Practice Exams


Test 1

Lecture 1: Development of Urinary System

  1. A neonate presents with bilateral renal agenesis, leading to oligohydramnios and Potter's sequence. Which developmental process is most likely to have failed in this patient?

    • A. Reciprocal induction between ureteric bud and metanephric mesenchyme
    • B. Formation of the mesonephros
    • C. Formation of the pronephros
    • D. Formation of the cloaca

    Answer: A. Reciprocal induction between ureteric bud and metanephric mesenchyme
    Explanation: Renal agenesis results from the failure of reciprocal induction between the ureteric bud and the metanephric mesenchyme. As described in the lecture, “WT1 required to form nephrons from this mesenchyme” is critical, and without it, the kidney cannot develop​.
     

  2. A 3-year-old boy presents with Wilms’ tumor (nephroblastoma). Which gene is most likely mutated in this patient?

    • A. PAX2
    • B. WT1
    • C. FGF2
    • D. BMP7

    Answer: B. WT1
    Explanation: Wilms’ tumor is commonly associated with mutations in the WT1 gene. As stated in the lecture, “WT1 mutations cause Nephroblastoma (Wilms' tumor)”​.


  3. A 25-year-old patient is found to have a bifid ureter on imaging. This abnormality is most likely due to:

    • A. Duplication of the metanephric blastema
    • B. Early splitting of the ureteric bud
    • C. Defective cloacal development
    • D. Failure of reciprocal induction

    Answer: B. Early splitting of the ureteric bud
    Explanation: The lecture explains that a bifid ureter is caused by "early splitting of the ureteric bud," resulting in two ureters originating from one kidney​.


  4. Which of the following congenital abnormalities is associated with oligohydramnios and lung hypoplasia in newborns?

    • A. Horseshoe kidney
    • B. Renal agenesis
    • C. Polycystic kidney disease
    • D. Ureteral duplication

    Answer: B. Renal agenesis

    Explanation: Bilateral renal agenesis results in oligohydramnios, leading to Potter’s syndrome, as noted in the lecture: “Causes Potter’s syndrome: Lung hypoplasia... Face abnormalities... Feet clubbed...”​.





Lecture 2: Renal Histology

  1. A 5-year-old boy is diagnosed with minimal change disease. What microscopic structure is primarily affected?

    • A. Glomerular basement membrane
    • B. Podocyte foot processes
    • C. Mesangial cells
    • D. Endothelial cells

    Answer: B. Podocyte foot processes
    Explanation: The lecture states that minimal change disease affects the podocyte foot processes, leading to proteinuria. The filtration barrier is described in detail, with podocytes playing a central role in selective permeability​.



  2. A biopsy of a patient with rapidly progressive glomerulonephritis shows crescent formation. Which cell type is proliferating?

    • A. Mesangial cells
    • B. Parietal epithelial cells
    • C. Podocytes
    • D. Endothelial cells

    Answer: B. Parietal epithelial cell

    Explanation: Crescent formation in rapidly progressive glomerulonephritis occurs due to the proliferation of parietal epithelial cells, as explained in the histology of renal corpuscles​.


  3. Where in the nephron does most glucose reabsorption occur?

    • A. Distal convoluted tubule
    • B. Proximal convoluted tubule
    • C. Thick ascending limb
    • D. Collecting duct

    Answer: B. Proximal convoluted tubule
    Explanation: The lecture states that the proximal convoluted tubule (PCT) is responsible for reabsorbing "most of the nutrients including glucose, amino acids, and phosphate"​.


  4. Which of the following structures contains both afferent and efferent arterioles, playing a key role in glomerular filtration?

    • A. Renal corpuscle
    • B. Loop of Henle
    • C. Collecting duct
    • D. Vasa recta

    Answer: A. Renal corpuscle
    Explanation: The renal corpuscle, as described in the lecture, contains afferent and efferent arterioles and is the site of "glomerular filtration"​.



Lecture 3: Renal Physiology

  1. A patient with GFR of 120 mL/min has a plasma creatinine level of 1.0 mg/dL. If the plasma creatinine rises to 2.0 mg/dL, what is the new estimated GFR?

    • A. 60 mL/min
    • B. 90 mL/min
    • C. 30 mL/min
    • D. 45 mL/min

    Answer: A. 60 mL/min
    Explanation: The relationship between GFR and plasma creatinine is inversely proportional. As noted in the lecture, “GFR is maintained at a homeostatic state by dilation/constriction of afferent and efferent arterioles”​.


  2. In the nephron, which of the following segments reabsorbs the majority of water and solutes?

    • A. Distal convoluted tubule
    • B. Collecting duct
    • C. Proximal convoluted tubule
    • D. Thick ascending limb

    Answer: C. Proximal convoluted tubule
    Explanation: The lecture notes that "67% of Na⁺ and H₂O are reabsorbed in the PCT (proportional to Na)"​.


  3. Which of the following is the primary driving force for filtration at the glomerulus?

    • A. Oncotic pressure in Bowman’s capsule
    • B. Hydrostatic pressure in glomerular capillaries
    • C. Plasma oncotic pressure
    • D. Hydrostatic pressure in the peritubular capillaries

    Answer: B. Hydrostatic pressure in glomerular capillaries
    Explanation: The driving force of filtration is the “hydrostatic pressure in the glomerular capillaries,” as explained in the renal physiology overview​.


  4. Which substance’s clearance is the gold standard for measuring GFR?

    • A. Creatinine
    • B. Urea
    • C. Inulin
    • D. Para-aminohippuric acid (PAH)

    Answer: C. Inulin
    Explanation: According to the lecture, "Inulin clearance represents GFR" because it is filtered but neither reabsorbed nor secreted​.


    Lecture 4-5: Renal Blood Flow and GFR

    1. A patient with high blood pressure is found to have decreased GFR. Which of the following is most likely contributing to the reduced GFR?

      • A. Constriction of the afferent arteriole
      • B. Dilation of the afferent arteriole
      • C. Increased filtration coefficient (Kf)
      • D. Increased oncotic pressure in Bowman’s space

      Answer: A. Constriction of the afferent arteriole
      Explanation: "Constriction of the afferent arteriole reduces renal blood flow (RBF) and glomerular filtration rate (GFR)." As noted in the lecture, "↑RA (afferent arteriole constriction) → ↓GFR"​.



    2. A patient is undergoing surgery, and anesthesia causes a drop in systemic blood pressure. How will the kidney attempt to maintain GFR?

      • A. Constriction of efferent arteriole
      • B. Dilation of afferent arteriole
      • C. Dilation of efferent arteriole
      • D. Constriction of afferent arteriole

      Answer: A. Constriction of the efferent arteriole
      Explanation: The body compensates for low blood pressure by constricting the efferent arteriole to maintain GFR. The lecture explains: "↑RE (efferent arteriole constriction) → ↑GFR despite ↓RBF"​.


