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Physiology Block 3 > 9 - Renal Endocrine Function, Diuretics, and Micturition > Flashcards

9 - Renal Endocrine Function, Diuretics, and Micturition Flashcards

1
Q

What role does the kidney play in endocrine function?

A

It’s important in the production of Vitamin D3, erythropoietin, and renin.

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2
Q

How do the kidneys produce active Vitamin D? What is the purpose of this?

A

25-dihydroxy D3 is hydroxylated to 1,25-dihydroxyvitamin D3 (calcitrol) in the proximal tubules.

Calcitrol is essential for calcium deposition in bone and reabsorptoin by the GI tract.

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3
Q

When is PTH stimulated? What is its action in the kidneys?

A

By low calcium.

Enhances thick ascending loop and distal tubular Ca reabsorption (paracellular).

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4
Q

What happens to 7-dehydrocholesterol in the skin?

A

It’s converted to cholecalciferol by UV rays.

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5
Q

How is erythropoietin (EPO) made before and after birth?

A

Mainly by hepatocytes during fetal stage.

After birth, 80-90% of EPO originates from peritubular fibroblast-like cells in the cortex.

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6
Q

What stimulates EPO production?

A

Tissue hypoxia mainly.

EPO production increases exponentially with decreased blood hemoglobin concentration.

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7
Q

What requires EPO? What happens when there is a lack of EPO? How it this treated?

A

RBC production.

Lack of EPO causes anemia associated with chronic renal failure.

Recombinant EPO used for treatment.

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8
Q

What are five factors that stimulate EPO production? What do they all have in common?

A
  1. Low blood volume
  2. Anemia
  3. Low Hb
  4. Poor blood flow
  5. Pulmonary disease

All factors that decrease tissue oxygenation.

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9
Q

How is EPO production stimulated?

A

Through stimulation of hematopoietic stem cells in bone marrow to develop into RBCs.

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10
Q

What is the function of renin? Where is it found?

A

Enzyme involved in the production of the vasoconstrictor and ANP AngII.

Renin is found in JG cells in the wall of the afferent arteriole.

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11
Q

What three things stimulate renin release?

A
  1. Increase renal sympathetic nerve stimulation
  2. Decreased delivery of NaCl to the macula densa
  3. Decreased renal perfusion pressure
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12
Q

In general terms, what occurs in renal gluconeogenesis? Where does this occur in the nephron?

A

Synthesis of glucose from amino acids and lactate in the proximal tubule cells.

Under normal conditions this is a minor function.

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13
Q

What happens to renal gluconeogenesis during prolonged fasting?

A

It becomes a major source of blood glucose, producing about 1/5 as much glucose as the liver.

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14
Q

What is the major amino acid substrate used for renal gluconeogenesis? What is a byproduct of this?

A

Glutamine.

Major byproduct is NH4+, which is important in renal acid secretion.

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15
Q

What effect does diuretic therapy have? What is the body’s response to this?

A

There is increased excretion of sodium and water, leading to a contraction of ECF volume.

Reduction of ECFV sensed by the body and mechanisms to conserve Na and water are activated.

This leads to a new steady-state where intake=output but at a new level of ECFV.

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16
Q

What is the function of osmotic diuretics? Where do these have the greatest effect? What is their effect?

A

Alter reabsorption of solute and water by altering osmotic driving forcees along nephron.

Greatest effect in high perm segments (PT and thick ascending).

Maximal effect is increased sodium excretion to 10% of filtered load.

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17
Q

What is an example of an exogenous osmotic diuretic? What is an example of two endogenous osmotic diuretics?

A

Mannitol, a sugar freely filtered, not reabsorbed, and trapped in the tubular lumen.

Glucose can act as one in uncontrolled diabetes mellitus, and urea can act as one during renal failure.

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18
Q

What are side effects of osmotic diuretics?

A

Increased potassium excretion, increased bicarb excretion, and increased Ca excretion.

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19
Q

What is the function of carbonic anhydrase inhibitors? Where does it have its greatest effect? What is its effect?

A

Inhibit CA and limit the activity of Na/H exchanger.

Major site of action is the PT. (will effect other segments too just not as much).

Increase sodium excretion to ~5-10% of filtered load.

