Pharmacology

PHARMACOLOGY NOTES
Drugs Affecting ANS
Nervous
System
23 December 2014
1. Central Nervous System.

2. Peripheral Nervous System.
Peripheral NS is subdivided into Afferent and
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.
vinupv.jak@gmail.com
Cholinergic Drugs
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.
23 December 2014
Adrenergic Drugs
1. Agrenergic Agonist:
Direct Acting:
These drugs act directly on or 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
or receptors.
Amphetamine, Cocaine, Tyramine.
Mixed:
Capacity both to stimulate adrenoceptors directly and to release norepinephrine from the adrenergic neuron.
Ephedrine, Pseudoephedrine.
2. Adrenergic Antagonist:
-Blockers:
Drugs that block -adrenoceptors profoundly affect blood pressure.
Doxazocin, Prazocin, Terazocin, Tamsulosin.
- 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.
23 December 2014
CNS Drugs
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.
23 December 2014
CNS Drugs
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.
23 December 2014
CNS Drugs
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.
23 December 2014
CVS Drugs
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. -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.
23 December 2014
CVS Drugs
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. -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.
23 December 2014
CVS Drugs
Anti-Anginal Drugs:
a. Organic Nitrates:
Nitrates decrease coronary vasoconstriction or spasm and
increase perfusion of the myocardium by relaxing
coronary arteries. In addition, they relax veins, decreasing
preload and myocardial oxygen consumption.
Isosorbide dinitrate & mononitrate, Nitroglycerin.
b. -Blockers:
They decrease the oxygen demands of the myocardium by
lowering both the rate and the force of contraction of the
heart.
Acebutolol, Atenolol, Metoprolol, Propranolol.
c. Ca Channel Blockers:
The calcium-channel blockers protect the tissue by inhibiting
the entrance of calcium into cardiac and smooth muscle
cells of the coronary and systemic arterial beds.
Amlodipine, Diltiazem, Verapamil, Nicardipine, Nifedipine.
23 December 2014
Anti-Hyperlipidemics:
a. HMG CoA Reductase Inhibitors:
Analogs of HMG(precursor of Cholesterol). Because of their
strong affinity for the enzyme, all compete effectively to
inhibit HMG CoA reductase, the rate-limiting step in
cholesterol synthesis (de novo synthesis).
Atorvastatin, Lovastatin, Provastatin, Simvastatin.
b. Fibrates:
Gemfibrozil, Fenofibrate.
c. Niacin:
Niacin strongly inhibits lipolysis in adipose tissue, the primary
producer of circulating free fatty acids.
d. Bile Acid Sequestrants:
Colestipol, Colestyramine, Colesevelam.
e. Cholesterol Absorption Inhibitors:
It inhibits intestinal absorption of dietary and biliary
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.
Ezetimibe.
10
CVS Drugs
Anti-Hypertensives:
a. Diuretics:
They cause increased water and sodium excretion leading to decreased extracellular volume & decreased cardiac output.
Bumetanide, Furosamide, Spironolactone, Hydrochlorthiazide.
b. -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. -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, -Methyldopa.
23 December 2014
11
CVS Drugs
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.
23 December 2014
12
Drugs Affecting Other Organs
Respiratory System:
a. Asthma:
2-Adrenergic Agonists, Corticosteroids, Montelukast(Cysteinyl leukotriene antagonist), Theophylline, Omalizumab.
b. Allergic Rhinitis:
-Adrenergic Agonists, Antihistamines, Corticosteroids, Cromolyn.
c. COPD:
-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.
23 December 2014
13
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. (Travellers diarrhea)
23 December 2014
14
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)
23 December 2014
15
Other Therapies
Erectile Dysfunction (PDE-5 Inhibitors):

