Pharmacology

High Yield USMLE Step 1 Notes

Welcome to the Pharmacology High-Yield Notes for Step 1.

These are the most commonly tested topics on the exam—ideal for quick review in your last
2 weeks before the exam, when you're short on time, or when you're just starting out and
want to focus on what is high yield. Created and peer-reviewed by physicians who scored
260+ on Step 1 in a Q&A style to reinforce active learning.

How to use this file

y
Read the question ➔ cover the answer ➔ self-quiz before revealing.

u
Review the NOTES ➔ they include high-yield details you don't want to
miss.

h G Need tutoring? Scan the QR code or visit The Match Guy Tutoring.

c
Watch the video explanations that go along with this file for deeper

t
understanding.

Ma
Pharmacokinetics & Pharmacodynamics

e
1. A 60M with alcoholic cirrhosis presents with confusion and signs of drug toxicity. He is

h
taking a highly protein-bound antiarrhythmic medication. How does his liver disease affect
the drug’s Vd?

T
➔ Increased

Note: Volume of distribution Vd is increased due to lower plasma protein binding.

Liver disease reduces albumin, increasing free drug levels and expanding Vd.
More drug in tissues reduces the efficacy of dialysis for removal

2. A 70M with CHF and significant peripheral edema is started on a hydrophilic diuretic. How
does fluid overload affect the drug dosing and volume of distribution?
➔ Fluid overload increases the volume of distribution, potentially requiring a higher
loading dose to achieve therapeutic plasma levels.

Note: Hydrophilic drugs stay mainly in extracellular fluid, which is expanded in

edema and CHF.
Increased Vd dilutes the drug concentration in plasma, reducing initial effectiveness
if dose isn’t adjusted.

© 2025 TheMatchGuy LLC. All rights reserved. Page 1

Version 1.0 May 2025. No part of this document may be reproduced or distributed without written permission. For personal study only. Medical information
herein is for educational purposes and does not constitute clinical advice. Always confirm with current guidelines and your institution’s policies.
 Mnemonic Dialysis
Drug Characteristics
“PET” Effectiveness

Large, charged, protein-bound ➞ Remains in High (easily

P
Plasma ➞ low Vd dialyzed)

Small, hydrophilic ➞ Stays mainly in ECF ➞

E Moderate
Medium Vd

Small, lipophilic ➞ Distributes into Tissues (incl. Low (poorly

T
fat) ➞ High Vd dialyzed)

3. A patient is prescribed a new medication that is eliminated at a constant rate regardless of

plasma concentration. After increasing the dose, the patient developed signs of toxicity.
Which elimination kinetics does this drug follow?

y
➔ Zero-order elimination

Gu
Note: Zero-order drugs eliminate at a constant amount per unit time due to enzyme
saturation.
Plasma concentration decreases linearly, not exponentially.
Examples: Phenytoin, ethanol, aspirin (at toxic doses)

tch
4. A 45-year-old man overdoses on aspirin and develops toxicity. Why does aspirin

a
elimination shift from first-order to zero-order kinetics at high doses?
➔ Enzyme saturation causes elimination to proceed at a constant rate, independent of

M
plasma concentration

e
Note: At therapeutic doses, aspirin elimination is first-order.
At toxic doses, elimination enzymes saturate, leading to zero-order kinetics and risk

h
of accumulation.

TKey Difference:
✔
Zero-order: Elimination rate is constant (enzyme saturation).
✔
First-order: Elimination rate varies with concentration (proportional elimination)

5. A factory worker collapses with lactic acidosis and cherry-red skin after inhaling fumes.
Increasing oxygen fails to improve symptoms. What explains this?
➔ Cyanide causes noncompetitive inhibition of cytochrome oxidase (Complex IV),
decreasing Vmax irreversibly

Note: Noncompetitive inhibitors bind allosteric sites ➞ ⇓ Vmax, no change in Km.

Increasing substrate (O₂) does not overcome inhibition.

6. A 45-year-old man ingests antifreeze and develops metabolic acidosis. He is treated with
IV ethanol. What is ethanol’s mechanism of action?
➔ Ethanol is a competitive inhibitor of alcohol dehydrogenase, preventing formation
of toxic metabolites from methanol.

© 2025 TheMatchGuy LLC. All rights reserved. Page 2

 Note: Competitive inhibitors resemble substrates and increase Km but do not
affect Vmax.
Increasing substrate concentration can overcome competitive inhibition.

