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* Rapid tolerance → tachyphylaxis.
* CYP450 induction → increased metabolism of substrate drugs.
* CYP450 inhibition → decreased metabolism of substrate drugs.
* Prodrugs may have reduced activity with enzyme inhibition.
* Codeine → CYP2D6 → morphine.
* Clopidogrel → CYP2C19 activation.
* Rifampin → CYP450 inducer.
* Grapefruit juice → intestinal CYP3A4 inhibition.
Test yourself: 5 high-yield MCQs
General Pharmacology Quiz
Q1. A drug has a half-life of 8 hours. Approximately how long will it take to reach steady state?
A. 8 hours
B. 16 hours
C. 32–40 hours
D. 64 hours
Q2. A competitive antagonist is added to a full agonist. What happens?
A. Decreased Emax
B. Increased EC50 without changing Emax
C. Decreased EC50
D. Increased Emax
Q3. Which drug follows classic zero-order kinetics?
A. Penicillin
B. Amoxicillin
C. Phenytoin
D. Metoprolol
Q4. A patient with hypoalbuminemia receives warfarin. What happens to its free fraction?
A. Decreases
B. Increases
C. Remains unchanged
D. Drug absorption decreases
Q5. A patient taking rifampin experiences reduced effectiveness of oral contraceptives. What is the mechanism?
A. CYP450 inhibition
B. CYP450 induction
C. Competitive receptor antagonism
D. Reduced renal clearance
Answers to the 5 General Pharmacology MCQs:
* C. 32–40 hours — Steady state occurs after 4–5 half-lives.
* B. Increased EC50 without changing Emax — Competitive antagonist.
* C. Phenytoin — Zero-order kinetics.
* B. Increases — Hypoalbuminemia increases the free fraction of warfarin.
* B. CYP450 induction — Rifampin increases metabolism of oral contraceptives.
#USMLE #USMLEStep1 #usmleprep #pharmacology
| 2 | * Hepatically metabolized drugs may accumulate.
* Reduced albumin can increase the free fraction of highly protein-bound drugs.
* Reduced hepatic metabolism can increase toxicity.
* Examples requiring caution include benzodiazepines, opioids, and warfarin.
Older adults
* Reduced renal function can increase drug accumulation.
* Reduced hepatic metabolism can prolong drug effects.
* Increased sensitivity to sedatives and anticholinergics is common.
* Polypharmacy increases the risk of drug interactions.
* Start with lower doses when clinically appropriate and titrate carefully.
20. Drug Transporters
* Transporters regulate drug movement across cellular membranes.
* P-glycoprotein (P-gp) is an efflux transporter.
* It pumps drugs out of cells.
* It is present in the intestine, liver, kidney, and blood-brain barrier.
* P-gp limits absorption of some drugs and restricts their entry into the brain.
Important examples:
* Digoxin is a P-gp substrate.
* Verapamil inhibits P-gp and can increase digoxin concentrations.
* Rifampin induces P-gp and can reduce digoxin exposure.
21. Important Drug Antidotes – General Pharmacology
These are frequently tested in pharmacology and toxicology.
* Acetaminophen overdose → N-acetylcysteine.
* Opioid overdose → Naloxone.
* Benzodiazepine overdose → Flumazenil (selected cases).
* Warfarin → Vitamin K; 4-factor PCC for major bleeding.
* Unfractionated heparin → Protamine sulfate.
* Dabigatran → Idarucizumab.
* Factor Xa inhibitors → Andexanet alfa in selected cases; PCC may be used depending on the situation.
* Methanol poisoning → Fomepizole.
* Ethylene glycol poisoning → Fomepizole.
* Methotrexate toxicity → Leucovorin.
* Digoxin toxicity → Digoxin-specific antibody fragments.
* Organophosphate poisoning → Atropine + pralidoxime.
* Iron overdose → Deferoxamine.
* Lead poisoning → Chelation therapy, such as succimer in appropriate cases.
* Cyanide poisoning → Hydroxocobalamin.
* Methemoglobinemia → Methylene blue.
* Malignant hyperthermia → Dantrolene.
* Isoniazid-induced seizures → Pyridoxine (vitamin B6).
* Beta-blocker overdose → Glucagon (among other treatments).
* Calcium-channel blocker overdose → IV calcium and high-dose insulin therapy.
22. Important USMLE Pharmacology Formulas
Memorize these formulas for calculation-based questions.
