM IS DESIGNED TO RESPOND TO PHYSIOLOGICAL STRESS
     16  16 ANATOMY OF ANS PARASYMPATHETIC NERVOUS SYSTEM NO VARICOSITIES ON POST-GANGLIONIC FIBERS, NO SYNAPSES EN PASSENT
     17  17 ANATOMY OF ANS PARASYMPATHETIC NERVOUS SYSTEM GANGLIA ARE LOCATED CLOSE TO OR WITHIN THE TARGET TISSUE (LONG PRE- AND SHORT POST-GANGLIONIC FIBERS) GANGLIA ARE NOT INTERCONNECTED RATIO OF POST- TO PRE-GANGLIONIC FIBER NUMBER = 1
     18  18 ANATOMY OF ANS PARASYMPATHETIC NERVOUS SYSTEM THE ANATOMY OF ANS IS STRUCTURALLY DESIGNED TO PRODUCE PRECISE PIN-POINT RESPONSES BY TARGETTING OF SPECIFIC TISSUES IN ADDITION TO THE ROUTINE HOMEOSTATIC MAINTENANCE OF VITAL FUNCTIONS, THE PARASYMPATHETIC NERVOUS SYTEM IS DESIGNED TO LIMIT RESPONSES TO PHYSIOLOGICAL STRESS
     19  19 SIGNAL TRANSMISSION IN THE ANS - I PRINCIPLES
     20  20 SIGNAL TRANSMISSION IN ANS ALONG THE PRE- AND POST GANGLIONIC FIBERS, ELECTRICAL PROPAGATION OF ACTION POTENTIAL BY FAST Na CHANNELS INHIBITION BY LOCAL AND GENERAL ANESTHETICS OR TTX
     21  21 SIGNAL TRANSMISSION IN ANS BETWEEN PRE-GANGLIONIC NERVE ENDING AND POST-GANGLIONIC CELL BODY, CHEMICAL NEUROTRANSMISSION GANGLIONIC TRANSMITTER - ACETYLCHOLINE (ACh) / NICOTINIC CHOLINERGIC RECEPTORS POST-GANGLIONIC TRANSMITTERS: PARASYMPATHETIC - Ach / MUSCARINIC CHOLINERGIC RECEPTORS SYMPATHETIC - NOREPINEPHRINE (NE) / ADRENERGIC RECEPTORS
     22  22 ACETYLCHOLINE NOREPINEPHRINE
     23  23 SIGNAL TRANSMISSION IN THE ANS - II TRANSMITTER SYNTHESIS
     24  24 SIGNAL TRANSMISSION IN ANSTRANSMITTER SYNTHESIS ACh SYNTHESIZED IN CHOLINERGIC NERVE ENDINGS FROM AcCoA AND CHOLINE BY CHOLINE-ACETYL TRANSFERASE CHOLINE ENTERS NERVE ENDINGS VIA A SPECIAL TRANSPORT SYSTEM INHIBITION BY HEMICHOLINIUM. HOWEVER, THERE IS NO THERAPEUTIC USE IN GENERALIZED INHIBITION OF Ach SYNTHESIS
     25  25 SIGNAL TRANSMISSION IN ANSTRANSMITTER SYNTHESIS NE SYNTHESIZED IN ADRENERGIC NERVE ENDINGS BY A SERIES OF REACTIONS: 1. TYROSINE->DOPA / TYROSINE HYDROXYLASE (TH) A PATHWAY BRANCHING POINT (AMINO ACIDS TO NEUROTRANSMITTERS), ALLOSTERICALLY AND TRANSCRIPTIONALLY REGULATED ENZYME, SENSITIVE TO CATECHOLAMINES CONCENTRATION INHIBITION BY ALPHA-METHYL TYROSINE - TRANSIENT AND WITH SERIOUS SIDE EFFECTS USED RARELY (E.G. PHEOCHROMOCYTOMA)
     26  26 SIGNAL TRANSMISSION IN ANSTRANSMITTER SYNTHESIS 2. DOPA -> DOPAMINE / DOPA DECARBOXYLASE 3. DOPAMINE ENTERS SECRETORY VESICLES BY VESICULAR TRANSPORT (H+ ANTIPORTER) IN DOPAMINERGIC NERVES THIS IS THE TERMINAL STEP IN SYNTHESIS VESICULAR TRANSPORT INHIBITABLE BY RESERPIN (ANTI-HYPERTENSIVE DRUG, NO LONGER IN USE, SIDE EFFECT - DEPRESSION) OR GUANETHIDINE (CURRENTLY SELDOM USED)
