Finals Practice

Question 1

1. What is the most likely acid-base disorder?
   A. Respiratory acidosis
   B. Metabolic acidosis with respiratory compensation
   C. Mixed respiratory and metabolic acidosis
   D. Metabolic alkalosis

Answer 1

B. Metabolic acidosis with respiratory compensation
💡 Rationale & Discussion:
* Low pH (7.18) = acidemia
* HCO₃⁻ low (14), AG high (24) = high anion gap metabolic acidosis
* PaCO₂ is appropriately low, suggesting respiratory compensation
* Common in DKA and sepsis
* No sign of mixed disorder based on ABG (Winter’s formula can confirm)

Question 2

2. What is the most appropriate initial management for this patient?
   A. Start IV insulin drip
   B. Give 2L bolus of 0.9% NSS and initiate oxygen
   C. Administer bicarbonate IV
   D. Start broad-spectrum oral antibiotics

Answer 2

B. Give 2L bolus of 0.9% NSS and initiate oxygen
💡 Rationale & Discussion:
* Patient is in shock + severe hypoxia → fluids + oxygen FIRST
* IV insulin needed but after initial resuscitation
* Bicarbonate not routinely given unless pH < 6.9
* Oral antibiotics inappropriate in unstable, possibly septic patient

Question 3

3. What is the most likely diagnosis?
   A. Diabetic ketoacidosis (DKA)
   B. Hyperosmolar hyperglycemic state (HHS)
   C. Sepsis with pneumonia, triggering DKA
   D. ARDS from aspiration pneumonia

Answer 3

C. Sepsis with pneumonia, triggering DKA
💡 Rationale & Discussion:
* Hyperglycemia + AG metabolic acidosis = DKA
* CXR: infiltrate = pneumonia
* WBC ↑, lactate ↑ = sepsis
* Likely infection precipitated DKA, not isolated DKA or HHS (no severe dehydration)

Question 4

4. Based on the CXR findings, what is the best initial antibiotic choice?
   A. Amoxicillin-clavulanate
   B. Ceftriaxone + azithromycin
   C. Piperacillin-tazobactam
   D. Vancomycin + meropenem

Answer 4

B. Ceftriaxone + azithromycin
💡 Rationale & Discussion:
* Community-acquired pneumonia: dual therapy covers S. pneumoniae + atypicals
* Piperacillin-tazo reserved for HAP/VAP or septic shock
* Vanco + meropenem = overkill unless MDR concern

Question 5

5. What ECG finding would most concern you in this patient?
   A. Sinus tachycardia
   B. ST depression in anterior leads
   C. Prolonged QTc
   D. T wave flattening

Answer 5

B. ST depression in anterior leads
💡 Rationale & Discussion:
* Tachycardia common in fever/sepsis
* ST changes = possible demand ischemia or MI, especially with hypoxia + shock
* ECG changes in sepsis must be watched for myocardial ischemia
* Monitor troponins & consider ischemic workup

Question 6

6. What is the target blood glucose for this patient once stabilized?
   A. <110 mg/dL
   B. 110–125 mg/dL
   C. 150–200 mg/dL
   D. <200 mg/dL at all times

Answer 6

C. 150–200 mg/dL
💡 Rationale & Discussion:
* Based on Harrison’s DKA target during treatment
* Avoids hypoglycemia & cerebral edema while acidosis resolves
* Tighter control is not needed during acute critical care phase

Question 7

7. Which electrolyte should be checked and corrected before giving insulin?
   A. Calcium
   B. Sodium
   C. Potassium
   D. Chloride

Answer 7

C. Potassium
💡 Rationale & Discussion:
* Insulin shifts K⁺ into cells → risk of hypokalemia → arrhythmia
* Must check K⁺ before insulin
* If K⁺ <3.3 mmol/L → hold insulin, give K⁺ first

Question 8

8. What complication is most likely if glucose is corrected too rapidly in this patient?
   A. Hypokalemia
   B. Pulmonary embolism
   C. Cerebral edema
   D. Acute kidney injury

Answer 8

C. Cerebral edema
💡 Rationale & Discussion:
* Rapid shifts in osmolarity → water moves into brain
* Most feared DKA complication, especially in children and elderly
* Emphasizes slow correction of hyperglycemia and fluids

Question 9

9. Which clinical sign indicates possible progression to ARDS?
   A. PaO₂/FiO₂ ratio <300
   B. Fever >39°C
   C. Blood glucose >400 mg/dL
   D. WBC >20,000

