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RP > L5: ADH > Flashcards

L5: ADH Flashcards

1
Q
  1. What is the compensation mechanism for positive water balance (gain of water)?
    a. Activation of thirst
    b. Increase in ADH secretion
    c. Increase excretion of hyposmotic urine
A

C

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2
Q
  1. How does the body compensate for negative water balance (loss of water)?
    a. Activation of thirst and excretion of concentrated urine
    b. Decreased ADH secretion
    c. Increased sweating
A

A

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3
Q
  1. In what situation might you experience uncontrollable water loss through breathing?
    a. High humidity
    b. Low humidity
    c. Cool environments
A

A

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4
Q
  1. How does heat contribute to increased water loss?
    a. Activation of thirst
    b. Sweating
    c. Decreased urine concentration
A

B

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5
Q
  1. What is the primary effect of low ADH levels on urine volume?
    a. Small volume of urine (antidiuresis)
    b. Large volume of urine (water diuresis)
    c. Concentrated urine
A

B

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6
Q
  1. How does ADH release change with high osmolarity sensed by osmoreceptors?
    a. Increases ADH secretion
    b. Decreases ADH secretion
    c. Has no effect on ADH
A

A

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7
Q
  1. What stimulates thirst based on osmolarity?
    a. Angiotensin II
    b. TRVP channels
    c. Hypothalamic osmoreceptors
A

C

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8
Q
  1. How does the osmoreceptor sense changes in osmolarity?
    a. Specific ion transporters
    b. TRVP channels
    c. Tight junctions
A

B

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9
Q
  1. What is the consequence of increased osmolarity on ADH release?
    a. Water conservation and decreased ADH
    b. Water reabsorption and increased ADH
    c. Increased urine volume
A

B

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10
Q
  1. How do low and high-pressure vascular receptors influence ADH release?
    a. Stimulate ADH release via CN IX & X
    b. Inhibit ADH release via CN IX & X
    c. Have no effect on ADH release
A

A

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11
Q
  1. What does ADH binding to V1 receptors induce?
    a. Arterial vasoconstriction
    b. Increased urine volume
    c. Decreased osmolarity
A

A

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12
Q
  1. Where are aquaporin 2 and 3 located in response to ADH?
    a. Only on the apical side
    b. Only on the basolateral side
    c. On both apical and basolateral sides
A

C

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13
Q
  1. In which segment of the nephron does ADH have no effect?
    a. Proximal convoluted tubule (PCT)
    b. Distal segment of the collecting duct
    c. Loop of Henle
A

A

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14
Q
  1. What is the primary role of aquaporin 2 & 3 in the presence of ADH?
    a. Decrease water reabsorption
    b. Increase water reabsorption
    c. Inhibit urea recycling
A

B

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15
Q
  1. What physiological consequences result from ADH action in the medulla?
    a. Decreased water reabsorption
    b. Increased water reabsorption
    c. Impermeability to water
A

B

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16
Q
  1. What is the primary role of ADH in the thick ascending loop of Henle?
    a. Impermeable to water
    b. Decreases urea concentration
    c. Increases water reabsorption
A

A

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17
Q
  1. How does diabetes insipidus affect ADH and water reabsorption?
    a. Inadequate release of ADH
    b. Increased ADH release
    c. Enhances signaling pathway
A

A

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18
Q
  1. What is the consequence of SIADH (Syndrome of Inappropriate Antidiuretic Hormone)?
    a. Increased water reabsorption
    b. Swelling of the brain
    c. Hypernatremia
A

B

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19
Q
  1. What condition results in loss of free water clearance?
    a. Losing fluid isosmolar to plasma
    b. Hyperosmolar urine excretion
    c. Increased osmolarity
A

A

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20
Q
  1. What inhibits thirst in response to hyperosmolar hypervolemia?
    a. Angiotensin II
    b. Relaxin
    c. Atrial Natriuretic Peptide (ANP)
A

C

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21
Q
  1. What is the primary role of the laminaterminalis in osmoregulation?
    a. Regulating blood pressure
    b. Sensing osmolarity to stimulate thirst
    c. Controlling sodium reabsorption
A

B

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22
Q
  1. How do TRVP channels sense changes in osmolarity?
    a. Measure the concentration of a singular ion
    b. Detect specific ion transporters
    c. Respond to total osmolarity
A

A

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23
Q
  1. What causes a response in osmoreceptors when TRVP channels open?
    a. Cell expansion
    b. Cell shrinkage
    c. Inhibition of osmoreceptor activity
A

B

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24
Q
  1. What conditions elicit a response from osmoreceptors?
    a. Small changes in osmolarity
    b. Large changes in osmolarity
    c. Lack of changes in osmolarity
A