     27  27 SIGNAL TRANSMISSION IN ANSTRANSMITTER SYNTHESIS 4. DOPAMINE -> NOREPINEPHRINE (NE)/ BETA HYDROXYLASE ALPHA-METHYLDOPA IS HANDLED BY ALL THE CATECHOLAMINES SYNTHETIC ENZYMES TO PRODUCE ALPHA-METHYL NE, A HIGHLY POTENT ALPHA-2-ADRENERGIC AGONIST, STORED AS NE ALPHA-METHYLDOPA (OR CLONIDINE) ACTS PRE-SYNAPTICALLY TO INHIBIT NE RELEASE AND CENTRALLY TO INHIBIT SYMPATHETIC OUTFLOW ANTI-HYPERTENSIVE
     28  28 SIGNAL TRANSMISSION IN THE ANS - III TRANSMITTER REMOVAL
     29  29 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-ACh ACh IS REMOVED BY NEURONAL (TRUE) ACETYLCHOLINE ESTERASE(AChE) NEURONAL AChE IS LOCATED IN CHOLINERGIC SYNAPSES IT IS A SERINE HYDROLASE AND ONE OF FASTEST ENZYMES KNOWN IT HYDROLYZES ACh TO CHOLINE AND ACETATE BY FORMING AN EXTREMELY UNSTABLE ACETATE ESTER WITH A SERINE AT THE ACTIVE SITE
     30  30 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-ACh AChE CAN BE INHIBITED BY: COMPETITIVE INHIBITORS (EDROPHONIUM, t1/2~2 MIN; AMBENONIUM, t1/2~3 HRS) REVERSIBLE COVALENT INHIBITORS (PHYSOSTYGMIN, NEOSTYGMINE, PYRIDOSTYGMINE THAT FORM RELATIVELY STABLE CARBAMOYL ESTER WITH THE ACTIVE SERINE) VIRTUALLY IRREVERSIBLE INHIBITORS, USUALLY ORGANOPHOSPHORUS COMPOUNDS (PARATHION, NERVE GASES, ECOTHIOPHATE)
     31  31 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-ACh EDROPHONIUM IS USED FOR DIAGNOSIS AND TITRATION OF ACh INHIBITORS DOSAGE IN MYASTHENIA GRAVIS AMBENONIUM, NEOSTYGMINE, PYRIDOSTYGMINE ARE USED IN MYASTHENIA GRAVIS PHYSOSTYGMIN AND ECOTHIOPHATE ARE USED IN POAG ORGANOPHOSPHORUS POISONING IS TREATED SYMPTOMATICALLY BY ATROPINE TO PREVENT MUSCARINIC OVERSTIMULATION AND BY PRALIDOXIME (TO RELEASE PHOSPHORUS ESTER FROM AChE AND PREVENT ”AGING”)
     32  32 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-NE NE IS REMOVED BY NEURONAL UPTAKE 1 AND BY TISSUE UPTAKE 2 (NOT ONLY INTO THE POST-SYNAPTIC CELL!) UPTAKE 1 AND 2 ARE ACTIVE, Na+ GRADIENT POWERED TRANSPORTERS UPTAKE 1 - HIGH-AFFINITY / LOW CAPACITY UPTAKE 2 - LOW AFFINITY / HIGH CAPACITY
     33  33 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-NE NE UPTAKE IS INHIBITED BY MANY DRUGS, THE MOST IMPORTANT ARE COCAIN (ACUTE) AND TRI-CYCLIC ANTIDEPRESSANTS (CHRONIC) ACUTE INHIBITION POTENTIATES THE ACTION OF ENDOGENOUSLY-RELEASED NE PERIFERALLY, ACUTE INHIBITION RESULTS IN INCREASED HEART RATE AND BLOOD PRESSURE (VASOCONSTRICTION) AND CENTRALLY BY A FEELING OF “HIGH” AND “RUSH” CHRONIC COCAIN USERS SUFFER FROM NASAL SEPTUM NECROSIS, DUE TO CELL DEATH FROM REPEATED ISCHEMIA