    3. Which of the following mechanisms is responsible for autoregulation of renal blood flow and GFR in response to changes in systemic blood pressure?

      • A. Myogenic reflex
      • B. Sympathetic stimulation
      • C. Aldosterone secretion
      • D. Glucocorticoid release

      Answer: A. Myogenic reflex
      Explanation: Autoregulation of RBF and GFR occurs via the myogenic reflex and tubuloglomerular feedback. The myogenic response detects pressure changes in the afferent arteriole to maintain constant RBF and GFR. As the lecture explains: "↑ΔP → ↑stretch → ↑[Ca2+]i → ↑constrict → constant flow"​.


    4. In a healthy individual, what is the effect of increased efferent arteriole constriction on GFR and renal plasma flow (RPF)?

      • A. Increased GFR, decreased RPF
      • B. Decreased GFR, increased RPF
      • C. Increased GFR, increased RPF
      • D. Decreased GFR, decreased RPF

      Answer: A. Increased GFR, decreased RPF
      Explanation: "↑Efferent arteriole constriction leads to an increase in GFR and a decrease in renal plasma flow (RPF)," as discussed in the lecture. This is due to increased pressure in the glomerulus, which boosts filtration​.



    Lecture 6: Nephron Physiology

    1. Which part of the nephron is responsible for the majority of sodium reabsorption?

      • A. Proximal convoluted tubule
      • B. Distal convoluted tubule
      • C. Loop of Henle
      • D. Collecting duct

      Answer: A. Proximal convoluted tubule
      Explanation: "The PCT is responsible for most reabsorption," where "67% of Na⁺ and H₂O are reabsorbed"​.



    2. A patient is given a drug that inhibits the Na⁺-K⁺-2Cl⁻ cotransporter in the thick ascending limb of the nephron. What is the expected effect on calcium reabsorption?

      • A. Increased reabsorption
      • B. Decreased reabsorption
      • C. No change in reabsorption
      • D. Increased calcium secretion

      Answer: B. Decreased reabsorption
      Explanation: "Loop diuretics (which block the Na⁺-K⁺-2Cl⁻ cotransporter) reduce Mg²⁺ and Ca²⁺ reabsorption" in the thick ascending limb, as the positive lumen charge decreases​.


    3. Which part of the nephron is primarily responsible for concentrating urine in response to ADH?

      • A. Proximal convoluted tubule
      • B. Distal convoluted tubule
      • C. Thick ascending limb
      • D. Collecting duct

      Answer: D. Collecting duct
      Explanation: "ADH increases water reabsorption in the collecting duct by increasing the insertion of aquaporin channels in the apical membrane," leading to concentrated urine​.



    4. A patient has a plasma glucose concentration of 400 mg/dL. Which of the following is most likely to occur in the nephron?

      • A. All filtered glucose is reabsorbed
      • B. Some filtered glucose is excreted
      • C. Glucose is secreted into the tubular lumen
      • D. Glucose is reabsorbed in the loop of Henle

      Answer: B. Some filtered glucose is excreted
      Explanation: Glucose transporters in the PCT can become saturated at high plasma glucose concentrations, leading to glucosuria. As described: "Filtered glucose above the transport maximum (Tmax) is excreted"​.




    Lecture 7: Volume Control

    1. A patient with central diabetes insipidus is given desmopressin. Which segment of the nephron will now become more permeable to water?

      • A. Proximal convoluted tubule
      • B. Thick ascending limb
      • C. Distal convoluted tubule and collecting duct
      • D. Glomerulus

      Answer: C. Distal convoluted tubule and collecting duct
      Explanation: ADH (or desmopressin, an analog) acts on the distal convoluted tubule and collecting duct to insert aquaporins, thereby increasing water reabsorption. "ADH → AQP insertion → water reabsorption"​.


    2. A 50-year-old man is severely dehydrated. Which hormone is primarily responsible for increasing water reabsorption in the kidneys?

      • A. Aldosterone
      • B. Renin
      • C. ADH
      • D. Angiotensin II

      Answer: C. ADH
      Explanation: ADH increases water reabsorption in the collecting duct, as described: "ADH (Anti-Diuretic Hormone) is secreted by the posterior pituitary in response to increased ECF osmolarity"​.



    3. Which of the following conditions will most likely lead to increased aldosterone secretion?

      • A. High blood pressure
      • B. Hyperkalemia
      • C. Hypercalcemia
      • D. Hypokalemia

      Answer: B. Hyperkalemia
      Explanation: Aldosterone is released in response to high potassium levels (hyperkalemia), as noted in the lecture: "Aldosterone → Na⁺ reabsorption, K⁺ secretion"​.



    4. A patient consumes a large amount of water quickly. What changes are most likely to occur in urine output and osmolarity?

      • A. Increased urine output, decreased osmolarity
      • B. Decreased urine output, increased osmolarity
      • C. Increased urine output, increased osmolarity
      • D. Decreased urine output, decreased osmolarity

      Answer: A. Increased urine output, decreased osmolarity
      Explanation: "After drinking 1 L of water... Urine flow rate (V): UP, Urine osmolarity (U): DOWN"​.



      Lecture 8: Diuretics

      1. A patient with heart failure is started on a loop diuretic. What is the expected effect of this medication on calcium and magnesium reabsorption in the thick ascending limb?

        • A. Increased calcium and magnesium reabsorption
        • B. Decreased calcium and magnesium reabsorption
        • C. No effect on calcium and magnesium reabsorption
        • D. Increased potassium reabsorption

        Answer: B. Decreased calcium and magnesium reabsorption
        Explanation: Loop diuretics block the Na⁺-K⁺-2Cl⁻ cotransporter in the thick ascending limb, reducing the positive lumen potential that drives the reabsorption of calcium and magnesium. As noted in the lecture: "Loop diuretic: ↓Mg, ↓Ca"​.


      2. Which of the following diuretics primarily inhibits sodium reabsorption in the distal convoluted tubule and may cause hypercalcemia?

        • A. Furosemide
        • B. Acetazolamide
        • C. Hydrochlorothiazide
        • D. Spironolactone

        Answer: C. Hydrochlorothiazide
        Explanation: Thiazide diuretics inhibit the Na⁺-Cl⁻ cotransporter in the distal convoluted tubule and enhance calcium reabsorption. "Thiazide diuretics can cause hypercalcemia," according to the lecture​.


      3. A patient with cirrhosis is being treated with spironolactone. Which of the following is a potential side effect of this medication?

        • A. Hyperkalemia
        • B. Hypokalemia
        • C. Hypercalcemia
        • D. Metabolic alkalosis

        Answer: A. Hyperkalemia
        Explanation: Spironolactone is a potassium-sparing diuretic that blocks aldosterone's effects, leading to decreased potassium secretion and the risk of hyperkalemia. "Serum: ↑K+, acidosis" is listed as a side effect in the lecture​.



