The action of a drug depends on multiple factors. Pharmacokinetics is the study of a drug's movements in the body and can be described as what the body does to the drug, while pharmacodynamics is the study of a drug's action and effects on a body and can be described as what the drug does to the body. The administration of a drug in combination with other drugs or substances can cause a variety of interactions that can synergistically or antagonistically modify the effect of those drugs (e.g., via the activation or inhibition of cytochrome P450 enzymes by certain medications). Knowledge of interactions and pharmacokinetics help determine the ideal route of administration (topical, oral, IV). Drugs that are eliminated by the liver may attain high serum concentrations when hepatic function is impaired, which increases the risk of drug toxicity. The same principle applies to drugs that are eliminated via the kidneys.
LADME is an acronym for the important phases of pharmacokinetics:
- Receptor types and their interaction with the drug
- Dose-response relationship
- Pharmacogenetics: deals with the effect of genetic variations on drug metabolism and drug action.
- Clinical trials: phases of drug development, testing, and regulatory approval (occur after preclinical studies)
Clinical trials phases
|Overview of clinical trial phases |
|Clinical trial phase||Purpose||Study population||Study design|
|Phase 0 trial|| || || |
|Phase I trial|| || |
|Phase II trial|| || || |
|Phase III trial|| || |
|Phase IV trial|| || || |
Before clinical trials begin, drugs are first tested in preclinical studies. Preclinical studies do not include human subjects.
Drug approval 
- In the US, all drugs must be approved by the Food and Drug Administration (FDA) for certain indications.
- Some drugs may be used for indications other than those they have been approved for. (See “Off-label use” below)
- Drugs that have not been approved by the FDA for any indication should generally not be prescribed, but there are exceptions. (See “Expanded access” below)
Development and general approval process
- Development of a substance with therapeutic potential or taking a decision to repurpose an existing substance
- Conducting pre-clinical studies (phase 0 clinical trial)
- Submitting investigational new drug (IND) application
- Investigator IND: submitted by a physician or representative of a company who will conduct the clinical trials to initiate the standard approval procedure
- Emergency use IND: asks for approval of an experimental drug in an emergency situation, in which the standard IND cannot be filed and there is no time for a standard approval procedure
- Treatment IND: requests approval of use of an experimental drug to treat serious or rare conditions that showed efficacy in clinical studies before their completion (e.g., during an interim analysis) and final approval by the FDA
- Research: submitted by a physician representing research or clinical institution
- Commercial: submitted by a representative of a commercial organization, e.g., drug company
- Phase 1 to 3 clinical trials
- Filing the New Drug Application
- A formal request to the FDA to approve the investigational agent for marketing and use in the US
- Should include all the information about the agent (manufacturing process, quality control, formula, pharmacodynamics, pharmacokinetics, risks, indications, proposed labeling, etc.)
- Application review
- Drug labeling
- Inspection of manufacturing facilities
Off-label use 
- Use of an FDA-approved drug for an unapproved indication or population, or in an unapproved form or dosage
- Examples: tricyclic antidepressants for the treatment of chronic pain, SSRIs for premature ejaculation, letrozole for infertility treatment in PCOS
Orphan drugs 
- A designation by the FDA for a medication or vaccine that can potentially be used to diagnose, prevent, or treat a rare disease (defined as affecting < 200,000 people in the US)
- Incentivizes the development of drugs for rare diseases (e.g., via tax benefits for clinical trials, exemption from user fees, market exclusivity for seven years after approval)
Expanded access 
- An FDA program that grants use of an investigational drug or medical device to treat a serious condition for which there is no comparable or satisfactory alternative treatment
- Examples: granting access to an investigational drug to a patient who lives too far from study centers or who does not meet eligibility criteria to participate in a drug trial
- Off-label use 
Drugs that do not have FDA approval for any indication should not be prescribed because the safety, efficacy, and quality of these drugs have not been proven. 