     34  34 SIGNAL TRANSMISSION IN ANSTRANSMITTER REMOVAL-NE NE IS METABOLIZED IN MANY TISSUES BY TWO ENZYMES: MONOAMINE OXIDASE (MAO) AND CATECHOL-O-METHYL TRANSFERASE (COMT) THE FINAL PRODUCTS RECOVERED IN URINE ARE VMA FROM PERIFERAL METABOLISM AND DOPEG FROM CENTRAL METABOLISM INHIBITION OF NE METABOLISM PREVENTS NE BREAKDOWN IN NON-SYNAPTIC SITES, HENCE NO ACUTE EFFECT INHIBITION OF MAO HAD BEEN USED TO TREAT HYPERTENSION (SEE BELOW) AND TO-DAY, TO TREAT PARKINSON
     35  35 SIGNAL TRANSMISSION IN THE ANS - IV TRANSMITTER RELEASE
     36  36 SIGNAL TRANSMISSION IN ANSTRANSMITTER RELEASE ACh IS ACUTELY AND MASSIVELY RELASED BY A BLACK WIDOW SPIDER VENOM COMPONENT (ALPHA-LATROTOXIN) AND THE RELEASE IS BLOCKED BY CLOSTRIDIUM BOTULINUM TOXIN CLOSTRIDIUM BOTULINUM TOXIN (BOTOX) IS USED IN NYSTAGMUS AND WRINKLE REMOVAL NE IS RELEASED BY INDIRECT SYMPATHOMIMETICS (AMPHETAMINE, EPHEDRINE, GUANETHIDINE, TYRAMINE...) THESE DRUGS ENTER THE NEURON VIA UPTAKE 1 AND THE GRANULE BY VESICULAR UPTAKE AND DISPLACE VESICULAR NE
     37  37 SIGNAL TRANSMISSION IN ANSTRANSMITTER RELEASE ACUTELY REPLACED VESICULAR NE IS PARTLY METABOLIZED AND PARTLY RELEASED INTO THE SYNAPSE, PROBABLY VIA REVERSAL OF UPTAKE 1 INHIBITION OF MAO POTENTIATES THE EFFECT OF INDIRECT SYMPATHOMIMETICS THE POOL OF NE AVAILABLE FOR RELEASE IS ONLY 10-20% OF TOTAL NEURONAL NE THIS LIMIT EXPLAINS THE PHENOMENON OF TACHYPHYLAXIS, I.E. DECREASING RESPONSES TO REPEATED EXPOSURES TO INDIRECT SYMPATHOMIMETICS
     38  38 ADRENERGIC SYNAPSE Beta1-receptor + M2-receptor
     39  39 SIGNAL TRANSMISSION IN ANSMAO AND “CHEEESE EFFECT” PERIPHERAL INHIBITION OF MAO PREVENTS INTESTINAL DEGRADATION OF TYRAMINE (FROM INTESTINAL FLORA, FOOD), WHICH SLOWLY REPLACES NE WITH FALSE TRANSMITTER OCTOPAMINE DECREASED RELEASE OF NE LEADS TO DECREASED BP, MOOD ELEVATION, BUT ALSO INCREASED DENSITY OF ALPHA-1 RECEPTORS (HYPERSENSITIVITY) LARGE AMOUNTS OF TYRAMINE (CHEESE, WINE, FISH...), WITH INHIBITED MAO, ACUTELY RELEASE SUFFICIENT NE TO PRODUCE HYPERTENSIVE CRISIS IN HYPERSENSITIVE VASCULAR MUSCLE
     40  40 SIGNAL TRANSMISSION IN THE ANS - V TARGET TISSUE RECEPTORS
     41  41 RECEPTORS IN ANSCHOLINERGIC NICOTINIC - SYMPATHETIC AND PARASYMPATHETIC GANGLIA, ADRENAL MEDULLA, STRIATED MUSCLE HETEROPENTAMER RECEPTOR-CHANNEL, Na+ CONDUCTANCE, EXTREMELY RAPID ACTIVATION/INACTIVATION PROLONGED ACTIVATION->DESENSITIZATION (E.G. FLACCID PARALYSIS) NATURAL AGONIST - ACh
     42  42 RECEPTORS IN ANSCHOLINERGIC MUSCARINIC - SMOOTH AND CARDIAC MUSCLE, EXOCRINE GLANDS GPCRs - TWO FAMILIES M1 (CORTICAL); M3 (GLANDULAR); M5 (CNS) SIGNAL TRANSDUCTION VIA PI-PLC-Ca PATHWAY M2 (CARDIAC); M4 (CNS) SIGNAL TRANSDUCTION VIA INHIBITION OF ADENYLYL CYCLASE OR DIRECT ACTIVATION OF CHANNELS (E.G. CARDIACK+ CHANNEL)
