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Batterjee Medical College - H⁺ & HCO₃⁻ Renal Handling: Complete Study Pack

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BMC Renal H HCO3 MCQ Pack

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The PDF contains 35 high-yield MCQs organized into 4 sections, with a separate answer section and a 2-page printable cheatsheet. Here is everything in full below:

SECTION 1 - MCQ BANK WITH FULL EXPLANATIONS

ACID-BASE BASICS (Q1-Q7)

Q1. The normal pH of arterial blood is:
  • A. 7.0
  • B. 7.2
  • C. 7.4 ✔ CORRECT
  • D. 7.6
Explanation: Normal arterial pH = 7.4 (range 7.35-7.45). Slightly alkaline. Free [H+] = 40 nmol/L. Death below pH 7.0 or above pH 7.8. (Guyton & Hall 13e, Unit V)
💡 Hint: Life-compatible range = 7.35-7.45. 7.4 is the midpoint.
📅 ★★★★★ | Appears in virtually every Batterjee physiology exam
Q2. Which of the following is a proton donor?
  • A. Base
  • B. Acid ✔ CORRECT
  • C. Buffer
  • D. Salt
Explanation: Acid = proton DONOR. Base = proton ACCEPTOR. (Lecture slide 5)
💡 Hint: "A for Acid, A for Add H+" - acids add protons to solution.
📅 ★★★★☆ | Early semester physiology tests
Q3. According to Henderson-Hasselbalch equation, pH is proportional to:
  • A. [HCO₃⁻] / [H₂CO₃] ✔ CORRECT
  • B. [H₂CO₃] / [HCO₃⁻]
  • C. PCO₂ × [HCO₃⁻]
  • D. pK − log [HCO₃⁻]
Explanation: pH = pK + log([HCO₃⁻]/[H₂CO₃]). HCO₃⁻ on top = alkaline; CO₂ in denominator = acidic. (Guyton 13e Ch 30; Ganong 25e Ch 37)
💡 Hint: Bicarbonate on TOP = alkaline tendency. Remember "HCO₃ rises → pH rises."
📅 ★★★★★ | Core equation for all acid-base MCQs
Q4. The pK of the bicarbonate buffer system is:
  • A. 6.8
  • B. 7.4
  • C. 6.1 ✔ CORRECT
  • D. 9.0
Explanation: Bicarbonate pK = 6.1. Despite being far from blood pH 7.4, it is the most important physiological buffer because both components are independently controlled (HCO₃⁻ by kidney; PCO₂ by lung). (Lecture slide 11)
💡 Hint: pK ladder = Bicarbonate 6.1 → Phosphate 6.8 → Ammonia 9.0 (ascending!)
📅 ★★★★★ | Classic "which pK belongs to which buffer?" MCQ
Q5. Which buffer is most effective INTRACELLULARLY?
  • A. Bicarbonate
  • B. Phosphate and proteins ✔ CORRECT
  • C. Ammonia
  • D. Haemoglobin
Explanation: ICF buffers = proteinate + organic phosphate. ECF = bicarbonate. Tubular DCT fluid = phosphate. (Lecture slide 12)
💡 Hint: ICF = Phosphate + Proteins. ECF = Bicarbonate.
📅 ★★★☆☆ | Compartment-distribution question
Q6. Which buffer has the HIGHEST buffering capacity in blood?
  • A. Plasma proteins
  • B. Bicarbonate
  • C. Haemoglobin ✔ CORRECT
  • D. Phosphate
Explanation: Haemoglobin has 6× the buffering capacity of all plasma proteins combined. ~750 g in adult male. Deoxy-Hb > oxy-Hb as a buffer. (Lecture slide 13)
💡 Hint: "6x plasma proteins" - memorise this number. It appears exactly like this.
📅 ★★★★☆ | Haemoglobin buffering comparison
Q7. Deoxyhemoglobin compared to oxyhemoglobin as a buffer is:
  • A. Equally effective
  • B. Less effective
  • C. More effective ✔ CORRECT
  • D. Inactive
Explanation: Deoxy-Hb is a BETTER buffer - physiologically important in tissues where O₂ is unloaded and CO₂/H+ is produced (Haldane effect). (Lecture slide 13)
💡 Hint: Tissues = O₂ released → deoxyHb forms → better H+ buffer. Perfect design!
📅 ★★★☆☆ | Haldane effect / Hb buffer property

