Renal Physiology – Chapter 6 Review

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A comprehensive set of flashcards covering nephron anatomy, renal blood flow, glomerular filtration and clearance, endocrine functions, sodium and water handling, diuretics, ADH, volume regulation, electrolyte balance, acid–base physiology, and micturition control, formatted in question-and-answer style for exam preparation.

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89 Terms

1
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What is the functional unit of the kidney?

The nephron.

2
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Approximately how many nephrons does each kidney contain?

About 500,000 – 800,000.

3
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Name the two major regions of the kidney.

Cortex (outer region) and medulla (inner region with renal pyramids).

4
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Which portion of the nephron is responsible for primary urine formation?

The glomerulus, enveloped by Bowman’s capsule.

5
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List the three segments of the Loop of Henle in order.

Thin descending limb, thin ascending limb, thick ascending limb.

6
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Which type of nephron has long loops of Henle and is crucial for urine concentration?

Juxtamedullary nephrons.

7
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What percentage of renal blood flow is normally received by the kidneys?

About 20 – 25 % of cardiac output.

8
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Which vessels supply and drain the glomerular capillary bed?

Afferent arteriole supplies; efferent arteriole drains.

9
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Define Glomerular Filtration Rate (GFR).

The volume of ultrafiltrate formed by all nephrons per minute (≈110-130 mL/min in healthy adults).

10
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What is the equation relating GFR to filtration pressures and permeability?

GFR = Kf × PUF, where Kf is filtration coefficient and PUF is net driving pressure.

11
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Which sympathetic neurotransmitter preferentially constricts the afferent arteriole?

Norepinephrine (NE).

12
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How does angiotensin II affect the efferent arteriole and GFR?

Constricts the efferent arteriole, reducing renal blood flow but helping maintain GFR.

13
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Name two common drug classes that can decrease GFR and their mechanisms.

NSAIDs (afferent vasoconstriction by ↓ prostaglandins) and ACE-inhibitors/ARBs (efferent vasodilation).

14
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What is renal clearance?

The volume of plasma cleared of a substance per minute.

15
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Which endogenous compound is commonly used to estimate GFR clinically?

Creatinine (creatinine clearance).

16
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If excretion rate (ER) < filtered load (FL), what has occurred in the tubule?

Net reabsorption.

17
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Define fractional excretion (FE).

The percentage of the filtered load of a solute that is excreted in the urine.

18
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Why does glucose appear in the urine of poorly controlled diabetics?

Plasma glucose exceeds the transport maximum (Tm) of tubular reabsorption.

19
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What is the daily filtered load of sodium relative to requirement?

It is far greater than needed; only ~5-7 % of filtered Na⁺ is normally excreted.

20
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Which nephron segment reabsorbs the largest fraction of filtered Na⁺?

The proximal tubule (~65-75 %).

21
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What is the primary mechanism of loop diuretics such as furosemide?

Inhibition of the Na⁺/K⁺/2Cl⁻ cotransporter in the thick ascending limb.

22
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Where do thiazide diuretics act?

On the Na⁺/Cl⁻ cotransporter in the early distal tubule.

23
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Which diuretic class is potassium-sparing by blocking aldosterone receptors?

Spironolactone and related K-sparing diuretics.

24
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List the three processes required for the kidney to vary urine concentration.

1) Adequate GFR to deliver filtrate; 2) Na⁺ reabsorption without water in ascending limb; 3) Variable water permeability in collecting duct controlled by ADH.

25
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Where is antidiuretic hormone (ADH) synthesized and released?

Synthesized in the hypothalamus; released from posterior pituitary.

26
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Which receptors mediate ADH’s vasoconstrictor effect?

V1 receptors.

27
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What are two major stimuli for ADH release?

Increased plasma osmolarity and decreased blood volume (>10 % loss).

28
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What is Syndrome of Inappropriate ADH (SIADH) commonly associated with?

Small-cell lung carcinoma, pneumonia, or head injury causing excess ADH and hyponatremia.

29
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Differentiate disorders of ECF volume vs. sodium concentration.

Volume disorders reflect problems with Na⁺ balance; sodium concentration disorders (hyper/hyponatremia) reflect water balance issues.

30
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Which kidney cells secrete renin and what triggers its release?

