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RABBE ZIDNI ILMA 21 April 2018 2
Rabbe Zidni Ilmaa

Qallat Heelati Anta Waseelati Adrikni

Ya Rasool Al ALLAH

Ass Salatu Wassalamo Alaika Ya

Rasool Al ALLAH

RABBE ZIDNI ILMA 21 April 2018 3

• 1. Central Nervous System.
• 2. Peripheral Nervous System.
• Peripheral NS is subdivided into Afferent and

Nervous Efferent System.

• Efferent System composed of Somatic and

Autonomic system.
• Autonomic further classified into Enteric,
Sympathetic n Parasympathetic.
• Enteric System is influenced by the Opoids.

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1. Cholinergic Agonist:
 Direct Acting:
Cholinergic agonists (also known as parasympathomimetics) mimic the effects of acetylcholine by binding directly to
Acetylcholine, Pilocarpine, Bethanecol, Carbachol.
 Indirect Acting:
Acetylcholinesterase is an enzyme that specifically cleaves acetylcholine to acetate and choline and, thus, terminates its actions.
Inhibitors of acetylcholinesterase indirectly provide a cholinergic action by prolonging the lifetime of acetylcholine.
Physostigmine, Neostigmine, Ecothiophate, Rivastigmine, Tacrine.
 Reactivation of Actylcholine-esterase:

2. Cholinergic Antagonist:
 Antimuscarinic:
Commonly known as antimuscarinics, these agents block muscarinic receptors, causing inhibition of all muscarinic functions.
Atropine, Scopolamine, Ipratropium.
 Ganglionic Bolckers:
Ganglionic blockers specifically act on the nicotinic receptors of both parasympathetic and sympathetic autonomic ganglia.
Except for nicotine, the other drugs mentioned in this category are nondepolarizing, competitive antagonists.
Mecylamine, Nicotine.
 Neuromuscular Bolckers:
These neuromuscular blockers are structural analogs of acetylcholine, and they act either as antagonists (nondepolarizing type)
or agonists (depolarizing type) at the receptors on the end plate of the neuromuscular junction. Neuromuscular blockers
are clinically useful during surgery for producing complete muscle relaxation
Atracurium, Doxacurium, Succinylcholine, Tubocurarine.

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1. Agrenergic Agonist:
 Direct Acting:
These drugs act directly on α or β receptors, producing effects similar to those that occur following stimulation of
sympathetic nerves or release of the hormone epinephrine from the adrenal medulla.
Dopamine, Epinephrine, Norepinephrine, Phenylephrine, Sameterol, Terbutaline.
 Indirect Acting:
These agents, which include amphetamine, cocaine and tyramine, may block the uptake of norepinephrine (uptake
blockers) or are taken up into the presynaptic neuron and cause the release of norepinephrine from the
cytoplasmic pools or vesicles of the adrenergic neuron. As with neuronal stimulation, the norepinephrine then
traverses the synapse and binds to the α or β receptors.
Amphetamine, Cocaine, Tyramine.
 Mixed:
Capacity both to stimulate adrenoceptors directly and to release norepinephrine from the adrenergic neuron.
Ephedrine, Pseudoephedrine.

2. Adrenergic Antagonist:
 α-Blockers:
Drugs that block α-adrenoceptors profoundly affect blood pressure.
Doxazocin, Prazocin, Terazocin, Tamsulosin.
 Β- Blockers:
All the clinically available B-blockers are competitive antagonists. Nonselective B-blockers act at both B1 and B2
receptors, whereas cardioselective B antagonists primarily block B1 receptors.
Atenolol, Esmolol, Labetalol, Pindolol.
 NT Uptake or Release:
Guanethidine, Reserpine.

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 Anti-Parkinsonism Drugs:
The disease is correlated with destruction of dopaminergic neurons in the substantia nigra.
Levodopa, Carbidopa, Amantidine, Apomorphine, Benzotropine.
 Alzheimer Drugs:
Major cause is loss of Cholinergic neurons.
Memantine, Rivastigmine, Tacrine.
 Anxiolytic Drugs:
a. Benzodiazepenes:
Alprazolam, Temazepam, Flurazepam, Lorazepam, Oxazepam.
b. Barbiturates:
Amobarbital, Phenobarbital, Pentobarbital, Thiopental.
c. Other Anxiolytic:
Buspirone(mediated by serotonin (5-HT1A) receptors), Hydroxyzine, Anti-depressants.
 CNS Stimulants:
a. Psychomotor Stimulants:
Psychomotor stimulants, cause excitement and euphoria, decrease feelings of fatigue, and increase motor
Amphetamine, Cocaine, Caffeine, Theobromine.
b. Hallucinogens:
The hallucinogens, or psychotomimetic drugs, produce profound changes in thought patterns and mood,
with little effect on the brainstem and spinal cord.
Lysergic Acid Diethylamide, Tetrahydro Cannabinol.

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 Anti-Depressants:
a. SSRIs:
Cetalopram, Fluoxetine, Fluvoxamine.
b. SNRIs:
Duloxetine, Venlafaxine.
c. Atypical Ads:
Bupropion, Trazodone.
d. TCAs (Older SNRIs):
Amitryptiline, Imipramine, Trimipramine.
e. MAO Inhibitors:
The MAO inhibitors may irreversibly or reversibly inactivate the mitochondrial enzyme (gut and
liver), permitting neurotransmitter molecules to escape degradation and, therefore, to both
accumulate within the presynaptic neuron and leak into the synaptic space.
Phenelzine, Selegiline.
f. Anti-Mania & Bipolar Disorders:
Valproic Acid, Lithium Salts.
 Anti-Epileptics:
By a variety of mechanisms, including blockade of voltage-gated channels (Na+ or Ca2+),
enhancement of inhibitory GABAergic impulses, or interference with excitatory glutamate
Barbiturates, BZDs, Carbamezepine, Gabapentin, Ethosuximide, Levetiracetam, Felbamate,
Phenytoin, Zonisamide.