     43  43 RECEPTORS IN ANSADRENERGIC ENDOGENOUS STIMULATION BY NE AND EPI BETA - SMOOTH AND CARDIAC MUSCLE, LIVER, FAT CELLS, ALMOST EVERY CELL (INCLUDING ERYTHROCYTES) GPCRs - THREE FAMILIES BETA-1 (CARDIAC, KIDNEY, FAT); BETA-2 (SMOOTH MUSCLE); BETA-3 (FAT) SIGNAL TRANSDUCTION VIA STIMULATION OF ADENYLYL CYCLASE
     44  44 RECEPTORS IN ANSADRENERGIC ALPHA - SMOOTH MUSCLE, LIVER, FAT CELLS, EXOCRINE GLANDS, PRESYNAPTIC ADRENERGIC ELEMENTS GPCRs - TWO FAMILIES ALPHA-1 (SMOOTH MUSCLE, LIVER, FAT, GLANDS) SIGNAL TRANSDUCTION VIA STIMULATION OF PI-PLC-Ca PATHWAY ALPHA-2 (CNS, PRESYNAPTIC) SIGNAL TRANSDUCTION VIA INHIBITION OF ADENYLYL CYCLASE AND DIRECT ACTIVATION OF ION CHANNELS
     45  45 AUTONOMIC DRUGS CHOLINERGIC
     46  46 AUTONOMIC DRUGSCHOLINERGIC-MUSCARINIC AGONISTS URECHOLINE: ACh ANALOG, AChE-RESISTANT, SELECTIVITY FOR INTESTINAL AND URINARY TRACT THAN FOR CARDIAC RECEPTORS USE: ATONIC (POSTOPERATIVE) ILEUS, BLADDER PILOCARPINE: ALKALOID, PARTIAL AGONIST USE: POAG (TOPICAL)
     47  47 AUTONOMIC DRUGSCHOLINERGIC-MUSCARINIC ANTAGONISTS ATROPINE: BELLADONNA ALKALOID, NON-SPECIFIC, HIGH AFFINITY, CNS STIMULANT USE: MAINLY TREATMENT OF AChE-I POISONING, SINUS BRADYCARDIA, PRE-OPERATIVE, GI HYPERMOTILITY SCOPOLAMINE: BELLADONNA ALKALOID, CNS DEPRESSANT USE: MOTION SICKNESS, NAUSEA IPRATROPIUM: USE: ASTHMA, BRONCHOSPASM INHALATIONS PIRENZEPINE: SYNTHETIC, M1-SELECTIVE USE: PEPTIC ULCER
     48  48 AUTONOMIC DRUGSCHOLINERGIC DRUGS-SIDE EFFECTS AGONISTS: BRADYCARDIA, INCREASED SECRETIONS (BRONCHIAL, SALIVARY, URINARY, GI, SWEAT), INCREASED GI MOTILITY, BRONCHOSPASM, MICTURITION, MIOSIS ANTAGONISTS: DECREASED SECRETIONS BRONCHIAL, SALIVARY, URINARY, GI, SWEAT- E.G. XEROSTOMIA, DRY SKIN), TACHYCARDIA,, ELEVATED TEMPERATURE SET-POINT, CNS STIMULATION >DEPRESSION, MYDRIASIS, CYCLOPLEGIA, URINARY RETENTION, BRONCHODILATION
     49  49 AUTONOMIC DRUGS ADRENERGIC
     50  50 AUTONOMIC DRUGSADRENERGIC-BETA AGONISTS ISOPROTERENOL: SYNTHETIC NE ANALOG, BETA 1,2,3 USE: ASTHMA, OBSOLETE DOBUTAMINE: SYNTHETIC NE ANALOG, BETA 1 USE: CARDIOGENIC SHOCK SALBUTAMOL, SALMETEROL, TERBUTALINE: SYNTHETIC, BETA 2-SELECTIVE USE: ASTHMA, BRONCHOSPASM
     51  51 AUTONOMIC DRUGSBETA-ADRENERGIC ANTAGONISTS PROPRANOLOL: SYNTHETIC, BETA 1,2 SPECIFIC USE: ANGINA, HYPERTENSION, ARRHYTHMIAS, ANXIETY TREMOR, HYPERTHYROIDISM ALPRENOLOL: AS PROPRANOLOL, BUT PARTIAL AGONIST USE: AS PROPRANOLOL PRACTOLOL, METOPROLOL:BETA-1 SPECIFIC USE: AS PROPRANOLOL
     52  52 AUTONOMIC DRUGSBETA DRUGS-SIDE EFFECTS AGONISTS: TACHYCARDIA, TACHYARRHYTHMIAS, NERVOUSNESS, ANXIETY, LIMB TREMOR, INCREASED BMR ANTAGONISTS: BRONCHOSPASM, BRADYCARDIA, AV BLOCK, HEART FAILURE, COLD EXTREMITIES, FATIGUE, DEPRESSION, HYPOGLYCEMIA, DEPRESSION OF SIGNS OF HYPOGLYCEMIA (DIABETES!)
