Topic 8 Part C Controlling Reabsorption Flashcards

1
Q

Glomerulartubular Balance allows an increase in what?

A

Allows an increase in reabsorption rate when there is an increase in tubular load (increased tubular inflow)

If GFR went from 125 mls/minute to 150 mls/minute rate of reabsorption in proximal tubule would go from 81 mls/minute [65% of GFR] to 97.5 mls/minute [65% of GFR] SAME PERCENT !!!!

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2
Q

Glomerulartubular Balance works to maintain Na and Volume homeostasis how?

A

Prevents large changes in fluid flow to distal tubules even though there have been significant changes in MAP

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3
Q

Peritubular Capillary & Interstitial Forces there is a relationship between what three things?

A

Relationship of hydrostatic and oncotic pressures AND filtration coefficient

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4
Q

Normal–net force for reabsorption

Peritubular Capillary & Interstitial

A

Normal–net force for reabsorption of 10 mmHg

IN (πc 32 + Pif 6 = 38) –OUT (Pc 13 + if π15 = 28) = 38-28

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5
Q

Peritubular Capillary & Interstitial Normal Reabsorption Rate? (ml/min)

A

Normal reabsorption rate of 124 mls/minute

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6
Q

Large filtration coefficient equation?

A

Reabsorption rate / net force
Affected by transfer surface area & hydraulic conductivity (permeability)

ex: 24 mls/min / 10 mmHg = 12.4 mls/min/mmHg

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7
Q

Factors Affecting Peritubular Capillary Reabsorption

A
Peritubular hydrostatic pressure (PHP)
Peritubular oncotic pressure (POP)
Filtration Coefficient (FC)
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8
Q

Increased PHP - (Peritubular hydrostatic pressure) does what to reabsorption?

A

DECREASES Reabsorption

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9
Q

Increased Arterial Pressure does what to PHP and Reabsorption?

A

INCREASE PHP and DECREASES Reabsorption

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10
Q

Increases Resistance of afferent & efferent arteriole does what to PHP and Reabsorption?

A

Decreases PHP and Increases Reabsorption

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11
Q

Increased Peritubular oncotic pressure (POP) does what to reabsorption?

A

INCREASES reabsorption

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12
Q

Increase Plasma protein concentration, does what to plasma oncotic pressure, POP, and reabsorption?

A

INCREASES plasma oncotic pressure, INCREASES POP, and INCREASES reabsorption

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13
Q

Filtration fraction equation

A

(GFR/RPF)

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14
Q

Increases Filtration Fraction

A

INCREASES protein concentration (more fluid is actually filtered)
INCREASES POP
INCREASES reabsorption

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15
Q

Renal interstitial hydrostatic and colloid osmotic pressures are affected by changes in what?

A

reabsorptive forces of peritubular capillaries

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16
Q

DECREASED capillary reabsorption does what to interstitial solute and water?

A

PRODUCES INCREASE in interstitial solute AND interstitial water

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17
Q

DECREASED capillary reabsorption does what to interstitial hydrostatic and oncotic pressure?

A

PRODUCES INCREASE in interstitial hydrostatic pressure AND in interstitial oncotic pressure

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18
Q

DECREASED capillary reabsorption does what to the net movement of solute and water from the renal tubules to renal interstitial space?

A

PRODUCES DECREASE in net movement (i.e. reabsorption) of solute & water from renal tubules to renal interstitial spaces

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19
Q

Decreased Peritubular reabsorption does what to solute & water accumulation in interstitial space

A

INCREASES solute & water accumulation in interstitial space

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20
Q

Decreased Peritubular reabsorption does what to backflow of solute and water from interstitial space into tubular lumen?

A

INCREASES backflow of solute and water from interstitial space into tubular lumen

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21
Q

Forces that increase peritubular capillary reabsorption also increase movement of solute and water from where?

A

solute and water (reabsorption) from the tubular lumen to the renal interstitial spaces [Reverse also true]

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22
Q

Increased Capillary surface area does what to FC & reabsorption?

A

Increases FC & reabsorption

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23
Q

Increased Capillary permeability area does what to FC and reabsorption?

