Rheumatology Boards Pearls
Master the 5-Step Method to Decode Complex Questions
A systematic approach to dissecting board questions and avoiding common cognitive traps
Introduction
Part 1: The 5-Step Dissection Method
Let me walk you through a systematic approach using modified examples:
How to Use the 5-Step Method to Decode Questions
01
Question Stem First
  • Identifies what they're actually testing
  • Determines your strategy (diagnosis vs. next step vs. treatment)
02
Scan for Anchors
  • Look for emergency flags
  • Find the most specific/unusual findings
  • Identify discordant details
03
Pattern Recognition
  • Match clinical constellation to disease patterns
  • Recall relevant guidelines/rules
04
Systematic Elimination
  • Give yourself a reason to eliminate each wrong answer
  • Keep finalists if truly stuck
05
Verify Your Answer
  • Check if your choice fits ALL the details
  • If two answers remain, consider context/timing/severity
EXAMPLE 1: The "What Are They Really Asking?" Question

Sample Question: A 76-year-old woman presents with a 3-week history of right-sided headache, scalp tenderness when brushing her hair, and fatigue. She mentions that chewing steak has become uncomfortable. She has a history of diabetes and hypertension. On exam, there is tenderness over the right temporal region. Labs show ESR 92 mm/hr, CRP 9.2 mg/dL. Fundoscopic exam shows a pale, swollen optic disc. What is the most appropriate NEXT step in management?
Answer choices:
  • A. Start oral prednisone 20 mg daily
  • B. Order temporal artery biopsy within 2 weeks
  • C. Start intravenous methylprednisolone immediately
  • D. Obtain MRI brain with contrast
LET'S WALK THROUGH THIS TOGETHER:
STEP 1: Read the QUESTION STEM First
(before diving into the vignette)
What I'm looking for:
"most appropriate NEXT step in management"
My thinking: This is asking what I do RIGHT NOW, not diagnosis, not long-term management. The word "NEXT" is critical—they want the immediate action.
Common trap: Students often jump to "temporal artery biopsy" because that's what you "should do" for GCA. But is it the NEXT step?
STEP 2: Scan for the Clinical Anchor
What catches my attention in the vignette:
  • 76 years old (elderly)
  • Headache + scalp tenderness + jaw claudication = classic triad
  • CRITICAL DETAIL: "pale, swollen optic disc" = this is describing ischemic optic neuropathy
My internal dialogue:
Wait—this isn't just suspected GCA. This patient has VISION INVOLVEMENT. This is an emergency. The fundoscopic finding tells me permanent blindness could happen.
STEP 3: Identify the Clinical Pattern
Pattern recognition:
Giant cell arteritis with vision loss = MEDICAL EMERGENCY
The rule I recall:
When GCA involves the eyes, you start high-dose steroids IMMEDIATELY to prevent permanent blindness. You don't wait for biopsy confirmation.
STEP 4: Eliminate Wrong Answers with Reasoning
Let me think through each option:
A. Oral prednisone 20 mg daily
My thinking: This is WAY too low a dose for GCA with vision involvement. Standard dosing is 1 mg/kg (usually 40-60 mg), and this patient needs even higher doses because of the optic nerve finding.
ELIMINATE ❌
B. Temporal artery biopsy within 2 weeks
My thinking: Yes, I need the biopsy for confirmation, but "within 2 weeks" is too slow. The question asks "NEXT step" and this patient could go blind in hours to days. Also, steroids don't significantly affect biopsy results for about 2 weeks, so I can start treatment first.
ELIMINATE ❌
C. IV methylprednisolone immediately
My thinking: This matches the urgency. High-dose IV steroids are indicated when there's visual involvement to prevent contralateral eye loss. This is the emergent action.
KEEP ✓
D. MRI brain with contrast
My thinking: This might show inflammation in the vessels, but it doesn't TREAT the patient. The question asks for management, not further workup. Also, imaging delays treatment.
ELIMINATE ❌
STEP 5: Verify My Choice Against the Clinical Scenario
Double-check: Does IV methylprednisolone make sense as the NEXT step?
