Give me MCQ 30 questions based on the files above and the answers give me at the end of 30 questions
python3 << 'EOF' import pdfplumber files = { "L14_Lungs_AcidBase": "/tmp/workspace/attachments/d8e195b8-1a27-4ca2-9409-4654cf9c1a90/MBBS B31 MRES L14 Role Lungs in Regultion of Acid Base.pdf", "Lec22_Biochem_Resp": "/tmp/workspace/attachments/d8e195b8-1a27-4ca2-9409-4654cf9c1a90/Lec 22 Biochemical basis of resp dis.pdf", "Lec15_Regulation_pH2": "/tmp/workspace/attachments/d8e195b8-1a27-4ca2-9409-4654cf9c1a90/Lec 15 Regulation of pH- 2 .pdf" } for name, path in files.items(): print(f"\n{'='*60}") print(f"FILE: {name}") print('='*60) with pdfplumber.open(path) as pdf: print(f"Pages: {len(pdf.pages)}") for i, page in enumerate(pdf.pages): text = page.extract_text() if text: print(f"\n--- Page {i+1} ---") print(text[:3000]) EOF
| Q | Answer | Explanation |
|---|---|---|
| 1 | B | Normal arterial blood pH is 7.35–7.45 |
| 2 | D | 70% of CO₂ is transported as bicarbonate |
| 3 | B | 23% is transported bound to hemoglobin |
| 4 | B | Carbonic anhydrase drives CO₂ + H₂O ⇌ H₂CO₃ |
| 5 | B | Lung compensation begins within 1–3 minutes |
| 6 | B | pKa of carbonic acid in blood at 37°C = 6.1 |
| 7 | B | Solubility coefficient of CO₂ = 0.03 |
| 8 | B | Respiratory mechanism is the 2nd line of defense |
| 9 | C | Respiratory acidosis = pCO₂ > 45 mmHg |
| 10 | C | Hyperventilation blows off CO₂ → respiratory alkalosis |
| 11 | C | Anxiety causes respiratory alkalosis, not acidosis |
| 12 | C | Citric Acid Cycle is the largest producer of CO₂ |
| 13 | C | Complete oxidation of glucose produces 6 CO₂ |
| 14 | C | Normal ctCO₂ = 23–29 mEq/L |
| 15 | B | Metabolic acidosis is compensated by hyperventilation |
| 16 | C | Chloride shift: HCO₃⁻ exits RBC in exchange for Cl⁻ |
| 17 | B | Vomiting causes loss of HCl → metabolic alkalosis |
| 18 | B | AG = Na⁺ − (Cl⁻ + HCO₃⁻) |
| 19 | C | Normal anion gap = 12 ± 2 mmol/L |
| 20 | C | Chronic resp. acidosis: HCO₃⁻ rises 3.5 mmol/L per 10 mmHg pCO₂ rise |
| 21 | B | CF is caused by mutation in the CFTR gene |
| 22 | C | CF is autosomal recessive |
| 23 | B | CFTR gene is on chromosome 7 |
| 24 | B | Alpha-1 antitrypsin inhibits elastase/proteases |
| 25 | C | Smoking increases neutrophil elastase → alveolar destruction |
| 26 | B | Surfactant is secreted by Type II alveolar cells |
| 27 | C | DPPC (dipalmitoyl phosphatidylcholine) is the main surfactant lipid |
| 28 | B | Leukotrienes are produced via 5-lipoxygenase |
| 29 | C | LTB₄ is a potent neutrophil chemoattractant |
| 30 | B | Breathing into a paper bag re-inhales CO₂ to correct alkalosis |
Give me 30 mcq questions based on the learning outcomes based on the files above and the answers give me at the end of question
| Q | Answer | Key Learning Outcome |
|---|---|---|
| 1 | B | Lungs regulate acid-base by controlling CO₂ elimination |
| 2 | B | CO₂ forms carbonic acid and is exhaled - hence "volatile" |
| 3 | B | Acidosis triggers hyperventilation to blow off CO₂ |
| 4 | B | Alkalosis triggers hypoventilation to retain CO₂ |
| 5 | B | Exhaling CO₂ shifts equation left - H⁺ consumed, pH rises |
| 6 | C | Respiratory centre is in the medulla oblongata |
| 7 | B | Diffusibility of CO₂ across pulmonary alveolar membrane |
| 8 | C | Citric Acid Cycle is the primary CO₂-producing pathway |
| 9 | C | Cannot eliminate fixed acids (sulfuric, lactic, keto acids) |
| 10 | C | Chemical buffers → Respiratory → Renal (1st, 2nd, 3rd) |
| 11 | B | Carbonic anhydrase in RBC (can increase rate up to 1 million-fold) |
| 12 | B | HCO₃⁻ diffuses into plasma in exchange for Cl⁻ (chloride shift) |
| 13 | B | Kidneys activate CA, generate HCO₃⁻, excrete H⁺ |
| 14 | C | Respiratory alkalosis caused by hyperventilation/CO₂ loss |
| 15 | C | 0.03 = solubility coefficient of CO₂ in blood plasma |
| 16 | C | Metabolic acidosis = HCO₃⁻ < 22 mmol/L |