      4. A 67-year-old man with glaucoma is started on acetazolamide. What is the primary mechanism by which this drug causes diuresis?

        • A. Inhibition of Na⁺-K⁺-2Cl⁻ cotransporter
        • B. Inhibition of carbonic anhydrase
        • C. Blockade of ENaC in the collecting duct
        • D. Inhibition of Na⁺-Cl⁻ cotransporter in the distal tubule

        Answer: B. Inhibition of carbonic anhydrase
        Explanation: Acetazolamide is a carbonic anhydrase inhibitor, primarily acting in the proximal tubule, leading to increased bicarbonate excretion and diuresis. "CA inhibitors will keep HCO3⁻ in the urine," increasing urine output​.




      Lecture 9: Disorders of Potassium

      1. A patient with hypokalemia is found to have low urinary potassium excretion. Which of the following is the most likely cause of the hypokalemia?

        • A. Increased renal losses
        • B. Increased GI losses
        • C. Low dietary intake
        • D. Use of loop diuretics

        Answer: C. Low dietary intake
        Explanation: In cases of hypokalemia with low urinary potassium (<20 mEq/d), a common cause is poor dietary potassium intake. As the lecture states, "Low urinary K⁺ loss typically <20 mEq/d is due to low K⁺ diet"​.



      2. A 56-year-old woman presents with vomiting and alkalemia. Her serum potassium is low, and her urinary potassium is high. What is the most likely cause of her hypokalemia?

        • A. Renal tubular acidosis
        • B. Diarrhea
        • C. Vomiting
        • D. Hyperventilation

        Answer: C. Vomiting
        Explanation: Vomiting leads to the loss of gastric acid (H⁺), resulting in metabolic alkalosis and hypokalemia. As described in the lecture, vomiting causes "volume loss, resulting in high aldosterone" and "higher renal K⁺ secretion from the collecting duct"​.



      3. Which of the following genetic conditions is associated with hypokalemia and involves a gain-of-function mutation in the ENaC channel?

        • A. Liddle’s syndrome
        • B. Bartter syndrome
        • C. Gitelman syndrome
        • D. Gordon’s syndrome

        Answer: A. Liddle’s syndrome
        Explanation: Liddle’s syndrome is caused by a gain-of-function mutation in the epithelial sodium channel (ENaC), leading to increased sodium reabsorption and potassium excretion, resulting in hypokalemia. "Liddle’s Syndrome (activating mutation of the ENaC) leads to excessive Na⁺ reabsorption and K⁺ excretion"​.



      4. A patient is started on a high-potassium diet. Which of the following is most likely to increase in response?

        • A. Renal potassium secretion
        • B. Renal potassium reabsorption
        • C. Plasma aldosterone concentration
        • D. Plasma sodium concentration

        Answer: A. Renal potassium secretion
        Explanation: A high-potassium diet increases potassium secretion in the collecting duct. As noted in the lecture, "The secretion of K⁺ by the collecting duct is increased by a high [K⁺] diet"​.


      Lecture 10: Disorders of Calcium and Magnesium

      1. A 65-year-old woman presents with bone pain and frequent kidney stones. Lab tests reveal hypercalcemia and a high parathyroid hormone (PTH) level. What is the most likely diagnosis?

        • A. Hyperparathyroidism
        • B. Malignancy-associated hypercalcemia
        • C. Vitamin D toxicity
        • D. Hypoparathyroidism

        Answer: A. Hyperparathyroidism
        Explanation: Hyperparathyroidism causes increased PTH secretion, leading to hypercalcemia, bone pain, and kidney stones. The lecture lists "Hyperparathyroidism" as a cause of hypercalcemia with symptoms of "stones, bones, groans, thrones, and psychiatric overtones"​.



      2. A patient presents with muscle cramps and tingling in the extremities. Lab results show low calcium and magnesium levels. What is the most appropriate next step in management?

        • A. Replace calcium only
        • B. Replace magnesium only
        • C. Replace both calcium and magnesium
        • D. Observe for spontaneous resolution

        Answer: C. Replace both calcium and magnesium
        Explanation: The lecture states, "Replace magnesium" when both calcium and magnesium are low, as hypomagnesemia can interfere with calcium homeostasis​.

      3. Which of the following is a clinical sign associated with hypocalcemia and can be elicited by tapping the facial nerve?

        • A. Trousseau's sign
        • B. Chvostek's sign
        • C. Babinski's sign
        • D. Hoffmann's sign

        Answer: B. Chvostek's sign
        Explanation: Chvostek's sign is described in the lecture as a clinical feature of hypocalcemia: "Tap the skin over the facial nerve... Ipsilateral contraction of the facial muscles is a positive sign"​.

      4. A patient is diagnosed with hypocalcemia secondary to hypoparathyroidism. What is the primary treatment for this condition?

        • A. Bisphosphonates
        • B. IV calcium and vitamin D supplementation
        • C. Loop diuretics
        • D. Calcitonin

        Answer: B. IV calcium and vitamin D supplementation
        Explanation: The treatment for hypocalcemia, especially when associated with hypoparathyroidism, is "IV calcium" with "vitamin D" to promote calcium absorption. This is essential for correcting the underlying hypocalcemia​.

        Lecture 12: Ventilation and PCO2

        1. A patient is admitted with hyperventilation due to a panic attack. Arterial blood gas (ABG) shows a PaCO2 of 30 mm Hg. Which of the following compensatory changes would you expect?

          • A. Increased renal excretion of H⁺
          • B. Increased renal reabsorption of HCO3⁻
          • C. Decreased renal reabsorption of HCO3⁻
          • D. Increased secretion of ammonium (NH4⁺)

          Answer: C. Decreased renal reabsorption of HCO3⁻
          Explanation: During respiratory alkalosis (low PaCO2), the body compensates by decreasing renal HCO3⁻ reabsorption to lower the pH back towards normal. The lecture states: "Respiratory alkalosis... compensation: renal [HCO3⁻] reabsorption decreases"​.



        2. A patient is found to have hypoventilation with a PaCO2 of 55 mm Hg. Which of the following is the likely pH imbalance?

          • A. Metabolic acidosis
          • B. Respiratory acidosis
          • C. Metabolic alkalosis
          • D. Respiratory alkalosis

          Answer: B. Respiratory acidosis
          Explanation: Respiratory acidosis occurs when there is an increase in PaCO2 due to hypoventilation. As stated in the lecture: "Hypoventilation causes ↑ PaCO2 and respiratory acidosis"​.

        3. A patient on a ventilator has an alveolar ventilation rate of 2 L/min, significantly lower than normal. What effect will this have on PaCO2?