  • Patient has visual involvement (optic disc changes) ✓
  • This is time-sensitive ✓
  • Treatment shouldn't be delayed for diagnosis confirmation ✓
  • I can still get the biopsy afterward ✓
ANSWER: C
KEY TEACHING POINTS FROM THIS QUESTION:
1
The question stem determines your strategy
"Next step" ≠ "best diagnostic test" ≠ "most likely diagnosis"
2
Scan for emergency flags
Vision changes, neurologic symptoms, hemodynamic instability—these change your answer strategy
3
Don't let "standard workup" fool you
Yes, temporal artery biopsy is part of the workup, but TIMING matters
4
The vignette gives you hints
"Pale, swollen optic disc" wasn't decoration—it was screaming "EMERGENCY!"
Part 2
Common Cognitive Traps
Let me show you how board questions exploit predictable thinking errors:
EXAMPLE 2: The "Buzzword Trap"

Sample Question: A 42-year-old woman with hepatitis C presents with 6 months of progressive joint pain in her hands and knees, a purplish rash on her lower legs, and numbness in her feet. She describes her joints as being "very stiff in the morning for about an hour." Labs show RF 280 IU/mL (normal <20), low C4, and elevated CRP. What is the most appropriate NEXT test?
Answer choices:
  • A. Anti-CCP antibodies
  • B. Cryoglobulins
  • C. Hepatitis C viral load
  • D. EMG/nerve conduction studies
LET'S DISSECT THE TRAP:
Where your brain wants to go:
"RF is elevated + morning stiffness + joint pain = rheumatoid arthritis, so I should check anti-CCP!"
Why that's the trap:
STEP 1: Question stem analysis
"Most appropriate NEXT test" = they're asking what will give me the diagnosis
STEP 2: Look for the DISCORDANT details
Let me list what DOESN'T fit RA:
Hepatitis C
Why mention this?
Purplish rash on lower legs
RA doesn't cause this—think vasculitis
Numbness in feet
Peripheral neuropathy—RA doesn't typically cause this
Low C4
Unusual for RA, common in cryoglobulinemia
STEP 3: Recognize the alternative pattern
This is the Meltzer's Triad of cryoglobulinemia:
1. Arthralgias
✓
2. Purpura
✓
3. Weakness/neuropathy
✓
Plus: Hepatitis C + high RF + low C4 = classic for type II/III cryoglobulinemia
STEP 4: Eliminate with reasoning
A. Anti-CCP
Would help diagnose RA, but this doesn't fit RA clinically
RF can be positive in cryo without RA
ELIMINATE ❌
B. Cryoglobulins
Directly tests for the disease I suspect
Explains ALL the findings: joints, rash, neuropathy, labs
KEEP ✓
C. Hepatitis C viral load
Sure, she has hep C, but knowing the viral load doesn't give me the rheumatologic diagnosis
This is a distractor using available history
ELIMINATE ❌
D. EMG/NCS
Would confirm neuropathy, but I already know she has numbness
Doesn't give me the unifying diagnosis
ELIMINATE ❌
ANSWER: B
THE LESSON:
"Buzzwords" can mislead you. The question WANTED you to see "RF positive + joint pain" and jump to RA. But boards test whether you can recognize when the FULL clinical picture doesn't match the buzzword diagnosis.
Strategy: When you see a buzzword, ask yourself: "What else in this vignette DOESN'T fit my initial diagnosis?"
EXAMPLE 2: The "Multiple Red Flags" Question

Sample Question: A 28-year-old woman with known SLE (on hydroxychloroquine and azathioprine) presents for contraception counseling. She is sexually active and wants to avoid pregnancy. Her SLE history includes arthritis, malar rash, and positive ANA. She has no history of nephritis or thrombosis. Recent labs show: lupus anticoagulant positive, anticardiolipin IgG 55 units (repeat testing 14 weeks ago also positive at 48 units), anti-beta-2-glycoprotein negative. She tried a progestin implant last year but had continuous spotting and wants a different option. What is the most appropriate contraceptive recommendation?
Answer choices:
  • A. Combined oral contraceptive pill
  • B. Copper intrauterine device
  • C. Transdermal estrogen-progestin patch
  • D. Progestin-only pill
STEP 1: Read the Question Stem First
What they're asking:
"Most appropriate contraceptive recommendation"
My thinking:
This is asking me to choose the BEST birth control option for THIS specific patient. Not just any contraception—it needs to be appropriate for her medical conditions.
Key recognition:
This is a "safety" question—which option won't harm her?