Feature Competitive Inhibitors Noncompetitive Inhibitors

Structure Resembles substrate Binds allosteric site

Overcome by ⇑ [S] Yes (e.g., statin vs. HMG-CoA) No

Effect on Km ⇑ Km (⇓ affinity) No change

Effect on
No change (reversible) ⇓ Vmax (e.g., lead poisoning)
Vmax

uy
7. A heroin-dependent patient develops sudden withdrawal after starting buprenorphine.
What explains this reaction?
➔ Buprenorphine displaces heroin but provides weaker μ-receptor activation

h G
Note: Buprenorphine = partial μ-opioid agonist ➞ high affinity, low efficacy.
Displaces full agonists (e.g., heroin) from receptors.

c
Weaker activation ➞ precipitated withdrawal in opioid-dependent patients.

at
e M
Th
Created with [Link]

8. In dose-response testing of two antihypertensive drugs: Drug X requires a low dose but
has a limited maximal effect; Drug Y requires a higher dose but achieves greater maximal
effect. Which drug is more potent and which is more efficacious?
➔ Drug X is more potent (lower dose needed), Drug Y is more efficacious (higher
maximal effect)

Note: Potency = dose needed for effect (related to affinity).

Efficacy = maximum effect achievable, independent of potency.

© 2025 TheMatchGuy LLC. All rights reserved. Page 3

 uy
Created by [Link]

Urine pH & drug elimination

h G
9. A 24-year-old woman presents to the ED after ingesting a large amount of aspirin. IV
sodium bicarbonate is administered. Primary mechanism of this intervention?

c
➔ Alkalinization of urine

at
Note: Aspirin is a weak acid.
Alkaline urine increases ionization, preventing reabsorption and enhancing excretion.

e M
10. A patient with amphetamine toxicity is given ammonium chloride. Rationale for this
intervention?

h
➔ Acidic urine increases ionization of amphetamines, preventing reabsorption.

T Note: Weak bases like amphetamines are better cleared in acidic urine.
Ionized form remains trapped in renal filtrate.

11. You are treating a patient who ingested an unknown substance with a pKa of 8.2. At
physiological pH (7.4), would the drug predominantly be ionized or non-ionized?
➔ Predominantly ionized

Note: Weak bases are ionized when PH <pka ➞ ⇑ absorption & reabsorption.

Non-ionized form crosses membranes easily ➞ ⇓ renal clearance.

Urine acidification traps the drug in ionized form ➞ ⇑ excretion.

© 2025 TheMatchGuy LLC. All rights reserved. Page 4

General anesthetics
12. A patient under general anesthesia with an inhaled agent develops severe muscle
rigidity, hypercarbia, tachycardia, and hyperthermia. Anesthetic likely responsible?
➔ Isoflurane (or any volatile anesthetic except nitrous oxide)

Note: Malignant Hyperthermia:

Due to excessive calcium release from the sarcoplasmic reticulum ➞ sustained
contraction, hypermetabolism.
Presents with muscle rigidity, hypercarbia, tachycardia, hyperthermia, acidosis,
rhabdomyolysis.

Triggering Agents: Volatile anesthetics (isoflurane, sevoflurane, desflurane) and

succinylcholine.

Treatment: Dantrolene (ryanodine receptor antagonist).

y
Halothane can cause hepatotoxicity. use Sevoflurane in those with liver diseases.

u
G
13. A patient requires rapid induction and recovery during surgery. Which inhaled anesthetic
is the best choice?

h
➔ Desflurane or Nitrous Oxide (lowest blood solubility ➞ fastest induction/recovery)

tc
Note: Desflurane has low potency but very low blood solubility.

a
Nitrous oxide has the lowest potency and fastest onset.

e M
Inhaled Anesthetic
Lipid Solubility (Potency -
MAC⇓)
Blood Solubility
(Induction/Recovery)

Th
Halothane

Nitrous Oxide
High (Very potent)

Very Low (Least potent)

High (Slow induction/recovery)

Very Low (Fastest induction)

📝 Trick to remember:
"High Lipid = High Potency = Low MAC"

"High Blood = Slow Induction"

© 2025 TheMatchGuy LLC. All rights reserved. Page 5

Maintenance & Loading Dose
14. A 65F with Hx of liver cirrhosis is prescribed warfarin, which is primarily metabolized by
the liver. Later, she presents with elevated INR levels. What pharmacokinetic change is
responsible for this?
➔ Liver cirrhosis ➞ ⇓ hepatic clearance ➞ ⇑ half-life ➞ drug accumulation ➞
increased bleeding risk

Note: Clearance (CL): Rate at which a drug is eliminated from the body.
Liver Cirrhosis Impact: Reduced metabolism ➞ prolonged drug action ➞ toxicity.
Clinical Implication: Lower doses or longer intervals may be required to prevent toxicity.