Volume of distribution
Vd=Amount of drug in body/Plasma concentration
Clearance
CL=Rate of eliminatio/Plasma concentration
Half-life
t1/2=0.693 * Vd/CL
Loading dose
LD=Vd * Target concentration/F
Maintenance dose rate
MD= CL * Target concentration/F
Therapeutic index
TI=TD50/ED50
Bioavailability
F= AUC(oral)/AUC(IV) * 100
(For equal doses.)
23. Last-Minute USMLE High-Yield MCQ Pearls
* IV administration → 100% bioavailability.
* First-pass metabolism → decreased oral bioavailability.
* High Vd → extensive tissue distribution.
* High plasma protein binding → generally low Vd.
* Hypoalbuminemia → increased free fraction of albumin-bound drugs.
* Increased clearance → decreased half-life.
* Increased Vd → increased half-life if clearance remains unchanged.
* Five half-lives → approximately 97% eliminated.
* Steady state → approximately 4–5 half-lives.
* Loading dose → depends primarily on Vd.
* Maintenance dose → depends primarily on clearance.
* First-order kinetics → constant fraction eliminated.
* Zero-order kinetics → constant amount eliminated.
* Phenytoin, ethanol, high-dose aspirin → classic zero-order examples.
* Competitive antagonist → increased EC50, unchanged Emax.
* Noncompetitive antagonist → decreased Emax.
* Partial agonist → lower maximal efficacy than full agonist.
* Lower EC50 → greater potency.
* Higher Emax → greater efficacy.
* Narrow therapeutic index → close monitoring.
* Chronic receptor blockade → upregulation.
* Chronic receptor stimulation → downregulation. | 168 |
| 3 | * Pharmacodynamic interactions affect the drug’s physiological effect.
* Additive effects occur when combined effects equal the sum of individual effects.
* Synergistic effects occur when the combined effect exceeds the expected additive effect.
* Antagonistic effects occur when one drug reduces the effect of another.
Important examples:
* Benzodiazepines + opioids → synergistic respiratory depression.
* Alcohol + benzodiazepines → increased CNS depression.
* NSAIDs + warfarin → increased bleeding risk.
* ACE inhibitors + spironolactone → hyperkalemia.
* Nitrates + sildenafil → severe hypotension.
* Metoprolol + verapamil → bradycardia and AV block.
* Rifampin + oral contraceptives → reduced contraceptive effectiveness.
17. Routes of Drug Administration
Intravenous (IV)
* Directly enters systemic circulation.
* Bioavailability = 100%.
* Fastest and most predictable systemic delivery.
* No absorption phase.
* Cannot be easily reversed once administered.
Intramuscular (IM)
* Drug is injected into muscle.
* Absorption depends on blood flow.
* Can be used for depot preparations.
* Some drugs have prolonged release from IM preparations.
Subcutaneous (SC)
* Drug is injected into subcutaneous tissue.
* Absorption is generally slower than IM.
* Examples: Insulin and heparin.
Oral (PO)
* Convenient and noninvasive.
* Subject to first-pass metabolism.
* Absorption can be affected by food and GI conditions.
* Not suitable for unconscious patients or patients unable to swallow safely.
Sublingual
* Drug is absorbed through oral mucosa.
* Bypasses hepatic first-pass metabolism.
* Rapid absorption.
* Example: Nitroglycerin.
Transdermal
* Drug crosses the skin into systemic circulation.
* Avoids first-pass metabolism.
* Provides sustained drug delivery.
* Examples: Nicotine patch, fentanyl patch, scopolamine patch.
Rectal
* Some rectal venous drainage bypasses the portal circulation.
* First-pass metabolism is partially avoided.
* Useful when oral administration is not possible.
18. Pharmacogenetics
* Pharmacogenetics studies how genetic variation affects drug response.
* Genetic differences can affect drug metabolism, transport, and receptor sensitivity.
* CYP450 polymorphisms can produce poor, intermediate, normal, or ultrarapid metabolizers.
High-yield examples:
CYP2D6
* Codeine requires CYP2D6 conversion to morphine.
* Poor metabolizers may have inadequate analgesia.
* Ultrarapid metabolizers may develop opioid toxicity.
CYP2C19
* Activates clopidogrel.
* Poor metabolizers have reduced antiplatelet response.
* May increase the risk of cardiovascular events.
TPMT / NUDT15
* Metabolize thiopurines such as azathioprine and 6-mercaptopurine.
* Reduced activity increases the risk of severe myelosuppression.
HLA-B*5701
* Associated with abacavir hypersensitivity.
* Test before starting abacavir.