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 Neuroleptic Drugs (Anti-Psychotic or Major Tranquilizers):
They inactivate Dopamine receptors.
a. Typical but low potency:
Chlorpromazine, Prochlorperazine.
b. Typical but high potency:
Haloperidol, Thiothixene.
c. Atypical:
Clozapine, Olanzapine, Risperidone.
 Opoids:
Activation of the opoid receptor decreases the Ca2+ influx and increases the K+ efflux. Decrease Ca+
influx decreases the release of excitatory NT and increased K+ efflux decreases the response of post-
synaptic neuron to excitatory NT (Glutamate).
a. Strong Agonists:
Meperadine, Methadone, Heroine, Fentanyl.
b. Moderate/Low Agonists:
Codeine, Propoxyphene.
c. Partial Agonists:
Buprenorphine, Pentazocine.
d. Antagonists:
Naloxone, Naltrexone.
e. Others:

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 Congestive Heart Failure(CHF):
a. Renin Angiotensin System Blockers:
These drugs block the enzyme that cleaves angiotensin I to form the potent vasoconstrictor angiotensin II. Also
diminish the rate of bradykinin inactivation. [Note: Vasodilation occurs as a result of the combined effects of
lower vasoconstriction caused by diminished levels of angiotensin II and the potent vasodilating effect of
increased bradykinin.] By reducing circulating angiotensin II levels, ACE inhibitors also decrease the secretion of
aldosterone, resulting in decreased sodium and water retention.
Captopril, Lisinopril, Quinapril, Ramipril, Enalapril (ACE Inhibitors)
ARBs are nonpeptide, orally active compounds that are extremely potent competitive antagonists of the angiotensin
type 1 receptor.
Losartan, Valsartan, Telmisartan (ARBs)
b. β-Blockers:
Atenolol, Metoprolol, Carvedilol.
c. Diuretics:
Diuretics decrease plasma volume and, subsequently, decrease venous return to the heart (preload). This decreases
the cardiac workload and the oxygen demand.
Bumetanide, Furesamide, Metolazone, Hydrochlorthiazide.
d. Direct Vasodilators:
Hydralazine, Isosorbide dinitrate, Sod nitroprusside.
e. Inotropic Agents:
Enhance cardiac muscle contractility and, thus, increase cardiac output.
Digitoxin, Digoxin, Dobutamine, Amrinone.
f. Aldosterone Antagonist:
*Dec. Angiotensin II cause dec. Aldosterone which cause decreased water & sod retention.
Plasma vol is decreased and hence preload also decreased & BP lowered.

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 Anti-Arrythmic Drugs:
Arrhythmias arise either from aberrations in impulse generation (abnormal automaticity) or
from a defect in impulse conduction.
a. Na+ Channel Blockers:
Quinidine, Procanamide, Propafenone.
b. β-Blockers:
Inhibits Phase 4 depolarization in SA & AV nodes.
Esmolol, Propranolol, Metoprolol.
c. K+ Channel Blockers:
Prolongs Phase 3 repolarization in ventricular muscle fibres.
Amiodarone, Sotalol, Dofetilide.
d. Ca2+ Channel Blockers:
Inhibits action potential in SA & AV nodes.
Diltiazem, Verapamil.
e. Others:
Adenosine, Digoxin.

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 Anti-Anginal Drugs:  Anti-Hyperlipidemics:
a. Organic Nitrates: a. HMG CoA Reductase Inhibitors:
Nitrates decrease coronary vasoconstriction or Analogs of HMG(precursor of Cholesterol). Because
spasm and increase perfusion of the of their strong affinity for the enzyme, all
myocardium by relaxing coronary arteries. In compete effectively to inhibit HMG CoA
addition, they relax veins, decreasing preload reductase, the rate-limiting step in cholesterol
and myocardial oxygen consumption. synthesis (de novo synthesis).
Isosorbide dinitrate & mononitrate, Nitroglycerin. Atorvastatin, Lovastatin, Provastatin, Simvastatin.
b. β-Blockers: b. Fibrates:
They decrease the oxygen demands of the Gemfibrozil, Fenofibrate.
myocardium by lowering both the rate and the c. Niacin:
force of contraction of the heart.
Niacin strongly inhibits lipolysis in adipose tissue,
Acebutolol, Atenolol, Metoprolol, Propranolol. the primary producer of circulating free fatty
c. Ca Channel Blockers: acids.
The calcium-channel blockers protect the tissue by d. Bile Acid Sequestrants:
inhibiting the entrance of calcium into cardiac Colestipol, Colestyramine, Colesevelam.
and smooth muscle cells of the coronary and
e. Cholesterol Absorption Inhibitors:
systemic arterial beds.
It inhibits intestinal absorption of dietary and biliary
Amlodipine, Diltiazem, Verapamil, Nicardipine,
cholesterol in the small intestine, leading to a
decrease in the delivery of intestinal cholesterol
to the liver. This causes a reduction of hepatic
cholesterol stores and an increase in clearance
of cholesterol from the blood.

