Lecture 35 4/9/24 Flashcards

1
Q

Which types of control mechanisms are in place around tubular reabsorption?

A

-nervous
-hormonal
-local

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2
Q

What is an important feature of tubular reabsorption?

A

reabsorption of some solutes can be regulated independently of others, esp. through hormonal control systems

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3
Q

What is glomerulotubular balance?

A

intrinsic ability of the tubules to increase their reabsorption rate in response to increased tubular load

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4
Q

Why does the percentage of GFR reabsorbed in the proximal tubule remain constant when filtered load increases?

A

because rate of reabsorption also increases

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5
Q

Besides the proximal tubule, which other segment of the nephron also sees a degree of glomerulotubular balance?

A

Loop of Henle

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6
Q

What is the overall goal of glomerulotubular balance?

A

prevent overloading of the distal tubular segments when GFR increases

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7
Q

Why is it important that glomerulotubular balance and tubuloglomerular feedback work together?

A

they both work to prevent changes in GFR from dramatically changing urine output

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8
Q

What percent of water and solutes is normally reabsorbed?

A

99%

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9
Q

What is the normal rate of peritubular capillary reabsorption?

A

124 ml/min

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10
Q

Which two determinants of peritubular capillary reabsorption are directly influenced by renal hemodynamic changes?

A

-hydrostatic pressure of the peritubular capillaries
-colloid osmotic pressure of the peritubular capillaries

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11
Q

How is peritubular capillary hydrostatic pressure influenced by arterial pressure?

A

increases in arterial pressure tend to raise peritubular capillary hydrostatic pressure and decrease reabsorption rate

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12
Q

How is peritubular capillary hydrostatic pressure influenced by afferent and efferent arteriole resistance?

A

increased resistance of the afferent or efferent arterioles reduces peritubular capillary hydrostatic pressure and increases reabsorption rate

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13
Q

Which factors influence the peritubular capillary oncotic pressure?

A

-systemic plasma colloid osmotic pressure
-filtration fraction

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14
Q

What are the characteristics of filtration fraction?

A

-the higher the filtration fraction, the greater the fraction of plasma filtered through glomerulus
-protein in the plasma left behind is more concentrated

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15
Q

What is filtration fraction?

A

GFR/RPF

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16
Q

How does angiotensin II raise filtration fraction?

A

by decreasing RPF

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17
Q

How do changes in the peritubular capillary physical forces influence tubular reabsorption?

A

by changing the physical forces in the renal interstitium

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18
Q

What is the net movement of water and solutes with the normal, high rate of peritubular capillary reabsorption?

A

net movement into the peritubular capillaries, with little back leak into the tubule lumen

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19
Q

What happens when peritubular capillary reabsorption is reduced?

A

-increased interstitial fluid hydrostatic pressure
-tendency for greater amounts of solute and water to leak back into tubular lumen
-reduced rate of net reabsorption

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20
Q

What is pressure natriuresis?

A

increased sodium excretion with increased arterial pressure

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21
Q

What is pressure diuresis?

A

increased water excretion with increased arterial pressure

22
Q

Why does urine output increase when systemic blood pressure increases?

A

-increased GFR
-slight increase in peritubular capillary and hydrostatic pressure
-decreased angiotensin II formation
-internalization of Na transporter

23
Q

What is the site of action for aldosterone?

A

collecting tubule and duct

24
Q

What are the effects of aldosterone?

A

-increased NaCl and H2O reabsorption
-increased K+ and H+ secretion

25
Q

What are the sites of action for angiotensin II?

A

-proximal tubule
-thick ascending LOH/distal tubule
-collecting tubule

26
Q

What are the effects of angiotensin II?

A

-increased NaCl and H2O reabsorption
-increased H+ secretion

27
Q

What is the site of action for ADH?

A

distal tubule/collecting tubule and duct

28
Q

What is the effect of ADH?

A

increased H2O reabsorption

29
Q

What is the site of action for atrial natriuretic peptide?

A

distal tubule/collecting tubule and duct

30
Q

What is the effect of atrial natriuretic peptide?

A

decreased NaCl reabsorption

31
Q

What are the sites of action for parathyroid hormone?

A

-proximal tubule
-thick ascending LOH/distal tubule

32
Q

What are the effects of parathyroid hormone?

A

-decreased PO4- reabsorption
-increased Ca++ reabsorption

33
Q

Which mechanisms are used by aldosterone?

A

-stimulation of Na+/K+ pump
-insertion of epithelial sodium channels

34
Q

What are the most important stimuli for aldosterone?

A

-increased extracellular potassium conc.
-increased angiotensin II levels

35
Q

How does aldosterone act on principal cells?

A

-stimulates Na+/K+ pump
-increases Na+ permeability while K+ diffuses out

36
Q

How does aldosterone act on alpha intercalated cells?

A

stimulates H+ ATPase pumps to increase H+ secretion

37
Q

How does aldosterone act on beta intercalated cells?

A

stimulates HCO3-/Cl- exchangers to increase HCO3- secretion and Cl- reabsorption

38
Q

What would be seen on a chemistry panel that would indicate Addison’s disease/deficit of aldosterone?

A

-low Na+
-high K+
-Na+/K+ ratio below 27:1

39
Q

What would be seen on a chemistry panel that would indicate hyperadolsteronism?

A

-high Na+
-low K+

40
Q

When does angiotensin II formation increase?

A

-low blood pressure
-low extracellular fluid volume

41
Q

What are the functions of angiotensin II?

A

-stimulates aldosterone release
-constricts efferent arterioles
-directly stimulates Na+ reabsorption

42
Q

What are the angiotensin II mechanisms of action?

A

-stimulates Na+/K+ ATPase pump
-stimulates Na+/H+ exchanger
-stimulates Na+/HCO3- co-transporter

43
Q

When is ADH released?

A

in response to increased extracellular osmolarity

44
Q

What are the mechanisms of action for ADH?

A

-binds receptors that stimulate cAMP activation of protein kinase A
-stimulates movement of aquaporins to luminal membranes
-forms channels for water to enter cells

45
Q

What are the two types of diabetes insipidus?

A

-lacking ADH secretion
-defect in renal receptors for ADH

46
Q

When is atrial natriuretic peptide released?

A

when specific cells of the cardiac atria undergo increased stretch/experience increased blood volume

47
Q

How does ANP act on the body?

A

-systemic vasodilation
-inhibits renin secretion and angiotensin II/aldosterone formation
-increases GFR and filtration fraction
-increases water excretion and reduces blood volume

48
Q

What are the mechanisms of action for parathyroid hormone?

A

-increased distal tubular reabsorption of Ca2+
-decreased proximal tubular reabsorption of P
-stimulates Mg2+ reabsorption

49
Q

What are the roles of the alpha adrenergic receptors in the kidney?

A

-alpha1-AR stimulates renal vasoconstriction
-alpha2-AR is responsible for Na+ reabsorption

50
Q

What are the roles of the beta adrenergic receptors in the kidney?

A

-beta1-AR and beta2-AR regulate renal blood flow, GFR, Na+ and H2O reabsorption, acid-base, and renin secretion
-beta3-AR regulates renal water and solute reabsorption

51
Q

What happens when the sympathetic nervous system is activated?

A

-constriction of renal arterioles
-reduced GFR and RPF
-increased sodium reabsorption
-increased renin release and angiotensin II formation