HLA-B*1502
* Associated with Stevens-Johnson syndrome/toxic epidermal necrolysis from carbamazepine, especially in certain Asian ancestry populations.
* Screening is recommended in at-risk populations before starting carbamazepine.
HLA-B*5801
* Associated with allopurinol-induced severe cutaneous adverse reactions.
* Consider screening in high-risk populations.
G6PD deficiency
* Oxidative medications can cause hemolytic anemia.
* Examples: Primaquine, dapsone, rasburicase, and nitrofurantoin.
19. Special Populations and Drug Dosing
Pregnancy
* Drugs can cross the placenta depending on molecular properties.
* Lipid-soluble, low-molecular-weight drugs generally cross more easily.
* Warfarin is teratogenic.
* ACE inhibitors and ARBs are contraindicated during pregnancy.
* Isotretinoin is highly teratogenic.
* Valproate increases neural tube defect risk.
* Tetracyclines can affect fetal teeth and bones.
Renal impairment
* Renally eliminated drugs may accumulate.
* Dose adjustment or longer dosing intervals may be needed.
* Examples include aminoglycosides, vancomycin, and digoxin.
* Monitor renal function and drug levels when indicated.
Hepatic impairment | 96 |
| 4 | * Leftward dose-response curve = increased potency.
* Higher maximum response = increased efficacy.
* Competitive antagonist = rightward shift without decreasing Emax.
* Noncompetitive antagonist = decreased Emax.
12. Therapeutic Index (TI)
* Therapeutic index measures the relative safety of a drug.
* It compares the toxic dose with the effective dose.
* A higher therapeutic index generally means a safer drug.
* A lower therapeutic index means the therapeutic and toxic concentrations are closer.
* Drugs with narrow therapeutic indices require close monitoring.
Formula:
TI=TD50/ED50
* TD50 = Dose producing toxicity in 50% of the population.
* ED50 = Dose producing the desired effect in 50% of the population.
Drugs with narrow therapeutic indices:
* Warfarin
* Digoxin
* Lithium
* Phenytoin
* Theophylline
* Aminoglycosides
* Cyclosporine
* Tacrolimus
USMLE clue: A patient develops toxicity despite a small increase in drug dose. Think narrow therapeutic index.
13. Receptor Regulation
Upregulation
* Upregulation means an increase in receptor number or sensitivity.
* It can occur after prolonged receptor blockade.
* Cells increase receptor expression to compensate for reduced stimulation.
Example:
* Chronic beta-blocker use increases beta-receptor expression.
* Abrupt discontinuation can cause rebound tachycardia and hypertension.
Downregulation
* Downregulation means a decrease in receptor number or sensitivity.
* It occurs after prolonged stimulation of receptors.
* It decreases cellular responsiveness to an agonist.
Example:
- Chronic exposure to beta-agonists can decrease beta-receptor responsiveness.
Remember:
* Chronic antagonist → receptor upregulation.
* Chronic agonist → receptor downregulation.
14. Tolerance and Tachyphylaxis
Tolerance
* Tolerance means decreased response to a drug after repeated administration.
* A higher dose may be required to achieve the same effect.
* It can occur because of receptor downregulation or increased drug metabolism.
* It generally develops over days to weeks, although the time course varies.
Examples:
* Opioids
* Benzodiazepines
* Alcohol
* Nitrates
Tachyphylaxis
* Tachyphylaxis is rapidly developing tolerance.
* It occurs after repeated doses over a short period.
* It may result from depletion of stored neurotransmitters or receptor desensitization.
Examples:
* Ephedrine: depletion of norepinephrine stores.
* Indirect sympathomimetics can develop tachyphylaxis.
USMLE clue: Repeated doses produce progressively smaller effects within a short time → tachyphylaxis.
15. Adverse Drug Reactions
Type A reactions
* Augmented pharmacologic effects.
* Dose-dependent.
* Predictable.
* Usually more common.
* Often preventable by adjusting the dose.
Examples:
* Insulin → hypoglycemia.
* Warfarin → bleeding.
* Opioids → respiratory depression.
* Antihypertensives → hypotension.
Type B reactions
* Bizarre reactions.
* Usually unpredictable.
* Not directly related to the usual pharmacologic effect.
* Often associated with allergy or idiosyncrasy.
* Can occur even at normal therapeutic doses.
Examples:
* Penicillin → anaphylaxis.
* Sulfonamides → severe hypersensitivity reactions.
* Genetic G6PD deficiency → hemolysis after certain oxidative drugs.