Answer 9

A. PaO₂/FiO₂ ratio <300
💡 Rationale & Discussion:
* ARDS diagnostic criteria: PaO₂/FiO₂ <300 + bilateral infiltrates + hypoxemia not explained by CHF
* Fever and WBC = infection but not specific for ARDS
* ARDS = non-cardiogenic pulmonary edema

Question 10

10. Which scoring tool can help determine severity and guide ICU admission?
    A. CURB-65
    B. Wells score
    C. CHADS2
    D. Ranson’s criteria

Answer 10

A. CURB-65
💡 Rationale & Discussion:
* CURB-65 = Confusion, Urea >7, RR ≥30, BP <90/60, Age ≥65
* Score ≥2 = consider hospitalization
* Used for pneumonia severity
* Wells = DVT/PE, CHADS2 = AFib, Ranson = pancreatitis

Question 11

❓1. What is the most likely diagnosis?
A. Acute transverse myelitis
B. Metastatic spinal tumor
C. Spinal cord infarct
D. Tuberculous spondylitis (Pott’s disease)

Answer 11

D. Tuberculous spondylitis (Pott’s disease)

💡 Rationale & Discussion:

Classic presentation: back pain + fever + progressive neurologic deficits

Imaging = vertebral body destruction + paravertebral abscess

History of TB + elevated ESR + caseating lesion = Pott’s disease

Sputum AFB often negative in extrapulmonary TB

Question 12

2. What is the most specific diagnostic test for confirmation?
   A. ESR
   B. Spine X-ray
   C. TB PCR or culture from biopsy/aspirate
   D. Mantoux (PPD) skin test

Answer 12

C. TB PCR or culture from biopsy/aspirate

💡 Rationale & Discussion:

Definitive dx = isolate M. tuberculosis from lesion

TB PCR = rapid; culture = gold standard

Imaging + ESR are supportive but not confirmatory

Mantoux = exposure, not diagnostic of active disease

Question 13

❓3. What is the most appropriate next step in management?
A. Immediate surgical decompression
B. Empiric anti-TB treatment + monitor response
C. IV steroids and antibiotics for presumed pyogenic abscess
D. Wait for culture confirmation before treatment

Answer 13

B. Empiric anti-TB treatment + monitor response

💡 Rationale & Discussion:

High clinical suspicion + imaging = treat empirically

Delay in TB treatment can cause permanent neurologic damage

Surgical decompression only if severe or progressive deficits

Question 14

❓4. What is the typical CSF profile in CNS TB?
A. ↓ protein, ↓ glucose, neutrophilic pleocytosis
B. ↑ protein, ↑ glucose, lymphocytic predominance
C. ↑ protein, ↓ glucose, lymphocytic predominance
D. Normal protein and glucose, mild lymphocytosis

Answer 14

C. ↑ protein, ↓ glucose, lymphocytic predominance

💡 Rationale & Discussion:

TB meningitis = chronic granulomatous inflammation

CSF:
📈 Protein ↑
📉 Glucose ↓
🔬 Lymphocytes ↑

Opening pressure often elevated

Neutrophils = early or bacterial cause

Question 15

❓5. A 36-year-old woman with weight loss and painless neck swelling is suspected to have TB lymphadenitis. What is the best diagnostic approach?
A. Fine needle aspiration biopsy with AFB staining and TB PCR
B. CT scan of the neck
C. ESR and Mantoux
D. Excisional biopsy followed by culture

Answer 15

A. Fine needle aspiration biopsy with AFB staining and TB PCR

💡 Rationale & Discussion:

FNAB = minimally invasive and diagnostic

AFB stain + TB PCR = rapid identification

Excisional biopsy is more invasive and often reserved for unclear cases

Question 16

❓6. In suspected CNS TB, which imaging finding supports the diagnosis?
A. Ring-enhancing lesion with central necrosis and mass effect
B. Diffuse meningeal enhancement, especially basal cisterns
C. Subdural hematoma over cerebral convexity
D. Diffuse white matter hyperintensity on T2

Answer 16

B. Diffuse meningeal enhancement, especially basal cisterns

💡 Rationale & Discussion:

Basal meningeal enhancement = hallmark of TB meningitis

Tuberculomas = may be ring-enhancing, but not exclusive

Subdural hematomas/white matter changes = seen in other conditions

Question 17

❓7. What is the standard duration of treatment for extrapulmonary TB with CNS or bone involvement?
A. 2 months intensive + 4 months continuation
B. 2 months intensive + 6–9 months continuation
C. 2 months intensive + 2 months continuation
D. 4 months intensive + 6 months continuation