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 Anti-Hypertensives:
a. Diuretics:
They cause increased water and sodium excretion leading to decreased extracellular volume & decreased cardiac
Bumetanide, Furosamide, Spironolactone, Hydrochlorthiazide.
b. β-Blockers:
Decrease Cardiac Output.
Atenolol, Carvedilol, Labetalol, Metoprolol.
c. ACE-Inhibitors:
ACE inhibitors decrease conversion into angiotensin II and increase bradykinin levels. Vasodilation occurs as a result
of the combined effects of lower vasoconstriction caused by diminished levels of angiotensin II and the potent
vasodilating effect of increased bradykinin.
Captopril, Enalapril,Fosinopril, Lisinopril, Ramipril.
d. ARBs:
Same As ACEIs but no Cough or Angiodema.
Candesartan, Losartan, Telmisartan, Valsartan.
e. Ca Channel Blockers:
Verapamil, Nifedipine, Nicardipine, Diltiazem, Amlodipine.
f. α-Blockers:
They decrease peripheral vascular resistance and lower arterial blood pressure by causing relaxation of both arterial
and venous smooth muscle.
Doxazocin, Prazocin, Terazocin.
g. Others:
Clonidine, Hydralazine, Sod. nitroprusside, Minoxidil, α-Methyldopa.

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 Diuretics:
a. Thiazides:
These drugs increase the concentration of Na+ and Cl- in the tubular fluid by decreasing
the reabsorption of Na in the distal convulated tubule.
Chlorothiazide, Chlorthalidone, Indapamide, Hydrochlorthiazide.
b. Loop Diuretics:
Loop diuretics inhibit the cotransport of Na+/K+/2Cl- in the luminal membrane in the
ascending limb of the loop of Henle. Therefore, reabsorption of these ions is
decreased. Most efficacious.
Bumetanide, Furosamide, Torsemide.
c. Potassium Sparing Diuretics:
Amiloride, Spironolactone, Triamterene.
d. Carbonic Anhydrase Inhibitors:
e. Osmotic Diuretics:
Mannitol, Urea.

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 Respiratory System:
a. Asthma:
β2-Adrenergic Agonists, Corticosteroids, Montelukast(Cysteinyl leukotriene antagonist), Theophylline, Omalizumab.
b. Allergic Rhinitis:
α-Adrenergic Agonists, Antihistamines, Corticosteroids, Cromolyn.
c. COPD:
β-Adrenergic Agonists, Corticosteroids, Ipratropium.
d. Cough:
Dextromethorphan, Opiates.
 GI Drugs:
Parietal cell is acted upon by Acetylcholine, Gastrin, Histamine & Prostaglandin. PG has inhibitory effect while others increase acid release.
a. Anti-Microbials:
Amoxycillin, Clarithromycin, Tetracycline, Metronidazole.
b. H2-Receptor Antagonist:
They are competitive antagonists of histamine and are fully reversible. These agents completely inhibit gastric acid secretion induced by
histamine or gastrin.
Cimetidine, Ranitidine, Famotidine.
c. PPIs:
They bind to the H+/K+-ATPase enzyme system (proton pump) of the parietal cell, thereby suppressing secretion of hydrogen ions into the
gastric lumen. The membrane-bound proton pump is the final step in the secretion of gastric acid
Esomeprazole, Omeprazole, Lansoprazole.
d. Prostaglandins:
Prostaglandin E2, produced by the gastric mucosa, inhibits secretion of HCl and stimulates secretion of mucus and bicarbonate.
Misoprostol (Prostaglandin E2 analog).
e. Antacids:
Aluminium Hydroxide, Magnesium Hydroxide.
f. Mucosal Protective Agents:

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 Anti-Emetics:
a. Phenothiazines:
Prochlorperazine (Block dopamine receptors)
b. 5-HT3 receptor blocker:
They selectively block 5-HT3 receptors in the periphery (visceral vagal afferent fibers) and in the
Ondansetron, Granisetron, Dolasetron.
c. Butyrophenones:
Droperidol, Haloperidol (Block Dopamine receptors).
d, Substance P/Neurokinin-I Blocker:
Aprepitant (It targets the neurokinin receptor in the brain and blocks the actions of the natural
 Anti-diarrheals:
a. Anti-motility agents:
Both are analogs of meperidine and have opioid-like actions on the gut, activating presynaptic
opioid receptors in the enteric nervous system to inhibit acetylcholine release and decrease
peristalsis. At the usual doses, they lack analgesic effects.
Diphenoxylate, Loperamide.
b. Adsorbents:
Bismuth subsalicylate, Methylcellulose, Aluminum hydroxide.
c. Agents that modify fluid and electrolyte transport:
Bismuth subsalicylate. (Traveller’s diarrhea)

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 Laxatives:
a. Irritants & Stimulants:
Senna, Bisacodyl.
b. Bulk Laxatives:
They form gels in the large intestine, causing water retention and intestinal distension,
thereby increasing peristaltic activity.
Methylcellulose, Psyllium seeds, Bran.
c. Stool softeners: (Emollient laxatives/Surfactants)
Docusate sodium, Docusate calcium, Docusate potassium.
d. Lubricant Laxatives:
Mineral oil & Glycerin suppositories. (Facilitate the passage of hard stools)

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 Erectile Dysfunction (PDE-5 Inhibitors):
Sildenafil, Vardenafil.
 Osteoporosis:
Alendronate, Ibandronate, Calcitonin, Zoledronic Acid.
 Obesity:
Orlistat (lipase inhibitor), Sibutramine (anorexiant), Phentermine (anorexiant).

