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Introduction
1. Anatomy
2. Microbiology
3. Physiology
4. Pathology
5. Pharmacology
5.1 Pharmacokinetics
5.2 Pharmacodynamics
5.3 Receptors, agonists and antagonists
5.4 Types of drug receptors
5.5 Anti-neoplastic drugs
5.6 Adverse effects of chemotherapeutic drugs
5.7 Newer chemotherapeutic drugs
5.8 Important drugs of the cardiovascular system
5.9 Antimicrobials
5.10 Drugs acting on the renal system
5.11 Drugs acting on the respiratory system
5.12 Drugs acting on the gastrointestinal system
5.13 Antidiabetics and insulin
5.14 Miscellaneous
5.15 Additional information
6. Immunology
7. Biochemistry
8. Cell and molecular biology
9. Biostatistics and epidemiology
10. Genetics
11. Behavioral science
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5.15 Additional information
Achievable USMLE/1
5. Pharmacology

Additional information

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Bioavailability of different routes of drug administration

Route Bioavailability (%)
Intravenous 100
Intramuscular 80-100
Subcutaneous 80-100
Oral 5- <100
Rectal 30-100 (highly variable)
Inhalational 5-100
Sublingual 30- <100%

First-pass metabolism is avoided with all routes except oral administration.

Succinylcholine

Succinylcholine is metabolized in plasma by cholinesterase (pseudocholinesterase) into inactive forms. Inherited differences in this enzyme can slow succinylcholine breakdown, leading to prolonged neuromuscular paralysis in some patients.

The involved gene is located on chromosome 3 (gene E1). The most common mutation is a substitution of aspartic acid to glycine, which reduces enzyme binding to succinylcholine.

Slow and fast acetylators: Drugs such as isoniazid, dapsone, hydralazine, sulfa drugs, and procainamide are metabolized by acetylation reactions catalyzed by acetyltransferases. The gene is NAT2. The rate of acetylation varies by ethnicity due to polymorphisms in the enzyme. About 50% of Caucasians and African Americans are slow acetylators, while most Asians are fast acetylators.

  • Slow acetylators are at risk of adverse effects.
  • Rapid acetylators are at risk of low blood levels, which can reduce the response to drug therapy.

Acetaminophen toxicity

Acetaminophen toxicity is a common cause of liver transplantation. Large doses of acetaminophen - especially in people with chronic liver disorders and in alcoholics - can saturate the usual hepatic detoxification mechanisms. This leads to excessive formation of a toxic metabolite called NAPQI (N-acetyl-p-benzoquinone imine).

Normally, NAPQI is detoxified by glutathione. In acetaminophen overdose, glutathione stores are depleted, allowing NAPQI to bind to hepatocytes and cause necrosis. Chronic alcoholism induces hepatic microsomal enzymes, increasing NAPQI formation. Alcohol also depletes glutathione.

Patients may be asymptomatic for up to 24 hours and then present with vomiting, RUQ pain, hypotension, liver failure, renal failure, coagulopathies, metabolic acidosis, and encephalopathy. Microscopically, the liver shows centrilobular necrosis.

Treatment is guided by time since ingestion:

  • Within 1 hour of ingestion, activated charcoal can be used.
  • Blood levels of acetaminophen are measured.
  • Definitive treatment is N-acetyl cysteine, which provides sulfhydryl groups that attach to NAPQI, preventing hepatic necrosis.

N-acetyl cysteine also reduces NAPQI to acetaminophen, acts as a precursor to glutathione, has antioxidant and anti-inflammatory properties, increases sulphate conjugation, and increases local nitric oxide and oxygen delivery. Severe cases may also require hemodialysis and liver transplantation.

Effect of ageing on drugs

  • Decreased hepatic and renal clearance
  • Increase in Vd of lipid soluble drugs*
  • Decrease in Vd of water soluble drugs**
  • Increased elimination half life
  • Decrease in first pass metabolism
  • Effects of drugs like verapamil, warfarin, morphine, diazepam are increased
  • Effects of drugs like furosemide, propranolol are decreased
  • Increased adverse effects of neuroleptics like delirium, arrhythmias, extrapyramidal symptoms and postural hypotension

* Includes digoxin, ethanol, theophylline, cimetidine, gentamicin. Reduce loading dose.

** Includes diazepam, lidocaine, thiopental. Increase in half life.

Types of chemotherapy

Type Description
Primary When chemotherapy alone can cure the cancer like in Hodgkin’s disease, Wilms tumor, small cell lung cancer, testicular cancer, Burkit’s lymphoma, large cell lymphoma, leukemias.
Adjuvant Administered prior to or after other methods like surgery, to increase the effectiveness of treatment, to prolong survival or decrease the risk of recurrence.
Palliative To minimize the discomfort caused by or slow progression of an incurable cancer
Neoadjuvant Given prior to surgery or radiation, to shrink the size of a tumor and make it easier to resect.
  • Vinca alkaloids cause microtubule depolymerization by binding to beta tubulin, resulting in apoptosis.
  • Paclitaxel binds to beta tubulin and enhances microtubule assembly, polymerization, and bundling.
  • Vinca destabilizes, while paclitaxel stabilizes, the microtubule.