STEP 2: Scan for Clinical Anchors (The Danger Signals)
What catches my attention:
  • Young woman with SLE (need to consider her underlying disease)
  • CRITICAL DETAILS:
Lupus anticoagulant POSITIVE
Anticardiolipin IgG 55 units (>40 = moderate-high titer)
Tested TWICE, 14 weeks apart (persistent = meets criteria!)
Tried progestin implant before (so progestins are tolerated)
My internal dialogue: Wait—she has antiphospholipid antibodies that are PERSISTENT. This means she meets criteria for antiphospholipid syndrome. Even though she hasn't had a clot YET, she's at high risk. This changes everything about contraception choices.
The alarm bell: ESTROGEN + ANTIPHOSPHOLIPID ANTIBODIES = THROMBOSIS RISK
STEP 3: Identify the Clinical Pattern & Rule
Pattern:
SLE with persistent antiphospholipid antibodies
The critical rule I need to recall:
  • Estrogen-containing contraceptives increase thrombosis risk in ANYONE
  • In patients with aPL antibodies, estrogen is contraindicated (even without prior clots)
  • Progestin-only methods are safe
What makes this tricky: She has no HISTORY of clots, so you might think estrogen is okay. WRONG. The persistent aPL antibodies alone are enough to avoid estrogen.
STEP 4: Eliminate Wrong Answers with Reasoning
Let me work through each systematically:
A. Combined oral contraceptive pill
My thinking: This contains ESTROGEN + progestin. The estrogen is the problem.
She has persistent aPL antibodies → estrogen is contraindicated
It doesn't matter that she hasn't had a clot yet—we're preventing the first one
ELIMINATE ❌
B. Copper IUD
My thinking: No hormones at all, so no thrombosis risk. This is SAFE.
Highly effective contraception
She didn't mention trying this before, so no known intolerance
Wait, but let me check the other options before committing...
KEEP ✓
C. Transdermal estrogen-progestin patch
My thinking: This ALSO contains estrogen, just delivered through the skin instead of orally
Route of administration doesn't matter—estrogen is still contraindicated with aPL
This is a classic distractor: "maybe a different formulation is okay?" Nope.
ELIMINATE ❌
D. Progestin-only pill
My thinking: Progestin-only = safe in aPL. No estrogen.
She tolerated the progestin implant (same hormone, just different delivery)
The spotting she had was from the implant formulation, not the hormone itself
POP is highly effective IF taken consistently
KEEP ✓
Now I have TWO possible answers: B and D. How do I choose?
STEP 5: Consider the Clinical Context to Choose Between Finalists
Copper IUD (B):
  • No hormones → definitely safe with aPL ✓
  • Highly effective (>99%) ✓
  • Long-acting (don't need to remember daily) ✓
  • No spotting issues like she had with progestin implant ✓
Progestin-only pill (D):
  • Safe with aPL ✓
  • Effective BUT requires perfect timing (same time daily)
  • If she misses pills, effectiveness drops significantly
  • She already expressed dissatisfaction with progestin side effects (spotting)
My decision-making: Both are medically safe, but the copper IUD is MORE effective and addresses her concern about the spotting she experienced with progestin. Also, IUDs are considered superior for long-acting reversible contraception.
FINAL ANSWER: B (Copper IUD)
However, in real guidelines, both B and D are acceptable. If the question specifically said "most appropriate" and both appeared, I'd choose copper IUD because it's more effective and avoids the progestin side effect she disliked.
KEY TEACHING POINTS:
1
"No history of thrombosis" doesn't mean estrogen is safe
in aPL patients
2
Persistent positive aPL tests
(2 positive results ≥12 weeks apart) = contraindication to estrogen
3
Different routes of estrogen
(oral, patch, ring) are all equally contraindicated
4
Progestin-only methods are safe:
IUD, POP, implant, depot injection
5
When multiple answers are medically correct
consider patient-specific factors (she didn't like progestin side effects)
EXAMPLE 3: The "Diagnosis vs Management" Question

A 58-year-old woman presents with a 3-week history of painful fingers, low-grade fever (100.8°F), and a facial rash. Her blood pressure has been difficult to control, and 8 weeks ago her physician started hydralazine 100 mg daily in addition to her hydrochlorothiazide and lisinopril. On exam, she has an erythematous macular rash across her cheeks. Labs: ANA 1:320, anti-histone antibody positive, anti-dsDNA 8 IU/mL (normal <10), C3 160 mg/dL (normal), C4 22 mg/dL (normal). What is the most likely diagnosis?
