L25 - Renal Function 4: Urine Concentration & Dilution Flashcards

1
Q

When is the renin-angiotensin-aldosterone system recruited?

A

when blood pressure drops

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2
Q

What is the role of angiotensin II in the nephron?

A

↑ sodium reabsorption in the proximal tubule and constricts the efferent arteriole as a means of protecting GFR during ↓ blood pressure

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3
Q

What is the role of aldosterone in the nephron?

A

↑ sodium reabsorption in the collecting duct

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4
Q

Where does the bulk of reabsorption occur in the nephron?

A

in the proximal end e.g. proximal convoluted tubule and loop of Henle

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5
Q

Where does fine-tuning occur in the nephron?

A

in the distal end e.g. distal tubule and collecting duct

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6
Q

How is fine-tuning possible in the distal nephron?

A

impermeable to Na+ and water unless this permeability is allowed
controlled independently

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7
Q

What stimulates renin release?

A

renin release is stimulated by volume depletion; fall in pressure at preglomerular arteriole, reduction in NaCl delivery to macula densa and sympathetic nerve activation

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8
Q

Which type of cells is renin released from?

A

granular cells

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9
Q

What are the effects of aldosterone in the collecting duct?

A

↑ activity of Na / K pump
↑ expression of ENaCs on luminal membrane
↑ potassium secretion
↑ activity of hydrogen ATPase on luminal membrane

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10
Q

What are the effects of the sympathetic nervous system (noradrenaline) on the nephron?

A

↑ reabsorption in the proximal convoluted tubule and constriction of the afferent arteriole in an attempt to reroute blood elsewhere

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11
Q

What are the effects of ANP on the nephron?

A

↓ sodium reabsorption in the collecting duct so that more sodium is excreted in the urine and dilates the afferent arteriole so that more sodium can be excreted by GFR

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12
Q

What is the balance of water in the body?

A
input:
diet (food and drink) = 2200mL
metabolism = 300mL
intravenous (5% dextrose) = 0mL
output:
urine = 1500mL
lungs = 500mL
skin = 400mL
feces = 100mL
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13
Q

A negative water balance will be most obvious as: (reduced plasma volume / reduced cardiac venous return / reduced ECF osmolarity / none of the above)

A

none of the above, not ↓ plasma volume or ↓ cardiac venous return because these also have to do with issues in sodium balance

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14
Q

How does the brain detect changes in osmolarity?

A

osmoreceptor cells in the anterior hypothalamus respond to changes in cell size

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15
Q

How do osmoreceptor cells respond to a negative water balance?

A

release antidiuretic hormone (vasopressin) to prevent urination

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16
Q

What things are needed to produce concentrated urine? (aldosterone / vasopressin / angiotensin II / all of the above)

A

vasopressin manages water balance, aldosterone and angiotensin II manage sodium balance

17
Q

What is concentration of vasopressin proportional to?

A

osmolarity

when osmolarity is higher, more vasopressin is released resulting in more concentrated urine

18
Q

How does the body respond to critically low ECF volume? (10% plasma volume or 500 mL of ECF volume loss)

A

decreased ECF volume results in increased vasopressin concentration so that water is retained as much as possible

19
Q

ANGII is involved in vasopressin release. Will ANGII stimulate vasopressin release most of the time?

A

no, only when ECF volume is particularly low

20
Q

Which action occurs at the proximal tubule?

A

bulk absorption

21
Q

Which action occurs at the ascending limb of the loop of Henle?

A

dilution of filtrate

22
Q

Which action occurs at the collecting ducts?

A

fine-tuning according to needs

23
Q

What is osmolarity?

A

solute concentration by volume

24
Q

What is osmolality?

A

solute concentration by weight

25
Q

What is normal urine osmolality?

A

ranges from 3 to 1200 mOsm/kgH2O

must excrete 600 mOsm of solute per day and at least 500 ml of water per day

26
Q

Tubular fluid leaving the loop of Henle is normally: (dilute / isosmotic / concentrated)

A

dilute

27
Q

How does osmolarity differ throughout the nephron?

A

isosmotic fluid leaving the PCT becomes more concentrated in the ↓ limb -> removal of solute in the thick ↑ limb creates hyposmotic fluid -> hormones control distal nephron permeability to water and solutes -> urine osmolarity depends on reabsorption in the collecting duct

28
Q

Why is it called the thick ascending limb?

A

because it is impermeable to water

29
Q

What is special about the distal nephron?

A

impermeable to everything unless permeability is allowed

30
Q

The medullary concentration gradient is mostly the result of: (sodium / urea / potassium / creatinine)

A

sodium and urea

31
Q

What are the two most metabolically active parts of the nephron?

A

ascending loop of Henle and proximal convoluted tubule

32
Q

What things are needed to produce concentrated urine?

A

Na/K/2Cl co-transporter, aquaporin 2 and cAMP

33
Q

What does activation of vasopressin receptor result in?

A

receptor activates cAMP second messenger system and cell inserts aquaporin-2 water pores into apical membrane resulting in absorption of water by osmosis into the blood

34
Q

What happens in the collecting duct when vasopressin is present?

A

urine concentration increases from 100 mOsM to 1200 mOsM

35
Q

What happens in the collecting duct when vasopressin is not present?

A

urine concentration remains at 100 mOsM which is dilute, however it can get more dilute depending on how much solute is reabsorbed

36
Q

Why is the Na-K-2Cl co-transporter essential?

A

if solute is not being reabsorbed from the ascending limb and the collecting duct then water is not going to move out as freely, therefore more water is lost