Tachyphylaxis

Tachyphylaxis is when a drug becomes less efficacious (or loses its effect) with continued use over a period of time. It is a type of tolerance (desensitization).

Mechanisms include:

  • Depletion of chemicals needed for pharmacological action (e.g., neurotransmitters)
  • Changes in receptor state (e.g., phosphorylation)
  • Changes in receptor number (e.g., downregulation)
  • Counterregulatory physiological changes that offset the drug’s action

It is seen with nitroglycerin, topical corticosteroids, local anesthetics, nicotine, etc. Temporarily withholding the drug or providing drug-free hours can restore sensitivity.

Metronidazole

Metronidazole is commonly used to treat anaerobic and protozoal infections. It is metabolized to nitro free radicals, which cause DNA damage and inhibit protein synthesis.

It is effective against E.histolytica, Trichomonas, Giardia lamblia, Bacteroides sp, Clostridium sp, Fusobacterium sp, Gardnerella vaginalis, H.pylori etc.

Adverse effects include nausea, metallic taste, headache, diarrhea, pruritus, peripheral neuropathy, seizures, and probable carcinogenicity. It can cause an antabuse-like reaction if alcohol is consumed concurrently.

Warfarin induced skin necrosis

Warfarin-induced skin necrosis typically occurs 2-5 days after starting warfarin therapy. It occurs due to depletion of vitamin K-dependent anticoagulant proteins C and S.

It is due to thrombosis in blood vessels of the skin, especially in areas with abundant fat. It presents with pain, a purplish rash, blistering, blue toe syndrome, and skin necrosis (commonly in the breast, thighs, buttocks, and abdomen).

Management includes stopping warfarin and giving vit K, heparin, and protein C concentrates.

Heparin induced thrombocytopenia

  • Can be immune or non-immune
  • Thrombocytopenia plus increased thrombosis in a patient on heparin therapy, more severe in immune type
  • More common with UFH, but also seen with LMWH
  • Due to antibodies to complex of heparin and platelet factor 4, which leads to platelet lysis
  • Platelet lysis causes clotting leading to DVT, PE, AMI, stroke, black toes, bruising, etc.
  • Typically occurs 1-2 weeks after initiation of heparin therapy
  • Laboratory findings are decreased platelet count and increased platelet factor 4 antibody
  • Treat by stopping heparin, anticoagulation with alternate agents like direct thrombin inhibitors, fondaparinux and/or warfarin
  • Platelet transfusion is contraindicated due to increased risk of thrombosis!

Cephalosporin generations

1st generation Cefazolin, cephalexin, cefadroxil
2nd generation Cefaclor, cefotetan, cefoxitin, cefprozil, cefuroxime
3rd generation Cefdinir, ceftriaxone, cefotaxime, cefpodoxime, ceftazidime, cefixime
4th generation Cefepime
5th generation Ceftaroline

Types of beta lactamases

  • Class A: Penicillinases, susceptible to clavulanic acid, sulbactam and tazobactam. TEM1, SHV1 in Enterobacteria; ESBL or extended spectrum beta lactamases confer resistance to penicillins, third generation cephalosporins, aztreonam but are sensitive to carbapenems and cephamycins like cefoxitin and cefotetan
  • Class B: Metallo-beta-lactamases, need metal ions like zinc for activity, not inhibited by clavulanic acid, sulbactam; resistant to carbapenems and aztreonam. They may be sensitive to colistin
  • Class C: Cephalosporinases, Amp C, resistant to clavulanic acid and all beta lactams except carbapenems
  • Class D: Oxacillin hydrolyzing enzymes, resistant to oxacillin, penicillin, cloxacillin, methicillin, weakly inhibited by clavulanic acid

Penicillin types

Penicillin type Characteristics
Natural penicillins Penicillin G, Penicillin V. Active against non-beta-lactamase producing Gram positive cocci like viridans streptococci, Group A streptococci, pneumococci, peptostreptococcus, Clostridia, Actinomycetes, meningococci, gonococci, Pasteurella multocida, Treponema pallidum
Penicillinase resistant penicillins Methicillin (not used now, causes interstitial nephritis), nafcillin, oxacillin, dicloxacillin. Active against penicillinase producing Staphylococci but no action on MRSA, MRSE and Enterococci
Aminopenicillins Ampicillin, amoxicillin; activity like natural penicillins plus also gram negative bacilli like H.influenzae, E.coli, Proteus, Salmonella, Shigella sp. Widespread resistance seen
Carboxypenicillins Carbenicillin, ticarcillin; greater Gram negative spectrum including Pseudomonas aeruginosa
Ureidopenicillins and piperazine penicillins Azlocillin, mezlocillin, piperacillin; coverage like carboxypenicillins plus more effective on Klebsiella, Serratia, Enterobacter, Enterococcus and P.aeruginosa;

Colchicine

Colchicine binds to tubulin and blocks microtubule assembly and polymerisation. It also inhibits neutrophil chemotaxis and the release of a crystal-derived chemotactic factor (CCF) from neutrophil lysosomes, superoxide formation, and phagocytosis.