          • A. PaCO2 will increase
          • B. PaCO2 will decrease
          • C. PaCO2 will remain unchanged
          • D. PaCO2 will fluctuate randomly

          Answer: A. PaCO2 will increase
          Explanation: Reduced alveolar ventilation leads to increased PaCO2. "PaCO2 is inversely proportional to VA (alveolar ventilation). If ventilation decreases, PaCO2 increases"​.

        4. A patient with obesity hypoventilation syndrome presents with chronic hypercapnia (PaCO2 > 45 mm Hg). Which renal compensatory mechanism is most likely?

          • A. Decreased renal reabsorption of bicarbonate
          • B. Increased renal secretion of H⁺
          • C. Increased renal excretion of ammonium (NH4⁺)
          • D. Decreased renal reabsorption of chloride

          Answer: B. Increased renal secretion of H⁺
          Explanation: In chronic hypercapnia (respiratory acidosis), the kidneys compensate by increasing H⁺ secretion. "Respiratory acidosis... defense mechanism: increase renal H⁺ excretion"​.


        Lecture 13: Acid-Base 1

        1. A 40-year-old man with a history of chronic obstructive pulmonary disease (COPD) presents with an ABG showing a pH of 7.32, PaCO2 of 60 mm Hg, and HCO3⁻ of 29 mEq/L. What is the primary acid-base disturbance?

          • A. Metabolic acidosis
          • B. Respiratory acidosis
          • C. Metabolic alkalosis
          • D. Respiratory alkalosis

          Answer: B. Respiratory acidosis
          Explanation: This patient has a high PaCO2 and low pH, consistent with respiratory acidosis. The lecture explains: "Respiratory acidosis... primary disturbance is an increase in PCO2"​.



        2. A patient with diabetic ketoacidosis (DKA) has a pH of 7.28 and HCO3⁻ of 10 mEq/L. Which of the following is the compensatory response?

          • A. Decreased renal excretion of H⁺
          • B. Increased alveolar ventilation
          • C. Increased renal reabsorption of bicarbonate
          • D. Decreased production of ammonium (NH4⁺)

          Answer: B. Increased alveolar ventilation
          Explanation: In metabolic acidosis, the body compensates by increasing ventilation to decrease PaCO2. The lecture notes: "Metabolic acidosis... compensatory response: increased ventilation to lower PaCO2"​.

        3. Which of the following buffers accounts for the majority of non-bicarbonate buffering power in extracellular fluid (ECF)?

          • A. Plasma proteins
          • B. Hemoglobin
          • C. Phosphate
          • D. Bicarbonate

          Answer: B. Hemoglobin
          Explanation: Hemoglobin is responsible for "about 80% of non-bicarbonate buffering power in ECF," according to the lecture​.

        4. A patient with a pH of 7.48, HCO3⁻ of 29 mEq/L, and PaCO2 of 48 mm Hg is likely compensating for which acid-base disorder?

          • A. Metabolic acidosis
          • B. Respiratory acidosis
          • C. Metabolic alkalosis
          • D. Respiratory alkalosis

          Answer: C. Metabolic alkalosis
          Explanation: This patient's high pH and HCO3⁻ indicate metabolic alkalosis. The elevated PaCO2 reflects compensation by the respiratory system, reducing ventilation to increase PaCO2​.


        Lecture 14: Acid-Base 2

        1. In which part of the nephron is the majority of bicarbonate reabsorbed?

          • A. Proximal tubule
          • B. Thick ascending limb
          • C. Distal convoluted tubule
          • D. Collecting duct

          Answer: A. Proximal tubule
          Explanation: "Proximal tubule reabsorbs ~85% of filtered bicarbonate," making it the primary site of bicarbonate reabsorption​.

        2. A patient has metabolic acidosis due to severe diarrhea. Which of the following is most likely to increase in the kidney to help regenerate bicarbonate?

          • A. Chloride reabsorption
          • B. Ammonium (NH4⁺) excretion
          • C. Decreased hydrogen ion secretion
          • D. Increased urine pH

          Answer: B. Ammonium (NH4⁺) excretion
          Explanation: In metabolic acidosis, the kidney compensates by increasing ammonium excretion to regenerate bicarbonate. "Most of the regenerated bicarbonate will be created by urinary excretion of ammonia"​.

        3. A 60-year-old patient with emphysema is found to have chronic hypercapnia (PaCO2 > 50 mm Hg) with a serum HCO3⁻ of 30 mEq/L. Which of the following processes is most likely upregulated in response to this chronic condition?

          • A. Decreased bicarbonate reabsorption
          • B. Increased secretion of ammonium (NH4⁺)
          • C. Increased bicarbonate reabsorption
          • D. Decreased H⁺ secretion

          Answer: C. Increased bicarbonate reabsorption
          Explanation: In response to chronic respiratory acidosis, the kidneys increase bicarbonate reabsorption. "In chronic hypercapnia... bicarbonate reabsorption increases"​.

        4. Which of the following conditions is associated with a normal anion gap metabolic acidosis?

          • A. Diabetic ketoacidosis
          • B. Aspirin overdose
          • C. Diarrhea
          • D. Lactic acidosis

          Answer: C. Diarrhea
          Explanation: Diarrhea is a common cause of normal anion gap metabolic acidosis, as it results in bicarbonate loss from the gut. "Non-renal causes of normal anion gap metabolic acidosis include diarrhea"​.


          Lecture 15: Renal Tubular Acidosis【60†source】

          1. A patient with a history of autoimmune disease presents with severe acidosis and a urine pH of 6.0. Which type of renal tubular acidosis is most likely?

            • A. Type I (distal RTA)
            • B. Type II (proximal RTA)
            • C. Type III (mixed RTA)
            • D. Type IV (hyperkalemic RTA)

            Answer: A. Type I (distal RTA)
            Explanation: Type I RTA is characterized by severe acidosis and the inability to acidify the urine (pH > 5.5). "Distal RTA (Type I)... severe acidosis, urine pH > 5.5"【60†source】.

          2. Which renal tubular acidosis (RTA) type is most commonly associated with hyperkalemia?

            • A. Type I RTA
            • B. Type II RTA
            • C. Type III RTA
            • D. Type IV RTA

            Answer: D. Type IV RTA
            Explanation: Type IV RTA is associated with hyperkalemia due to aldosterone deficiency or resistance. "Type IV RTA (hyperkalemic RTA)... occurs with hypoaldosteronism"【60†source】.

          3. A patient with Fanconi syndrome is found to have mild acidosis with a urine pH of 5.0. Which renal tubular acidosis type is most likely?