Juxtaglomerular cells; triggered by decreased afferent arteriolar stretch (low effective circulating volume).

31
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Name two actions of angiotensin II.

Vasoconstriction and stimulation of aldosterone secretion.

32
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Where is atrial natriuretic peptide (ANP) released and what does it do?

Released from cardiac atria when stretched; increases Na⁺ and water excretion by kidneys.

33
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What is Brain Natriuretic Peptide (BNP) used clinically for?

As nesiritide for acute congestive heart failure to promote natriuresis and vasodilation.

34
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Which nephron segments reabsorb most magnesium?

Thick ascending limb and distal tubule.

35
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Why can loop diuretics cause hypomagnesemia?

They inhibit Na⁺/K⁺/2Cl⁻ transport in thick ascending limb, disrupting Mg²⁺ reabsorption.

36
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How does antidiuresis affect blood urea nitrogen (BUN)?

Water reabsorption concentrates urea, increasing BUN—often seen in dehydration.

37
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Which hormones increase distal tubular Ca²⁺ reabsorption?

Parathyroid hormone (PTH), active vitamin D, and thiazide diuretics.

38
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Why are thiazides useful in patients with recurrent calcium oxalate stones?

They reduce urinary Ca²⁺ excretion by increasing distal Ca²⁺ reabsorption.

39
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Where is phosphate reabsorption restricted in the nephron?

To the proximal tubule via Na⁺/phosphate cotransporters.

40
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Which hormone is the most important regulator of renal phosphate handling?

Parathyroid hormone (PTH).

41
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State the normal extracellular potassium range.

3.5 – 5.5 mEq/L.

42
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How does aldosterone affect potassium balance?

Increases K⁺ secretion in principal cells while promoting Na⁺ reabsorption.

43
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List two rapid shifts that move K⁺ into cells (internal K homeostasis).

Insulin and β2-adrenergic (epinephrine) stimulation.

44
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What acid-base disturbance causes K⁺ to move out of cells?

Metabolic acidosis (H⁺ enters cells, K⁺ exits → hyperkalemia).

45
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Which diuretic classes increase distal Na⁺ delivery and thus K⁺ loss?

Loop and thiazide diuretics.

46
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Describe the reciprocal relationship of H⁺ and K⁺ secretion in CCD.

Increased H⁺ secretion (acidosis compensation) reduces K⁺ excretion and vice versa.

47
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What is the normal arterial pH range?

7.35 – 7.45.

48
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Give the normal arterial PCO₂ and HCO₃⁻ values.

PCO₂ ≈ 40 mmHg; HCO₃⁻ ≈ 24 mmol/L.

49
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Which buffer system is most important in extracellular fluid?

The bicarbonate buffer system (CO₂/HCO₃⁻).

50
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What is the primary respiratory response to metabolic acidosis?

Hyperventilation to decrease PCO₂ (compensatory respiratory alkalosis).

51
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Define titratable acid in urine.

Acid excreted as H₂PO₄⁻; represents ~25 % of renal H⁺ excretion.

52
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What fraction of renal H⁺ excretion is via ammonium (NH₄⁺)?

About 75 % during ammonia production in proximal tubule.

53
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Name the diuretic that causes bicarbonaturia and why.

Acetazolamide; it inhibits carbonic anhydrase, impairing HCO₃⁻ reabsorption.

54
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Which acid-base disorder is characterized by PaCO₂ > 45 mmHg?

Respiratory acidosis.

55
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Which acid-base disorder involves HCO₃⁻ < 22 mEq/L?

Metabolic acidosis.

56
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What mnemonic helps relate pH changes to respiratory vs metabolic disorders?

ROME – Respiratory Opposite, Metabolic Equal (pH vs PCO₂/HCO₃⁻).

57
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Give two common causes of metabolic acidosis with an increased anion gap.

Diabetic ketoacidosis and lactic acidosis.

58
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Which disorder is termed ‘contraction alkalosis’?

Metabolic alkalosis due to volume depletion (e.g., vomiting) with HCO₃⁻ retention.

59
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How does aspirin overdose create a mixed acid-base disorder?

It causes metabolic lactic acidosis (uncouples oxidative phosphorylation) and respiratory alkalosis (stimulates respiratory center).