It is used to treat acute gout, familial meditteranean fever, Behcet’s disease, and inflammatory disorders.

Adverse effects include diarrhea, nausea, vomiting, neutropenia, neuropathy, and organ failure. Doses should be decreased in renal and/or hepatic failure. Colchicine has a narrow therapeutic index.

Rhabdomyolysis can occur when colchicine is given with statins. The dose should be reduced when cyt P450 inhibitors are co-prescribed.

Ultra fast acting insulin or Fiasp

Ultra fast acting insulin (Fiasp) is a recently FDA-approved form of insulin aspart designed to speed up absorption of subcutaneous insulin by adding vitamin B3 (niacin) and L-arginine.

It is used in type 1 and 2 DM and can be injected up to 20 minutes after starting a meal. Onset of action is within 15-20 minutes, and duration of action is 7 hours.

Commonly used antidotes

Antidote Uses
Activated charcoal Typically within 1 hour and maximum within 4 hours of oral ingestion of a toxin; can be used in carbamazepine, dapsone, theophylline, phenobarbitone, quinine etc. Do not use in alcohol, acid, alkali or metal poisoning
Dimercaprol Arsenic, gold, mercury and lead poisonings
Digi-Fab (antibody to digoxin) Digoxin toxicity
Urinary alkalinization with sodium bicarbonate TCA, salicylates, phenobarbital
Naloxone Opioids, repeat doses every 2-3 minutes, onset of action <2 minutes in intravenous dosing
Flumazenil Benzodiazepines
Fomepizole Methanol and ethylene glycol
Pralidoxime and atropine Organophosphorus
N acetyl cysteine Paracetamol
Sodium thiosulfate Cyanide poisoning
Vitamin K Warfarin
Pyridoxine or Vit B6 Isoniazid
Folinic acid Methotrexate
Beta blockers Theophylline
Octreotide Oral hypoglycemics
Physostigmine Anticholinergic poisoning
Protamine sulfate Heparin
Glucagon, calcium, high dose insulin with glucose Beta blockers and calcium channel blockers

Comparison between proton pump inhibitors and H2 blockers

PPIs (omeprazole, lansoprazole, rabeprazole, pantoprazole, esomeprazole)

  • Bind to and inhibit H+/K+ ATPase (the proton pump) located in parietal cells
  • Used to treat GERD, peptic ulcers, H.pylori gastritis, prevention of stress ulcers, and NSAID induced gastritis
  • Adverse effects include nausea, headache, diarrhea, vomiting, hypergastrinemia, pneumonia, fractures, hypomagnesemia, Vit B12 deficiency, Cl.difficile colitis, acute interstitial nephritis, SLE
  • Interfere with the absorption of ketoconazole, itraconazole, isoniazid, oral iron supplements, protease inhibitors
  • Inhibit CYP2C19 and may decrease the hepatic activation of clopidogrel and reduce it’s antiplatelet activity
  • Bind to and inhibit histamine H2 receptors on the basolateral surface of gastric parietal cells thereby decreasing acid production and secretion
  • Used to treat GERD, duodenal and peptic ulcers and prevention of stress ulcers
  • Less potent than PPIs
  • Adverse effects include diarrhea, constipation, fatigue, drowsiness, headache, muscle aches, prolongation of QTc in renal failure (famotidine), rarely liver failure and CNS effects
  • Cimetidine is a potent inhibitor of cyt P450 and should be avoided with warfarin, theophylline and SSRIs
  • Cimetidine may cause galactorrhea, gynecomastia, impotence and reduced sperm count

Treatment options for resistant bacteria

Resistance type Treatment
MRSA Soft tissue infections: oral doxycycline, trimethoprim-sulfamethoxazole, clindamycin, minocycline, linezolid, tedizolid, delafloxacin, omadacycline; Complicated infections: Intravenous vancomycin, daptomycin or linezolid
VRSA and VISA Daptomycin, telavancin, ceftaroline, linezolid, tedizolid, oritavancin
VRE Ampicillin plus gentamicin/streptomycin, ceftriaxone, ampicillin-sulbactam, linezolid, daptomycin
MDR Pseudomonas aeruginosa Ceftazidime-avibactam, ceftolozane-tazobactam, colistin, polymyxin B, imipenem-cilastatin, relebactam
ESBL Carbapenems (imipenem, meropenem, ertapenem), piperacillin tazobactam, cefepime, fosfomycin (UTIs), temocillin
Carbapenem resistant Enterobacteriaceae Avibactam plus ceftazidime, meropenem plus vaborbactam, fosfomycin (UTIs)
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