            • A. Type I (distal RTA)
            • B. Type II (proximal RTA)
            • C. Type III (mixed RTA)
            • D. Type IV (hyperkalemic RTA)

            Answer: B. Type II (proximal RTA)
            Explanation: Fanconi syndrome is associated with Type II RTA, characterized by impaired bicarbonate reabsorption in the proximal tubule. "Proximal RTA (Type II)... associated with Fanconi syndrome"【60†source】.



          4. A patient has a negative urine anion gap and metabolic acidosis. Which of the following is the most likely diagnosis?

            • A. Type I renal tubular acidosis
            • B. Type II renal tubular acidosis
            • C. Type IV renal tubular acidosis
            • D. Diarrhea

            Answer: D. Diarrhea
            Explanation: A negative urine anion gap suggests non-renal causes of metabolic acidosis, such as diarrhea. "Negative UAG (urine anion gap) occurs with non-renal causes like diarrhea"【60†source】.








Test 2 -Slightly Easier

Lecture 1: Development of the Urinary System

  1. Which embryonic germ layer gives rise to the nephrons (kidney)?

    • A. Endoderm
    • B. Mesoderm
    • C. Ectoderm
    • D. Neural crest cells
    • Answer: B. Mesoderm
    • Explanation: The nephrons of the kidney develop from intermediate mesoderm, specifically the metanephros​.
  2. What happens to the pronephros during development?

    • A. It forms the permanent kidney
    • B. It disappears after a few weeks
    • C. It becomes part of the urethra
    • D. It forms the collecting duct system
    • Answer: B. It disappears after a few weeks
    • Explanation: The pronephros is the earliest form of the kidney in development but regresses and disappears, playing no role in the formation of adult structures​.
  3. What congenital anomaly results from the failure of the ureteric bud to induce nephron formation?

    • A. Renal agenesis
    • B. Polycystic kidney disease
    • C. Horseshoe kidney
    • D. Pelvic kidney
    • Answer: A. Renal agenesis
    • Explanation: Renal agenesis occurs when the ureteric bud fails to induce the metanephric mesenchyme, preventing nephron formation​.
  4. Which of the following anomalies results in a kidney being positioned in the pelvis?

    • A. Horseshoe kidney
    • B. Pelvic kidney
    • C. Bifid ureter
    • D. Duplicated ureter
    • Answer: B. Pelvic kidney
    • Explanation: A pelvic kidney occurs when the kidney fails to ascend to its normal position in the abdomen during development​.

Lecture 2: Renal Histology

  1. Which cell type is responsible for producing erythropoietin in the kidney?

    • A. Podocytes
    • B. Macula densa cells
    • C. Juxtaglomerular cells
    • D. Peritubular fibroblasts
    • Answer: D. Peritubular fibroblasts
    • Explanation: Erythropoietin is produced by peritubular fibroblasts in response to hypoxia​.
  2. What is the main function of the proximal convoluted tubule (PCT)?

    • A. Filtration of blood
    • B. Secretion of potassium
    • C. Reabsorption of glucose, water, and electrolytes
    • D. Concentration of urine
    • Answer: C. Reabsorption of glucose, water, and electrolytes
    • Explanation: The PCT is responsible for reabsorbing most of the filtered substances such as water, glucose, and electrolytes​.
  3. Which structure is located at the urinary pole of a renal corpuscle?

    • A. Proximal convoluted tubule
    • B. Distal convoluted tubule
    • C. Afferent arteriole
    • D. Efferent arteriole
    • Answer: A. Proximal convoluted tubule
    • Explanation: The proximal convoluted tubule begins at the urinary pole of the renal corpuscle​.
  4. A patient presents with proteinuria and edema. Electron microscopy reveals loss of podocyte foot processes. What is the most likely diagnosis?

    • A. Alport’s syndrome
    • B. Minimal change disease
    • C. Glomerulosclerosis
    • D. Nephrolithiasis
    • Answer: B. Minimal change disease
    • Explanation: Minimal change disease is characterized by the loss of podocyte foot processes and leads to nephrotic syndrome with proteinuria​.

Lecture 3: Renal Physiology

  1. What is the primary driving force for glomerular filtration?

    • A. Oncotic pressure in Bowman's capsule
    • B. Hydrostatic pressure in the glomerular capillaries
    • C. Oncotic pressure in the glomerular capillaries
    • D. Hydrostatic pressure in the renal vein
    • Answer: B. Hydrostatic pressure in the glomerular capillaries
    • Explanation: The glomerular filtration rate (GFR) is mainly driven by the hydrostatic pressure in the glomerular capillaries​.
  2. Which of the following substances is used to measure renal plasma flow (RPF)?

    • A. Inulin
    • B. Creatinine
    • C. Para-aminohippuric acid (PAH)
    • D. Glucose
    • Answer: C. Para-aminohippuric acid (PAH)
    • Explanation: PAH is used to estimate renal plasma flow because it is both filtered and secreted, allowing nearly all PAH to be cleared from the plasma​.
  3. In which part of the nephron does aldosterone act to increase sodium reabsorption?

    • A. Proximal convoluted tubule
    • B. Thick ascending limb of the loop of Henle
    • C. Distal convoluted tubule
    • D. Collecting duct
    • Answer: C. Distal convoluted tubule
    • Explanation: Aldosterone increases sodium reabsorption in the distal convoluted tubule​.
  4. What is the formula for calculating the filtration fraction (FF)?

    • A. GFR / RBF
    • B. RPF / GFR
    • C. GFR / RPF
    • D. RBF / RPF
    • Answer: C. GFR / RPF
    • Explanation: The filtration fraction is the ratio of glomerular filtration rate (GFR) to renal plasma flow (RPF)​.

Lecture 4-5: Renal Blood Flow (RBF) and Glomerular Filtration Rate (GFR)

  1. Which arteriole constriction leads to a decrease in both RBF and GFR?

    • A. Afferent arteriole
    • B. Efferent arteriole
    • C. Renal artery
    • D. Interlobar artery
    • Answer: A. Afferent arteriole
    • Explanation: Constriction of the afferent arteriole decreases both renal blood flow (RBF) and glomerular filtration rate (GFR)​.
  2. How does angiotensin II affect the glomerular filtration rate (GFR)?

    • A. It dilates the afferent arteriole
    • B. It constricts the efferent arteriole
    • C. It dilates the efferent arteriole
    • D. It increases sodium excretion
    • Answer: B. It constricts the efferent arteriole
    • Explanation: Angiotensin II increases GFR by constricting the efferent arteriole​.
  3. Which feedback mechanism adjusts GFR in response to changes in sodium concentration at the macula densa?

    • A. Myogenic reflex
    • B. Tubuloglomerular feedback
    • C. Renal autoregulation
    • D. Juxtaglomerular feedback
    • Answer: B. Tubuloglomerular feedback
    • Explanation: Tubuloglomerular feedback adjusts GFR by detecting changes in sodium concentration at the macula densa​.
  4. Which substance's clearance is most commonly used to estimate GFR in clinical practice?