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 Cell Wall Inhibitors:
These drugs interfere with the last step of bacterial cell wall synthesis (transpeptidation or cross-
linkage), resulting in exposure of the osmotically less stable membrane. Cell lysis can then
occur, either through osmotic pressure or through the activation of autolysins. These drugs are
thus bactericidal.
a. B-lactams:
i- Penicillins:
Amoxicillin, Ampicillin, Piperacillin, Oxacillin, Methicillin, Nafcillin.
ii- Cephalosporins:
1st Generation (Cefadroxil, Cefalexin)
2nd Generation (Cefaclor, Cefoxitin, Cefprozil)
3rd Generation (Cefixime, Cefotaxime, Cefibuten, Ceftriaxone)
4th Generation (Cefepime)
iii- Carbapenems:
Meropenem, Imipenem.
Iv- Monobactam:
b. Other Antibiotics:
Bacitracin, Vancomycin, Daptomycin.

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 Protein Synthesis Inhibitors:
a. Tetracyclines:
The drug binds reversibly to the 30S subunit of the bacterial ribosome, thereby blocking access of
the amino acyl-tRNA to the mRNA-ribosome complex at the acceptor site. By this mechanism,
bacterial protein synthesis is inhibited.
Doxycycline, Minocycline, Tetracycline.
b. Glycylcyclines:
Also binds reversibly to the 30S of the ribosomal unit.
c. Aminoglycosides (derived from Streptomyces have -mycin suffixes, whereas those derived from
Micromonospora end in –micin):
Also binds reversibly to the 30S ribosomal subunit & inhibiting protein translation.
All aminoglycosides should be given parenterally except neomycin.
Amikacin, Gentamicin, Neomycin, Tobramycin, Streptomycin.
d. Macrolides/Ketolides:
The macrolides bind irreversibly to a site on the 50S subunit of the bacterial ribosome, thus
inhibiting the translocation steps of protein synthesis.
Azithromycin, Clarithromycin, Erythromycin, Telithromycin.
e. Chloramphenicol (50S subunit)
f. Clindamycin
g. Dalfopristin/Quinupristin (50S subunit)
h. Linezolid (binds to a site on the 50S subunit near the interface with the 30S subunit)

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 Fluoroquinolones:
These drugs enter the bacterium by passive diffusion through water-filled protein channels
(porins) in the outer membrane and then inhibit the replication of bacterial DNA by interfering
with the action of DNA gyrase (topoisomerase II) and topoisomerase IV during bacterial growth
and reproduction.
Nalidixic Acid, (Ciprofloxacin, Ofloxacin, Norfloxacin), Levofloxacin, Moxifloxacin.
 Folate Synthesis Inhibitors:
Silver Sulfadiazene, Sulfamethoxazole, Sulfasalazine, Sulfisoxazole.
 Folate Reduction Inhibitors:
Pyrimethamine, Trimethoprim.
 Combination of Above two:
 UTI Antiseptics:
Methenamine, Nitrofurantoin(urine discoloration).

 Where Sulfonamides and Trimethoprim act ??

Pteridine + p-ABA + Glutamate synthetase Dihydrofolic Acid (Sulfonamide) (microbes)
Dihydrofolic Acid Tetra hydro folic Acid (Trimethoprim) (humans)

Tetrahydrofolic Acid Amino Acid Synthesis + Purine Synthesis + Thymidine Synthesis

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 Anti-TB drugs:
Isoniazid(altering cell membrane function), Ethambutol(inhibit normal arabinogalactin cell
wall), Rifampicin(inhibits synthesis of mRNA), Pyrazinamide(unknown). (1st line drugs)
Aminoglycosides, Macrolides, Cycloserine, Ethionamide,. (2nd line drugs)
 Anti-Leprosy Drugs:
Clofazimine, Dapsone, Rifampin.
 Subcutaneous and Systemic Mycoses:
Amphitericin B, Fluconazole, Ketoconazole, Micafungin, Capsofungin.
 Cutaneous Mycoses:
Butoconazole, Griseofulvin, Nystatin, Terbinafine.

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 Amebiasis:
Chloroquine, Emetine, Dehydroemetine, Metronidazole, Paramomycin.
 Malaria:
Artemisinin, Primaquine, Pyrimethamine, Mefloquine, Quinine/Quinidine.
 Trypanosomiasis:
Benznidazole,Suramin, Nifurtimox, Melarsoprol.
 Leishmaniasis:
Sodium stibogluconate.
 Toxoplasmosis:
 Giardiasis:
Metronidazole, Nitazoxanide, Tinidazole.
 Anti-Nematodes (Ascaris, Hookworms, Filarias. Enterobius, Trichinella):
Ivermectin, Pyrantel pamoate, Diethylcarbamazine.
 Anti-Trematodes (Schistosomes):
 Anti-Cestodes (Tapeworms):
Niclosamide, Albendazole.

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 Respiratory Virus Infections:
Amantadine, Rimantadine, Ribavirin, Zanamivir.
 Hepatic Viral Infections:
Interferon, Adefovir, Entecavir.
 HIV Infections:
Abacavir, Didanosine, Etravirine, Fosamprenavir, Tenofovir.