     53  53 AUTONOMIC DRUGSALPHA-ADRENERGIC AGONISTS METARAMINOL: ALPHA 1 SELECTIVE USE: MAINLY TO RAISE AND MAINTAIN BLOOD PRESSURE IN SHOCK PHENYLEPHRINE: ALPHA 1-SELECTIVE USE: DECONGESTANT CLONIDINE: ALPHA-2 PARTIAL AGONIST USE: HYPERTENSION, MIGRAINE
     54  54 AUTONOMIC DRUGSALPHA-ADRENERGIC ANTAGONISTS PHENOXYBENZAMINE: ALPHA 1,2, IRREVERSIBLE, UPTAKE-1 INHIBITOR USE: PHEOCHROMOCYTOMA PRAZOSIN: ALPHA 1-SELECTIVE USE: HYPERTENSION YOHIMBINE: ALPHA-2 SELECTIVE USE: NOT USED, BUT APHRODYSIAC?
     55  55 AUTONOMIC DRUGSALPHA DRUGS-SIDE EFFECTS AGONISTS: HYPERTENSION, REFLEX BRADYCARDIA ANTAGONISTS: HYPOTENSION, TACHYCARDIA, NASAL CONGESTION, IMPOTENCE
     56  56 AUTONOMIC DRUGSMIXED ADRENERGIC AGONISTS NE: ALPHA 1,2- BETA 1 SELECTIVE USE: NOT USED EPINEPHRINE: ALPHA/BETA NON-SPECIFIC USE: ANAPHYLACTIC SHOCK, ASTHMA, CARDIAC ARREST, VASOCONSTRICTOR IN LOCAL ANESTHETICS AND SUPERFICIAL BLEEDING
     57  57 AUTONOMIC DRUGSMIXED ADRENERGIC ANTAGONISTS LABETALOL: ALPHA-BETA USE: HYPERTENSION, ESPECIALLY IN PREGNANCY
     58  58 AUTONOMIC DRUGS ORGAN CONTROL - CVS
     59  59 AUTONOMIC CONTROL OF CVS
     60  60 AUTONOMIC CONTROL OF CVS ISO – VASODILATION, INCREASED HR, DECREASED MEAN BP, SYMPATHETIC REFLEX NE – VASOCONSTRICTION, INCREASED MEAN BP, VAGAL REFLEX, DECREASED HR EPI – VASODILATION & VASOCONSTRICTION, NO CHANGE IN MEAN BP, NO REFLEX, INCREASED HR
     61  61 AUTONOMIC CONTROL OF CVS DOPAMINE – (LOW - DARs) VASODILATION OF SPLANCHNIC BED, DECREASED PERIFERAL RESISTANCE, INCREASED URINE OUTPUT DOPAMINE – (MEDIUM -betaRs) VASODILATION OF SEVERAL BEDS, DECREASED PERIFERAL RESISTANCE, INCREASED URINE OUTPUT & CO DOPAMINE – (HIGH - alphaRs) VASODILATION & VASOCONSTRICTION, DECREASED PERIFERAL RESISTANCE, INCREASED URINE OUTPUT, INCREASED CO, INCREASED BP
     62  62 GLAUCOMA THERAPY Primary Open-Angle Glaucoma (POAG)
     63  63 GLAUCOMA CILLIARY BODY LENS IRIS CORNEA SCLERA PUPIL TRABECULAR MESH AQUEOUS OUTFLOW
     64  64 GLAUCOMA THERAPY Primary Open-Angle Glaucoma (POAG) ETHIOLOGY? INCREASED IOP (BUT ALSO NORMOTENSIVE GLAUCOMA) (BUT ALSO INCREASED IOP W/O GLAUCOMA – OCULAR HYPERTENSION) PROGRESSIVE DEATH OF GANGLION CELLS PROGRESSIVE DAMAGE TO OPTIC NERVE HEAD PROGRESSIVE LOSS OF VISION NEURODEGENERATIVE SYNDROME?
     65  65 PROGRESSIVE LOSS OF VISION
     66  66 POAG THERAPY DRUG CLASS – BETA BLOCKERS
     67  67 POAG THERAPY DRUG CLASS – MUSCARINIC STIMULATION
     68  68 POAG THERAPY DRUG CLASS – ALPHA AGONISTS
     69  69 POAG THERAPY DRUG CLASS – CARBONIC ANHYDRASE INHIBITORS
     70  70 POAG THERAPY DRUG CLASS – PROSTAGLANDINS
     71  71 ESSENTIAL HYPERTENSION THERAPY
     72  72 ESSENTIAL HYPERTENSION