RENAL H⁺ & HCO₃⁻ HANDLING (Q8-Q15)

Q8. Where is H⁺ secreted in the renal tubule?
  • A. All segments including thin limbs
  • B. PCT only
  • C. All segments EXCEPT thin limbs of loop of Henle ✔ CORRECT
  • D. Collecting duct only
Explanation: H+ secreted in ALL renal tubule segments EXCEPT the thin limbs. Includes PCT (85%), thick ascending loop (10%), DCT, and collecting ducts (4.8%). (Lecture slide 17; Guyton 13e Ch 31)
💡 Hint: "Thin limbs = NO. Everything else = YES." The most classic exam trap in this lecture.
📅 ★★★★★ | MOST FREQUENTLY ASKED - appears in nearly every past Batterjee paper
Q9. What percentage of filtered HCO₃⁻ is reabsorbed in the PCT?
  • A. 50%
  • B. 65%
  • C. 85% ✔ CORRECT
  • D. 95%
Explanation: PCT = 85% of filtered HCO₃⁻. Thick ascending loop = ~10%. Collecting ducts = ~4.8%. (Lecture slide 17)
💡 Hint: "85% PCT" - the single most important percentage number in this topic.
📅 ★★★★★ | Classic percentage question, every year
Q10. The renal threshold for HCO₃⁻ reabsorption is:
  • A. 20 mEq/L
  • B. 22 mEq/L
  • C. 24 mEq/L
  • D. 26 mEq/L ✔ CORRECT
Explanation: Threshold = 26 mEq/L. Normal plasma HCO₃⁻ = 24 mEq/L. Above 26 mEq/L → HCO₃⁻ appears in urine (bicarbonaturia → alkaline urine). (Lecture slide 17)
💡 Hint: Normal = 24, Threshold = 26. Two numbers, two different clinical meanings.
📅 ★★★★★ | Pure recall threshold value, every exam
Q11. Carbonic anhydrase type II (CA-II) is located in:
  • A. Tubular lumen
  • B. Brush border of PCT
  • C. Inside tubular cells (cytoplasm) ✔ CORRECT
  • D. Peritubular capillary
Explanation: CA-II = intracellular (cytoplasm) - generates H+ + HCO₃⁻ from CO₂ + H₂O inside the cell. CA-IV = brush border/luminal membrane of PCT - dehydrates H₂CO₃ in the lumen → H₂O + CO₂. (Brenner & Rector's Kidney; Campbell-Walsh)
💡 Hint: CA-II = INside (intracellular). CA-IV = outside at the brush border. Roman numerals help: II = inner, IV = outer (vessel/surface).
📅 ★★★★☆ | CA-II vs CA-IV location distinction
Q12. The mechanism of H⁺ secretion in the PCT is:
  • A. Primary active transport via H+/K+-ATPase
  • B. Secondary active transport via Na+/H+ antiporter (NHE3) ✔ CORRECT
  • C. Passive diffusion
  • D. Facilitated diffusion
Explanation: PCT (+ loop of Henle + early DCT) = SECONDARY active via NHE3. Na+ diffuses in (down gradient) while H+ is secreted out (against gradient). Energy from basolateral Na+/K+-ATPase. (Lecture slide 20; Ganong 26e; Guyton 13e)
💡 Hint: PCT = NHE3 = SECONDARY (uses Na+ gradient). Late DCT/CDs = H+/K+-ATPase = PRIMARY. This contrast is a guaranteed MCQ.
📅 ★★★★★ | Primary vs secondary mechanism distinction - extremely high yield
Q13. Primary active H⁺ secretion in the kidney occurs in:
  • A. PCT
  • B. Thick ascending loop
  • C. Early DCT
  • D. Late DCT and collecting ducts ✔ CORRECT
Explanation: Late DCT + collecting ducts: Na+-INDEPENDENT primary active secretion via H+/K+-ATPase pump on type A (alpha) intercalated cells. Stimulated by aldosterone up to ×900. (Lecture slide 20)
💡 Hint: "LATE = PRIMARY." Alpha-intercalated cells. H+/K+-ATPase. Aldosterone.
📅 ★★★★★ | Segment-specific mechanism, core exam topic
Q14. Type A (alpha) intercalated cells of the collecting duct:
  • A. Secrete HCO₃⁻ into urine
  • B. Secrete H⁺ via H+/K+-ATPase into tubular lumen ✔ CORRECT
  • C. Reabsorb H+ from tubular lumen
  • D. Have NHE3 on their luminal surface
Explanation: Alpha (A) = Acid secretion (H+/K+-ATPase on luminal side, HCO₃⁻ exits basolateral). Beta (B) = Bicarbonate secretion (into lumen, in alkalosis). Opposite roles! (Lecture slide 20; Brenner & Rector)
💡 Hint: Alpha = Acid. Beta = Bicarbonate. Perfect alphabetical pairing.
📅 ★★★★★ | Alpha vs Beta intercalated cell - very frequently tested
Q15. Aldosterone stimulates H⁺ secretion in the collecting duct by how much?
  • A. 10-fold
  • B. 100-fold
  • C. 500-fold
  • D. Up to 900-fold ✔ CORRECT
Explanation: Aldosterone can increase primary active H+ secretion by up to 900-fold in late DCT and collecting ducts. This explains metabolic alkalosis in Conn's/Cushing's syndrome. (Lecture slide 20)
💡 Hint: The trick answer - not 100, not 500. It is 900. This specific number appears.
📅 ★★★★☆ | Aldosterone magnitude - number-based MCQ