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 Antimetabolites:
Methotrexate, Gemcitabine, 6-Mercaptopurine, Cytarabine.
 Antibiotics:
Bleomycin, Doxorubicin, Daunorubicin.
 Alkylating Agents:
Cyclophosphamide, Busulfan, Ifosfamide, Mechlorethamine, Streptozocin.
 Microtubule Inhibitors:
Docetaxel, Vincristine, Vinblastine, Vinorelbine.
 Steroids, Hormones and their Antagonists:
Prednisone, Tamoxifen, Estrogens, Goserelin, Letrozole.
 Monoclonal Antibodies:
Cetuximab, Rituximab.
 Others:
Asparaginase, Interferons, Cisplatin, Etoposide, Imanitib, Topotecan, Oxaliplatin.

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Aspirin, Diclofenac, Indomethacin, Fenamates, Ibuprofen, Piroxicam, Sulindac.
 CoX-2 Inhibitors:
 Other Analgesics:
 Anti-Arthritis:
Adalimumab, Anakinra, Infliximab, Gold salts, D-Penicillamine.
 Drugs for Gout:
Allopurinol, Colchicine, Probenecid, Sufinpyrazone.

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 Prostaglandins:
 H1-Antihistamines:
H1 receptors present in exocrine excretion, bronchial smooth muscles, intestinal smooth
muscles and sensory nerve endings.
H1 & H2 receptors present in CVS & Skin.
H2 receptors found only in stomach.
First Generation (Chlorpheniramine, Diphenhydramine, Dimenhydrinate)
Second Generation (Cetrizine, Fexofenadine, Loratadine)
 Migraine Headache:
Almotriptan, Naratriptan, Riztriptan, Sumatriptan, Zolmitriptan.

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 Substance P Blocker: APREPITANT
 Isoniazid written as INH represents IsoNicotinic acid Hydrazide.
 Uterus Parts: Fundus; Body; Corporis; Cervix.
 Fallopian tube connects ovary with uterus.
 Female Reproductive System: Ovary; Fallopian Tube; Uterus; Vagina.
 Embryo life cycle: 1-8weeks
 Fetus: After 8weeks
 Uterus walls: Endometrium Myometrium; Parametrium.
 Endo & Myometrial walls involved in the production of Prostaglandins.
 F2α: Vasoconstrictor(dysmenorrhia)
 E2: Vasodilator (menorraghia)
 I2: Myometrial relaxation; vasodialtion; anti-platelets.
 Menarchie: First Periods of a woman (8-16yrs) Avg: 13yrs.
 Most regularized periods:20-40yrs.
 Average cycle: 28days (24-36days)
 Average Flow: 3-7days; Typical Flow: 5days
 Starts light then heavy then again light.
 ACEIs contraindicated in bilateral renal artery stenosi.
 Desmopressine used in nocturnal enuresis.

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 Ovulation: Release of ova from the ovary.
 Range: Day 8th-20th (14th day).
 A woman has almost 2000days of periods in her life (400cycles) except pregnancy and illness.
 Menstrual cycle: Menstruation; Proliferation; Ovulation; Secretory.
 Menstruation: Day 1-5.
 Proliferation: Day 6-13.
 Ovulation: Day 14th.
 Secretory: Day 15-28.
 Graffian Follicle before ovulation secrete estrogen and after ovulation is is known as Corpeus
Luteum and secretes Progesterone which develops thick wall of uterus (endometrium).
 Cervix: Neck of uterus.
 Basal Body Temperature (BBT):Temp at relaxed body state.
 Nociceptives: Nerve Endings that sense pain.
 Anhedonia: An unprovoked stimuli could result in painful sensation normally not painful.
 Gestational Diabetes: Diabetes that occurs during pregnancy and soon disappears after child
 Major Adverse effect of Adenosine { is Dyspnea.
 Verapamil is contraindicated with CNS Depressants.
 Daily dose of Folic Acid is 400-500µg.

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 Types of Pain:
a. Nociceptive: Pain due to sensitization of nociceptive nerve endings due to certain tissue
b. Neuropathic: Any lesion or damage to the nerve fibres, resulting in pain. E.g. Diabetic
Peripheral Neuropathy (DPN)
c. Mixed: Low back pain; Ankolysing Spondylitis.
 Mechanism of Feeling pain:
a. Reception: Stimulation of nociceptives by PGs.
b. Conduction: From Nerve ending to brain.
c. Perception: Cortex & Thallamus receive impulse.
d. Suffering: Reaction.
 Pain & Inflammation Mediators: Histamine; Bradykinins; Kinins; Substace P; PGs.
 PGs increase blood flow to the injury site and accelerate the transfer of WBCs and Platelets.
 Inflammation: Natural response to the injury to inactivate causative agent.
 PGs increase vascular permeability and WBCs migration and sensitization of Nociceptives.
 PAE: The postantibiotic effect (PAE) is a persistent suppression of microbial growth that occurs
after levels of antibiotic have fallen below the MIC.
 Myasthenia gravis: (Muscle weakness)Autoimmune disorder due to blockade of cholinoceptors
by circulating antibodies. Treatment by Neostigmine, physostigmine.
 Diabetes Type-I: Insulin Dependant; when the body stops making insulin. Also called brittle or
labile diabetes.
 Diabetes Type-II: Non Insulin Dependant; body is making insulin either in insufficient amount
or the cells do not respond to body made insulin.