Sildenafil, Vardenafil.
Osteoporosis:
Alendronate, Ibandronate, Calcitonin, Zoledronic Acid.
Obesity:
Orlistat (lipase inhibitor), Sibutramine (anorexiant), Phentermine (anorexiant).
23 December 2014
16
Antibiotics (Antimicrobials)
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.
23 December 2014
17
Protein Synthesis Inhibitors:

a. Tetracyclines:
The drug binds reversibly to the 30S subunit of the bacterial ribosome, thereby blocking access of the amino acyltRNA 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)
23 December 2014
18
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
Dihydrofolic Acid (Sulfonamide) (microbes)
Dihydropteroate
synthetase
Tetra hydro folic Acid
(Trimethoprim) (humans)
reduction
Tetrahydrofolic Acid
23 December 2014
Amino Acid Synthesis + Purine Synthesis + Thymidine Synthesis
19
Antimycobacterials And Antifungals
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.
23 December 2014
20
Antiprotozoals & Antihelminthics
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.
23 December 2014
21
Anti-Virals
Respiratory Virus Infections:

Amantadine, Rimantadine, Ribavirin, Zanamivir.
Hepatic Viral Infections:

Interferon, Adefovir, Entecavir.
HIV Infections:
Abacavir, Didanosine, Etravirine, Fosamprenavir, Tenofovir.
23 December 2014
22
Anti-Cancers
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.
23 December 2014
23
Anti-Inflammatory
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.
23 December 2014
24
Autocoids & Their Antagonists
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.
23 December 2014
25
Facts to Remember
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.
F2: 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.
23 December 2014
26
Facts to Remember
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 400-500g.
23 December 2014
27
Facts to Remember
a.
b.
c.
a.
b.
c.
d.
Types of Pain:
Nociceptive: Pain due to sensitization of nociceptive nerve endings due to certain tissue damage.
Neuropathic: Any lesion or damage to the nerve fibres, resulting in pain. E.g. Diabetic Peripheral Neuropathy
(DPN)
Mixed: Low back pain; Ankolysing Spondylitis.
Mechanism of Feeling pain:
Reception: Stimulation of nociceptives by PGs.
Conduction: From Nerve ending to brain.
Perception: Cortex & Thallamus receive impulse.
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.
23 December 2014
28
Facts to Remember
Menorrhagia: Excess Blood flow in frequency, duration or amount; upto 80ml. (20-30ml)
PGE2: Inc. vasodilation; Dec. platelet adhesion & aggregation Inc. Blood Flow.
PGF2: 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.
23 December 2014
29
Facts to Remember
a.
b.
c.
d.
Receptor: Biological molecule to which drug binding produce measurable response.

Receptor Types:
Ligand gated Ion Channels: GABA (Fastest reception)
G-protein Coupled: Sildenafil
Enzyme Linked: Insulin
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.
23 December 2014
30
Facts to Remember
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 Dales 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
Dukes 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 -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.
23 December 2014
31
Facts to Remember
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).
23 December 2014
32
Adrenal Hormones
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
Corticotropinreleasing Factor
a.
b.
c.
Corticotropin
ACTH
Corisol
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:
Short Acting (1-12 hrs): Hydrocortisone, Cortisone.
Intermediate Acting (12-36hrs): Prednisone, Prednisolone, Methylprednisolone.
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 Cushings disease (Overproduction of
glucocoricoids)
23 December 2014
33
Diabetes Mellitus-II Treatment
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
Increased
Yes
Meglitinides
Nateglinide;
Repaglinide
Increased
Rarely
Biguanides
Metformin
Inhibiting Gluconeogenesis
Decreased
No
Glitazones
Pioglitazone;
Rosglitazone
Binds to Peroxisome Perforator

Activated Receptor & decrease
Insulin Resistance
Highly
decreased
No
-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
23 December 2014
34
Toxicology
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
23 December 2014
35
Common Latin Abbreviations
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
23 December 2014
36
Facts to Remember
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
Alzheimers Disease
Ecothiphate
Open Angle Glaucoma.
23 December 2014
37
Facts to Remember
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.
23 December 2014
38
Facts to Remember
Adrenergic Agonists
Drugs
Receptor Specificity
Therapeutic Uses
Epinephrine
1, 2, 1, 2
Acute Asthma; Anaphylactic Shock;

In local anesthetics.
Norepinephrine
1, 2, 2
Shock Treatment
Isoproterenol
1, 2
Cardiac Stimulant
Dopamine
1, 1, Dopaminergic
CHF, Raise BP
Dobutamine
CHF
Methoxamine
Supraventricular tachycardia
Clonidine
Treatment of hypertension
Phenylephrine
Nasal decongestant
Albuterol; Terbutaline
Short acting bronchospasm
Salmeterol; Formoterol
Long acting bronchospasm
Amphetamine
, , CNS
CNS stimulant in children, ADHD,