Drug scheduling 
- Definition: legal classification of substances based on their abusive potential
|Overview of drug scheduling|
Pharmacokinetics deals with drug absorption, distribution, metabolism, and excretion.
- The process by which the drug is released from its pharmaceutical form (e.g., capsule, tablet, suppository, etc.)
- The most common routes of drug administration are:
- Injection (the drug is introduced directly into the bloodstream or into tissue)
- Peroral administration
- Dermal administration
- Rectal administration
- Less common routes
- Intra-articular administration
The process by which the drug reaches the bloodstream. The following factors affect drug absorption:
- Describes the rate and concentration at which a drug reaches systemic circulation
- Expressed as a percentage of the dose that was initially administered
- Drugs administered intravenously have a bioavailability of 100%.
- Can be calculated using the area under curve (AUC) of the plotted graph concentration versus time: (F) = (AUCoral/AUCIV) x 100
Bioavailability is affected by two mechanisms:
- Ability to pass through lipid membranes: dependent on the nature of the substance (see the table below)
First pass effect
- Orally administered drugs are absorbed in the GI tract and reach the liver via portal circulation
- In the liver they undergo first pass metabolism before they enter systemic circulation → ↓ bioavailability of the drug (F < 100%).
- Rectal or sublingual administration bypasses first pass metabolism, as the drug is absorbed directly into the bloodstream.
- Bioequivalence: Two proprietary preparations of a drug are said to be bioequivalent if they exhibit the same bioavailability when administered in equal doses.
|Abilities of chemical compounds|
|Characteristic||Chemical nature||Clinical significance||Example|
|Lipophilic|| || || |
|Hydrophilic|| || || |
|Amphiphilic|| || |
Changes in older adults
- Despite slowing of gastric emptying and an increase in gastric pH, absorption remains typically unaffected in older adults.
- Due to older adults often having multiple drug regimens, this group is at particular risk of drug and food interactions.
Distribution coefficient: measure of hydrophobicity/hydrophilicity of a drug
- Corganic = drug concentration in an organic solvent
- Cwater = drug concentration in water
- Corganic/ Cwater
Volume of distribution
Vd = M/Cplasma
- Vd = volume of distribution (usually expressed in liters/kg body weight)
- M = amount of drug in the body at a specific time
- Cplasma = plasma concentration of the drug at a specific time
- The theoretical volume a drug would occupy if it was distributed evenly in fluids at plasma concentration.
- Provides information about a drug tendency to distribute in other compartments (e.g., muscle or adipose tissue) rather than in the plasma.
- Drugs can distribute in more than one compartment.
- The Vd of plasma protein-bound drugs may be increased in patients with renal and liver disease due to loss of plasma proteins.
- Vd = M/Cplasma
|Volumes of distribution|
|Drugs|| || || |
|Compartment|| || |
Binding to plasma proteins: Different drugs have different affinities to bind to plasma proteins (e.g., albumin).
- Only the unbound fraction of the drug has a pharmacological effect.
- Different drugs may compete to bind to plasma proteins
Redistribution (pharmacology): transfer of a drug between the different compartments within the human body
- Lipophilic substances (e.g., inhalation anesthetics) are redistributed from plasma into fat tissue → initially decreased action of the applied drug
- Drug is stored but over time is released again from fat tissue into plasma → delayed elimination and prolonged action of the specific drug ).
Changes in advanced age
- Hydrophilic drugs (e.g., digoxin): ↓ total body water → ↓ Vd
- Acidic drugs: ↓ albumin → ↓ binding
- Lipophilic drugs (e.g., propofol): ↑ body fat content → ↑ Vd
After the drug reaches the bloodstream, it is initially distributed in the most vascularized organs.
Renal and liver disease can increase the apparent volume of distribution of drugs bound to plasma proteins.
- Chemical alteration of substances (e.g., drugs) within the body by the action of enzymes and mainly takes place in the liver.