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 Menorrhagia: Excess Blood flow in frequency, duration or amount; upto 80ml. (20-30ml)
 PGE2: Inc. vasodilation; Dec. platelet adhesion & aggregation…… Inc. Blood Flow.
 PGF2α: Inc. vasospasm; Inc. uterine contractions…… Painful Menses.
 Hyperalgesia: Intensed Pain.
 Articular: Bones & Joints.
 Non-Articular: Tendons; Ligaments; Bursa.
 Epicondyl: Bony projections at the end of long bones.
 Sprains: Injury to the ligament.
 Stills Disease: Juvenile Idiopathic Arthritis.
 In enteral route duodenum is the major site for drug absorption.
 Bioavailability: Fraction of the drug that reaches the blood stream.
 Total body water in 70kg human=42litres.
 Intracellular( 28ltrs) + Interstitial(10ltrs) + Plasma(4ltrs)= 42 litres.
 Volume of Distribution: Hypothetical volume of fluids into which drug is dispersed.
 Albumin has the strongest affinity with anionic and hydrophobic drugs.
 Each cell may have 10,000 receptors e.g. heart has B-receptor for norepinephrine and
muscarinic receptor for acetylcholine.
 Potassium is administered as Slow IV infusions.

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 Receptor: Biological molecule to which drug binding produce measurable response.
 Receptor Types:
a. Ligand gated Ion Channels: GABA (Fastest reception)
b. G-protein Coupled: Sildenafil
c. Enzyme Linked: Insulin
d. Intracellular Receptors: Steroids (Slowest reception)
 Competitive Antagonism: Same site on same receptor e.g. Prazocin & Norepinephrine.
 Non-competitive Antagonism/Allosteric: Different sites on same receptor e.g. Protamine & Heparin.
 Functional/Physiologic Antagonism: Different receptors involved e.g. Epinephrine & Histamine.
 Quantal-Dose Response: Study of dose-response on a population that responds.
 Therapeutic Index: Ratio of toxic dose to effective dose.
 Drugs with High Therapeutic Index is SAFER to use.
 Catecholamines have brief duration & rapid onset of action and do not cross BBB.
 Non-catecholamines have longer duration of action and can be administered orally.
 Narcolepsy: Narcolepsy is a relatively rare sleep disorder that is characterized by uncontrollable bouts
of sleepiness during the day. It is sometimes accompanied by catalepsy, a loss in muscle control, or
even paralysis brought on by strong emotions, such as laughter.
 P450 enzyme INDUCERS: Smoking, Omeprazole, Rifampicin, Carbamazepine, Phenytoin,
 P450 enzyme INHIBITORS: Cimetidine, Fluvoxamine, Isoniazid Quinidine, Macrolides,

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 INR: A laboratory test to called INTERNATIONAL NORMALISED RATIO measures the time it takes for a
blood sample to clot and compares it with average clotting time(5-11min). Average CT measured by
Dale’s method (taking a blood sample in a thin capillary and the end of tube is broken every 30sec until
clot formed).
 Bleeding Time: It is the time until which the blood continues oozing from the injured site(1-5min).
Measured by Duke’s method (pricking a finger and taking the blood sample every 30sec. on a filter
paper until blood stops coming).
 Norepinephrine is ineffective orally.
 Alpha Methyldopa is the only ani-hypertensive used in pregnancy.
 Major side effect of Doxorubicin is tissue necrosis.
 Oxidation is Phase-I reaction.
 In overdosage of Digoxin we use Antidote FAB fragment.
 Digitoxin toxicity reflects in ECG as to prolong PR interval.
 Myxodema (Hypothyroidism) treated by Thyroid sodium.
 Vit A daily dose is 30,000-50,000 IU.
 Vit C daily dose is 400mg for both men and women.
 Floxapen (flucloxacillin) is resistant to penicilinnase.
 Chelators are drugs that form covalent bonds with cationic metals.
 Antibiotics showing Conc. dependant killing involve aminoglycosides, flouroquinolones, carbapenems.
 While those showing time dependant killing involve β-lactams, macrolides, clindamycin.
 Narrow Spectrum: Covering single or limited group of microbes. e.g Isoniazid.
 Extended Spectrum: Covering gram +ve and also significant gram –ve bacteria. e.g Ampicillin
 Broad Spectrum: Covering a wie variety of microbes; also the beneficial microbes causing Candida
albicans. e.g Tetracyclines, Chloramphenicol.

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 Angina Pectoris: It is a characteristic sudden, severe, pressing chest pain radiating to the neck, jaw,
back, and arms. It is caused by coronary blood flow that is insufficient to meet the oxygen demands of
the myocardium, leading to ischemia.
 Stable Angina(Typical): It is characterized by a burning, heavy, or squeezing feeling in the chest. It is
caused by the reduction of coronary perfusion due to a fixed obstruction produced by coronary
 Unstable Angina: In unstable angina, chest pains occur with increased frequency and are precipitated
by progressively less effort.(lies b/w Angina and MI)
 Prinzmetal/Variant/Vasopastic Angina: It is an uncommon pattern of episodic angina that occurs at
rest and is due to coronary artery spasm. Symptoms are caused by decreased blood flow to the heart
muscle due to spasm of the coronary artery.
 Mixed Angina: Patients with advanced coronary artery disease may present with angina episodes during
effort as well as at rest, suggesting the presence of a fixed obstruction associated with endothelial
 Angiodema: Angioedema or Quincke's edema is the rapid swelling (edema) of
the dermis, subcutaneous tissue, mucosa and submucosal tissues. Also known as angioneurotic
oedema. Due to increased bradykinin(vasodilator) levels which occurs in ACEIs treatment.
 Hydralazine causes Lupus Like Syndrome.
 Hypothyroidism & Antidepressants causes Weight Gain.
 Low Density Lipoproteins LPLs act as Carriers of cholesterol in Plasma.
 HDLs cause atherosclerosis.
 Sites of Antibiotics: Cell wall synthesis(B-lactams); metabolism(sulfonamides); protein
synthesis(macrolides); nucleic acid function or synthesis(cipro); cell membrane function(isoniazid).