15. A 68M with sepsis is started on vancomycin. His physician notes an increased volume of
distribution (Vd) due to his body habitus. How should the loading dose be adjusted?
➔ Increased Vd ➞ drug distributes more widely ➞ higher loading dose needed to

y
achieve therapeutic levels

tissues.

u
Note: Volume of Distribution (Vd): Indicates how extensively a drug spreads into body

G
Obesity ➞ more tissue mass ➞ greater distribution ➞ higher loading dose
required.

ch
Clinical Implication: Dosing must account for Vd to reach effective plasma
concentration.

t
a
Key takeaway:
✔⇑ Vd ➞ ⇑ t₁/₂
✔⇑ CL ➞ ⇓ t₁/₂

e M
Impaired liver or kidney function ➞ ⇓ clearance ➞ ⇑ half-life ➞ prolonged drug
exposure ➞ increased toxicity risk.

Th
16. A 72-year-old woman with chronic kidney disease is started on digoxin. A week later, she
presents with nausea, visual disturbances, and bradycardia. What explains the toxicity?
➔ Renal impairment ➞ ⇓ clearance ➞ ⇑ half-life ➞ digoxin accumulation ➞ toxicity

Note: In patients with renal impairment, the dose of digoxin must be reduced, and
serum levels should be monitored to prevent toxicity.
Management: Monitor renal function regularly, adjust dose based on GFR, and
consider digoxin-specific antibody (Digibind) if toxicity is severe.
Renal dysfunction reduced insulin and morphine metabolite clearance, causing
hypoglycemia and sedation, requiring dose reduction.
Adjust the loading dose based on Vd and the maintenance dose based on CL to
ensure proper drug levels and avoid toxicity.

© 2025 TheMatchGuy LLC. All rights reserved. Page 6

Drug & enzyme reactions
17. A 60-year-old patient with atrial fibrillation is started on warfarin. He is also taking
rifampin. How would this affect his maintenance dose?
➔ Rifampin ➞ increased clearance of warfarin ➞ higher maintenance dose required

Note: Enzyme Induction: Rifampin accelerates warfarin metabolism.

Monitor INR frequently and adjust the dose.

18. A 72F with generalized anxiety is prescribed diazepam. She experiences confusion and
excessive sedation. Which phase of drug metabolism is most likely impaired in elderly
patients?
➔ Phase I (Oxidation)

Note: Phase I Reactions: Oxidation, Reduction, Hydrolysis (Old Rats Hide)

y
Elderly lose Phase I first ➞ "Old People Fade First"

Gu
19. A patient on warfarin is started on ciprofloxacin for a UTI. One week later, her INR is
significantly elevated. Which drug interaction is responsible?

h
➔ CYP450 Inhibition (Ciprofloxacin)

tc
Note: CYP450 Inhibitors: [Link]
Effect: ⇓ Warfarin breakdown ➞ ⇑ INR and bleeding risk

a
e M
CYP-450 Inhibitors
("[Link]")
Sodium valproate, Isoniazid, Cimetidine, Ketoconazole,
Fluconazole, Alcohol (acute), Chloramphenicol,
Erythromycin, Sulfonamides, Ciprofloxacin, Omeprazole,

h
Metronidazole

TCYP-450 Inducers ("CRAP

GPS")
Carbamazepine, Rifampin, Alcohol (chronic), Phenytoin,
Griseofulvin, Phenobarbital, St. John’s Wort

20. A 45M with COPD on theophylline presents with vomiting, insomnia, tremors,
palpitations. He recently started ciprofloxacin for a UTI. Likely cause of his Sx?
➔ Theophylline toxicity due to CYP450 inhibition by ciprofloxacin

Note: Theophylline has a narrow therapeutic index — small changes in dose or

metabolism can lead to toxicity.
CYP1A2 inhibitors (e.g., ciprofloxacin, cimetidine, erythromycin, verapamil) reduce
metabolism ➞ toxic accumulation.
Toxicity signs:
GI: nausea, vomiting
CNS: tremors, insomnia, seizures
CV: palpitations, tachyarrhythmias

