Pharmacology notes

By: Mohammad Alauddin
PHARMACOLOGY
NOTES

December 3, 2015 2RABBE ZIDNI ILMA

1. Cholinergic Agonist:
 Direct Acting:
Cholinergic agonists (also known as parasympathomimetics) mimic the effects of acetylcholine by binding directly to cholinoceptors.
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:
Pralidoxime.
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.

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.

 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 activity.
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.

 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 transmission.
Barbiturates, BZDs, Carbamezepine, Gabapentin, Ethosuximide, Levetiracetam, Felbamate, Phenytoin,
Zonisamide.

 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:
Tramadol.

 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:
Spironolactone.
*Dec. Angiotensin II cause dec. Aldosterone which cause decreased water & sod retention. Plasma
vol is decreased and hence preload also decreased & BP lowered.

 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.

 Anti-Hypertensives:
a. Diuretics:
They cause increased water and sodium excretion leading to decreased extracellular volume & decreased cardiac output.
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.

 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:
Acetazolamide.
e. Osmotic Diuretics:
Mannitol, Urea.

 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:
Sucralfate.

 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 brain.
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 substance)
 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)

 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)

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

 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:
Aztreonam.
b. Other Antibiotics:
Bacitracin, Vancomycin, Daptomycin.

 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.
Tigecycline.
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)

 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:
Co-trimoxazole.
 UTI Antiseptics:
Methenamine, Nitrofurantoin(urine discoloration).
 Where Sulfonamides and Trimethoprim act ??
Pteridine + p-ABA + Glutamate Dihydrofolic Acid (Sulfonamide)
(microbes)
Dihydrofolic Acid Tetra hydro folic Acid (Trimethoprim)
(humans)
Tetrahydrofolic Acid Amino Acid Synthesis + Purine Synthesis + Thymidine
Synthesis
reduction
Dihydropteroate
synthetase

 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.

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

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

 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.

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

 Prostaglandins:
Misoprostol.
 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.

 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.

 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 birth.
 Major Adverse effect of Adenosine { is Dyspnea.
 Verapamil is contraindicated with CNS Depressants.
 Daily dose of Folic Acid is 400-500µg.

 Types of Pain:
a. Nociceptive: Pain due to sensitization of nociceptive nerve endings due to certain tissue damage.
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.

 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.

 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, Phenobarbital.
 P450 enzyme INHIBITORS: Cimetidine, Fluvoxamine, Isoniazid Quinidine, Macrolides, Chloramphenicol.

 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.

 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 atherosclerosis.
 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 dysfunction.
 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).

 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:
Hypothalamus A Pituitary Adrenal Gland
 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
glucocoricoids)
December 3, 2015RABBE ZIDNI ILMA 33
Corticotropin-
releasing
Factor
Corticotropi
n ACTH
Aldosterone
Corisol
Androgens

 Types of Insulin: Lispro, Aspart, Glulisine, Glargine, Detemir, Neutral Protamine Hagedorn
(NPH).
Drug Class Drugs MoA Plasma
Insulin
Risk of
HYPO
Sulfonylurea (1st Gen) Tolbutamide Increase Insulin secretion Increased Yes
Sulfonylurea (2nd
Gen) Glipizide;
Glimepiride
Increase Insulin secretion Increased Yes
Meglitinides Nateglinide;
Repaglinide
Increase Insulin secretion Increased Rarely
Biguanides Metformin Inhibiting Gluconeogenesis Decreased No
Glitazones Pioglitazone;
Rosglitazone
Binds to Peroxisome Perforator
Activated Receptor & decrease
Insulin Resistance
Highly
decreased
No
α-Glucosidase
Inhibitors
Acarbose;
Miglitol
Decrease breakdown of starch
and oligosaccharides & glucose
absorption.
Little or no
change
No
DPP-IV Inhibiotrs Sitagliptin;
Vildagliptin
Prolongs Incretin thus increase
insulin & decrease glucagon
production
Increased No

Poison or Syndrome Antidote Mechanism
Acetaminophen N-acetylcystine Accelerate detoxification of toxic
agents
Anticholinergic agents
(Muscarine)
Physostigmine Inhibits Acetylcholine-esterase
Benzodiazepene Flumazenil Antagonist
Cyanide Amyl nitrite pearls or Sodium
nitrite then Sod. thiosulfate
Provide alternative target
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 (pesticides);
Carbamates; Nerve gases
Atropine; Pralidoxime Pharmacological antagonist

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 /
sinistra
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
prescripto
q.h Every hour quaque hour et and et
q.s A sufficient
quantity
quantum sufficiat ft make fiat
Rx Prescription recipe gtt drop gutta
sig. / S. Directions signa mist mix mistura
stat. Immediately statim m.d.u used as directed more dicto
utendus
u.d as directed ut dictum mitte send mitte
q.o.d Every other day quaque otram
diem
mane in morning mane
noct. at night nocte non rep. no repeats non repetatur
36December 3, 2015RABBE ZIDNI ILMA

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
Tubocurarine.
Rivastigmine Alzheimer’s Disease
Ecothiphate Open Angle Glaucoma.

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 hypertension.

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

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

 Metabolism can happen in two phases.
 Phase I reactions involve hydrolysis, oxidation and reduction (results in low hydrophilicity).
 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 drug.
 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.

 Pharmacokinetic Models are imaginary compartments.
 Central Compartment represents plasma and tissues which rapidly equilibrate with drugs.
 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)

 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.

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

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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