Other important adverse reactions
* Type C: Chronic use-related reactions.
* Type D: Delayed reactions.
* Type E: End-of-use or withdrawal reactions.
* Type F: Failure of therapy.
High-yield examples:
* Long-term glucocorticoids → osteoporosis (Type C).
* Teratogenicity → delayed effect (Type D).
* Abrupt clonidine discontinuation → rebound hypertension (Type E).
* Antibiotic treatment failure due to resistance → Type F.
16. Drug Interactions
* Drug interactions occur when one drug alters the effect of another drug.
* Pharmacokinetic interactions affect absorption, distribution, metabolism, or excretion. | 82 |
| 5 | * Fluoxetine and paroxetine inhibit CYP2D6.
* Amiodarone inhibits several CYP enzymes.
* Ritonavir inhibits CYP3A4.
Clinical examples:
* Erythromycin + simvastatin → increased statin concentration → rhabdomyolysis risk.
* Fluoxetine + metoprolol → increased metoprolol exposure → bradycardia risk.
* Grapefruit juice inhibits intestinal CYP3A4 → increased levels of certain medications.
Important exception: CYP induction or inhibition does not always produce the same clinical effect with prodrugs.
* Inhibition of codeine activation by CYP2D6 can decrease morphine formation and analgesia.
* Inhibition of clopidogrel activation by CYP2C19 can decrease its antiplatelet effect.
8. First-Order vs Zero-Order Kinetics
First-order kinetics
* Most drugs follow first-order kinetics.
* A constant fraction of the drug is eliminated per unit time.
* The elimination rate is proportional to drug concentration.
* Half-life remains constant.
* Increasing drug concentration increases the amount eliminated per unit time.
Examples:
* Penicillin
* Most beta-blockers
* Most antibiotics
Zero-order kinetics
* A constant amount of drug is eliminated per unit time.
* Elimination enzymes become saturated.
* Half-life is not constant.
* A small increase in dose can cause a disproportionately large increase in plasma concentration.
* Drug accumulation and toxicity are important concerns.
Three classic USMLE examples:
* Phenytoin
* Ethanol
* Aspirin at high doses
MCQ clue: A drug’s elimination becomes saturated, and its plasma concentration rises disproportionately after a small dose increase.
Answer: Zero-order kinetics.
9. Pharmacodynamics
Pharmacodynamics = What the drug does to the body.
* Pharmacodynamics describes the relationship between drug concentration and drug effect.
* Drugs act by interacting with receptors, enzymes, ion channels, or transporters.
* Agonists activate receptors.
* Antagonists block receptor activation.
* Partial agonists produce a submaximal response even when all receptors are occupied.
* Inverse agonists decrease constitutive receptor activity.
10. Agonists and Antagonists
Full agonist
* Binds to a receptor.
* Has affinity for the receptor.
* Has intrinsic activity.
* Produces maximal receptor activation when sufficient receptors are available.
Example: Morphine is a full agonist at the mu-opioid receptor.
Partial agonist
* Binds to the same receptor as a full agonist.
* Produces a lower maximal response.
* Has lower intrinsic efficacy than a full agonist.
* Can act as a functional antagonist in the presence of a full agonist.
Examples:
* Buprenorphine = partial mu-opioid agonist.
* Aripiprazole = partial dopamine D2 agonist.
* Pindolol = partial beta-adrenergic agonist.
Competitive antagonist
* Competes with an agonist for the same receptor binding site.
* Its effect can be overcome by increasing agonist concentration.
* It causes a rightward shift in the dose-response curve.
* It increases EC50.
* It does not change Emax.
Example: Naloxone competitively antagonizes opioid receptors.
Noncompetitive antagonist
* Binds irreversibly to the receptor or binds to an allosteric site.
* Cannot be overcome by simply increasing agonist concentration.
* Decreases the maximal response (Emax).
* Reduces the number of functional receptors or receptor signaling.
Example: Phenoxybenzamine irreversibly blocks alpha receptors.
11. Potency vs Efficacy
Potency
* Potency refers to the amount of drug required to produce a particular effect.
* More potent drugs require lower doses to produce the same effect.
* EC50 is the concentration producing 50% of maximal effect.
* Lower EC50 means higher potency.
Efficacy
* Efficacy refers to the maximum effect a drug can produce.
* Emax measures maximal efficacy.
* A full agonist has greater efficacy than a partial agonist at the same receptor system.
* Increasing the dose of a partial agonist cannot produce the same maximum response as a full agonist in the same system.