- Detoxifies drugs and facilitates their elimination
Types of drug kinetics
- Zero order kinetics: The rate of metabolism and/or elimination remains constant and is independent of the plasma concentration of a drug at steady state (Cp decreases linearly over time)
First order kinetics: The rate of metabolism and/or elimination is directly proportional to the plasma concentration of the drug (Cp decreases exponentially over time)
- First-order is a flow-dependent elimination.
- Applies to most drugs
It takes zero PHEN-tAS-E (fantasy) to remember the drugs that are eliminated by zero-order kinetics: PHENytoin, ASpirin, Ethanol.
Phases of biotransformation
Phase I reaction: A drug is transformed into a polar, water-soluble metabolite by cytochrome P450 via one or more of the following reactions:
- Oxidation (most common reaction)
Phase II reaction: A drug is conjugated and thereby transformed into a very polar metabolite (can be excreted renally) via one or more of the following reactions:
- Glucuronidation (most common coupling reaction)
- Acetylation (e.g., isoniazid)
- Detoxification: In most cases, the drug is inactivated and modified into a hydrophilic metabolite, allowing excretion of the drug via the kidneys or in bile.
- Activation; : Certain drugs are transformed in the liver from their inactive prodrug state into active forms (e.g., the ACE inhibitor enalapril is transformed through ester hydrolysis into the active form enalaprilat).
- Formation of toxic metabolites (e.g., the breakdown of paracetamol gives rise to toxic metabolites that may cause severe liver damage in large doses)
- In individuals who are slow drug acetylators, the decreased rate of metabolism increases the risk of side effects (e.g., isoniazid).
Changes in advanced age: ↓ metabolization (due to ↓ hepatic mass and ↓ hepatic blood flow)
- Because phase I metabolism decreases (affecting drugs like diazepam), drugs predominantly metabolized in phase II (e.g., acetaminophen, lorazepam) are considered safer.
- Consequently, lower therapeutic doses should be considered in elderly individuals.
In the elderly population, phase I reactions will usually become impaired before phase II reactions.
Drug clearance (CL): a measure of the rate of drug elimination.
- It is defined as the plasma volume that can be completely cleared of the drug in a given period of time (e.g., creatinine clearance).
CL = Vd x Ke = rate of drug elimination/plasma drug concentration
- Vd = volume of distribution
- Ke = elimination constant
- CL = rate of elimination / plasma concentration
- CL can be impaired in patients with cardiac, hepatic, or renal dysfunction.
Half-life (t½): the time required for the plasma concentration of a drug to reach half of its initial value
- Dynamic equilibrium
- Drug concentration stays constant because the rate of drug elimination equals the rate of drug administration
In first-order kinetics
- t½ = (0.7 x Vd) / CL
- It takes 1 half-life to reach 50% of the steady-state level, 2 half-lives to reach 25%, 3 half-lives to reach 12.5%, and 4 half-lives to reach 6.25%.
- Complete steady-state attainment takes 4–5 half-lives for drugs infused at a constant rate; 90% of steady-state level is reached after 3.3 half-lives
- Steady state
- The time it takes for a drug's plasma concentration to reach 50% of its initial value during the most clinically important phase of its kinetics
- For drugs with atypical kinetics (e.g., those with a high volume of distribution), the effective half-life may be shorter than the terminal elimination half-life but more predictive of the drug's duration of effect and accumulation.
Defects in renal, hepatic, or cardiac function can impair drug clearance.
After 4 half-lives, more than 90% of the drug will be eliminated.
Drugs and/or their metabolites are excreted from the body in one or more of the following ways:
Renal elimination: mostly hydrophilic drugs
- Main renal elimination mechanisms include
- Glomerular filtration
- Tubular secretion
- Tubular reabsorption
Ionized substances cannot cross renal tubular membranes and are cleared quickly.