Answer choices:
  • A. Drug-induced lupus from hydralazine
  • B. Drug-induced lupus from hydrochlorothiazide
  • C. Systemic lupus erythematosus
  • D. Undifferentiated connective tissue disease
STEP 1: Read the Question Stem
What they're asking:
"Most likely diagnosis"
My thinking:
They want me to differentiate between types of lupus and identify which diagnosis best fits the clinical picture.
Strategy for "diagnosis" questions:
Build a case for AND against each option
STEP 2: Scan for Discriminating Features
What I notice:
  • Recent medication change (hydralazine started 8 weeks ago)
  • Symptoms started 3 weeks ago (after the medication)
  • Key lab findings:
ANA positive (consistent with either drug-induced or SLE)
Anti-histone POSITIVE (this is a clue!)
Anti-dsDNA LOW/negative
C3 and C4 NORMAL (not low!)
My internal dialogue: The timing is suspicious—new drug, then new symptoms. But I need to differentiate between drug-induced lupus and real SLE. The lab pattern is KEY here.
STEP 3: Identify Discriminating Patterns
What distinguishes drug-induced lupus from SLE?
Pattern match: Anti-histone positive + normal complements + dsDNA negative = drug-induced lupus
STEP 4: Eliminate with Reasoning
A. Drug-induced lupus from hydralazine
Timing fits: started 8 weeks ago, symptoms began 3 weeks ago
Dose is 100 mg daily (higher doses >50mg increase risk)
Lab pattern fits perfectly: anti-histone+, dsDNA-, normal C3/C4
Hydralazine is a well-known cause of drug-induced lupus
KEEP ✓
B. Drug-induced lupus from hydrochlorothiazide
My thinking: HCTZ can cause lupus-like reactions BUT much less common than hydralazine
She's been on HCTZ longer (implied by "difficult to control BP")
If HCTZ was the cause, why did symptoms start only recently?
Timing doesn't fit as well
ELIMINATE ❌
C. Systemic lupus erythematosus
My thinking: The lab pattern argues AGAINST this
SLE usually has low complements and positive dsDNA
No mention of renal involvement, severe cytopenias, serositis
The temporal relationship with hydralazine is too coincidental
ELIMINATE ❌
D. Undifferentiated connective tissue disease
My thinking: This is a "wastebasket" diagnosis when you can't classify
But I CAN classify this based on the clear drug-induced pattern
UCTD would be considered if there was no drug association
ELIMINATE ❌
STEP 5: Verify Against Clinical Scenario
Double-check my choice:
  • Hydralazine started recently ✓
  • Appropriate dose to cause drug-induced lupus (>50mg) ✓
  • Classic lab findings (anti-histone+, normal complements) ✓
  • Clinical manifestations fit (arthritis, rash, fever) ✓
  • No features strongly suggesting true SLE (no renal/CNS disease, normal labs) ✓
ANSWER: A
KEY TEACHING POINTS:
Timing matters
New drug → new symptoms suggests drug-induced
Anti-histone antibodies are the CLUE
Very sensitive for drug-induced lupus
Normal complements favor drug-induced
over active SLE
Hydralazine dose >50 mg daily
increases risk significantly
Other drugs causing lupus
procainamide, isoniazid, minocycline, TNF inhibitors
EXAMPLE 4: The "Atypical Presentation" Question

Sample Question: A 40-year-old man with Behçet's disease presents with 8 weeks of worsening headaches and difficulty walking. He describes the room "spinning" when he stands. His Behçet's has been controlled on colchicine for oral ulcers, but he developed recurrent uveitis last year requiring addition of mycophenolate. MRI brain shows T2 hyperintensity and enhancement in the brainstem with mild atrophy. MR venography is negative for thrombosis. CSF shows lymphocytic pleocytosis with elevated protein. He is offered pulse IV cyclophosphamide plus steroids but declines cyclophosphamide due to fertility concerns. What alternative therapy is most appropriate?
Answer choices:
  • A. Azathioprine
  • B. Apremilast
  • C. Infliximab
  • D. Cyclosporine
STEP 1: Identify the Question Type
What they're asking:
"Most appropriate alternative therapy"
My thinking:
This is a treatment question, but with a twist—the first-line agent was declined. I need to know what the NEXT best option is, not just standard treatment.