Answer 17

B. 2 months intensive + 6–9 months continuation

💡 Rationale & Discussion:

For CNS TB or Pott’s disease, longer duration (total 9–12 months)

RIPE (Rifampin, Isoniazid, Pyrazinamide, Ethambutol) x 2 months

Then INH + Rifampin for 6–9 months

Question 18

❓8. When should adjunctive corticosteroids be given in extrapulmonary TB?
A. Always in lymphadenitis
B. In spinal TB with cord compression
C. In hepatic TB
D. Only in HIV-negative patients

Answer 18

B. In spinal TB with cord compression

💡 Rationale & Discussion:

Steroids reduce inflammatory edema and neurologic compromise

Also indicated in TB meningitis

Not routinely given in lymphadenitis or hepatic TB

Question 19

❓9. Which lab finding supports a chronic inflammatory process typical of TB?
A. ESR >70 mm/hr
B. Eosinophilia
C. Low CRP
D. Pancytopenia

Answer 19

A. ESR >70 mm/hr

💡 Rationale & Discussion:

ESR = nonspecific marker of chronic inflammation

TB often has very high ESR (>50–70 mm/hr)

CRP also rises, but ESR more classic

Pancytopenia suggests marrow infiltration, not isolated TB

Question 20

❓1. What does the ABG suggest?
A. Metabolic alkalosis
B. Acute respiratory alkalosis
C. Chronic compensated respiratory acidosis
D. Uncompensated respiratory acidosis

Answer 20

C. Chronic compensated respiratory acidosis

💡 Rationale & Discussion:

pH low-normal (7.32), PaCO₂ high (58), HCO₃⁻ slightly elevated (28)

= chronic CO₂ retention with renal compensation

Classic in COPD with chronic hypercapnia

Question 21

❓2. What ECG finding supports cor pulmonale (chronic RV strain)?
A. Left bundle branch block
B. Peaked P waves in II, III, aVF
C. ST depression in lateral leads
D. Q waves in anterior leads

Answer 21

B. Peaked P waves in II, III, aVF

💡 Rationale & Discussion:

P pulmonale = peaked P waves → right atrial enlargement

Suggests RV strain from chronic pulmonary hypertension

LBBB and Q waves = ischemia

ST changes = less specific

Question 22

3. What chest x-ray finding supports COPD over pneumonia?
   A. Right lower lobe consolidation
   B. Blunting of costophrenic angle
   C. Flattened diaphragm with hyperlucent lungs
   D. Pleural effusion

Answer 22

C. Flattened diaphragm with hyperlucent lungs

💡 Rationale & Discussion:

Hyperinflation + flattened diaphragm = classic for COPD

No infiltrates → less likely pneumonia

Effusion/blunting = not common in uncomplicated COPD

Question 23

4. Which of the following treatments should be started immediately?
   A. IV steroids + IV antibiotics + furosemide
   B. Nebulized bronchodilators + systemic corticosteroids + oxygen
   C. High-dose aspirin + clopidogrel + oxygen
   D. Intubation and mechanical ventilation

Answer 23

B. Nebulized bronchodilators + systemic corticosteroids + oxygen

💡 Rationale & Discussion:

Standard for COPD exacerbation:
🔹 SABA + SAMA nebulized
🔹 Systemic steroids (e.g., prednisone 40 mg PO)
🔹 O₂ therapy to keep SpO₂ 88–92%

Intubation only if in respiratory failure

No need for antiplatelets unless ACS is suspected

Question 24

❓5. What is the target oxygen saturation for this patient?
A. >95%
B. 90–94%
C. 88–92%
D. <88% to prevent CO₂ retention

Answer 24

C. 88–92%

💡 Rationale & Discussion:

In COPD with CO₂ retention, avoid over-oxygenation

Too much O₂ → hypoventilation, worsening hypercapnia

Target: SpO₂ 88–92% (per GOLD + Harrison’s)

Question 25

❓6. Which finding suggests acute worsening of chronic respiratory failure? A. pH 7.48, PaCO₂ 30 B. pH 7.20, PaCO₂ 70, HCO₃⁻ 20 C. pH 7.35, PaCO₂ 58, HCO₃⁻ 29 D. pH 7.42, PaCO₂ 40, HCO₃⁻ 24

Answer 25

B. pH 7.20, PaCO₂ 70, HCO₃⁻ 20 💡 Rationale & Discussion: Indicates acute decompensation with uncompensated acidosis Likely due to infection, poor ventilation Requires urgent respiratory support