© 2025 TheMatchGuy LLC. All rights reserved. Page 7

21. A 55-year-old man on isoniazid therapy tests positive for anti-histone antibodies. What
genetic trait is responsible?
➔ Slow Acetylation

Note: SHIP Drugs: Sulfasalazine, Hydralazine, Isoniazid, Procainamide ➞ Drug-

induced lupus
Mechanism: Slow metabolism ➞ drug accumulation

Key takeaway:

✔ Slow acetylators ➞ More drug accumulation ➞ Higher toxicity risk

✔ Fast acetylators ➞ Rapid clearance ➞ Lower drug efficacy
Sympathetic and Parasympathetic

y
22. A 30M presents with excessive sweating and is diagnosed with primary hyperhidrosis. He
is prescribed a topical drug. Which neurotransmitter is blocked by the drug to reduce

u
sweating?
➔ Acetylcholine

h G
Note: Sweat glands are sympathetic but use ACh (M₃), not NE.
Blocking M₃ reduces sweating.

✔
atc
Key takeaway:
✔Sweat glands = Sympathetic but use ACh instead of norepinephrine.
Adrenal medulla = Direct preganglionic innervation

e M
23. A 72M with BPH is prescribed tamsulosin. A week later, he reports dizziness when
standing. MOA of this side effect?

h
➔ Blocks α₁ receptors ➞ vasodilation ➞ orthostatic hypotension

T Note: α₁ blockers (tamsulosin) relax prostate smooth muscle but may cause postural
hypotension by blocking α₁ receptors in vessels.

24. A patient with asthma uses albuterol during an acute episode and gets better. Which
receptor is stimulated?
➔ β₂ agonist ➞ bronchodilation

Note: β₂ activation ➞ ⇑cAMP ➞ smooth muscle relaxation ➞ bronchodilation.

However, at high doses, β₁ receptors in the heart can be secondarily stimulated,
causing tachycardia and palpitations.
Avoid in patients with CAD.

25. A 30-year-old man develops sudden-onset wheezing, hypotension, and urticaria after a
bee sting. What is DOC?
➔ IM epinephrine

© 2025 TheMatchGuy LLC. All rights reserved. Page 8

 Note: Epinephrine (α ≈ β):
α₁ ➞ vasoconstriction ➞ ⇑ BP, ⇓ mucosal edema
β₁ ➞ ⇑ HR & CO
β₂ ➞ bronchodilation
Rapidly reverses airway obstruction and hypotension ➞ first-line treatment for
anaphylaxis.

26. A 43M presents with distended abdomen after inguinal hernia repair. USG shows post-
void retention. Which muscarinic agonist would be most appropriate?
➔ Bethanechol

Note: M₃ agonist ➞ activates detrusor muscle ➞ promotes urination.

Used for post-op or neurogenic bladder.
blocking M₃ by oxybutynin= useful for urinary urgency and incontinence.

uy
27. A 38-year-old woman exposed to insecticides develops miosis, bradycardia, and
salivation. DOC?
➔ Atropine

h G
Note: Organophosphate Poisoning
Cause: Inhibition of acetylcholinesterase ➞ Excess acetylcholine ➞ Cholinergic toxicity

c
Some mushrooms produce similar effects.

t
Clinical Features (DUMBBELLS): Diarrhea, Urination, Miosis, Bradycardia,

a
Bronchospasm, Bronchorrhea, Emesis, Lacrimation, Lethargy, Salivation, Sweating
Treatment:

M
1. Atropine (muscarinic antagonist)
2. Pralidoxime (2-PAM) (reactivates acetylcholinesterase)

The
28. A 50-year-old man with CKD presents with hypertensive emergency. He is given IV
fenoldopam. MOA?
➔ D₁ receptor agonist ➞ vasodilation of renal arteries ➞ ⇓BP

Note: Fenoldopam is a short-acting D₁ agonist.

Used in hypertensive emergencies, especially in patients with renal insufficiency.
It promotes natriuresis and maintains renal blood flow

29. A 60-year-old man with GERD is prescribed famotidine. What is its target and
mechanism?
➔ H₂ receptor antagonist ➞ ⇓gastric acid secretion

Note: H₂ blockers (e.g., ranitidine, famotidine) are used to treat GERD & peptic
ulcers by blocking histamine in parietal cells.
H1- blockers like diphenhydramine are used for allergic rhinitis

© 2025 TheMatchGuy LLC. All rights reserved. Page 9

30. A 65-year-old with Alzheimer’s disease is started on donepezil. What receptor is
targeted and what is the effect?
➔ M₁ agonist (via cholinesterase inhibition) ➞ enhances cognition

Note: M₁ receptors in CNS help with memory.