USMLE clue: | 86 |
| 6 | Answer: Approximately 24–30 hours.
4. Steady-State Concentration
* Steady state occurs when the rate of drug administration equals the rate of drug elimination.
* It usually takes 4–5 half-lives to achieve steady state.
* Increasing the dose increases steady-state concentration.
* Increasing the dosing frequency increases steady-state concentration if the dose per administration remains unchanged.
* Decreasing clearance increases steady-state concentration.
* Steady state can be achieved faster with a loading dose.
* A loading dose is used when rapid therapeutic drug concentrations are needed.
* A maintenance dose maintains the desired steady-state concentration.
Important formulas:
Loading dose:
LD=Target concentration * Vd/F
Maintenance dose rate:
MD rate=Target concentration * CL/F
Clinical examples:
* Digoxin: Loading dose may be used when rapid therapeutic effect is required.
* Vancomycin: Loading doses can be used in selected severe infections.
* Phenytoin: Loading dose can rapidly achieve therapeutic concentrations in seizures.
5. Drug Metabolism
* Drug metabolism is the chemical modification of drugs, mainly in the liver.
* The liver is the major site of drug metabolism.
* Metabolism usually makes drugs more water-soluble for renal excretion.
* Some drugs are converted into inactive metabolites.
* Some drugs are converted into active metabolites.
* Some drugs are prodrugs that require metabolism for activation.
Phase I reactions
* Phase I reactions include oxidation, reduction, and hydrolysis.
* Cytochrome P450 enzymes are important in Phase I metabolism.
* Phase I reactions introduce or expose functional groups.
* CYP450 enzymes are mainly located in the smooth endoplasmic reticulum of hepatocytes.
* Phase I metabolism may activate, inactivate, or occasionally produce toxic metabolites.
Examples:
* Diazepam → active metabolites.
* Codeine → morphine through CYP2D6.
* Clopidogrel → active metabolite through CYP2C19.
Phase II reactions
* Phase II reactions involve conjugation.
* Glucuronidation is a major Phase II reaction.
* Other reactions include sulfation, acetylation, methylation, and glutathione conjugation.
* Conjugation generally increases water solubility.
* Phase II reactions usually produce inactive metabolites, although exceptions exist.
High-yield examples:
* Acetaminophen is metabolized mainly by glucuronidation and sulfation.
* A small fraction is metabolized by CYP450 to NAPQI, a toxic metabolite.
* Glutathione detoxifies NAPQI.
* In acetaminophen overdose, glutathione becomes depleted.
* N-acetylcysteine replenishes glutathione and treats acetaminophen toxicity.
6. Cytochrome P450 Enzyme Inducers
* Enzyme induction increases CYP450 enzyme activity.
* It increases metabolism of drugs that are CYP substrates.
* It can decrease plasma concentrations and therapeutic effects of active drugs.
* Enzyme induction can take days to weeks because new enzyme synthesis is required.
* Prodrugs may become more active if induction increases their activation.
Mnemonic: CRAP GPS
* C = Carbamazepine
* R = Rifampin
* A = Alcohol (chronic use)
* P = Phenytoin
* G = Griseofulvin
* P = Phenobarbital
* S = St. John’s wort
Additional important inducer:
- Smoking induces CYP1A2.
Clinical examples:
* Rifampin decreases the effectiveness of oral contraceptives.
* Carbamazepine can decrease warfarin concentrations.
* Phenytoin can decrease the effectiveness of many drugs.
* Smoking increases metabolism of CYP1A2 substrates, such as theophylline.
7. Cytochrome P450 Enzyme Inhibitors
* Enzyme inhibition decreases CYP450 enzyme activity.
* It decreases metabolism of active drugs.
* This can increase plasma drug concentrations.
* Increased drug concentration can cause toxicity.
* Enzyme inhibition can occur relatively quickly.
Mnemonic:
* C = Cimetidine
* C = Ciprofloxacin
* M = Macrolides (especially erythromycin and clarithromycin)
* A = Azole antifungals
* G = Grapefruit juice
* I = Isoniazid
* V = Valproate
* S = Sulfonamides
Additional examples: | 113 |
| 7 | General Pharmacology: If you go through this thoroughly, I promise you won’t miss a single General Pharmacology question 🔥🔥💯
1. Pharmacokinetics
Pharmacokinetics = What the body does to the drug.
Four major processes:
* Absorption
* Distribution
* Metabolism
* Excretion
Absorption
* Absorption is the movement of a drug from its administration site into systemic circulation.
