Finals Practice Flashcards
- 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
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)
- 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
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
- 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
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)
- Based on the CXR findings, what is the best initial antibiotic choice?
A. Amoxicillin-clavulanate
B. Ceftriaxone + azithromycin
C. Piperacillin-tazobactam
D. Vancomycin + meropenem
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
- 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
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
- 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
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
- Which electrolyte should be checked and corrected before giving insulin?
A. Calcium
B. Sodium
C. Potassium
D. Chloride
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
- 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
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
- 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
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
- Which scoring tool can help determine severity and guide ICU admission?
A. CURB-65
B. Wells score
C. CHADS2
D. Ranson’s criteria
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
❓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)
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
- 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
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
❓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
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
❓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
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
❓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
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
❓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
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
❓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
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
❓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
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
❓9. Which lab finding supports a chronic inflammatory process typical of TB?
A. ESR >70 mm/hr
B. Eosinophilia
C. Low CRP
D. Pancytopenia
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
❓1. What does the ABG suggest?
A. Metabolic alkalosis
B. Acute respiratory alkalosis
C. Chronic compensated respiratory acidosis
D. Uncompensated respiratory acidosis
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
❓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
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
- 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
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
- 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
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
❓5. What is the target oxygen saturation for this patient?
A. >95%
B. 90–94%
C. 88–92%
D. <88% to prevent CO₂ retention
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)
❓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
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
❓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
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
❓8. Which cardiac complication is most common in COPD exacerbation?
A. Pericarditis
B. Right heart strain / cor pulmonale
C. Bradyarrhythmia
D. Aortic dissection
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
❓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
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
❓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)
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
- 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
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
- What does the elevated lactate signify in this patient?
A. Respiratory failure
B. Liver dysfunction
C. Tissue hypoperfusion
D. Hemolysis
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
- 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
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
- 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
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
- 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
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
- 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
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
❓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
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
❓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
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
❓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
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
❓4. Which beta-blocker is preferred in thyrotoxic heart failure with AFib?
A. Atenolol
B. Propranolol
C. Bisoprolol
D. Carvedilol
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
❓5. What is the target HR in managing AFib in acute HF?
A. <60 bpm
B. <80 bpm
C. <100 bpm
D. <130 bpm
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
❓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
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
❓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
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
❓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
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