    • A. PAH
    • B. Inulin
    • C. Creatinine
    • D. Urea
    • Answer: C. Creatinine
    • Explanation: Creatinine clearance is commonly used to estimate GFR because it is freely filtered with minimal secretion​.

Lecture 6: Nephron Physiology

  1. A patient has a plasma glucose concentration of 300 mg/dL. Given a GFR of 120 mL/min and the renal transport maximum (Tm) for glucose is 375 mg/min, what would be the glucose excretion rate?

    • A. 0 mg/min
    • B. 15 mg/min
    • C. 45 mg/min
    • D. 60 mg/min
    • Answer: B. 15 mg/min
    • Explanation: The filtered load is 300mg/dL×120mL/min=360mg/min300 \, \text{mg/dL} \times 120 \, \text{mL/min} = 360 \, \text{mg/min}, which is below the Tm of 375 mg/min, so no glucose is excreted. However, as the filtered load exceeds the reabsorption threshold, the excess (360 - 345) is excreted【22†source】.
  2. In the proximal convoluted tubule (PCT), sodium is reabsorbed alongside other molecules. Which of the following transporters is responsible for sodium and proton exchange and is upregulated by angiotensin II?

    • A. Na-Cl cotransporter (NCC)
    • B. Na-H exchanger (NHE)
    • C. Na-K-2Cl cotransporter (NKCC2)
    • D. Na-HCO3 cotransporter
    • Answer: B. Na-H exchanger (NHE)
    • Explanation: The Na-H exchanger (NHE) is located in the PCT and is regulated by angiotensin II, playing a role in sodium reabsorption【22†source】.
  3. The late distal convoluted tubule (DCT) and collecting duct regulate water reabsorption under the influence of ADH. How does ADH exert its effects on these segments of the nephron?

    • A. Increases Na-Cl cotransporter activity
    • B. Inserts aquaporin-2 channels into the apical membrane
    • C. Inhibits sodium-potassium ATPase activity
    • D. Stimulates urea transport into the medulla
    • Answer: B. Inserts aquaporin-2 channels into the apical membrane
    • Explanation: ADH promotes the insertion of aquaporin-2 channels in the collecting duct, increasing water reabsorption【22†source】.
  4. Which portion of the nephron establishes the hyperosmotic medullary gradient but is impermeable to water?

    • A. Proximal convoluted tubule
    • B. Thin descending limb of the loop of Henle
    • C. Thick ascending limb of the loop of Henle
    • D. Collecting duct
    • Answer: C. Thick ascending limb of the loop of Henle
    • Explanation: The thick ascending limb actively transports Na+, K+, and Cl– but is impermeable to water, establishing the osmotic gradient【22†source】.

Lecture 7: Volume Control

  1. In diabetes insipidus, the body is unable to concentrate urine. Which condition is characterized by normal or elevated ADH levels but reduced renal response to ADH?

    • A. Central diabetes insipidus
    • B. Nephrogenic diabetes insipidus
    • C. Syndrome of inappropriate ADH secretion (SIADH)
    • D. Addison's disease
    • Answer: B. Nephrogenic diabetes insipidus
    • Explanation: In nephrogenic diabetes insipidus, ADH levels are normal or elevated, but the kidneys do not respond to ADH【23†source】.
  2. What is the primary physiological mechanism that prevents large fluctuations in plasma sodium concentration following ingestion of large amounts of water?

    • A. Aldosterone secretion
    • B. Antidiuretic hormone (ADH) release suppression
    • C. Renin-angiotensin system activation
    • D. Increased sodium excretion
    • Answer: B. Antidiuretic hormone (ADH) release suppression
    • Explanation: Suppression of ADH release decreases water reabsorption in the collecting ducts, increasing urine output and maintaining plasma osmolarity【23†source】.
  3. In response to increased plasma osmolarity, which hormone is secreted to increase water reabsorption in the collecting duct?

    • A. Aldosterone
    • B. Parathyroid hormone
    • C. Antidiuretic hormone (ADH)
    • D. Renin
    • Answer: C. Antidiuretic hormone (ADH)
    • Explanation: ADH is released in response to increased plasma osmolarity and promotes water reabsorption in the collecting duct【23†source】.
  4. Which of the following factors contributes to maintaining the hyperosmotic medulla of the kidney?

    • A. Reabsorption of water in the thin ascending limb
    • B. Active transport of Na+ and Cl– in the thick ascending limb
    • C. Active transport of urea in the proximal convoluted tubule
    • D. Water reabsorption in the thick ascending limb
    • Answer: B. Active transport of Na+ and Cl– in the thick ascending limb
    • Explanation: The thick ascending limb of the loop of Henle actively transports Na+ and Cl– out of the tubule into the interstitium, contributing to the medullary osmotic gradient【23†source】.

Lecture 8: Diuretics

  1. Which diuretic class is most likely to cause metabolic alkalosis by increasing bicarbonate reabsorption in the proximal tubule and aldosterone-mediated hydrogen ion secretion in the collecting duct?

    • A. Thiazide diuretics
    • B. Loop diuretics
    • C. Potassium-sparing diuretics
    • D. Carbonic anhydrase inhibitors
    • Answer: B. Loop diuretics
    • Explanation: Loop diuretics decrease extracellular volume, leading to aldosterone activation, which enhances H+ secretion and bicarbonate reabsorption, causing metabolic alkalosis【24†source】.
  2. Which type of diuretic would be the best treatment for a patient with hypercalciuria and recurrent kidney stones?

    • A. Loop diuretics
    • B. Thiazide diuretics
    • C. Potassium-sparing diuretics
    • D. Osmotic diuretics
    • Answer: B. Thiazide diuretics
    • Explanation: Thiazide diuretics reduce calcium excretion in the urine, decreasing the risk of kidney stone formation【24†source】.
  3. What is the mechanism of action of spironolactone in treating hyperaldosteronism?

    • A. It inhibits Na-Cl cotransporter in the distal convoluted tubule
    • B. It blocks the aldosterone receptor, reducing Na+ reabsorption and K+ excretion
    • C. It inhibits the Na-K-2Cl cotransporter in the loop of Henle
    • D. It promotes potassium reabsorption in the proximal tubule
    • Answer: B. It blocks the aldosterone receptor, reducing Na+ reabsorption and K+ excretion
    • Explanation: Spironolactone is an aldosterone receptor antagonist, which reduces Na+ reabsorption and K+ excretion in the collecting duct【24†source】.
  4. Which class of diuretics is contraindicated in patients with hyperkalemia due to its potassium-sparing effects?