BUFFER FATE IN RENAL TUBULES (Q16-Q24)

Q16. In the PCT, secreted H⁺ is mainly buffered by:
  • A. Phosphate buffer
  • B. Ammonia (NH₃)
  • C. Bicarbonate (NaHCO₃) ✔ CORRECT
  • D. Haemoglobin
Explanation: PCT: H+ + HCO₃⁻ → H₂CO₃ → H₂O + CO₂ (CA-IV at brush border). CO₂ re-enters the cell. Tubular fluid pH barely changes in PCT because most H+ is immediately neutralised. (Lecture slide 22)
💡 Hint: PCT = Bicarbonate buffer (abundant). DCT/CDs = Phosphate + Ammonia.
📅 ★★★★★ | Buffer-segment matching - tested every exam
Q17. In the DCT and collecting ducts, secreted H⁺ is buffered by:
  • A. Bicarbonate only
  • B. Phosphate buffer and ammonia system ✔ CORRECT
  • C. Haemoglobin
  • D. Bicarbonate and haemoglobin
Explanation: DCT/CDs: (1) Phosphate: H+ + Na₂HPO₄ → NaH₂PO₄ + Na+ (= titratable acidity in urine). (2) Ammonia: NH₃ + H+ → NH₄+ → excreted as NH₄Cl. Bicarbonate exhausted by DCT. (Lecture slides 23-25)
💡 Hint: DCT = "PA" - Phosphate + Ammonia.
📅 ★★★★★ | Two-buffer system of distal nephron
Q18. The pK of the ammonia/ammonium buffer system is:
  • A. 6.1
  • B. 6.8
  • C. 7.4
  • D. 9.0 ✔ CORRECT
Explanation: pK for NH₃/NH₄+ = 9.0. At pH 7.4, [NH₄+]/[NH₃] = 100:1 (almost all as NH₄+). NH₃ (lipid-soluble) diffuses into lumen → combines with H+ → NH₄+ (lipid-insoluble = TRAPPED). (Lecture slides 24-25)
💡 Hint: pK order - Bicarbonate=6.1, Phosphate=6.8, Ammonia=9.0.
📅 ★★★★☆ | pK values comparison
Q19. Ammonia (NH₃) is synthesized in renal tubular cells mainly from:
  • A. Alanine
  • B. Glutamine ✔ CORRECT
  • C. Aspartate
  • D. Glycine
Explanation: Glutamine → (glutaminase) → glutamate + NH₃; glutamate → (glutamate dehydrogenase) → α-ketoglutarate + NH₃. 2 NH₃ per glutamine molecule. (Lecture slide 24; Goldman-Cecil Medicine)
💡 Hint: "GlutaMINE provides aMINEonia" - the only amino acid you need to know here.
📅 ★★★★★ | Glutamine→NH₃→NH₄Cl pathway - core exam topic
Q20. The limiting pH for H⁺ secretion in the DCT/collecting ducts is:
  • A. 5.0
  • B. 4.5 ✔ CORRECT
  • C. 6.0
  • D. 5.5
Explanation: H+ secretion in DCT/CDs continues as long as tubular fluid pH > 4.5. Below pH 4.5, secretion STOPS. Phosphate and ammonia buffers prevent rapid acidification and allow continued H+ secretion. (Lecture slide 25)