Donepezil is an AChE inhibitor used in Alzheimer’s.

31. A 62-year-old man with newly diagnosed CHF is started on dobutamine. Which receptor
does this drug primarily act on and what is the effect?
➔ β₁ receptor agonist ➞ ⇑ heart rate and contractility

Note: β₁ receptors are found in the heart and kidneys.

Dobutamine = β₁ agonist ➞ used in acute heart failure to increase cardiac output.

y
32. A 47-year-old woman is prescribed metoclopramide for nausea. What is the drug’s

u
mechanism of action?
➔ D₂ receptor antagonist ➞ blocks dopamine in the CTZ (chemoreceptor trigger zone)

G
Note: D₂ blockade in the CNS ➞ antiemetic effect.
Commonly used in gastroparesis and chemo-induced nausea.

h
at
action?
c
33. A 10-year-old boy is started on methylphenidate for ADHD. What is the mechanism of

➔ Reverses NET ➞ ⇑ NE and dopamine in the synapse ➞ improves attention and

M
focus

e
Note: ADHD stimulants (methylphenidate, amphetamines) enhance catecholamine
release by reversing NET and DAT. used in ADHD and Narcolepsy.

Th
34. A 45-year-old woman on MAO inhibitors uses cocaine recreationally. She presents with
severe hypertension, headache, and agitation. Why is her crisis worse?
➔ Cocaine blocks NE reuptake (⇑ NE); MAOIs prevent NE breakdown ➞ massive NE
buildup ➞ hypertensive crisis

Note: Combining reuptake inhibitors (like cocaine/TCAs) with MAOIs causes

catecholamine storm.
Avoid tyramine-containing foods too (aged cheese).

35. A 70-year-old man is admitted with fever, dysuria and warm extremities, low BP (75/40),
and elevated HR (110). What is the vasopressor of choice?
➔ Norepinephrine

Note: Norepinephrine (α1 > β1) — increases MAP via vasoconstriction and
maintains perfusion.
NE is the DOC for septic shock. It increases both systolic and diastolic BP, leading to
reflex bradycardia sometimes.

© 2025 TheMatchGuy LLC. All rights reserved. Page 10

 Receptor Location Effect Drugs

Bladder detrusor, SM contraction, 🟢Bethanechol ➞ Urinary retention

M₃
GI, glands, eye ⇑Secretions 🔴Oxybutynin ➞ Urinary urgency
α₁
Vascular SM,
bladder sphincter
Vasoconstriction,
urinary retention
🔴Tamsulosin, prazosin ➞ BPH
Heart (SA/AV
⇑HR,
🔴Metoprolol ➞ HTN,arrhythmias
β₁
node), JG cells
⇑Contractility
⇑Renin
🟢Dobutamine ➞ CHF
Bronchial SM,
β₂ uterus, skeletal
Bronchodilation,
SM relaxation
🟢Albuterol ➞ Asthma, preterm labor
vessels

🔴Haloperidol ➞ Psychosis

y
⇓Prolactin,
D₂
CNS (striatum,
⇓Nausea/Vomitin 🟢Bromocriptine ➞

u
pituitary)
g hyperprolactinemia

G 🔴Loratadine, Diphenhydramine ➞
⇑Mucus,
Respiratory tract,
H₁ bronchoconstrict
skin Allergic rhinitis, urticaria

h
ion

H₂

atc Gastric parietal

cells

Kidney (collecting
⇑Acid secretion

⇑Water
🔴Famotidine ➞ GERD, peptic ulcers
🟢Desmopressin ➞ Central DI,

M
V₂ reabsorption via nocturnal enuresis
duct)
AQP2 🔴Conivaptan ➞ SIADH

T e
🟢:Agonist 🔴:Antagonist

h
36. A patient receives botulinum toxin for blepharospasm. What is the mechanism of action?
➔ Inhibits ACh release at NMJ ➞ prevents muscle contraction

Note: Botulinum toxin blocks presynaptic ACh release

Used for muscle spasm, cosmetic use, and Diffuse Esophageal Spasm (DES)