* Most drugs are absorbed by passive diffusion.
* Lipid-soluble drugs cross cell membranes more easily.
* Nonionized drugs cross membranes more easily than ionized drugs.
* Weak acids are more nonionized in acidic environments.
* Weak bases are more nonionized in alkaline environments.
* Most drug absorption occurs in the small intestine because of its large surface area.
* First-pass metabolism occurs when an orally administered drug passes through the intestinal wall and liver before reaching systemic circulation.
* First-pass metabolism decreases oral bioavailability.
* Sublingual, transdermal, and IV administration bypass hepatic first-pass metabolism.
Bioavailability (F)
* Bioavailability is the fraction of an administered drug that reaches systemic circulation unchanged.
* IV administration has 100% bioavailability.
* Oral drugs usually have less than 100% bioavailability.
* First-pass metabolism decreases bioavailability.
* Bioavailability can be affected by absorption and hepatic metabolism.
Distribution
* Distribution is the movement of a drug from blood into tissues.
* Highly lipid-soluble drugs distribute widely into tissues.
* Highly protein-bound drugs remain more in the plasma.
* Albumin mainly binds acidic drugs.
* Alpha-1 acid glycoprotein mainly binds basic drugs.
* Only the free (unbound) drug is pharmacologically active, freely filtered by the glomerulus, and available for metabolism.
* Hypoalbuminemia increases the free fraction of highly albumin-bound drugs.
* This can increase drug toxicity.
Volume of Distribution (Vd)
* Vd = Amount of drug in the body / Plasma drug concentration.
* High Vd means the drug is extensively distributed into tissues.
* Low Vd means the drug remains mainly in the bloodstream.
* Lipid-soluble drugs generally have a high Vd.
* Highly plasma protein-bound drugs generally have a low Vd.
* Edema and ascites can increase Vd of water-soluble drugs.
High-yield clinical example:
Digoxin has a large volume of distribution because it accumulates in tissues, particularly skeletal and cardiac muscle.
2. Drug Clearance
* Clearance is the volume of plasma cleared of a drug per unit time.
* Clearance measures the body’s ability to eliminate a drug.
* Total clearance = Renal clearance + Hepatic clearance + Other clearance.
* Increased clearance decreases plasma drug concentration.
* Decreased clearance increases plasma drug concentration.
* Renal impairment decreases clearance of renally eliminated drugs.
* Liver disease can decrease clearance of drugs metabolized by the liver.
* Creatinine clearance is commonly used to estimate renal function for drug dosing.
* Drugs with narrow therapeutic indices require closer monitoring when renal or hepatic function changes.
High-yield formula:
CL = \frac{\text{Rate of elimination}}{\text{Plasma concentration}}
3. Half-life (t½)
* Half-life is the time required for plasma drug concentration to decrease by 50%.
* After one half-life, 50% of the drug remains.
* After two half-lives, 25% remains.
* After three half-lives, 12.5% remains.
* After four half-lives, 6.25% remains.
* After five half-lives, approximately 3% remains.
* Approximately 4–5 half-lives are required to reach steady state.
* Approximately 4–5 half-lives are also required to eliminate most of a drug after discontinuation.
* Long half-life means the drug remains in the body longer.
* Short half-life means the drug is eliminated more rapidly.
* Decreased renal or hepatic clearance can increase half-life.
* Increased volume of distribution can increase half-life.
Formula:
t1/2=0.693 * Vd/CL
USMLE clue: A drug has a half-life of 6 hours. How long will it take to reach steady state? | 218 |
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Happy Irreechaa🥰 | 1 729 |
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| 17 |  Sin texto... | 1 410 |
| 18 |  Happy Ethiopian New Year 🎊🎊🎊 | 1 235 |
| 19 | WHO guidelines for malaria - 10 September 2026 | 1 595 |
| 20 |  🌼 መልካም አዲስ ዓመት! | Happy Enkutatash! 🌼
Baga Bara Haaraa Geessan!
To all members of Pharmacy News:
May this New Year bring fresh energy, academic triumphs, clinical excellence, and boundless success to your journey in healthcare!
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℞: Peace, Robust Health, Joy & Prosperity
Sig: Take daily all year long. Refills: Unlimited! 💊✨
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Wishing you and your families a blessed and prosperous Ethiopian New Year!
Warm regards,
Pharmacist Kenenisa S.
Founder & Admin, Pharmacy News
(#Enkutatash #PharmacyNews #MelkamAddisAmet 🌼🇪🇹) | 1 724 |