A

Increases FC and reabsorption

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24
Q

Filtration Coefficient will be affected by what?

A

Coefficient remains constant under most physiologic conditions. Will be affected by renal disease

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25
Q

When arterial pressure is increased what happens to angiotensin II release? and does what?

A

Angiotensin II release is decreased
Less stimulation of sodium reabsorption by angiotensin II
Less stimulation of aldosterone production which means less stimulation of sodium reabsorption

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26
Q

Angiotensin II works where? (4)

A

Proximal tubule; Thick ascending loop of Henle / distal tubule; Collecting duct

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27
Q

Antidiuretic Hormone works where? (3)

A

Distal tubule; Collecting tubule & duct

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28
Q

Atrial natriuretic peptide works where? (3)

A

Distal tubule; Collecting tubule & duct

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29
Q

Parathyroid Hormone works where? (3)

A

Proximal tubule; Thick ascending loop of Henle; Distal tubule

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30
Q

Aldosterone works where? (2)

A

Collecting tubule & duct

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31
Q

Aldosterone increases what 3 things?

A

⬆️ NaCl reabsorption, ⬆️ H2O reabsorption

⬆️ K+ secretion

32
Q

Angiotensin II increases what 3 things?

A

⬆️ NaCl reabsorption, ⬆️ H2O reabsorption

⬆️ K+ secretion

33
Q

Antidiuretic Hormone increases what?

A

⬆️ H2O reabsorption

34
Q

Atrial natriuretic peptide

A

⬇️ NaCl reabsorption

35
Q

Parathyroid Hormone

A

⬇️ PO4—reabsorption

⬆️ Ca++ reabsorption

36
Q

Aldosterone is secreted by what?

A

Secreted by zona glomerulosa cell in adrenal cortex

37
Q

Aldosterone principal site of action is where?

A

Principal cells of cortical collecting tubule

38
Q

Aldosterone stimulates increased what?

A

Stimulates increased Na-K ATPase activity (basolateral locations)
Increases permeability of luminal side membrane to sodium

39
Q

Aldosterone increased release is stimulated by what 2 things?

A

Increased extracellular potassium concentration

Increased angiotensin II levels (i.e. sodium / volume depletion or low arterial pressure)

40
Q

Aldosterone Absence caused/s what?

A

Absence (adrenal malfunction or destruction) (Addison’s disease)
(decreases BP)

41
Q

Aldosterone Excess caused/s what?

A

Excess (adrenal tumors) (Conn’s syndrome)

increased BP

42
Q

Aldosterone is a very important regulator of what 2 things?

A

Na reabsorption

K secretion

43
Q

Most powerful sodium-retaining hormone

A

Angiotensin II

44
Q

Angiotensin II increased production is caused by what?

A

Low blood pressure and/or low ECF volume

45
Q

Angiotensin II actions? (3)

A

Stimulates aldosterone secretion (sodium reabsorption)
Constricts efferent arterioles (sodium and water reabsorption)
Direct stimulation of sodium reabsorption in proximal tubules, LOH, distal tubules, and collecting tubules

46
Q

Angiotensin II constriction of efferent arterioles does what?

A

Helps ensure that normal exertion rates of metabolic wastes are maintained by helping to maintain normal rates of GFR
Able to retain sodium & water without retaining metabolic waste

47
Q

Angiotensin II’s Direct stimulation of sodium reabsorption in proximal tubules, LOH, distal tubules, and collecting tubules is caused by what 3 mechanisms?

A

Stimulate increased Na-K ATPase activity of tubular epithelial cells (basolateral membrane)
Stimulate Na-H exchange in proximal tubule (luminal membrane)
Stimulate Na-Bicarb co-transport (basolateral membrane)- which increases H+ secretion

48
Q

ADH (Vasopressin) made where?

A

Made in the hypothalamus
Two types of magnocellular (large) neurons produce
(stored and released from post pituitarty gland)

49
Q

Neurons located in supraoptic and paraventricular nuclei produce what %’s of ADH?

A

83% in supraoptic

17% in paraventricular nuclei

50
Q

Stimulation of what causes release of AHD?