60
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What are the primary sensors for effective circulating volume in the kidney?

Afferent arteriolar baroreceptors (juxtaglomerular apparatus).

61
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What peptide is secreted when the atria are stretched by volume expansion?

Atrial natriuretic peptide (ANP).

62
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Why is the renal medulla susceptible to ischemic injury?

It receives low blood flow to preserve hypertonicity; hypotension or vasoconstriction can cause ischemia.

63
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What maintains medullary hypertonicity for urine concentration?

Counter-current multiplication and low vasa recta blood flow.

64
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Define the guarding reflex in micturition.

A spinal reflex that prevents involuntary bladder emptying by keeping the external urethral sphincter contracted.

65
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Which nerve innervates the external urethral sphincter?

The pudendal nerve (S2-S4).

66
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Parasympathetic fibers that contract the detrusor muscle travel via which nerves?

Pelvic splanchnic nerves (S2-S4).

67
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Which receptor subtype mediates detrusor contraction?

Muscarinic M3 receptors activated by acetylcholine.

68
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How do sympathetic nerves affect bladder function?

They relax the detrusor (β3) and contract the internal sphincter (α1) to inhibit voiding.

69
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What is the usual arterial perfusion pressure needed to maintain renal blood flow?

Approximately 90-100 mmHg.

70
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Why does low blood flow in the vasa recta enhance urine concentration?

Minimizes washout of medullary osmotic gradient while still allowing some oxygen delivery.

71
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State the stages of chronic kidney disease based on GFR (moderate and severe).

Moderate: GFR 30-59 mL/min; Severe: GFR 15-29 mL/min.

72
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Which endocrine hormone from the kidney stimulates red blood cell formation?

Erythropoietin (EPO).

73
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What happens to EPO levels in chronic renal failure?

They decrease, leading to anemia.

74
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How is inactive vitamin D (25-OH) converted to its active form?

In the kidney to 1,25-OH vitamin D under regulation by PTH.

75
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Which acid-base disorder can result from hyperaldosteronism and why?

Metabolic alkalosis due to excessive H⁺ secretion in distal nephron.

76
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How does ethanol affect ADH secretion?

It inhibits ADH release, leading to diuresis.

77
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Differentiate prerenal, renal, and postrenal acute renal failure causes.

Prerenal: hypoperfusion (e.g., hypovolemia); Renal: intrinsic parenchymal damage (e.g., glomerulonephritis); Postrenal: urinary tract obstruction (e.g., BPH).

78
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What is the main driving pressure for glomerular ultrafiltration?

Glomerular capillary hydrostatic pressure (P_GC).

79
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Name the three layers of the glomerular filtration barrier.

Fenestrated endothelium, basement membrane, and podocyte slit diaphragm (nephrin).

80
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Why is albumin normally not filtered despite its size (~70 kDa)?

Negative charges in the filtration barrier repel negatively charged albumin, preventing its passage.

81
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What renal complication is seen in minimal-change disease?

Loss of nephrin leads to heavy proteinuria (nephrotic syndrome).

82
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Explain glomerulotubular balance.

Proximal tubule adjusts Na⁺ reabsorption to a constant fraction (~67 %) of the filtered load despite changes in GFR.

83
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Which natriuretic peptide is longer-acting and more potent than ANP?

Brain Natriuretic Peptide (BNP).

84
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What is the primary site and mechanism for bicarbonate reabsorption?

Early proximal tubule via Na⁺/H⁺ exchange and carbonic anhydrase activity.

85
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Which intercalated cell type reabsorbs potassium during K deficiency?

α-Intercalated cells via H⁺/K⁺-ATPase.

86
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What is the effect of nicotine on ADH release?

Nicotine increases ADH secretion.

87
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Why does metabolic alkalosis often present with hypokalemia?

Increased distal Na⁺ delivery and aldosterone drive K⁺ secretion; also reciprocal H⁺/K⁺ exchange favors K⁺ loss.

88
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State the life-sustaining arterial pH limits.

Approximately 6.8 to 7.8.

89
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What is the primary therapeutic approach to acute life-threatening hyperkalemia?

Calcium gluconate (membrane stabilization) plus insulin/glucose, β2-agonist, and/or Kayexalate to shift or remove K⁺.