Weak acidic drugs (e.g., phenobarbital, methotrexate, aspirin) are trapped in a basic environment
- Overdoses with these drugs can be treated via alkalinization of urine (sodium bicarbonate)
- RCOOH (lipid soluble) ⇄ RCOO– + H+ (trapped form)
Weak basic drugs (e.g., tricyclic antidepressants, amphetamines) are trapped in an acidic environment
- Overdoses with these drugs can be treated via acidification of urine (ammonium chloride)
- RNH3+ (trapped form) ⇄ RNH2 + H+ (lipid soluble)
- The elimination of tricyclic antidepressants, which are basic, can be increased by acidification of urine, but toxicity is generally treated with sodium bicarbonate.
- Weak acidic drugs (e.g., phenobarbital, methotrexate, aspirin) are trapped in a basic environment
- Neutral substances can be reabsorbed.
- Main renal elimination mechanisms include
Biliary elimination 
- Lipophilic and hydrophilic substances
- Lipophilic substances that have undergone biliary elimination may be reabsorbed from the gut and then secreted again in bile (enterohepatic circulation)
- Pulmonary elimination: primarily in inhaled anesthetic drugs
- Changes in advanced age
LADME is an acronym for the important phases of pharmacokinetics: Liberation, Absorption, Distribution, Metabolism, Excretion.
- Definition: the amount of an initial dose of a certain drug needed to reach a target plasma concentration
Formula: loading dose = (Cp x Vd) / F
- Cp = target peak plasma concentration at steady state (mg/L or units/L)
- Vd = volume of distribution (L/kg)
- F = bioavailability
- In patients with renal and/or liver dysfunction, loading dose (which does not depend on drug clearance) and time to steady-state are usually unaffected.
- Definition: The amount of a certain drug needed to achieve a steady target plasma concentration.
Formula: maintenance dose = (Cp x Cl * τ) / F
- Cp = target plasma concentration at steady state (mg/L)
- Cl = clearance (L/h)
- τ = dosing interval (hours)
- F = bioavailability
- In patients with renal and/or liver dysfunction, maintenance dose is decreased (because of impaired drug clearance) and time to steady-state is unchanged (time to steady state depends on t½).
Renal or liver conditions lower the maintenance dose without affecting the loading dose.
The main factor influencing the time to steady-state is t½, not dose or administration frequency.
Pharmacodynamics deals with the effect of a drug at its site of action, the dose-response relationship of the drug, and the influence of other factors on the drug effect.
Types of drug targets
Every functioning molecule in an organism is a potential site of action for a drug. Means through which drugs act include:
- Interaction with receptors
- Cell membrane receptors
- Intracellular receptors (e.g., receptors for glucocorticoids, NO)
- Interaction with enzymes
- Interaction with DNA (e.g., cytostatics)
- A physical/chemical effect (e.g., osmotic diuretics, antacids)
Drug affinity: a measure of the tendency of a drug to bind to its receptor
- Most drug-receptor bonds are reversible
- Covalent drug-receptor bonds, which are less common, are almost always irreversible (e.g., the binding of aspirin to cyclooxygenase enzyme).
Drug efficacy (correlates with Emax): the maximum degree to which a drug activates receptors after binding and triggers a cell response
- On an efficacy graph, the difference in efficacy of the two drugs is determined by the difference in the maximal effect exerted by each of them (shown on the y-axis); drugs with different efficacy will have different heights, with the difference in efficacy represented on the y-axis.
- Not related to potency (drugs with a high efficacy can have a low potency)
- Partial agonists are less efficacious than full agonists.
Structure-activity relationship 
- The relationship between a chemical compound's structure and its biological activity
- Modeling of the structure-activity relationship can help predict the biological action of a substance and, accordingly, plays a major role in the development of drugs with a specific target. 
- Residence time: : the lifespan of a drug‑receptor complex
Antagonists have zero efficacy, agonists have maximum efficacy, and partial agonists (see below) have submaximal efficacy.