💡 Hint: Limiting pH = 4.5. Without buffers → pH 4.5 quickly → secretion halted.
📅 ★★★★★ | Limiting pH value - appears every year
Q21. NH₄⁺ (ammonium) is excreted in urine together with:
  • A. HCO₃⁻
  • B. SO₄²⁻
  • C. Cl⁻ (as NH₄Cl) ✔ CORRECT
  • D. PO₄³⁻
Explanation: NH₄+ + Cl- → NH₄Cl excreted in urine. Cl- from NaCl. Na+ reabsorbed with HCO₃⁻ from tubular cell to blood. Net: acid excreted + HCO₃⁻ generated. (Lecture slide 25)
💡 Hint: NH₄Cl = ammonium chloride in urine. Na+ is saved.
📅 ★★★☆☆ | Final product of NH₃ buffering
Q22. Which of the following INCREASES H⁺ secretion in the renal tubule?
  • A. Inhibition of carbonic anhydrase
  • B. K+ excess in cells
  • C. Aldosterone ✔ CORRECT
  • D. Intracellular alkalosis
Explanation: Increases H+ secretion: (1) Aldosterone, (2) ↑ intracellular PCO₂ (respiratory acidosis), (3) K+ depletion (intracellular acidosis). Decreases: CA inhibitors, K+ excess. (Lecture slide 26)
💡 Hint: Aldosterone = "A for Acid" - always increases H+ secretion.
📅 ★★★★★ | Regulation MCQ - factors affecting H+ secretion
Q23. In hypokalaemia (K⁺ depletion from cells), H⁺ secretion is:
  • A. Decreased
  • B. Unchanged
  • C. Increased (intracellular acidosis) ✔ CORRECT
  • D. Abolished
Explanation: K+ leaves cells → H+ moves IN to maintain electroneutrality → intracellular acidosis → kidney secretes MORE H+ → metabolic alkalosis. The opposite (hyperkalaemia) inhibits H+ secretion. (Lecture slide 26; Guyton 13e)
💡 Hint: Low K+ outside → H+ enters cells → cells acidic → kidney pumps MORE H+ out → urine acidic + blood alkalotic = paradoxical aciduria.
📅 ★★★★★ | K+/H+ relationship - classic clinical MCQ, repeated yearly
Q24. Carbonic anhydrase inhibitors (e.g. acetazolamide) cause:
  • A. Metabolic alkalosis
  • B. Metabolic acidosis with proximal RTA ✔ CORRECT
  • C. Respiratory acidosis
  • D. Respiratory alkalosis
Explanation: CA inhibitors block intracellular CA-II → less H+ generation → less H+ secretion → less HCO₃⁻ reabsorption in PCT → HCO₃⁻ wasted in urine → metabolic acidosis (proximal/type 2 RTA). (Lecture slide 26; Brenner & Rector)
💡 Hint: Acetazolamide → HCO₃⁻ wasted → TYPE 2 (proximal) RTA.
📅 ★★★★☆ | CA inhibitor clinical application

ACID-BASE DISTURBANCES & COMPENSATION (Q25-Q35)