Question 26

❓7. Which is an indication for intubation in COPD exacerbation? A. RR 22/min B. SpO₂ 91% on 2L O₂ C. Confusion with rising CO₂ and worsening acidosis D. Crackles on auscultation

Answer 26

C. Confusion with rising CO₂ and worsening acidosis 💡 Rationale & Discussion: Altered mental status + hypercapnia = impending respiratory failure Noninvasive ventilation (BiPAP) if possible Intubate if patient can’t protect airway or fails BiPAP

Question 27

❓8. Which cardiac complication is most common in COPD exacerbation? A. Pericarditis B. Right heart strain / cor pulmonale C. Bradyarrhythmia D. Aortic dissection

Answer 27

B. Right heart strain / cor pulmonale 💡 Rationale & Discussion: Chronic hypoxia → pulmonary hypertension → RV hypertrophy and failure Can cause edema, JVD, hepatomegaly in advanced stages Look for P pulmonale, RAD on ECG

Question 28

❓1. What is the most likely source of sepsis in this patient? A. Community-acquired pneumonia B. Acute cholangitis C. Urinary tract infection with possible pyelonephritis D. Clostridium difficile colitis

Answer 28

C. Urinary tract infection with possible pyelonephritis 💡 Rationale & Discussion: Dysuria + flank pain + pyuria/nitrites → upper UTI AKI + sepsis symptoms → suspect urosepsis CXR clear, no GI symptoms = less likely other sources

Question 29

❓2. What organ systems are already showing sepsis-related dysfunction? (Select ALL that apply) A. Renal (acute kidney injury) B. Hepatic (liver injury) C. CNS (encephalopathy) D. Circulatory (hypotension/shock) E. Respiratory (ARDS)

Answer 29

Renal (AKI), CNS (encephalopathy), Circulatory (hypotension) 💡 Rationale & Discussion: A. Renal ✅: ↑ Creatinine from baseline (2.1 mg/dL from 1.0) and oliguria = AKI C. CNS ✅: Disorientation + GCS drop = septic encephalopathy D. Circulatory ✅: BP 85/55 mmHg = septic shock B. Hepatic ❌: No liver enzyme abnormalities or jaundice E. Respiratory ❌: No hypoxemia or infiltrates on CXR = no ARDS

Question 30

3. What is the most appropriate immediate management? A. Blood transfusion + steroids B. IV ceftriaxone, IV fluids, urine culture C. Wait for culture results before starting antibiotics D. Foley removal and discharge if improved

Answer 30

B. IV ceftriaxone, IV fluids, urine culture 💡 Rationale & Discussion: Sepsis bundle = fluids + empiric antibiotics + cultures Don’t wait for results to start empiric therapy Ceftriaxone covers gram-negative uropathogens

Question 31

4. What does the elevated lactate signify in this patient? A. Respiratory failure B. Liver dysfunction C. Tissue hypoperfusion D. Hemolysis

Answer 31

C. Tissue hypoperfusion 💡 Rationale & Discussion: Lactate >2 mmol/L = marker of anaerobic metabolism Indicates poor tissue perfusion, even if BP seems adequate Key component of septic shock definition

Question 32

5. What is the minimum amount of IV fluids to give initially? A. 100 mL/hour B. 10 mL/kg bolus C. 30 mL/kg bolus within the first 3 hours D. 500 mL bolus, then re-evaluate in 8 hours

Answer 32

C. 30 mL/kg bolus within the first 3 hours 💡 Rationale & Discussion: Sepsis guidelines: rapid fluid resuscitation 30 mL/kg = approx. 2 L for 70-kg adult Critical to restore perfusion and prevent shock progression

Question 33

6. Which finding confirms progression to septic shock? A. Fever >39°C and WBC >20,000 B. Creatinine >2.0 mg/dL C. BP remains <90 systolic despite 2L fluids and lactate >2 D. Positive blood culture

Answer 33

C. BP remains <90 systolic despite 2L fluids and lactate >2 💡 Rationale & Discussion: Septic shock = hypotension requiring vasopressors + lactate >2 mmol/L despite adequate fluids Infection + organ dysfunction = sepsis Shock = refractory hypotension

Question 34

7. What is the best marker to track renal recovery in this case? A. Serial creatinine levels B. Serum urea C. Urine protein D. Sodium levels