Types of drug-receptor interactions
Agonist: a drug that has a similar effect to that of the endogenous receptor activator (e.g., β2 agonists)
- Full agonist: a molecule that binds to a receptor and activates the receptor with the highest response it can elicit
- A substance that has some agonistic action at a receptor but does not elicit the complete response of a true agonist
- Act at the same site as full agonists
Antagonist: a drug that binds to a receptor and prevents its activation.
- Agonist and the antagonist compete to bind to the same receptor.
Inhibition of the effect of the agonist in a dose-dependent fashion → higher concentration of the agonist is needed to achieve same efficacy (e.g., there is a decrease in potency)
- Reversible competitive antagonists
- Irreversible competitive antagonists
- Non-competitive antagonist
- Functional (physiological) antagonist; : In this type of antagonism, two different molecules working through separate receptors produce physiologically opposite effects.
- Competitive antagonist
- Inverse agonist: Binds to the same receptor as an agonist, but not to the same active site. It elicits a response that is opposite to the agonistic response and has a negative efficacy.
- Allosteric modulator: Binds at a different site than the agonist and initiates conformational changes that induce modulation of ligand-binding.
- Binds at a site other than the agonist-binding site (also called allosteric site) and changes the structure of the active binding site to increase affinity to the substrate
- For more information on enzyme kinetic, see also “Enzymes and biocatalysis.”
|Overview of drug-receptor interactions|
|Competitive antagonist||Noncompetitive antagonist||Partial agonist|
|Potency|| || || |
|Efficacy|| || || |
|Drug example|| || || |
The following terms are used to describe dose-response relationships:
Potency (EC50): The potency of a drug is measured as the concentration required to produce a pharmacological response of a specified intensity.
- Not related to efficacy (drugs with a high potency can have a low efficacy) but dependent on affinity
- EC50 = the effective concentration required to produce 50% of the maximum possible response (Emax)
- A left shift of the curve is a sign of decreased EC50 and increased potency, meaning a lower concentration of the drug is needed.
- EC50 is not to be confused with ED50; ED50 is the median effective dose that produces a desired beneficial effect in 50% of the population.
Therapeutic index (TI): a measurement of the safety of a drug
- TI = median toxic dose (TD50)/median effective dose (ED50)
The greater the therapeutic index, the safer the drug
- High therapeutic index: e.g., glucocorticoids, penicillin
- Narrow therapeutic index: Drugs with a narrow TI require monitoring (e.g., lithium, theophylline, warfarin, digoxin, and antiepileptic drugs).
- Therapeutic window: the range of doses that is effective for treating a condition with a minimum of adverse effects
- Lethal dose (LD50): The dose that is lethal for 50% of the test population in animal experiments.
TILE: Therapeutic Index = TD50/ED50
Drug tolerance and tachyphylaxis
The effect of a drug can decrease with repeated dosing:
Drug tolerance (e.g., opioids, benzodiazepines, barbiturates, alcohol)
- The mechanisms responsible for the development of drug tolerance include:
- Down-regulation of receptors
- Increased synthesis of enzymes that metabolize the drug
- Can be overcome by increasing the dose
- Develops slowly over a few weeks
- The mechanisms responsible for the development of drug tolerance include:
- The underlying mechanism responsible for the decreased effect of a drug involves depletion of the body's stores of an endogenous mediator and downregulation of receptors.
- Cannot be overcome by increasing the drug dose.
- Develops quickly (within a few hours of dosing)
- Indirect sympathomimetic drugs (e.g., ephedrine)
- Direct sympathomimetic drugs (e.g., phenylephrine, niacin, LSD, MDMA; ): the response to the repeated use of nasal decongestants (e.g., oxymetazoline) reduces the response over a short period of time and may cause rebound congestion
- Pharmacogenetics deals with genetic variation in the expression of enzymes that metabolize drugs.