Q25. In respiratory acidosis, the kidney compensates by:
  • A. Increasing HCO₃⁻ loss in urine
  • B. Increasing H⁺ secretion and HCO₃⁻ generation ✔ CORRECT
  • C. Reducing NH₃ synthesis
  • D. Reducing phosphate buffer secretion
Explanation: Resp. acidosis (↑PCO₂) → more CO₂ enters tubular cells → ↑ H₂CO₃ → ↑ H+ secretion → ↑ HCO₃⁻ generated → raised plasma [HCO₃⁻] → compensates acidosis. Takes 12-24 hours. (Lecture slides 29-30)
💡 Hint: Resp. Acidosis → Kidney gives MORE HCO₃⁻. Compensation takes DAYS (vs minutes for lungs).
📅 ★★★★★ | Compensation mechanism - acid-base MCQ staple
Q26. Respiratory acidosis is characterized by:
  • A. pH > 7.45 and PCO₂ < 35 mmHg
  • B. pH < 7.35 and PCO₂ > 44 mmHg ✔ CORRECT
  • C. pH < 7.35 and HCO₃⁻ < 22 mEq/L
  • D. pH > 7.45 and HCO₃⁻ > 26 mEq/L
Explanation: Resp. acidosis = pH < 7.35 (acidosis) + PCO₂ > 44 mmHg (hypercapnia). C describes metabolic acidosis; D describes metabolic alkalosis. (Lecture slide 30)
💡 Hint: Resp. ACID = HIGH CO₂. Resp. ALK = LOW CO₂. Metabolic = changes in HCO₃⁻.
📅 ★★★★★ | ABG interpretation - most clinically tested topic
Q27. A patient has pH 7.52, PCO₂ 28 mmHg, HCO₃⁻ 22 mEq/L. This is:
  • A. Metabolic alkalosis
  • B. Respiratory alkalosis with partial renal compensation ✔ CORRECT
  • C. Metabolic acidosis
  • D. Respiratory acidosis
Explanation: pH 7.52 → alkalosis. Low PCO₂ = primary respiratory alkalosis. Low HCO₃⁻ 22 = renal compensation (kidneys reduce HCO₃⁻ generation). (Lecture slide 31)
💡 Hint: Step approach: 1) pH>7.45 = alkalosis. 2) PCO₂ low → primary respiratory. 3) Low HCO₃⁻ = renal compensation.
📅 ★★★★☆ | ABG clinical scenario interpretation
Q28. Which causes metabolic acidosis with a HIGH anion gap?
  • A. Diarrhea
  • B. Diabetic ketoacidosis ✔ CORRECT
  • C. Renal tubular acidosis type I
  • D. Pancreatic fistula
Explanation: High AG metabolic acidosis (MUDPILES): Methanol, Uraemia, DKA, Propylene glycol, Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates. Diarrhea/RTA/pancreatic fistula = normal AG (hyperchloraemic). (Lecture slide 32; Goldman-Cecil)
💡 Hint: DKA = ketoacids ADDED → high AG. Diarrhea = HCO₃⁻ LOST → normal AG (hyperchloraemic).
📅 ★★★★★ | Anion gap distinction - clinical reasoning
Q29. A patient on prolonged vomiting develops:
  • A. Metabolic acidosis
  • B. Respiratory alkalosis
  • C. Metabolic alkalosis ✔ CORRECT
  • D. Respiratory acidosis
Explanation: Vomiting → loses HCl (H+ and Cl-) → HCO₃⁻ added to plasma → ↑ plasma [HCO₃⁻] → metabolic alkalosis. (Lecture slide 34)
💡 Hint: Vomiting = loses ACID (HCl) = blood becomes BASIC = metabolic ALKalosis.
📅 ★★★★★ | Classic clinical MCQ, repeated every year
Q30. Conn's syndrome causes:
  • A. Metabolic acidosis
  • B. Respiratory acidosis
  • C. Metabolic alkalosis ✔ CORRECT
  • D. Respiratory alkalosis
Explanation: Conn's (excess aldosterone) → ×900 H+ secretion → excess H+ loss + K+ loss → metabolic alkalosis + hypokalaemia. (Lecture slide 34; Guyton 13e)