Key phrase:
"Alternative therapy" = second-line option
STEP 2: Scan for the Critical Diagnosis
What I identify:
  • Known Behçet's disease
  • NEW neurologic symptoms: headaches, vertigo, gait difficulty
  • MRI findings: Brainstem involvement (T2 hyperintensity)
  • This is NEURO-BEHÇET'S = serious complication
My internal dialogue: This isn't just regular Behçet's flaring. Brainstem involvement is neuro-Behçet's, which has different treatment considerations. The standard immunosuppression for mucocutaneous or joint disease won't be enough.
The critical recognition: Neuro-Behçet's requires more aggressive therapy
STEP 3: Recall the Treatment Algorithm
What I need to remember:
  • Neuro-Behçet's is a severe manifestation
  • First-line: cyclophosphamide + high-dose steroids
  • Patient declined cyclophosphamide
  • What's the next best option for neuro-Behçet's?
  • TNF inhibitors (especially infliximab) have shown efficacy in neuro-Behçet's
  • They're used when: (1) first-line fails, OR (2) first-line not tolerated/declined
  • Other immunosuppressants (azathioprine) are used for NON-neurologic Behçet's
STEP 4: Systematic Elimination
A. Azathioprine
My thinking: Azathioprine IS used in Behçet's disease
HOWEVER: It's used for mucocutaneous disease, arthritis, uveitis
For NEURO-Behçet's, azathioprine is less effective
This would be appropriate for his uveitis but not for brainstem involvement
ELIMINATE ❌
B. Apremilast
My thinking: Apremilast is a PDE4 inhibitor used for oral ulcers in Behçet's
It's not immunosuppressive enough for neuro-Behçet's
This treats mild disease, not CNS involvement
ELIMINATE ❌
C. Infliximab
My thinking: TNF inhibitor with proven efficacy in neuro-Behçet's
Used in combination with steroids for severe disease
Specifically recommended in guidelines for parenchymal neurologic involvement
Appropriate when cyclophosphamide is contraindicated or declined
KEEP ✓
D. Cyclosporine
My thinking: Cyclosporine is used in Behçet's for uveitis
HOWEVER: There's a WARNING about cyclosporine in neuro-Behçet's
Some evidence suggests it may WORSEN neurologic manifestations
Generally avoided in patients with CNS involvement
ELIMINATE ❌
STEP 5: Verify the Choice
Checking infliximab:
  • Proven efficacy for neuro-Behçet's in studies ✓
  • Guideline-recommended for severe/refractory cases ✓
  • Can be used when cyclophosphamide is not an option ✓
  • Works for both neurologic AND his uveitis ✓
  • Addresses fertility concerns (doesn't affect sperm like cyclophosphamide) ✓
ANSWER: C
KEY TEACHING POINTS:
1
Neuro-Behçet's ≠ regular Behçet's
Treatment escalation required
2
Location matters
Parenchymal (brainstem) involvement is more serious than vascular
3
Cyclosporine WARNING
May worsen neuro-Behçet's—avoid!
4
TNF inhibitors
Effective for severe organ-threatening Behçet's
5
Always address patient concerns
Fertility is a legitimate reason to seek alternatives
EXAMPLE 5: The "Diagnosis with Multiple Findings" Question

Sample Question: A 62-year-old man is admitted with 6 months of recurrent fevers (102-103°F), fatigue, and a rash on his chest and arms. The fevers occur every 3-4 weeks and last 1-2 weeks. He has tried colchicine without benefit. Prednisone 30 mg daily controls symptoms but they return when tapered below 15 mg. He's otherwise healthy with no prior medical problems. When he tried anakinra for presumed adult-onset Still's disease, he developed severe injection site reactions requiring discontinuation. Labs: WBC 11,500, Hgb 9.8 g/dL with MCV 108 fL, platelets 88,000, ESR 95 mm/hr, ferritin 850 ng/mL. Bone marrow biopsy shows hypercellular marrow with vacuoles in myeloid and erythroid precursor cells. What genetic test should be ordered?
Answer choices:
  • A. ADA2 gene sequencing
  • B. MEFV gene for familial Mediterranean fever
  • C. TNFRSF1A gene
  • D. UBA1 gene sequencing
STEP 1: Question Stem Analysis
What they're asking:
"What genetic test should be ordered?"