- These genetic differences can cause a drug response to deviate from the expected response and/or increase the risk of side effects:
If the enzyme in question is responsible for the breakdown of a drug, the following effects are possible:
- A hyperactive variant of the enzyme decreases the drug response.
- A hypoactive variant of the enzyme can cause cumulative drug effects and thus increase the risk of side effects.
- The reverse is true if the enzyme is responsible for the activation of a drug.
- If the enzyme in question is responsible for the breakdown of a drug, the following effects are possible:
Examples of clinically relevant variations
- There are hyperactive and hypoactive variants.
- CYP2D6 is involved in the metabolism of many drugs (e.g., the breakdown of antiarrhythmics and tricyclic antidepressants; the activation of codeine).
- Gender-specific differences in CYP2D6 have been observed (e.g., CYP2D6-mediated breakdown of beta blockers (such as metoprolol) is greater among women).
- There are hyperactive (rapid acetylators) and hypoactive (slow acetylators) variants.
- N-acetyltransferase breaks down isoniazid, sulfasalazine, and hydralazine.
- Pseudocholinesterase is responsible for the breakdown of succinylcholine through ester hydrolysis.
- Atypical pseudocholinesterase breaks down succinylcholine slowly and thus prolongs the duration of muscle relaxation during anesthesia from a few minutes to a few hours; this may cause respiratory depression.
- Thiopurine-methyltransferase polymorphism (TPMT): involved in the breakdown of azathioprine.
Drug interactions and the cytochrome P450 system
- Drug interactions can cause an increase or decrease in the potency of a drug or result in additional side effects.
- The greater the number of coadministered drugs, the greater the chance of drug interaction
- Beers criteria is a list of over 50 drugs with potentially decreased effectiveness or increased risk of side effects or interactions in the elderly population; (see “Introduction to geriatrics” for further information).
- The most common form of drug interaction results from the induction of the cytochrome P450 enzyme system; interactions as a result of drug inhibition are less common.
Types of interactions
Additive drug interaction: the effect of two substances interacting with each other corresponds to the sum of their individual effects
- A + B = AB
- Example: aspirin coadministered with acetaminophen
Synergistic drug interaction: the effect produced by the interaction of two substances is greater than the sum of their individual actions
- A + B > AB
- Example: aspirin coadministered with clopidogrel
Drug potentiation: the therapeutic effect of a substance is enhanced by another substance with no therapeutic action
- A + 0 > A
- Carbidopa coadministered with levodopa (carbidopa blocks the peripheral conversion of levodopa)
- Cobicistat: used in antiretroviral therapy of HIV infection to decrease breakdown of antiretrovirals (e.g., darunavir, atazanavir)
Permissive drug interaction: the effect of a substance can only be achieved in the presence of another substance
- A - B = 0
- Example: cortisol coadministered with catecholamine (cortisol increases the sensitivity of adrenoreceptors to catecholamines)
Antagonistic drug interaction: the effect produced by the interaction of two substances is smaller than the sum of their individual actions
- A + B < AB
- Example: Ethanol is used to treat methanol toxicity (ethanol binds alcohol dehydrogenase with higher affinity than methanol and thereby competitively inhibits the formation of toxic metabolites),
- Cytochrome P450 is a superfamily of heme-containing, primarily oxidative enzymes that take part in phase 1 reactions.
- There are 200 cytochrome P450 enzymes, which are classified into 43 subfamilies and 18 families based on the similarity of amino acid sequences.
- The highest concentration of CYP enzymes is found within the centrilobular hepatocytes.
- Nomenclature: the prefix "CYP" (which stands for cytochrome P450)- PLUS family number PLUS a letter representing the subfamily PLUS isoenzyme number (e.g., CYP2D6 means isoenzyme no. 6 of subfamily "D" of the 2nd main family)
- Induction and inhibition: CYP induction increases the rate of metabolism of the substrate, while CYP inhibition decreases it.