💡 Hint: Excess aldosterone → loses H+ AND K+ → alkalosis + hypokalaemia.
📅 ★★★★★ | Conn's syndrome acid-base effect - high yield
Q31. DKA causes metabolic acidosis because of:
  • A. Excessive CO₂ retention
  • B. Loss of HCO₃⁻ in urine
  • C. Accumulation of acetoacetate and beta-hydroxybutyrate ✔ CORRECT
  • D. Excess protein intake only
Explanation: Lack of insulin → ↑ fat metabolism → ketoacids (acetoacetate, 3-β-OH-butyrate, acetone) → H+ added to ECF → depletes HCO₃⁻ → high AG metabolic acidosis. Respiratory compensation = Kussmaul breathing. (Lecture slide 32)
💡 Hint: DKA = ketoacids added → consume HCO₃⁻ → metabolic ACIDOSIS. Kussmaul = respiratory compensation.
📅 ★★★★★ | DKA mechanism - pathophysiology + acid-base
Q32. The respiratory system returns pH how far back to normal?
  • A. 1/3 of the way
  • B. 1/2 of the way
  • C. 2/3 of the way ✔ CORRECT
  • D. Fully back to normal
Explanation: Respiratory system restores pH 2/3 of the way toward normal within 1-12 minutes. Its buffering power = 1-2× all chemical buffers combined. Limited because changes in PCO₂ have opposite effects on ventilation. (Lecture slide 15)
💡 Hint: Respiratory = 2/3 in minutes. Renal = FULL correction in 12-24 hours.
📅 ★★★★☆ | Efficacy comparison between regulatory systems
Q33. Which organ is the "most efficient and most powerful" regulator of acid-base?
  • A. Lungs
  • B. Liver
  • C. Kidneys ✔ CORRECT
  • D. Red blood cells
Explanation: Kidneys = most efficient + most powerful. Excrete fixed acids, restore ECF buffers, fully correct pH within 12-24 hours. Lungs = fast (minutes) but partial (2/3 correction only). (Lecture slide 15)
💡 Hint: Kidneys = SLOWEST but MOST POWERFUL and COMPLETE. Quote from lecture used verbatim.
📅 ★★★★★ | System comparison - almost guaranteed in every exam
Q34. Sources of H⁺ in the body include all EXCEPT:
  • A. Metabolism of carbohydrates (CO₂)
  • B. Ketoacids from fat metabolism
  • C. Lactic acid from anaerobic exercise
  • D. Synthesis of bicarbonate by liver ✔ CORRECT
Explanation: True H+ sources: ingested food, CHO→CO₂→H₂CO₃ (12,000-20,000 mmol/day), protein/lipid→H₂SO₄/H₃PO₄ (40-80 mmol/day), lactic acid (exercise), ketoacids (DM). HCO₃⁻ synthesis is not an H+ source - it is alkaline. (Lecture slides 6-7)
💡 Hint: Everything that generates H+ = source. Bicarbonate = alkaline, not H+ source.
📅 ★★★☆☆ | Negative MCQ (EXCEPT type) - sources of H+
Q35. In metabolic acidosis, the respiratory compensation is:
  • A. Hypoventilation to retain CO₂
  • B. Hyperventilation (Kussmaul breathing) to blow off CO₂ ✔ CORRECT
  • C. No respiratory response
  • D. Increased tidal volume only
Explanation: ↑[H+] in metabolic acidosis → stimulates peripheral chemoreceptors → stimulates resp. centre → HYPERVENTILATION (Kussmaul) → ↓ PCO₂ → ↓[H+] toward normal. Insufficient to fully restore pH. (Lecture slide 33)
💡 Hint: Metabolic ACIDOSIS → HYPERVENTILATION (blow off CO₂ = acid). "Kussmaul" = deep, rapid breathing.
📅 ★★★★★ | Kussmaul breathing + compensation of metabolic acidosis