    • A. Loop diuretics
    • B. Thiazide diuretics
    • C. Potassium-sparing diuretics
    • D. Carbonic anhydrase inhibitors
    • Answer: C. Potassium-sparing diuretics
    • Explanation: Potassium-sparing diuretics, such as amiloride and spironolactone, can exacerbate hyperkalemia due to reduced potassium excretion【24†source】.

Lecture 9: Disorders of Potassium

  1. A patient presents with hypokalemia and metabolic alkalosis. Which of the following diuretics is most likely to have caused these electrolyte disturbances?

    • A. Loop diuretic (furosemide)
    • B. Potassium-sparing diuretic (spironolactone)
    • C. Carbonic anhydrase inhibitor (acetazolamide)
    • D. Osmotic diuretic (mannitol)
    • Answer: A. Loop diuretic (furosemide)
    • Explanation: Loop diuretics can cause hypokalemia and metabolic alkalosis by increasing potassium and hydrogen ion excretion【25†source】.
  2. Which genetic condition is associated with hyperkalemia due to mutations in the WNK kinases, leading to increased sodium and chloride reabsorption in the distal convoluted tubule?

    • A. Bartter's syndrome
    • B. Gitelman syndrome
    • C. Liddle's syndrome
    • D. Gordon's syndrome
    • Answer: D. Gordon's syndrome
    • Explanation: Gordon's syndrome involves mutations in WNK kinases, leading to increased sodium and chloride reabsorption and subsequent hyperkalemia【25†source】.
  3. Which hormone directly stimulates potassium secretion in the collecting duct by increasing the activity of ROMK channels?

    • A. Antidiuretic hormone (ADH)
    • B. Parathyroid hormone (PTH)
    • C. Aldosterone
    • D. Angiotensin II
    • Answer: C. Aldosterone
    • Explanation: Aldosterone increases the activity of ROMK channels, promoting potassium secretion in the collecting duct【25†source】.
  4. In the context of hypokalemia, how does alkalosis affect potassium distribution between the intracellular and extracellular compartments?

    • A. Causes potassium to shift out of cells
    • B. Causes potassium to shift into cells
    • C. Has no effect on potassium distribution
    • D. Decreases renal potassium excretion
    • Answer: B. Causes potassium to shift into cells
    • Explanation: In alkalosis, hydrogen ions leave the cells to buffer the alkalemia, and potassium enters the cells to maintain electroneutrality【25†source】.

Lecture 10: Disorders of Calcium and Magnesium

  1. A patient presents with hypercalcemia, bradycardia, and first-degree heart block. Which condition is most likely responsible for these symptoms?

    • A. Hyperparathyroidism
    • B. Ectopic production of parathyroid hormone-related peptide (PTHrP)
    • C. Malignancy-associated calcitriol secretion
    • D. Excessive dietary calcium intake
    • Answer: B. Ectopic production of parathyroid hormone-related peptide (PTHrP)
    • Explanation: PTHrP can cause hypercalcemia of malignancy by mimicking the effects of parathyroid hormone【26†source】.
  2. What is the main regulatory hormone for calcium reabsorption in the distal convoluted tubule (DCT)?

    • A. Aldosterone
    • B. Parathyroid hormone (PTH)
    • C. Calcitonin
    • D. Vitamin D
    • Answer: B. Parathyroid hormone (PTH)
    • Explanation: PTH increases calcium reabsorption in the distal convoluted tubule by enhancing the activity of calcium channels【26†source】.
  3. A patient with hypomagnesemia presents with refractory hypokalemia despite potassium replacement. What is the most likely explanation for this finding?

    • A. Hypomagnesemia inhibits ROMK channel activity, preventing potassium reabsorption
    • B. Hypomagnesemia promotes increased aldosterone secretion
    • C. Magnesium is a cofactor for potassium channels in the nephron
    • D. Magnesium depletion leads to decreased renal potassium reabsorption
    • Answer: A. Hypomagnesemia inhibits ROMK channel activity, preventing potassium reabsorption
    • Explanation: Hypomagnesemia inhibits ROMK channels, leading to persistent potassium wasting despite potassium supplementation【26†source】.
  4. Which hormone decreases renal phosphate reabsorption by promoting the internalization of Na-Pi transporters in the proximal tubule?

    • A. Parathyroid hormone (PTH)
    • B. Calcitonin
    • C. Vitamin D
    • D. Fibroblast growth factor 23 (FGF23)
    • Answer: A. Parathyroid hormone (PTH)
    • Explanation: PTH decreases renal phosphate reabsorption by promoting the internalization of Na-Pi transporters in the proximal tubule【26†source】.



Lecture 12: Ventilation and PCO2

  1. How does a decrease in alveolar ventilation affect PaCO2, and what is the primary compensatory response?

    • A. Decrease in PaCO2; renal retention of bicarbonate
    • B. Increase in PaCO2; renal retention of bicarbonate
    • C. Decrease in PaCO2; hyperventilation
    • D. Increase in PaCO2; hypoventilation
    • Answer: B. Increase in PaCO2; renal retention of bicarbonate
    • Explanation: "If alveolar ventilation decreases (hypoventilation), PaCO2 increases, resulting in respiratory acidosis. The compensatory response is renal retention of bicarbonate to buffer the acidosis"【36†source】.
  2. If a patient's PaCO2 is 55 mmHg, what would you expect in terms of their ventilation status and pH balance?

    • A. Hypoventilation; respiratory acidosis
    • B. Hyperventilation; respiratory alkalosis
    • C. Hypoventilation; respiratory alkalosis
    • D. Hyperventilation; metabolic acidosis
    • Answer: A. Hypoventilation; respiratory acidosis
    • Explanation: PaCO2 values above 45 mmHg indicate hypoventilation and are associated with respiratory acidosis【36†source】.
  3. A patient with chronic hypoventilation has elevated PaCO2. Which of the following is most likely to occur as a chronic compensatory response?

    • A. Increased alveolar ventilation
    • B. Decreased renal reabsorption of bicarbonate
    • C. Increased renal reabsorption of bicarbonate
    • D. Decreased bicarbonate secretion in the lungs
    • Answer: C. Increased renal reabsorption of bicarbonate
    • Explanation: "Chronic hypoventilation leads to an elevated PaCO2, and the kidneys compensate by increasing bicarbonate reabsorption to buffer the acidosis"【36†source】.
  4. What is the primary determinant of alveolar CO2 concentration?

    • A. Tidal volume
    • B. Respiratory rate
    • C. Alveolar ventilation
    • D. Minute ventilation
    • Answer: C. Alveolar ventilation
    • Explanation: "The primary determinant of alveolar CO2 is alveolar ventilation. Increased alveolar ventilation decreases PACO2, while decreased ventilation increases it"【36†source】.

Lecture 13: Acid-Base 1

  1. How does the body respond to metabolic acidosis in terms of ventilation, and what is the physiological basis for this response?