- Activity of CYP2D6 is increased in individuals with a duplication on chromosome 22.
- These individuals require a significantly higher dose to achieve the desired effect.
- Role in carcinogenesis: metabolic activation of certain pro-carcinogens (e.g., aflatoxin, sterigmatocystin) → induction of cancer (e.g., hepatocellular carcinoma) 
Carbamazepine acts as both substrate and inducer of CYP3A4.
Rifampicin and carbamazepine are some of the strongest inducers of cytochrome P450 enzymes and can thus interact with many drugs.
P450 inducers: ↓ warfarin levels (Chronic Alcoholics Steal Phen-Phen and Never Refuse Greasy Carbs): C - Chronic alcohol use, S - St. John's wort, P - Phenytoin, P - Phenobarbital, N - Nevirapine, R - Rifampin, G - Griseofulvin, C - Carbamazepine
P450 inhibitors can be remembered with “sickfaces.com group”: S - Sulfonamides, I - Isoniazid, C - Cimetidine, K - Ketoconazole, F - Fluconazole, A - Alcohol (binge drinking), C - Ciprofloxacin, E - Erythromycin, S - Sodium valproate, C - Chloramphenicol, O - Omeprazole, M - Metronidazole, G - Grapefruit juice
The P450 substrates beta-BLOCKers, THEophylline, WARfarin, STATins, ORAL contraceptives, and antiPSYCHOtics: Let's BLOCK THE WAR between STATes with ORAL and PSYCHOlogical tools.
Adverse effects of substances can be classified into the following groups:
We list the most important adverse effects. The selection is not exhaustive.
Cardiovascular adverse effects
|Overview of substances causing cardiovascular adverse effects|
|Cardiovascular adverse effects||Substance||Main clinical use|
|Coronary vasospasm|| |
|Cutaneous flushing|| |
| || |
|Torsades de pointes after QT prolongation|| || |
| || |
| || |
Dilated cardiomyopathy caused by Doxorubicin and Danurobicin can be prevented with Dexrazoxane.
ABCDE to recall the 5 class of drugs potentially causing torsades de pointes: antiArrhythmic, antiBiotics, antiCychotics, antiDepressants and antiEmetics.
Endocrine adverse effects
|Overview of substances causing endocrine adverse effects|
|Endocrine adverse effects||Substance||Main clinical use|
| || |
|Hot flashes|| |
|Hyperprolactinemia|| || |
Hydrochlorotiazide, Niacin, Tacrolimus and corticoSteroids can lead to High amouNT of Sugars in your blood.
SUlfonamides, Lithium and AMiodarone may induce SUdden Lethargy And Myxedema (hypothyroidism).
If patients taking Carbamazepine, Cyclophosphamide or SSRI get SIADH, they Can't Concentrate Serum Sodium!
Gastrointestinal adverse effects
|Overview of substances causing gastrointestinal adverse effects|
|Gastrointestinal adverse effects||Substance||Main clinical use|
|Acute cholestatic hepatitis with jaundice|| || |
| || |
|Pseudomembranous colitis|| || |
Diuretics, Alcohol, Corticosteroids, Valproic acid, Azathioprine and Didanosine are Drugs that Abrupty Cause Violent Abdominal Distress.
Hematologic adverse effects
|Overview of substances causing hematologic adverse effects|
|Hematologic adverse effects||Substance||Main clinical use|
Autoimmune hemolytic anemia (positive direct Coombs test)
Drug reaction with eosinophilia and systemic symptoms (DRESS)
|Megaloblastic anemia|| |
Thrombotic complications (this side effect is mediated by increased estrogen level)
Clozapine, Propylthiouracile, Methimazole, Carbamazepine, Ticlopidine, Dapsone, Colchicine, Chemotherapeutics and Gangiclovir Causes Pretty Major Collapse To Defense Cells Called Granulocytes (agranulocytosis).