A

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25
Q
  1. Why do osmoreceptors lack a blood-brain barrier (BBB)?
    a. To change brain osmolarity
    b. To measure total osmolarity
    c. To maintain brain environment
A

C

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26
Q
  1. What inhibits thirst in response to hypervolemia?
    a. Angiotensin II
    b. Relaxin
    c. Atrial Natriuretic Peptide (ANP)
A

C

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27
Q
  1. What is the primary effect of negative feedback on the regulation of thirst?
    a. Increases thirst
    b. Inhibits thirst
    c. Stimulates ADH release
A

B

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28
Q
  1. What is the primary consequence of increased plasma osmolarity?
    a. Decreased water reabsorption
    b. Increased water excretion
    c. Activation of thirst and ADH secretion
A

C

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29
Q
  1. How does diabetes insipidus affect signaling in the nephron?
    a. Enhances signaling
    b. Causes a defect in signaling
    c. Increases water reabsorption
A

B

30
Q
  1. What is the role of aquaporin 1 in the proximal convoluted tubule (PCT)?
    a. Increases water reabsorption
    b. Has no effect on water reabsorption
    c. Decreases water reabsorption
A

A

31
Q
  1. What does ADH binding to V2 receptors in the inner medullary collecting duct induce?
    a. Decreased urea concentration
    b. Increased urea permeability
    c. Enhanced water reabsorption
A

B

32
Q
  1. How does ADH influence blood volume and MAP?
    a. Directly affects blood volume
    b. Indirectly affects blood volume through osmolarity
    c. Has no effect on blood volume
A

B

33
Q
  1. What does an increase in blood volume in shock conditions preserve?
    a. Fluid dilution
    b. Volume for perfusion
    c. Increased urea concentration
A

B

34
Q
  1. What is the primary role of V1 receptors when activated by ADH?
    a. Arterial vasoconstriction
    b. Venous vasodilation
    c. Increased urine volume
A

A

35
Q
  1. In the absence of ADH, what is the collecting duct’s permeability to water?
    a. Permeable to water with aquaporin 2 & 3
    b. Impermeable to water
    c. Highly permeable to water
A

B

36
Q
  1. What causes water reabsorption in the collecting duct with ADH presence?
    a. Activation of aquaporin 1
    b. Presence of aquaporin 2 & 3
    c. Inhibition of urea recycling
A

B

37
Q
  1. How does increased blood flow in Vasa Recta affect hyperosmolarity?
    a. Decreases hyperosmolarity
    b. Enhances hyperosmolarity
    c. Has no effect on hyperosmolarity
A

A

38
Q
  1. What is the primary effect of decreased V1 receptor stimulation in Vasa Recta?
    a. Increased blood flow
    b. Decreased washout of solutes
    c. Reduced vasoconstriction
A

C

39
Q
  1. What is the consequence of increased urea concentration in the interstitium due to ADH?
    a. Inhibits urea recycling
    b. Enhances urea transporter 1 expression
    c. Promotes urea recycling
A

C

40
Q
  1. How does ADH affect blood flow through Vasa Recta in hypertensive patients?
    a. Decreases blood flow
    b. Increases blood flow
    c. Maintains constant blood flow
A

B

41
Q
  1. What is the primary outcome of positive free water clearance?
    a. Hyposmolar urine excretion
    b. Isosmotic urine excretion
    c. Concentrated urine excretion
A

A

42
Q
  1. How does negative free water clearance affect hyperosmolar patients?
    a. Induces cell swelling
    b. Preserves water with concentrated urine
    c. Increases osmolar clearance
A

B

43
Q
  1. What is the significance of increased urea transporter 1 expression in the presence of ADH?
    a. Inhibits urea recycling
    b. Decreases urea permeability
    c. Promotes concentrated urine
A

C

44
Q
  1. What causes decreased blood flow through Vasa Recta in response to ADH?
    a. Increased washout of solutes
    b. Enhanced urea recycling
    c. Increased hyperosmolarity
A

C

45
Q
  1. How does ADH influence V1 receptors in Vasa Recta?
    a. Increases V1 receptor stimulation
    b. Decreases V1 receptor stimulation
    c. Has no effect on V1 receptors
A

A

46
Q
  1. What is the primary impact of high blood flow in Vasa Recta in hypertensive patients?
    a. Increased urea recycling
    b. Reduced hyperosmolarity
    c. Decreased water reabsorption
A

C

47
Q
  1. What is the primary function of aquaporin 2 & 3 in the collecting duct during diuresis?
    a. Decreases water reabsorption
    b. Increases water reabsorption
    c. Promotes urea recycling
A

A

48
Q
  1. What causes urea to move into the interstitium and the thin ascending limb of the loop of Henle?
    a. Decreased urea transporter expression
    b. Concentration gradient created by ADH
    c. Increased urea excretion
A