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 Structure: Inner part Medulla secreting Epinehprine. Outer part cortex. Cortex is further divided
into three parts. Inner most of cortex is Reticularis which secretes Adrenal androgens; Middle
part called Fasciculata secreting Glucocorticoids and outer most is the Glomerulosa which
secretes Mineralocorticoids.
 Physiology: Aldosterone
Hypothalamus A Pituitary Adrenal Gland Corisol
Corticotropin- Corticotropin
releasing Factor ACTH Androgens

 Glucocorticoids & Mineralocorticoids are collectively known as Corticosteroids.

 Cortisol also acts as a feedback mechanism and inhibits both processes from hypothalamus to
anterior pituitary and pituitary to adrenal glands.
 Glucocorticoids:
a. Short Acting (1-12 hrs): Hydrocortisone, Cortisone.
b. Intermediate Acting (12-36hrs): Prednisone, Prednisolone, Methylprednisolone.
c. Long Acting (36-55hrs): Betamethasone, Dexamethasone.
 Mineralocorticoids: Deoxycorticosterone, Fludrocortisone.
 Glucocorticoids act as anti inflammatory by inhibiting PGs and Leukotrienes & also
redistribute WBCs to other body sites; also reduce histamine release from mast cells and
basophils; decrease ability of macrophages and leukocytes to antigens and mitogens.
 Also used in Treatment of Allergies and Diagnosis of Cushing’s disease (Overproduction of

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 Types of Insulin: Lispro, Aspart, Glulisine, Glargine, Detemir, Neutral Protamine
Hagedorn (NPH).

Drug Class Drugs MoA Plasma Risk of

Insulin HYPO
Sulfonylurea (1st Gen) Tolbutamide Increase Insulin secretion Increased Yes

Sulfonylurea (2nd Gen) Glipizide; Increase Insulin secretion Increased Yes

Meglitinides Nateglinide; Increase Insulin secretion Increased Rarely
Biguanides Metformin Inhibiting Gluconeogenesis Decreased No

Glitazones Pioglitazone; Binds to Peroxisome Perforator Highly No

Rosglitazone Activated Receptor & decrease decreased
Insulin Resistance
α-Glucosidase Acarbose; Decrease breakdown of starch Little or no No
Inhibitors Miglitol and oligosaccharides & glucose change
DPP-IV Inhibiotrs Sitagliptin; Prolongs Incretin thus increase Increased No
Vildagliptin insulin & decrease glucagon

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Poison or Syndrome Antidote Mechanism
Acetaminophen N-acetylcystine Accelerate detoxification of
toxic agents
Anticholinergic agents Physostigmine Inhibits Acetylcholine-
(Muscarine) esterase
Benzodiazepene Flumazenil Antagonist
Cyanide Amyl nitrite pearls or Sodium Provide alternative target
nitrite then Sod. thiosulfate
Digitalis Digoxin Immune Fab
Methanol Ethylene Glycol Fomepizole Reduce metabolic activation
Heparin Protamine sulphate Antagonist
Lead Dimercaptosuccinic aid Chelators
Mercury; Arsenic; Gold Dimercaprol Chelators
Methemoglobinemia Methylene Blue Chelators
Opiates Naloxone; Naltrexone Antagonist
Organophosphates Atropine; Pralidoxime Pharmacological antagonist
(pesticides); Carbamates;
Nerve gases

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Abbreviations Meanings Latin Origin Abbreviations Meanings Latin Origin
a.c before meals ante cibum ad Upto ad
a.m Morning ante meridiem a.d Right ear Auris dextra
b.i.d Twice a day bis in die admov. apply admove
gtt drop gutta agit stir/shake agita
h.s at bed time hora somni a.r / a.s left ear auris laeva /
p.c After food post cibum a.u both ears auris utraque
p.m Afternoon post meridiem bol. single large dose bolus
p.o Orally per oral BUCC in cheek bucca
p.r.n as needed pro re nata c.c with food cum cibo
q.d Every day / daily quaque die e.m.p as directed ex modo
q.h Every hour quaque hour et and et
q.s A sufficient quantum ft make fiat
quantity sufficiat
Rx Prescription recipe gtt drop gutta
sig. / S. Directions signa mist mix mistura
stat. Immediately statim m.d.u used as directed more dicto
u.d as directed ut dictum mitte send mitte
q.o.d Every other day quaque otram mane in morning mane
noct. at night nocte non rep. no repeats non repetatur
RABBE ZIDNI ILMA 21 April 2018 38
Cholinergic Agonists
Drugs Therapeutic Uses
Bethanecol Treatment of Urinary Retention
Carbachol Miosis during Ocular Surgery; Topically to
reduce IO pressure.

Pilocarpine Reduce intraocular pressure in open angle &

narrow angle glaucoma

Physostigmine Increase bladder motility; reverse CNS effects

of Antidepressants & Atropine.

Neostigmine Treat Myasthenia Gravis; Antidote for


Rivastigmine Alzheimer’s Disease

Ecothiphate Open Angle Glaucoma.