Narcolepsy.
Ephedrine; Pseudo Ephedrine
, , CNS
Asthma, Nasal decongestant
23 December 2014
39
Facts to Remember
Adrenergic Antagonists
Drugs
Receptor Specificity
Therapeutic Uses
Propranolol
1, 2
Hypertension, Glaucoma,
Migraine, Angina pectoris, MI
Nadolol; Timolol
1, 2
Glaucoma, Hypertension
Atenolol; Esmolol; Metoprolol
Hypertension
Pindolol (Partial Agonist)
1, 2
Hypertension
Carvedilol; labetalol
1, 1, 2
Hypertension, CHF
*Pindolol and Aebutolol are Partial Agonists
23 December 2014
40
Biopharm Concepts
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 NonLinear Kinetics. Generally described by Michelis Menten Equation.
23 December 2014
41
Biopharm Concepts
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)
23 December 2014
42
Biopharm Concepts
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.
23 December 2014
43
Common Gram +ve Bacteria

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
23 December 2014
44
Common Gram -ve Bacteria

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).
23 December 2014
45
23 December 2014
46

Pharmacology

Hochgeladen von

Dokumentinformationen

Originalbeschreibung:

Copyright

Verfügbare Formate

Dieses Dokument teilen

Dokument teilen oder einbetten

Freigabeoptionen

Stufen Sie dieses Dokument als nützlich ein?

Sind diese Inhalte unangemessen?

Copyright:

Verfügbare Formate

Pharmacology

Hochgeladen von

Copyright:

Verfügbare Formate

PHARMACOLOGY NOTES

Drugs Affecting ANS

1. Central Nervous System.

Neuroleptic Drugs (Anti-Psychotic or Major Tranquilizers):

Congestive Heart Failure(CHF):

Drugs Affecting Other Organs

Drugs Affecting Other Organs

Drugs Affecting Other Organs

Erectile Dysfunction (PDE-5 Inhibitors):

Cell Wall Inhibitors:

Protein Synthesis Inhibitors:

Folate Synthesis Inhibitors:

Folate Reduction Inhibitors:

Combination of Above two:

Where Sulfonamides and Trimethoprim act ??

Pteridine + p-ABA + Glutamate

Dihydrofolic Acid (Sulfonamide) (microbes)

Tetra hydro folic Acid

Amino Acid Synthesis + Purine Synthesis + Thymidine Synthesis

Antimycobacterials And Antifungals

Subcutaneous and Systemic Mycoses:

Antiprotozoals & Antihelminthics

Anti-Nematodes (Ascaris, Hookworms, Filarias. Enterobius, Trichinella):

Respiratory Virus Infections:

Hepatic Viral Infections:

Steroids, Hormones and their Antagonists:

Drugs for Gout:

Autocoids & Their Antagonists

Substance P Blocker: APREPITANT

Ovulation: Release of ova from the ovary.

Receptor: Biological molecule to which drug binding produce measurable response.

Glucocorticoids & Mineralocorticoids are collectively known as Corticosteroids.

Diabetes Mellitus-II Treatment

Sulfonylurea (1st Gen)

Increase Insulin secretion

Sulfonylurea (2nd Gen)

Increase Insulin secretion

Increase Insulin secretion

Binds to Peroxisome Perforator

Decrease breakdown of starch

Prolongs Incretin thus increase

Accelerate detoxification of toxic

Anticholinergic agents (Muscarine)

Amyl nitrite pearls or Sodium

Provide alternative target

Digoxin Immune Fab

Methanol Ethylene Glycol

Reduce metabolic activation

Mercury; Arsenic; Gold

Common Latin Abbreviations

auris laeva / sinistra

single large dose

Every day / daily

more dicto utendus

Every other day

quaque otram diem

Treatment of Urinary Retention

Miosis during Ocular Surgery; Topically to reduce IO

Reduce intraocular pressure in open angle & narrow

Increase bladder motility; reverse CNS effects of

Treat Myasthenia Gravis; Antidote for Tubocurarine.

Open Angle Glaucoma.

Mydriasis and cycloplegia prior to refraction.