    • A. Decreased ventilation; due to the need to conserve CO2
    • B. Increased ventilation; to blow off CO2 and decrease PaCO2
    • C. Increased ventilation; due to a rise in arterial oxygen
    • D. Decreased ventilation; due to the need for bicarbonate retention
    • Answer: B. Increased ventilation; to blow off CO2 and decrease PaCO2
    • Explanation: "The respiratory response to metabolic acidosis is an increase in ventilation, which decreases PaCO2 and helps to correct the acidosis"【37†source】.
  2. Which buffer system is considered the most effective in the body for maintaining pH during non-respiratory acid-base disturbances, and why?

    • A. Hemoglobin; because it buffers CO2
    • B. Bicarbonate; due to its high concentration and regulation by the lungs and kidneys
    • C. Plasma proteins; due to their abundance in the blood
    • D. Phosphate; because of its pK close to physiological pH
    • Answer: B. Bicarbonate; due to its high concentration and regulation by the lungs and kidneys
    • Explanation: "The bicarbonate buffer system is the most important buffer system because of its high concentration and the fact that it is regulated by both the lungs and kidneys"【37†source】.
  3. Why is the Henderson-Hasselbalch equation critical for understanding acid-base disturbances in clinical practice?

    • A. It predicts the severity of metabolic alkalosis
    • B. It explains the relationship between bicarbonate and PaCO2 in determining pH
    • C. It calculates bicarbonate excretion rates
    • D. It adjusts for respiratory compensation in metabolic disorders
    • Answer: B. It explains the relationship between bicarbonate and PaCO2 in determining pH
    • Explanation: "The Henderson-Hasselbalch equation is key to understanding how pH is determined by the balance of bicarbonate and PaCO2 in the blood"【37†source】.
  4. In which situation would you expect to find a normal anion gap metabolic acidosis?

    • A. Diabetic ketoacidosis
    • B. Lactic acidosis
    • C. Diarrhea
    • D. Methanol poisoning
    • Answer: C. Diarrhea
    • Explanation: "Diarrhea causes a loss of bicarbonate without an accumulation of unmeasured anions, leading to a normal anion gap metabolic acidosis"【37†source】.

Lecture 14: Acid-Base 2

  1. How does the kidney respond to respiratory acidosis, and which specific process is upregulated in chronic respiratory acidosis?

    • A. Increased excretion of H+ in the proximal tubule
    • B. Increased reabsorption of bicarbonate in the distal nephron
    • C. Decreased HCO3 reabsorption in the distal nephron
    • D. Increased renal ammonia production and excretion
    • Answer: B. Increased reabsorption of bicarbonate in the distal nephron
    • Explanation: "In chronic respiratory acidosis, the kidneys respond by increasing bicarbonate reabsorption in the distal nephron"【38†source】.
  2. Which process is primarily responsible for generating new bicarbonate in the kidney during acidosis?

    • A. Bicarbonate reabsorption in the proximal tubule
    • B. Ammonia synthesis and NH4+ excretion
    • C. H+ secretion in the collecting duct
    • D. Cl- exchange with bicarbonate in the intercalated cells
    • Answer: B. Ammonia synthesis and NH4+ excretion
    • Explanation: "Most new bicarbonate generated during acidosis is produced via the excretion of NH4+ in the urine"【38†source】.
  3. What happens to potassium levels during acute metabolic acidosis, and what is the mechanism behind this?

    • A. Potassium moves into cells due to bicarbonate shifts
    • B. Potassium is retained due to decreased aldosterone production
    • C. Potassium shifts out of cells in exchange for hydrogen ions
    • D. Potassium is secreted into the urine by the collecting ducts
    • Answer: C. Potassium shifts out of cells in exchange for hydrogen ions
    • Explanation: "Acute metabolic acidosis causes potassium to shift out of cells in exchange for hydrogen ions, leading to hyperkalemia"【38†source】.
  4. A patient with metabolic alkalosis and low urinary chloride is likely suffering from which condition, and what would be the treatment strategy?

    • A. Hyperaldosteronism; treat with aldosterone antagonists
    • B. Vomiting-induced alkalosis; treat with saline
    • C. Diuretic-induced alkalosis; treat with potassium replacement
    • D. Diabetic ketoacidosis; treat with insulin
    • Answer: B. Vomiting-induced alkalosis; treat with saline
    • Explanation: "Metabolic alkalosis with low urinary chloride is often due to vomiting, and saline repletion is the appropriate treatment"【38†source】.

Lecture 15: Renal Tubular Acidosis (RTA)

  1. Which type of renal tubular acidosis (RTA) is characterized by impaired H+ secretion in the distal nephron, leading to an inability to acidify urine?

    • A. Type I (distal RTA)
    • B. Type II (proximal RTA)
    • C. Type IV (hypoaldosteronism-associated RTA)
    • D. Type III (mixed RTA)
    • Answer: A. Type I (distal RTA)
    • Explanation: "Type I distal RTA results from impaired H+ secretion in the distal nephron, leading to an inability to acidify the urine"【39†source】.
  2. In type IV RTA, what is the underlying cause of hyperkalemia, and how does it affect acid excretion?

    • A. Increased aldosterone production; increased H+ secretion
    • B. Decreased aldosterone activity; impaired K+ and H+ secretion
    • C. Decreased bicarbonate reabsorption; increased K+ secretion
    • D. Increased sodium reabsorption; increased H+ secretion
    • Answer: B. Decreased aldosterone activity; impaired K+ and H+ secretion
    • Explanation: "In type IV RTA, decreased aldosterone activity leads to impaired secretion of both K+ and H+, resulting in hyperkalemia and acidosis"【39†source】.
  3. How does type II RTA affect bicarbonate reabsorption, and what is the typical urinary pH in this condition?

    • A. Decreased bicarbonate reabsorption; urinary pH > 5.5
    • B. Increased bicarbonate reabsorption; urinary pH < 5.5
    • C. Decreased bicarbonate reabsorption; urinary pH < 5.5
    • D. Increased bicarbonate reabsorption; urinary pH > 5.5
    • Answer: C. Decreased bicarbonate reabsorption; urinary pH < 5.5
    • Explanation: "In type II (proximal) RTA, there is decreased bicarbonate reabsorption in the proximal tubule, leading to a urinary pH that is typically less than 5.5"【39†source】.
  4. What laboratory finding distinguishes type I distal RTA from other forms of RTA?

    • A. Hyperkalemia
    • B. Hypokalemia and urine pH > 5.5
    • C. Hyperkalemia and urine pH < 5.5
    • D. Elevated serum bicarbonate
    • Answer: B. Hypokalemia and urine pH > 5.5
    • Explanation: "Type I distal RTA is characterized by hypokalemia and an inability to acidify the urine, resulting in a urine pH greater than 5.5"【39†source】.