My thinking:
This is a diagnosis question disguised as a "which test" question. I need to figure out what disease this is, then I'll know which gene to test.
STEP 2: Scan for Unique/Pathognomonic Findings
Let me list the findings in order of specificity:
Common findings (not helpful for differentiation):
  • Recurrent fevers
  • Elevated inflammatory markers
  • Steroid-responsive
Unusual findings (more specific):
  • Macrocytic anemia (MCV 108) - not typical for inflammatory conditions
  • Thrombocytopenia - suggests marrow involvement
  • Severe reaction to anakinra - interesting drug response pattern
  • Bone marrow vacuoles in precursor cells - THIS IS VERY SPECIFIC!

My internal dialogue: That bone marrow finding is NOT something I see in typical autoinflammatory diseases. Vacuoles in myeloid and erythroid precursors is pathognomonic for something specific.
STEP 3: Pattern Recognition
What disease presents with this unique constellation of findings in an older adult male?
Clinical Picture
  • Older adult male (>50)
  • Recurrent fevers, rash
  • Steroid-dependent (autoinflammatory features)
Hematologic Clues
  • Macrocytic anemia
  • Thrombocytopenia
  • Pathognomonic bone marrow vacuoles
Treatment Response
  • Severe reactions to biologics (e.g., anakinra)
  • Poor response to standard immunosuppressants
This distinct pattern points directly to a rare, recently described autoinflammatory condition: VEXAS syndrome.
Key features to recall about VEXAS:
Caused by a UBA1 gene mutation on the X chromosome, affecting myeloid and erythroid precursors.
Typically affects males over 50, explaining the patient's demographics.
The acronym stands for Vacuoles, E1 enzyme, X-linked, Autoinflammatory, Somatic.
Characterized by treatment-resistant autoinflammation and progressive cytopenias with macrocytic anemia.
The bone marrow finding of vacuoles in myeloid and erythroid precursor cells is pathognomonic.
STEP 4: Eliminate Based on Disease Patterns
A. ADA2 gene sequencing
My thinking: ADA2 deficiency causes polyarteritis nodosa-like vasculitis. Usually presents in CHILDHOOD, not at age 62. Doesn't cause bone marrow vacuoles or macrocytic anemia.
ELIMINATE ❌
B. MEFV gene (FMF)
My thinking: Familial Mediterranean Fever presents in youth, not at age 62. Typical FMF episodes are 1-3 days, not 1-2 weeks. Doesn't cause bone marrow changes. Colchicine failure makes FMF less likely (it usually responds).
ELIMINATE ❌
C. TNFRSF1A gene
My thinking: This causes TNF receptor-associated periodic syndrome (TRAPS). It can present in adults, and episodes can be 1-2 weeks. HOWEVER: It doesn't cause bone marrow vacuoles, macrocytic anemia, or thrombocytopenia.
ELIMINATE ❌
D. UBA1 gene sequencing
My thinking: UBA1 mutation = VEXAS syndrome. This matches the older male demographic, pathognomonic bone marrow vacuoles, macrocytic anemia + thrombocytopenia, severe reaction to anakinra, and treatment-resistant autoinflammation.
KEEP ✓
STEP 5: Confirm the Answer
I'm confident in UBA1 because the bone marrow finding is the KEY. Vacuolization of myeloid and erythroid precursors is essentially pathognomonic for VEXAS; no other autoinflammatory condition causes this.
Demographics: Older male ✓
Hematologic: Macrocytic anemia ✓
Marrow: Vacuoles ✓
Treatment: Biologic failure/reactions ✓
Steroid-dependent ✓
ANSWER: D
Summary: How to Use the 5-Step Method
1
STEP 1: Question Stem First
Identifies what the question is truly testing, guiding your strategy (diagnosis, next step, treatment, etc.).
2
STEP 2: Scan for Anchors
Pinpoint critical information: emergency flags, unique findings, or discordant details that challenge common patterns.
3
STEP 3: Pattern Recognition
Match the clinical constellation to known disease patterns and recall relevant guidelines or rules.
4
STEP 4: Systematic Elimination
Articulate a specific reason to eliminate each incorrect answer, leaving only the most plausible options.
5
STEP 5: Verify Your Answer
Confirm that your chosen answer aligns with all clinical details. If multiple answers remain, evaluate context, timing, and severity.