Answer 34

A. Serial creatinine levels 💡 Rationale & Discussion: Creatinine trend is the most reliable marker for AKI monitoring Urine output also important (≥0.5 mL/kg/hr target) Urea affected by hydration and catabolism

Question 35

8. What is the best way to monitor improvement in mental status? A. Daily cranial CT B. EEG monitoring C. Glasgow Coma Scale (GCS) tracking D. Serum ammonia

Answer 35

C. Glasgow Coma Scale (GCS) tracking 💡 Rationale & Discussion: GCS is quick, repeatable, bedside neurologic assessment Useful in all septic patients CT/EEG only if deterioration or structural cause suspected

Question 36

❓1. What is the most likely diagnosis? A. Acute coronary syndrome with arrhythmia B. Thyrotoxic heart failure with atrial fibrillation C. Diabetic ketoacidosis with high-output failure D. Hypertensive heart failure with preserved EF

Answer 36

B. Thyrotoxic heart failure with atrial fibrillation 💡 Rationale & Discussion: Classic signs: weight loss, anxiety, goiter, AFib, HF TSH suppressed, FT₄ ↑ = thyrotoxicosis Thyroid hormone ↑ myocardial contractility + HR = high-output HF, AFib trigger

Question 37

❓2. What is the most appropriate initial management step? A. Electrical cardioversion B. IV furosemide and beta-blocker C. Methimazole and steroids only D. Start warfarin immediately

Answer 37

B. IV furosemide and beta-blocker 💡 Rationale & Discussion: Initial goals: relieve congestion + control HR IV furosemide = reduce pulmonary edema Beta-blocker (e.g., propranolol) = rate control + block T₄→T₃ conversion Definitive thyroid tx comes after stabilization

Question 38

❓3. What is the mechanism of heart failure in thyrotoxicosis? A. Decreased afterload with diastolic dysfunction B. Increased preload and afterload with bradycardia C. High-output failure from ↑ metabolic demand D. Hypovolemia causing diastolic collapse

Answer 38

C. High-output failure from ↑ metabolic demand 💡 Rationale & Discussion: Thyroid hormones ↑ HR, contractility, oxygen consumption Leads to high-output failure, especially with AFib Over time, may transition into low-output HF if untreated

Question 39

❓4. Which beta-blocker is preferred in thyrotoxic heart failure with AFib? A. Atenolol B. Propranolol C. Bisoprolol D. Carvedilol

Answer 39

B. Propranolol 💡 Rationale & Discussion: Non-selective β-blocker Blocks T₄ to T₃ conversion in peripheral tissues Ideal in thyroid storm or thyrotoxic AFib Other cardioselectives lack thyroid-blocking effect

Question 40

❓5. What is the target HR in managing AFib in acute HF? A. <60 bpm B. <80 bpm C. <100 bpm D. <130 bpm

Answer 40

C. <100 bpm 💡 Rationale & Discussion: Acute rate control target: <100 bpm Avoid bradycardia in patients with borderline CO Aggressive rate control reduces O₂ demand and improves filling

Question 41

❓6. What is the next endocrine management step after rate control? A. IV hydrocortisone + Lugol’s solution B. Methimazole or PTU initiation C. Immediate thyroidectomy D. Radioiodine therapy

Answer 41

B. Methimazole or PTU initiation 💡 Rationale & Discussion: Methimazole = first-line antithyroid (except in 1st trimester) PTU preferred in thyroid storm due to added T₄→T₃ inhibition Radioiodine/surgery only after patient is euthyroid

Question 42

❓7. In AFib with new heart failure and thyrotoxicosis, when should anticoagulation be considered? A. Only if EF <40% B. Only after TSH normalizes C. Based on CHA₂DS₂-VASc score D. Not needed if HR controlled

Answer 42

C. Based on CHA₂DS₂-VASc score 💡 Rationale & Discussion: Thyrotoxicosis increases AFib risk, but stroke risk is based on score If ≥2 → anticoagulate Don’t delay due to thyroid status alone

Question 43

❓8. What is the most likely CXR finding in thyrotoxic heart failure? A. Bilateral pleural effusion with Kerley B lines B. Cardiomegaly with upper lobe vascular diversion C. Lung consolidation in midzones D. Flattened diaphragm with hyperinflation

Answer 43

B. Cardiomegaly with upper lobe vascular diversion 💡 Rationale & Discussion: Signs of congestive HF: 🔹 Enlarged cardiac silhouette 🔹 Pulmonary vascular congestion 🔹 Cephalization of flow No evidence of consolidation or COPD pattern