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20
Q

What is a commonly used CA inhibitor? What are side effects that can occur?

A

Acetazolamide.

Side effects: Increased potassium excretion, increased bicarb excretion, increased calcium excretion.

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21
Q

What is the function of loop diuretics? Where do they have their effect? What is their effect?

A

Inhibit sodium reabsorption in the thick ascending loop by blocking Na/K/2CL transporter.

They also impair ability of kidney to concentrate or dilute urine.

Acutely increase sodium excretion up to 20% of the filtered load.

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22
Q

What are some commonly used loop diuretics?

A

Bumetanide, furosemide, and ethacrynic acid.

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23
Q

What are side effects of loop diuretics?

A

Increase potassium excretion, increased calcium and magnesium excretion, and an impaired urinary concentrating and diluting ability.

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24
Q

What is the function of thiazide diuretics? What is their effect?

A

Inhibit sodium reabsorption in the early DT (diluting segment) by blocking Na/Cl symporter in apical membrane.

Decreases ability to dilute tubular fluid.

Acutely increase sodium excretion to 5-10% of filtered load.

25
Q

What are two commonly used thiazide diuretics? What are the side effects of thiazide diuretics?

A

Chlorothiazide and metolazone.

Side effects include increased potassium excretion and decreased urinary diluting ability.

26
Q

What is the function of potassium-sparing diuretics? What effect do they have?

A

Inhibit sodium reabsorption and potassium secretion in the principal cells of the late DT and CCD.

Called K sparing because interruption of sodium reabsorption does not increase potassium secretion/excretion.

Increase sodium excretion to 3-% of filtered load.

27
Q

What are two types of K-soaring diuretics?

A

One type antagonizes aldosterone action in principal cells - spironolactone and eplerenone

Second class blocks K channels in the principal cells - amiloride and triamterene

28
Q

What are side effects of K-sparing diuretics?

A

Decreased potassium excretion and increased bicarb excretion.

29
Q

Urine expelled from the bladder is unchanged from what?

A

The fluid that left the collecting ducts.

30
Q

What is the structure of ureters?

A

Lumen lined with transitional epithelium which is above a submucosal later of connective tissue and an inner longitudinal and outer circular later of smooth muscle.

31
Q

How does the ureter pass fluid from the renal pelvis to the bladder? How does the pressure change during this movement of fluid?

A

Peristaltic contractile waves, 2-6/min, which originate from proximal portion.

Hydrostatic pressure changes from 0-5 cm H2O at baseline to 20-80 cm H2O during peristaltic contraction.

32
Q

What triggers peristaltic contraction of the ureters?

A

Mechanical stimuli (stretch), chemical stimuli, or membrane depolarization all trigger an action potential and an associated contraction.

33
Q

How does ureteral smooth muscle function? What permits peristaltic contractions?

A

As a syncytium.

The muscle unit has an action potential of the extended plateau type, which permits extended peristaltic contractions.

This type of contraction also seen in the bladder.

34
Q

Can ureteral peristalsis occur without innervation? What can modulate peristalsis?

A

Yes.

Modulated by sympathetic stimulation (aortic, hypogastric, and ovarian/spermatic plexuses) - inhibits ureteral contraction

Parasympathetic (pelvic splanchnic nerve) - stimulate contraction

Some autonomic nerve pain fibers too.

35
Q

What covers the ureteral orifice? What function does this serve?

A

A flaplike mucous membrane valve that, in conjunction with the oblique path the ureter follows through the detrusor muscle, prevents reflux.

36
Q

What effect does the detrusor muscle have on the bladder? Where it this located?

A

Contraction can increase pressure to 40-60 mmHg.

At the neck of the bladder
(elastic tissue also present), serves as an internal sphincter which prevents emptying until pressure reaches threshold.

37
Q

What is the external urethral sphincter made of? Where is it located?

A

Adjacent to internal sphincter, located in urogenital diaphragm.

Made of skeletal muscle under voluntary control.

38
Q

How are the bladder and sphincters innervated? What is the function of each?

A

By sympathetic, parasympathetic, and somatic nerves.

Primary nerve supply is pelvic nerve which contains sensory and motor.

  • sensory detects stretch and initiate emptying
  • motor are parasympathetic and innervate detrusor muscle

Somatic fibers in pudendal nerve innervate and control the external sphincter.