| 17 | C | Respiratory alkalosis = deficit of H₂CO₃ (carbonic acid) |
| 18 | C | High pCO₂ (55 mmHg) with low pH = respiratory acidosis |
| 19 | B | pCO₂ decreases 1 mmHg per 1 mmol/L drop in HCO₃⁻ |
| 20 | C | Compensation restores pH toward normal but cannot fully correct it |
| 21 | C | Metabolic alkalosis compensated by hypoventilation → increased pCO₂ |
| 22 | C | Diarrhea causes loss of HCO₃⁻ → metabolic acidosis |
| 23 | C | ABG drawn from the radial artery |
| 24 | B | Hypoventilation as compensation is limited by hypoxia |
| 25 | B | High anion gap = unmeasured acids (lactate, ketones) present |
| 26 | B | Imbalance between proteases and antiproteases destroys alveolar walls |
| 27 | C | Alpha-1 antitrypsin deficiency → panacinar emphysema |
| 28 | B | Defective CFTR → Cl⁻ channel loss → salty sweat |
| 29 | B | Surfactant reduces surface tension, prevents alveolar collapse |
| 30 | B | Cysteinyl leukotrienes cause bronchoconstriction and inflammation |
Give me another 30 MCQ questions same as the conditions of above but in this u can add some case based scenario questions
| Q | Answer | Explanation |
|---|---|---|
| 1 | B | Lactic acid is a fixed acid - cannot be exhaled, only renally excreted |
| 2 | C | Normal HCO₃⁻ : H₂CO₃ ratio = 20:1, maintaining pH 7.4 |
| 3 | B | Retaining CO₂ shifts equation right → more H⁺ released → pH drops |
| 4 | C | Pyruvate oxidation produces 2 CO₂ (one per pyruvate, 2 pyruvates per glucose) |
| 5 | D | Carbonic anhydrase increases the reaction rate up to 1,000,000-fold |
| 6 | B | CO₂ is eliminated in expired air through the lungs |
| 7 | C | COPD with CO₂ retention causes respiratory ACIDOSIS, not alkalosis |
| 8 | C | K⁺ exits cells in exchange for H⁺ during alkalosis → hypokalemia |
| 9 | B | Dissolved CO₂ contributes approximately 1.2 mEq/L to arterial plasma |
| 10 | D | Metabolic alkalosis = excess HCO₃⁻ |
| 11 | C | Chronic respiratory alkalosis: HCO₃⁻ decreases 4 mmol/L per 10 mmHg fall in pCO₂ |
| 12 | B | Alveolar macrophages express cathepsins and MMPs in emphysema |
| 13 | C | CFTR protein consists of 1,480 amino acids |
| 14 | B | ROS cause endothelial dysfunction and disruption in ARDS |
| 15 | B | Leukotrienes use autocrine (self) and paracrine (neighboring cells) signaling |
| 16 | C | Emphysema = protease-antiprotease imbalance; elastase destroys alveolar walls |
| 17 | B | Salty sweat + recurrent infections + malabsorption = Cystic fibrosis; autosomal recessive |
| 18 | C | Leukotriene antagonists (e.g., montelukast) specifically block cysteinyl leukotrienes |
| 19 | B | Smoke inhalation → ARDS → reduced surfactant (DPPC) |
| 20 | C | pH low + pCO₂ very high + HCO₃⁻ slightly elevated = respiratory acidosis with partial renal compensation |
| 21 | B | Panic attack → hyperventilation → respiratory alkalosis; treat with rebreather mask/paper bag |
| 22 | B | Kussmaul breathing = respiratory compensation (hyperventilation) for metabolic acidosis (DKA) |
| 23 | B | Vomiting → loss of HCl → metabolic alkalosis; high pH + high HCO₃⁻ confirm this |
| 24 | B | Altitude hypoxia stimulates peripheral chemoreceptors → hyperventilation → CO₂ blow-off |
| 25 | B | CKD → accumulation of phosphates, sulfates, organic acids = high anion gap metabolic acidosis |
| 26 | B | C4 spinal injury paralyses respiratory muscles → neuromuscular hypoventilation → CO₂ retention |
| 27 | C | DPPC (dipalmitoyl phosphatidylcholine) is the principal lipid in surfactant therapy |
| 28 | C | Tetany and hyperactive reflexes are classic symptoms of metabolic alkalosis |
| 29 | B | Dual mechanism: smoking attracts neutrophils + polymerised abnormal antitrypsin as chemoattractant, with no antiprotease defence |
| 30 | C | Opioid-induced respiratory depression → acute respiratory acidosis; treat with naloxone and restore ventilation |