37. Which drug class should be started first in a patient with pheochromocytoma preparing
for surgery, and why is it is preferred over phentolamine?
➔ Phenoxybenzamine ➞ irreversible α-blockade

Note: Phenoxybenzamine = irreversible α-blocker

Phentolamine = reversible α-blocker
Starting β-blockers before α-blockade risks unopposed α stimulation ➞
hypertensive crisis

© 2025 TheMatchGuy LLC. All rights reserved. Page 11

Drug metabolism & elderly
38. A 78M on digoxin presents with nausea, visual changes, and confusion. Labs show
impaired renal function and high digoxin levels. Why does toxicity develop despite normal
dosing?
➔ ⇓ Total body water in elderly ➞ ⇓ Vd for hydrophilic drugs like digoxin ➞ drug
accumulation

Note: Elderly = ⇓ renal clearance, ⇓ total body water, altered

distribution/metabolism.
Renally cleared, narrow-TI drugs (digoxin, lithium) require dose adjustment.

39. A 60-year-old man with a history of peptic ulcer disease is started on ibuprofen for
chronic back pain. What is the most important complication to consider?
➔ ⇑ Risk of GI bleeding

uy
Note: NSAIDs inhibit prostaglandin synthesis ➞ ⇓ gastric mucus and bicarbonate
➞ mucosal injury.

G
Risk is higher in older adults and those with prior ulcers.
Co-prescribe a PPI to reduce GI complications.

tch
40. A 75F is given diphenhydramine for allergic rhinitis. She returns with confusion, dry
mouth, and urinary retention. Why should diphenhydramine be avoided in older adults?

Ma
➔ Due to anticholinergic effects

Note: Diphenhydramine = strong anticholinergic ➞ ⇑ risk of delirium, falls, urinary

retention.

e
Elderly have ⇓ cholinergic reserve and slower clearance.

h
Listed in Beers Criteria — avoid in older adults.

T
41. A 68-year-old man is taking multiple medications. His new drug is highly protein-bound.
What happens if he has hypoalbuminemia?
➔ ⇑ Free (active) drug concentration ➞ ⇑ toxicity risk

Note: Low albumin (e.g., in liver disease, elderly) ➞ less protein binding ➞ more
free drug ➞ enhanced effect/toxicity of protein-bound drugs (e.g., warfarin,
phenytoin).

42. A 74-year-old man started on diazepam for anxiety. What pharmacokinetic property
makes this drug risky in the elderly?
➔ ⇓ Phase I metabolism ➞ prolonged half-life and sedation

Note: Diazepam undergoes Phase I metabolism (oxidation), which declines with

age.
Safer options like lorazepam use Phase II (unchanged in elderly).

© 2025 TheMatchGuy LLC. All rights reserved. Page 12

43. A 70-year-old woman on amitriptyline for neuropathic pain reports dizziness and near-
syncope on standing. Vitals show orthostatic hypotension. What is the likely cause?
➔ α₁ receptor blockade by a tricyclic antidepressant (TCA)

Note: TCAs (e.g., amitriptyline, nortriptyline) inhibit NET, block muscarinic, H₁, and
α₁ receptors.
α₁ blockade ➞ vasodilation ➞ orthostatic hypotension, especially in elderly.
Other TCA side effects: anticholinergic toxicity, sedation, QT prolongation.
Use caution in older adults.

Common drugs to avoid in elderly according to BEER’S criteria

α-blockers: ⇑ risk of hypotension
Anticholinergics, TCAs, antihistamines, opioids: ⇑ delirium, falls, constipation,
urinary retention
Benzodiazepines: ⇑ sedation, falls, cognitive impairment

y
NSAIDs: ⇑ GI bleeding (esp. with anticoagulants)
PPIs (long-term): ⇑ risk of C. difficile infection

Gu
🏁 Final Thoughts

ch
You made it to the end—well done! These high-yield notes are designed to save you time

t
and keep you focused on what actually matters for Step 1. Review these vignettes regularly

a
—steady practice beats cramming.

M
Need one-on-one tutoring? Scan the QR code or visit The Match Guy Tutoring — we’ve
helped hundreds of students reach their score goals.

The
🎥 Don’t forget to watch the video lessons that go with this file—they break down tricky
concepts and reinforce key takeaways.

📂 Want access to all our high-yield files for Step 1?

If you haven’t signed up yet, you can join here

Good luck—and we’re rooting for you all the way to Match Day! 🎯
© 2025 TheMatchGuy LLC. All rights reserved. Page 13