39
Q

Describe the micturition reflex?

A

Bladder stretch receptors conducted to sacral cold via pelvic nerves and reflexively back to bladder by parasympathetics that lead to contractions.

40
Q

What happens to bladder contractions caused by parasympathetics at low volumes? What occurs after that if micturition does not occur?

A

Low vol - contractions relax spontaneously.

As bladder filled, contractions are more freq and of greater duration and intensity.

Unsucessful micturition reflex followed by inhibition state (min-hrs).

41
Q

What does the micturition reflex consist of?

A
  1. rapid and . progressive increase in pressure
  2. Period of sustained pressure
  3. Return of pressure to basal tone
42
Q

What happens during bladder filling? What is this process called?

A

Distention causes low level afferent firing, which stimulates sympathetic outflow to base and urethra and pudendal outflow to external sphincter.

This occurs by spinal reflex pathways and represent “guarding reflexes” which promote continence.

(sympathetic firing also inhibits detrusor muscle and transmission of bladder ganglia)

43
Q

What is the micturition reflex-1 ?

A

Periods of increased luminal pressure (miturition waves) which last from sec-min are imposed upon tonic pressure from bladder filling.

As bladder fills, contractions increase in strength and freq. They are self-regenerative and last up to a min. Upon cessation, they may be quiet for minutes to an hour.

44
Q

What happens when the micturition waves of the micturition reflex-1 become powerful enough?

A

It initiates reflex through the pudendal nerves to inhibit contraction of the external sphincter.

Urination will occur unless voluntary signals through the pudendal nerve are more potent.

45
Q

What exerts the final control on micturition?

A

Higher cortical centers, which partially inhibit reflec and inhibit micturition by voluntary contraction of external bladder sphincter.

46
Q

What happens at initiation of micturition?

A

Intense afferent activity activates the brainstem micturition center which inhibits spinal guarding reflexes.

The pontine center also stimulates parasympathetic outflow to the bladder and internal sphincter smooth m.

47
Q

How is the voiding reflex maintained?

A

Ascending afferent input from the spinal cord, which reaches the pontine micturition center.

48
Q

What is voluntary cessation of voiding associated with? What is resumption of voiding associated with?

A

An initial increase in sphincter and detrusor pressure.

A resumption of voiding is associated with sphincter relaxation and decreases detrusor pressure that continues as the bladder empties and relaxes.

49
Q

How does reflex voiding in infants differ from that of healthy adults?

A

The reciprocal relationship between sphincter relaxation and detrussor activity is intact but it is not under voluntary control.

50
Q

How does reflex voiding in paraplegic patients differ from that in healthy adults?

A

The reciprocal relationship between bladder and sphincter is abolished and thus interferes with bladder emptying.

51
Q

How do you calculate urine flow rate (V)?

A

Urine Flow Rate (V) = Urine volume/ time of collection

52
Q

How do you calculate urine excretion rate?

A

Clearance rate X volume

53
Q

How do you calculate fractional excretion?

A

Excretion/filtered load

(Us X V ) / (Ps X GFR)

Us = clearance rate 
V = urine flow rate 
Ps = plasma concentration
54
Q

What is net reabsorption rate equal to?

A

Filtered load - excretion rate

55
Q

What is net secretion rate equal to?

A

Excretion rate - filtered load

56
Q

How do you calculate renal clearance of a substance?

A

Cx = (Ux) X (V) / Px

Where 
Cx = clearance of substance X 
Ux = urine concentration of X 
V = urine flow rate 
Px = plasma concentration of substance X
57
Q

What is the renal clearance rate of glucose? Sodium? Chloride? Potassium?

A

Glucose - 0
Sodium - 0.9
Chloride - 1.3
Potassium - 12

58
Q

How do you calculate osmolar clearance?

A

Cosm = Uosm X V / Posm

Uosm = Urine osmolarity 
V = urine flow rate 
P = plasma osmolarity
59
Q

What is free water clearance rate and how do you calculate it?

A

Rate at which solute-free water is excreted by the kidneys.

Ch2O = V - Cosm

V = urine flow rate 
Cosm = osmolar clearance

Physiology Block 3 (17 decks)

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