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Y2 Renal > Physiology II > Flashcards

Physiology II Flashcards

1
Q

What is the two solute hypothesis

A

Concentration of urea in the kidney is dependent on the concentration gradient created by active transport of NaCl
The presence of these 2 solutes allows kidney to concentrate urea in the urine and excrete it

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2
Q

How does urea contribute to the cortico-medullary concentration gradient

A
  1. The ascending limb of loop of Henle actively transports out NaCl without water
  2. Water is drawn out of the descending limb of loop of Henle without solute moving
  3. The concentration gradient in medulla established by NaCl draws water out of the collecting duct which dips into the medulla
  4. This makes the tubular fluid in collecting duct concentrated with urea
  5. Hence urea moves out of the collecting duct to interstitial fluid -> reabsorbed back into the ascending limb -> contribute to the concentration of urine
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3
Q

The distal tubule and collecting duct are major sites for

A

regulation of ion and water balance

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4
Q

Distal tubule and collecting duct ability to regulate ion and water balance can be affected by

A

ADH
Aldosterone
PTH
Atrial natriuretic hormone (ANP)

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5
Q

What factor allows the production of hypertonic urine in presence of ADH

A

Cortico-medullary concentration gradient

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6
Q

How does the cortico-medullary concentration gradient allow the production of hypertonic urine in presence of ADH

A
  1. The function of ascending and descending limbs of loop of Henle creates a highly concentrated interstitial fluid in medulla
  2. The tubular fluid flowing into the collecting duct is less concentrated because NaCl was pumped out to contribute to the gradient
  3. Collecting duct had low permeability to water but in presence of ADH, it becomes more permeable
  4. Water can then flow from collecting duct into the interstitial fluid to be reabsorbed due to the osmotic gradient established by the countercurrent flow
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7
Q

Function of ADH

A

Increase water reabsorption to decrease plasma osmolarity

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8
Q

Function of aldosterone

A

Increase Na+ reabsorption
Increase K+ secretion (so less K+ in blood; this is why hyperaldosteronism causes high BP and hypokalaemia)

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9
Q

Function of ANP

A

Decrease Na+ reabsorption

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10
Q

Function of PTH

A

Increase Ca2+ reabsorption
Decrease phosphate reabsorption

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11
Q

Distal tubule is in the cortex / medulla

A

Cortex

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12
Q

Osmolarity of the fluid entering distal tubule

A

Hypoosomtic

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13
Q

Describe the permeability of distal tubule

A

Low to water and urea
But can be affected by ADH

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14
Q

Low permeability to urea in distal tubule means that

A

Tubular fluid is concentrated with urea

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15
Q

Early distal tubule function

A

NaCl reabsorption using Na K Cl transporter (triple transporter)

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16
Q

Late distal tubule function

A

Reabsorption of
Ca2+
Na+
K+
Secretion of H+ and aldosterone

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17
Q

How does aldosterone alter the late distal tubule function

A

Instead of reabsorbing K+, aldosterone will cause the secretion of K+ into tubular fluid -> excreted

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18
Q

The collecting tubule is located at

A

Going down from cortex to medulla

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19
Q

Describe the interstitial fluid around medulla

A

Progressively increasing concentration (osmolarity)

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20
Q

Late collecting duct function

A

Low ion, water, urea permeability
But can be influenced by ADH

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21
Q

Triggers of ADH release

A

Increase in plasma osmolarity
Decrease in blood pressure
Nicotine

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22
Q

What inhibits ADH release

A

Alcohol

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23
Q

How does drastic decrease in blood volume (trauma) cause ADH secretion

A

Decrease in blood volume -> decrease in blood pressure -> decreased atrial pressure activates left atrial stretch receptors -> stimulates ADH release

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24
Q

How does ADH decrease plasma osmolarity

A

Increase aquaporin channels on the collecting duct
Increase thirst -> increase H2O intake

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25
Q

Effect of ADH on urine

A

Small, concentrated (hypertonic) urine

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26
Q

Triggers of aldosterone release

A

Increase in K+ plasma concentration
RAAS

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27
Q

90% of K+ is reabsorbed in

A

proximal tubule
10% in distal tubule

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28
Q

Is there K+ urine

A

No, all are reabsorbed in either the proximal or distal tubule

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29
Q

What triggers the release of renin from granular cells in juxtaglomerular apparatus

A

Decrease in blood pressure
Decrease in NaCl in blood
Decrease in blood volume
Sympathetic nervous system due to decrease in BP

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30
Q

Which cells sense the amount of NaCl in distal tubule hence triggers renin release

A

Macula dena cells

31
Q

ANP is produced by ___ and stored in ____

A

Produced by the heart
Stored in atrial muscle cells

32
Q

Trigger of release of ANP

A

When atrial cells are stretched due to an increase in plasma volume

33
Q

Effect of ANP

A

Decrease reabsorption of Na+ -> increase in H2O excretion in urine -> lower BP

Afferent arteriolar vasodilation -> increase in GFR so more Na+ and H2O filtered out

Reduce cardiac output -> lower BP
Reduce vascular resistance -> lower BP

34
Q

Micturition is controlled by

A

Micturation reflex
Voluntary tightening of external sphincter

35
Q

What is the micturition reflex

A

Involuntary response initiated by stretch receptors in the bladder wall
Contraction of detrusor muscle and opening of the internal and external urethral sphincters