B

49
Q
  1. How does ADH affect the solute concentration in the interstitium of the medulla?
    a. Decreases solute concentration
    b. Increases solute concentration
    c. Has no effect on solute concentration
A

B

50
Q
  1. What is the primary outcome of decreased water reabsorption in the lower segments of the loop of Henle?
    a. Increased urea concentration
    b. Reduced solute movement into the interstitium
    c. Enhanced vasoconstriction in the vasa recta
A

B

51
Q
  1. How does ADH affect blood flow through Vasa Recta in hypertensive patients?
    a. Decreases blood flow
    b. Increases blood flow
    c. Maintains constant blood flow
A

B

52
Q
  1. What is the consequence of increased urea concentration in the interstitium due to ADH?
    a. Inhibits urea recycling
    b. Enhances urea transporter 1 expression
    c. Promotes urea recycling
A

C

53
Q
  1. What is the primary impact of countercurrent multiplication in the loop of Henle?
    a. Decreases medullary osmolarity
    b. Promotes hyperosmolarity in the medulla
    c. Inhibits urea recycling
A

B

54
Q
  1. How does ADH influence blood flow through Vasa Recta in hypertensive patients?
    a. Increases blood flow
    b. Decreases blood flow
    c. Maintains constant blood flow
A

B

55
Q
  1. What is the primary consequence of decreased blood flow through Vasa Recta in response to ADH?
    a. Increased washout of solutes
    b. Enhanced urea recycling
    c. Increased hyperosmolarity
A

C

56
Q
  1. What is the primary outcome of hyperosmolarity in the medullary interstitium?
    a. Decreased water reabsorption
    b. Increased aquaporin expression
    c. Facilitates increased water reabsorption
A

C

57
Q
  1. How does ADH affect the osmotic gradient in the loop of Henle?
    a. Decreases osmolarity
    b. Increases solute diffusion into the interstitium
    c. Increases osmolarity by promoting urea recycling
A

B

58
Q
  1. What is the significance of countercurrent multiplication in the loop of Henle?
    a. Decreases medullary osmolarity
    b. Promotes hyperosmolarity in the medulla
    c. Inhibits urea recycling
A

B

59
Q
  1. How does ADH influence blood flow through Vasa Recta in hypertensive patients?
    a. Increases blood flow
    b. Decreases blood flow
    c. Maintains constant blood flow
A

B

60
Q
  1. What is the primary consequence of decreased blood flow through Vasa Recta in response to ADH?
    a. Increased washout of solutes
    b. Enhanced urea recycling
    c. Increased hyperosmolarity
A

C

61
Q
  1. In diabetes insipidus, what is the primary cause of inadequate ADH release?
    a. Damage to osmoreceptors
    b. Enhanced signaling pathway
    c. Increased V2 receptor expression
A

A

62
Q
  1. How does lithium contribute to drug-induced diabetes insipidus?
    a. Inhibits action of ADH on renal tubules
    b. Enhances signaling in the nephron
    c. Increases V2 receptor sensitivity
A

A

63
Q
  1. What is the consequence of nephrogenic polyuria in the absence of ADH?
    a. Increased urea recycling
    b. Decreased urea concentration in the interstitium
    c. No effect on the kidney
A

C

64
Q
  1. In SIADH, what is the result of high plasma ADH levels?
    a. Dehydration
    b. Increased water retention and brain swelling
    c. Hypernatremia
A

B

65
Q
  1. What is the primary cause of Central Diabetes Insipidus?
    a. Defect in V2 receptor signaling
    b. Damage to osmoreceptors, neurons, or axons
    c. Inhibition of urea recycling
A

B

66
Q
  1. What is the consequence of a defect in intracellular signaling pathways in Nephrogenic Diabetes Insipidus?
    a. Decreased water reabsorption
    b. Increased V1 receptor stimulation
    c. Impaired response to ADH
A

C

67
Q
  1. How does SIADH affect urine concentration?
    a. Increases urine concentration
    b. Decreases urine concentration
    c. Has no effect on urine concentration
A

B

68
Q
  1. In diabetes insipidus, what is the result of defective water channels (AQP2 & AQP3)?
    a. Increased water reabsorption
    b. Impaired response to ADH
    c. Enhanced V1 receptor sensitivity
A

B

69
Q
  1. What is the role of SIADH in brain swelling?
    a. Decreases water retention
    b. Increases water excretion
    c. Causes water retention and brain swelling
A

C

70
Q
  1. In negative free water clearance, what does a hyperosmolar patient excrete more of?
    a. Concentrated urine
    b. Isosmotic urine
    c. Diluted urine
A

A

RP (4 decks)

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