A

Stimulation of the supraoptic and paraventricular nuclei (increased osmolarity) sends impulses down the magnocellular neurons which stimulates release of ADH from storage vesicles located in the nerve endings

51
Q

ADH stimulates formation of what?

A

water channels across luminal membrane

52
Q

ADH - HOW does it work in the tubular cell?

binds with what?, which increases formation of what? then what things come together? and they do what?

A

Binds with specific V2 receptors which increases formation of cyclic AMP and activation of protein kinases
Protein kinase activation results in movement of aquaporin-2 (intracellular protein) to luminal side of cell
Aquaporin-2 molecules come together and fuse with cell membrane to form water channels which increases membrane permeability to water (water reabsorption)

53
Q

Chronic increases in ADH causes what?

A

an increase in formation of aquaporin-2 molecules

54
Q

DECREASED [ADH] results in movement of the

aquaporin-2 where?

A

molecules back into the cytoplasm which reduces the number of water channels and DECREASING water permeability

55
Q

Atrial Natriuretic Peptide Secreted by what?

A

cardiac atrial cells when atria distended by plasma volume expansion

56
Q

Atrial Natriuretic Peptide Actions? (2)

A

Direct inhibition of sodium & water reabsorption (especially collecting ducts)
Inhibits renin secretion (thus inhibits angiotensin II formation)

57
Q

Atrial Natriuretic Peptide is an Important response to help prevent sodium and water retention during what?

A

heart failure

58
Q

Most important hormone for regulating calcium

A

Parathyroid Hormone

59
Q

Parathyroid Hormone three actions?

A

Increases calcium reabsorption (distal tubules)
Inhibits phosphate reabsorption (proximal tubule)
Increases magnesium reabsorption (loop of Henle)

60
Q

SNS severe stimulation results in what effect to GFR ?

A

Severe stimulation results in constriction of renal arterioles which DECREASE GFR

61
Q

SNS low levels of stimulation activate what on renal tubular epithelial cells? and what does it stimulate?

A

activate alpha-receptors on renal tubular epithelial cells (proximal tubule, thick ascending limb of loop of Henle, maybe distal tubule)
Receptor activation stimulates sodium reabsorption which sodium and water excretion

62
Q

SNS stimulates release of what which adds to tubular reabsorption of Na?

A

Stimulates release of renin (angiotensin II)

63
Q

Renal Clearance

A

Volume of plasma that is completely cleared (i.e. all of specified solute) by kidneys per unit time
Not realistic as no volume of blood completely cleared

64
Q

Renal Clearance PROVIDES:

A
Way to quantify excretory function of kidneys
Way to quantify renal blood flow
Way to quantify glomerular filtration
Way to quantify tubular reabsorption
Way to quantify tubular secretion
65
Q

Renal Clearance equation?

A
C(ml/min) = U x V/P
Clearance = Urinary excretion rate / Plasma concentration
GFR = U x V/P
66
Q

If solute freely filtered and neither reabsorbed or secreted, then excretion rate is equal to what?

A

is the filtration rate

67
Q

Inulin clearance used as measure of what?

A

GFR

68
Q

What substance is usually used clinically to measure GFR?

A

Creatinine usually used clinically although small amount is reabsorbed
Rough estimate of changes in GFR is to look at changes in creatinine concentration
–A four fold increase in creatinine concentration means the GFR is one-fourth normal

69
Q

If a substance is completely cleared then clearance rate should equal what flow?

A

renal plasma flow

70
Q

PAH clearance provides reasonable estimation of renal plasma flow bc what % is cleared?

A

90% cleared

71
Q

Actual renal plasma flow can be calculated by what calculation with the PAH

A

PAH clearance rate by the PAH extraction rate

PAH Clearance / 0.9

72
Q

Absorption - equation

A

Filtered load–Excretion rate

73
Q

Secretion - equation

A

Excretion rate–Filtered load

74
Q

Clearance Rate If equal to inulin clearance

A

Substance only filtered, not reabsorbed, not secreted

75
Q

Clearance Rate - If less than inulin clearance

A

Substance must be reabsorbed

76
Q

Clearance Rate - If greater than inulin clearance

A

Substance must be secreated