Carbamazepine, Methimazole, NSAIDs, Benzene, Chloramphenicol, Propylthiouracile Can't Make New Blood Cells Properly (aplastic anemia).
MetHyldopa, Penicilline, and Cephalosporins may induce HeMolytic anemia (Positive Coombs test).
YoU'RE Having a MEGA BLAST with Plays, Music, and Snacks! (HydroxyUREa, Phenytoin, Methotrexate and Sulfonamides may induce MEGAloBLASTic anemia)
Musculoskeletal/skin/connective tissue adverse effects
|Overview of substances causing musculoskeletal/skin/connective tissue adverse effects|
|Musculoskeletal/skin/connective tissue adverse effects||Substance||Main clinical use|
| || |
Stevens-Johnson syndrome (rash)
Methyldopa, Phenytoin, Hydralazine, Isoniazid, Procainamide, Sulfonamides, Minocycline and Etanercept may provoke Malar rash, Painful HIPS, & Myalgia (Systemic Lupus Erythematous).
Protease Inhibitors and Corticosteroids PICk your FAT somewhere else!
Cyclosporine, CA2+ channel blockers, and Phenytoin can Cause Chubby Puffy Gums!
Pyrazinamide, Furosemide, Niacin, Cyclosporine and Thiazides may induce Pain on your Feet, Needle-shaped Crystals, and Tophi (gout).
With 5-FLuorouracil, Amiodarone, Sulfonamides & Tetracyclines you may geT sunburn in a FLASh (photosensitivity)!
AntiEpiLEpTIC drugs, Penicillin, ALlopurinol and SULFonamides may provoke STEVE JOHNSON (syndrome), an EcLEcTIC PAL who loves SUrF!
TETracyclines may discolor your TEeTh!
Neurologic adverse effects
|Overview of substances causing neurologic adverse effects|
|Neurologic adverse effects||Substance||Main clinical use|
Parkinson-like syndrome and/or tardive dyskinesia
|Peripheral neuropathy|| |
| || |
|Idiopathic intracranial hypertension|| |
| || |
Antipsychotics, Reserpine, and Metoclopramide may make your ARMs rigid as in Parkinson's disease.
Isoniazide, Bupropion, Imipenem/cilastatin, Tramadol and Enflurane lower seizures threshold (I BITE my tongue).
Topiramate, Digoxin, Isoniazid, Ethambutol, Vigabatrin and PDE-5 inhibitors: These Drugs Induce Problems to Vision and Eyes!
Multiorgan adverse effects
|Overview of substances causing multiorgan adverse effects|
|Multiorgan adverse effects||Substance||Main clinical use|
Nephrotoxicity and/or ototoxicity
| || |
To remember that Sulfonylureas, Cephalosporines, Metronidazole, Griseofulvin and Procarbazine can cause disulfiram-like reaction: Sorry, Can't Mess with Gin and Port wine.
If you use Loop diuretics, Amphotericin B, cisPlatin, Vancomycin, or Aminoglycosides Listening And Peeing Vanish Away.
Respiratory adverse effects
|Overview of substances causing respiratory adverse effects|
|Respiratory adverse effects||Substance||Main clinical use|
|Pulmonary fibrosis|| |
CArmustine, NiTrofurantoin, Busulfan, Amiodarone, Bleomycin, Methotrexate: I CAN'T Breathe Air Because of these Medications.
Renal and genitourinary adverse effects
|Overview of substances causing renal and genitourinary adverse effects|
|Renal and genitourinary adverse effects||Substance||Main clinical use|
|Fanconi syndrome|| || |
| || |
|Hemorrhagic cystitis|| || |
Diuretics, Penicillins, Sulfonamides, PPIs, NSAIDs and Rifampin may cause blooDy Pee, Sterile Pyuria, 'N' Rash (interstitial nephritis).