SECTION 2 - PRINTABLE CHEATSHEET (2-PAGE SUMMARY)

PAGE 1: Fundamentals

ParameterNormal ValueClinical Note
Arterial pH7.35-7.45 (mean 7.4)Below 7.35 = Acidosis; Above 7.45 = Alkalosis
[H+] free in ECF40 nmol/LVery low vs Na+ (140 mmol/L)
Death rangepH < 7.0 or > 7.8Incompatible with life
Plasma [HCO₃⁻]24 mEq/LRegulated by kidneys
Arterial PCO₂35-45 mmHgRegulated by lungs
Renal HCO₃⁻ threshold26 mEq/L>26 → HCO₃⁻ in urine
Limiting tubular pH4.5Below this = H+ secretion STOPS
Henderson-Hasselbalch: pH = 6.1 + log([HCO₃⁻]/[H₂CO₃]) = 6.1 + log(24/1.2) = 7.4
pK Ladder (ascending): Bicarbonate 6.1 → Phosphate 6.8 → Ammonia 9.0
DisorderpHPrimary ChangeCompensationKey Causes
Resp. Acidosis<7.35↑PCO₂ >44↑Renal HCO₃⁻ (12-24h)Narcotics, COPD, asthma
Resp. Alkalosis>7.45↓PCO₂ <35↓Renal HCO₃⁻ (days)Anxiety, altitude, fever
Metabolic Acidosis<7.35↓HCO₃⁻Hyperventilation (min)DKA, diarrhea, RTA, RF
Metabolic Alkalosis>7.45↑HCO₃⁻Hypoventilation (limited)Vomiting, Conn's, diuretics

PAGE 2: Nephron Mechanism Diagram

GLOMERULUS → PCT [85%] → Thick Loop [10%] → [Thin Limb: NO H+] → Early DCT → Late DCT + CDs [4.8%]
                ↓                                                                      ↓
          NHE3 (2° active)                                                    H+/K+-ATPase (1° active)
          Na+→cell, H+→lumen                                                  α-IC cells, ×900 aldosterone
          Buffer: HCO₃⁻ → CO₂                                                Buffer: HPO₄²⁻ → NaH₂PO₄
          (CA-IV brush border)                                                 NH₃ → NH₄⁺ → NH₄Cl (urine)
★ TOP 12 MEMORY AIDS (Most Common Batterjee Exam Traps):
  1. Thin limb = NO H+ secretion (all other segments = YES)
  2. PCT = 85% HCO₃⁻ reabsorption via NHE3 (secondary active, Na-dependent)
  3. Late DCT/CDs = H+/K+-ATPase (primary active, Na-INDEPENDENT, aldosterone ×900)
  4. Limiting pH = 4.5 (H+ secretion stops below this)
  5. pK: 6.1 / 6.8 / 9.0 (Bicarbonate / Phosphate / Ammonia)
  6. NH₃ from GLUTAMINE → lipid-soluble → NH₄+ trapped → NH₄Cl excreted
  7. HCO₃⁻ threshold = 26 mEq/L (above = bicarbonaturia)
  8. Kidneys = most powerful (12-24h); Lungs = 2/3 correction in minutes
  9. Hypokalaemia → intracellular acidosis → ↑H+ secretion → metabolic ALKALOSIS
  10. Vomiting = loses HCl → metabolic alkalosis | Diarrhea = loses HCO₃⁻ → metabolic acidosis
  11. DKA = high AG metabolic acidosis | Kussmaul = respiratory compensation
  12. Conn's = metabolic alkalosis + hypokalaemia

QUICK ANSWER KEY

Q1:C | Q2:B | Q3:A | Q4:C | Q5:B | Q6:C | Q7:C | Q8:C | Q9:C | Q10:D | Q11:C | Q12:B | Q13:D | Q14:B | Q15:D | Q16:C | Q17:B | Q18:D | Q19:B | Q20:B | Q21:C | Q22:C | Q23:C | Q24:B | Q25:B | Q26:B | Q27:B | Q28:B | Q29:C | Q30:C | Q31:C | Q32:C | Q33:C | Q34:D | Q35:B
Sources cited throughout:
  • Guyton & Hall Medical Physiology, 13th ed., Unit V Ch 30-31
  • Ganong's Review of Medical Physiology, 25th/26th ed., Section VII Ch 37
  • Brenner & Rector's The Kidney, Acid-Base Regulation chapters
  • Goldman-Cecil Medicine, Renal Dysplasia / Acid-Base sections
  • Dr. Hader I. Sakr's BMC lecture slides (direct reference)
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