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Cholinergic Antagonists
Drugs Therapeutic Uses
Atropine Mydriasis and cycloplegia prior to refraction.
Organophosphate poisoning.
Suppress respiratory secretions.
Scopolamine In obstetrics, to produce amnesia and
sedation(with morphine)
Motion Sickness.
Ipratropium Asthma

Nicontine None

Mecamylamine Treatment of moderate to severe


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Adrenergic Agonists
Drugs Receptor Specificity Therapeutic Uses
Epinephrine α1, α2, β1, β2 Acute Asthma; Anaphylactic
Shock; In local anesthetics.
Norepinephrine α1, α2, β2 Shock Treatment
Isoproterenol β1, β2 Cardiac Stimulant
Dopamine α1, β1, Dopaminergic CHF, Raise BP
Dobutamine β1 CHF
Methoxamine α1 Supraventricular tachycardia
Clonidine α2 Treatment of hypertension
Phenylephrine α1 Nasal decongestant
Albuterol; Terbutaline β2 Short acting bronchospasm
Salmeterol; Formoterol β2 Long acting bronchospasm
Amphetamine α, β, CNS CNS stimulant in children,
ADHD, Narcolepsy.
Ephedrine; Pseudo Ephedrine α, β, CNS Asthma, Nasal decongestant

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Adrenergic Antagonists
Drugs Receptor Specificity Therapeutic Uses
Propranolol β1, β2 Hypertension, Glaucoma,
Migraine, Angina pectoris, MI
Nadolol; Timolol β1, β2 Glaucoma, Hypertension
Atenolol; Esmolol; Metoprolol β1 Hypertension
Pindolol (Partial Agonist) β1, β2 Hypertension
Carvedilol; labetalol α1, β1, β2 Hypertension, CHF

*Pindolol and Aebutolol are Partial Agonists

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 Metabolism can happen in two phases.
 Phase I reactions involve hydrolysis, oxidation and reduction (results in low
 Phase II reactions involve glucoronidation, sulfonation, acetylation, methylation,
conjugation with glutathione or amino acids(cause high hydrophilicity).
 Phase I may or may not precede Phase II.
 Clearance is the volume of plasma cleared off drug per unit time. Its unit is ml/min.
 Pharmacokinetics involves the movement of drug or its metabolites into or out of the
body and also evaluates its metabolism rates.
 Zero order kinetics is independent of drug concentrations; usually seen when reaction
system is saturated.e.g Metabolism of Phenytoin, Constant rate IV Infusion.
 In First order kinetics rate of drug elimination at particular time is directly proportional
to the amount of drug in the body at that time; Semi Logarithmic plot of Plasma Drug
Conc vs time is a straight line.
 Elimination rate constant, Vd, clearance and half life are independent of the dose of the
 First order kinetics is also known as monoexponential kinetics; in which rate of reaction
is directly proportional to the drug concentration in the reaction.
 Mixed Order Kinetics depends on the dose of the drug and are thus known as Dose
Dependant or Non-Linear Kinetics. Generally described by Michelis Menten Equation.

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 Pharmacokinetic Models are imaginary compartments.
 Central Compartment represents plasma and tissues which rapidly equilibrate with
 Peripheral Compartments represents tissues or organs which equilibrate slowly.
 Number and site of compartments is determined by the blood perfusion capacity and
drug physicochemical properties.
 Michelis Menten Equation:
-dc = Vmax x C
dt Km + C
 Plasma albumin has 4 binding sites .i.e Warfarin, Diazepam, Tamoxifen, Digoxin.
 Total body tissue comprises 40% of the total body.
 Pharmaceutical Equivalents: If two drugs contain same amount of active ingredient in
same dosage form. They may contain different excipients.
 Pharmaceutical Alternatives: If two drugs contain same drug molecule but in different
chemical form e.g different salt or strength.
 Bioavailability: Rate and extent to which a drug is absorbed from the site of
administration and become available at the site of action.
 Bioeuivalence: Drugs showing same bioavailability are said to be bioequivalent.
 Essentially Similar Product: A copy of the research or Innovator Product. (ME 2)

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 Therapeutic Equivalents: If two drugs provide the same desired therapeutic effect with
same safety and efficacy.
 Cmax: Maximum Drug Plasma concentration partly depends on the rate of release of drug
from the formulation.
 Tmax: Time required to reach maximum Plasma drug concentration; also dependant on
rate of drug release.
 T1/2: Elimination half life.
 Mean Residence Time (MRT): Time a drug molecule spends in the body before it gets
excreted out.
 Metabolism reactions are also said to be Bioactivation reactions.
 Metabolism is basically involved in converting a drug more hydrophilic to facilitate its
excretion from the body.

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Bacteria Disease Caused
Actinomyces Respiratory disease; Cavities
Bacillus anthracis Anthrax
Clostridium tetani Tetanus
Cornyebacterium diphteriae Diphtheria
Mycobacterium tuberculosis Tuberculosis
Staphylococcus aureus; S. epidermis
Streptococcus pneumonia; S. pyogenes Alpha hemolysis; Beta hemolysis.
Mycoplasma Walking pneumonia
Listeria Fetal pathogens; Newborn meningitis
Nocardia Respiratory Diseases

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Bacteria Disease Caused
Borrelia Lymes Disease
Campylobacter GI Diseases
Chlamydia STD; Trachoma(blindness); Pneumonia
Enterobacter UTIs
Escherichia coli Normal GI tract
Helicobacter Peptic Ulcer
Hemophilus influenzae Upper RTIs; Epiglottitis; Meningitis; Otitis
Legionella Pneumonia
Neisseria gonorrheae; N. meningitidis STD; Meningitis
Salmonella typhi Typhoid
Shigella Dysentry
Vibrio cholera Cholera
Yersinia Plague
Treponema pallidum Syphilis
Pseudomonas Nosocomiel Infections(acquired at hospial).

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