36
Q

What is the normal pH of arterial blood

A

7.45

37
Q

What is the normal pH of venous blood

A

7.35

38
Q

Why is it important to regulate pH

A

H+ can affect enzyme activity
Changes in H+ influence K+ levels
Changes in CNS and peripheral nervous system

39
Q

Weak acid dissociates partially / completely in solution

A

Partially

40
Q

Strong / weak acid sets up an equilibrium

A

Weak because it dissociates partially only

41
Q

Adding H+ to the buffer system will cause the equilibrium to

A

Shift to the left
= more HA less A-

42
Q

Adding a base to the buffer system will cause the equilibrium to

A

Shift to the right; because the base is reacting with H+ so less H+
Less H+ = HA will dissociate more to replenish the lost H+ so pH does not change
So Less HA more A-

43
Q

What is the most important physiological buffer system and what is its significance

A

CO2 and HCO3 buffer
To control the acid-base balance in body

44
Q

H2CO3 in the CO2 HCO3 buffer is formed from

A

CO2 + H2O by carbonic anhydrase

45
Q

What controls the concentration of HCO3-

A

Kidneys

46
Q

What controls the concentration of CO2

A

Lungs

47
Q

How do kidneys maintain the acid base balance

A

It controls the excretion of H+ and reabsorption of HCO3-

48
Q

How do kidneys excrete fixed amount of H+ to maintain acid base balance

A

Excretion of H+ as titratable acid (H2PO4)
Excretion of H+ as ammonia (NH4+)

49
Q

How does the kidney control the concentration of HCO3-

A

Reabsorption of filtered HCO3-
Formation of new HCO3- to add to the blood

50
Q

The mechanisms that control the concentration of HCO3- is dependant on

A

how much H+ is in the tubule - the excretion of H+ is accompanied by synthesis and reabsorption of HCO3- in order to replenish the HCO3- used for buffering

51
Q

Are all HCO3- reabsorbed

A

Yes, mainly in proximal tubule

52
Q

The reabsorption of HCO3- mainly occurs at

A

Proximal tubule

53
Q

Describe the formation of new HCO3-

A

Occurs when the HCO3- in tubular fluid is low
- Secreted H+ into urine in exchange for HCO3- combines with phosphate to form a titratable acid (H2PO4)
- net gain of HCO3-

54
Q

What is the titratable acid and what is its use

A

H2PO4; it is the by product for formation of new HCO3- and it can be measured to use as an indicator for body’s acid-base balance

55
Q

If 40mmol/day of titratable acid is excreted, what does it imply

A

40mmol/day new HCO3- is gained by the circulation

56
Q

If 40mmol/day of NH4- is excreted, what does it imply

A

40mmol/day new HCO3- is gained by the circulation

57
Q

Total H+ secreted into the tubule Is 4360 mmol/day but total H+ excreted is 60mmol/day. Why isn’t there acidosis

A

Because most of the H+ secretion is used for HCO3- (base) reabsorption

58
Q

What is used to assess glomerular function

A

GFR
Proteinuria

59
Q

What is used to assess GFR

A

Serum creatinine
or serum creatinine / urine creatinine

60
Q

Why is creatinine used to assess GFR

A

Because it is filtered by the glomerulus freely at a constant rate

61
Q

Concerns of using creatinine to assess GFR

A

It isn’t sensitive to changes in GFR until GFR is quite low
Different factors such as muscle mass and diet can confound the measurement

62
Q

What is eGFR

A

estimated glomerular filtration rate that is calculated taking into account a person’s age, sex, race, and serum creatinine level

63
Q

Limitation of eGFR

A

still not accurate at high GFR level

64
Q

How is proteinuria (if any) assessed

A

24 hour urinary collection
Urine dipstick
Protein creatinine ratio
Albumin creatinine ratio

65
Q

Proteinuria of what value indicates significant glomerular damage

A

> 150mg/day

66
Q

Normal dipstick reading, PC, 24 hour protein, and ACR values

A

Dipstick - negative
PCR - <15
24 hr protein - <0.150
ACR
- female - <3.5
- Male - <2.5

67
Q

Microalbuminuria lab results

A

Dipstick - negative
PCR - <15
24hr Urine - <0.15
ACR
- 2.5-30 in males
- 3.5-30 in females

68
Q

Microalbuminuria is an early sign of

A

Diabetic nephropathy

69
Q

What is used to assess tubular function

A

Urine osmolarity

70
Q

If tubules are not functioning, the urine osmolarity will be

A

Urine osmolarity = serum osmolarity

71
Q

What are the 2 systems that regulate the physiological pH

A

HCO3- - regulated by kidneys
CO2 - regulated by the lungs

72
Q

What happens in respiratory acidosis

A

There is a retention of CO2 by the body
This drives the equilibrium to the right, increasing H+ and HCO3-
The increase in H+ causes acidosis and the overall change in HCO3- is not enough to correct the acidosis due to small changes in H+ causing large changes in pH

73
Q

What are the compensations for respiratory acidosis

A

Blood CO2 stimulates H+ secretion into the filtrate
All filtered HCO3- is reabsorbed
H+ continues to be secreted and generate titratable acid and NH4+
Through these processes, acid is excreted and new HCO3- is added to blood
However, because changes in H+ causes a bigger change in pH, the increase in HCO3- cannot fully compensate

Y2 Renal (12 decks)

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