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Renal 2 Test 1 > Renal Physiology Part 3 > Flashcards

Renal Physiology Part 3 Flashcards

1
Q

Countercurrent multiplier mechanism

A
  • concentrates solute in medullary interstitium via 2 primary mechanisms:
  • Na-K-2Cl cotransporter reabsorption of Na in the TAL
  • reabsorption of urea initiated by ADH
  • high solute concentration enables kidneys to excrete highly concentrated urine, conserve water during periods of dehydration
  • this mechanism requires integrated function of descending, ascending limbs; vasa recta capillaries; collecting ducts
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2
Q

Any drugs which increase renal blood flow to vasa recta or inhibit the loop transporter will

A

decrease the renal medullary interstitial osmolarity and reduce the kidney’s ability to produce a concentrated urine

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3
Q

ADH

A
  • increase H2O and urea permeability of late distal tubule, collecting duct
  • stimulates water reabsorption in principal cells via V2 receptor
  • also vasoconstrictor arterioles (V1 receptor) and thus can serve as a hormonal regulator of vascular tone
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4
Q

2 primary regulators of ADH are

A
  • plasma osmolality: an increase stimulates, while a decrease inhibits
  • blood pressure/volume: an increase inhibits, while a decrease stimulates
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5
Q

In well-hydrated individuals (diuresis) collecting duct

A

is normally impermeable to water

  • water remains in tubular lumen; dilute urine is excreted
  • low ADH
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6
Q

In dehydrated individuals (antidiuresis) collecting duct

A

is highly water-permeable

  • water is reabsorbed; low volume of concentrated urine is excreted
  • high ADH
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7
Q

ADH promotes urea

A

reabsorption from inner medullary collecting duct by increasing expression of urea transporters

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8
Q

Antidiuresis: high ADH

A
  • ADH makes the collecting duct epithelial highly water permeable
  • water is reabsorbed in this segment, and a low volume, highly concentrated urine is excreted
  • SIADH, dehydration
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9
Q

Water diuresis: low ADH

A
  • high volume of dilute urine is excreted
  • collecting duct epithelium is impermeable to water
  • lower solute concentrations in medullary interstitium
  • diabetes insipidus, volume expansion
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10
Q

ANP

A
  • increases GFR: afferent arteriolar dilation, efferent arteriolar constriction
  • inhibits Na+ reabsorption in medullary CD
  • suppresses renin secretion
  • suppresses aldosterone secretion
  • a systemic vasodilator
  • suppresses AVP secretion, actions
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11
Q

Free water clearance (Ch2o)

A

excretion of solute-free water by the kidneys

-Ch2o=V-Cosm

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12
Q

If Uosm

A

positive; pure water is cleared from the body

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13
Q

If Uosm > Posm, Ch2o

A

is negative; pure water is retained

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14
Q

Fractional Excretion

A

(Una x Pcreat)/(Pna x Ucr) x 100

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15
Q

Fractional excretion below 1%

A
  • prerenal and AGN

- Na avidly reabsorbed

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16
Q

Fractional excretion greater than 2%

A
  • ATN, renal

- tubular damage disrupts normal Na reabsorption

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17
Q

3 lines of defense against pH changes

A
  • chemical buffers
  • respiration
  • kidneys
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18
Q

6 factors control renal H+ secretion

A

-intracellular pH, plasma Pco2, carbonic anhydrase, Na+ reabsorption, extracellular K+, aldosterone

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19
Q

Respiratory acid-base disturbances:

A

-primary changes in Pco2 cause H+ and HCO3- to change

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20
Q

Metabolic acid-base disturbances

A

-gains or losses of H+ and HCO3-; respiratory, renal responses

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21
Q

H+ competes with

A

Ca2+ for binding sites on plasma proteins

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22
Q

Acidemia

A

increased [H+] = increase plasma free [Ca2+]

  • hypercalcemia
  • decreased pH–H+ displaces Ca2+ from proteins
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23
Q

Alkalemia

A

decreased [H+] = decreased plasma free [Ca2+]

-hypocalcemia

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24
Q

Acidosis

A
  • increased H+
  • hyperkalemia
  • K+ shifting out of cell into ECF
  • Na+ shifting out of cell into ECF
  • H+ moving into cell
25
Q

Alkalosis

A
  • hypokalemia
  • decreased H+
  • H+ moving out of cell
  • K+ moving into cell
  • Na+ moving into cell
26
Q

Respiratory alkalosis

A
  • decreased CO2+; equation shifted towards CO2
  • compensate by decreasing HCO3-; pH increases
  • PCO2
27
Q

Respiratory acidosis

A
  • increased CO2+; equation shifted towards HCO3-
  • compensate by increasing HCO3-; pH decreases
  • PCO2>40
  • renal compensation
28
Q

Metabolic alkalosis

A
  • increased HCO3-; equation shifted towards CO2
  • compensate by increasing CO2; pH increases
  • HCO3- > 24
  • respiratory compensation
29
Q

Metabolic acidosis

A
  • decreased HCO3-; equation shifted towards HCO3-
  • compensate by decreasing CO2; pH decreases
  • PCO2
30
Q

Anion gap

A
  • differential diagnosis of metabolic acidosis
  • cations - anions (sodium - (chloride + bicarbonate)
  • Normal range: 8-11
  • anion gap is either normal or increased, depending on cause of metabolic acidosis
31
Q

Anion Gap Hyperchloremic acidosis

A
  • AG is unchanged

- loss of HCO3- is matched by gain of Cl-

32
Q

High Anion Gap acidosis

A

-HCO3- is replaced by unmeasured anion (lactate, ketoacidosis, poisoning)

33
Q

Causes of high anion gap acidosis

A
  • Ethanol
  • Ethylene glycol
  • Lactic acid
  • Methanol
  • Paraldehyde
  • Aspirin
  • Renal Failure
  • Ketone bodies
34
Q

Renin

A

-catalyzes conversion of angiotensinogen to angiotensin I, which in turn is converted to Ang II by ACE

35
Q

3 primary regulators of renin are

A
  • perfusion pressure to the kidney: an increase inhibits, while a decrease stimulates
  • sympathetic stimulation to the kidney (direct effect via B-1 receptors)
  • Na+ delivery to the macula densa: an increase inhibits, while a decrease stimulates
36
Q

A patient with essential hypertension has

A
  • increased renal artery pressure leading to vasoconstriction of the afferent arterioles and vasodilation of the efferent arterioles
  • high pressure in the juxtaglomerular apparatus leads to decreased renin secretion–>low angiotensin II–>vasodilation of the efferent arterioles
37
Q

A patient with renal artery stenosis has

A

low renal artery pressures, leading to low pressures at the afferent arterioles
-vasodilation of the afferent arterioles and vasoconstriction of the efferent arterioles (increased renin secretion leads to increased angiotensin II)

38
Q

For a patient who has diarrhea, vomiting, or hemorrhaging, it is important to

A

preserve extracellular volume

-one way to do so is to increase reabsorption of fluid an electrolytes at the proximal tubules

39
Q

In nephrogenic diabetes insipidus,

A
  • ADH receptors are not functioning and it is not possible to increase reabsorption at the CD.
  • the patient loses free water and develops hypernatremia
  • treatment is reduction of ECF volume with a thiazide diuretic.
  • this increases peritubular oncotic pressure, in turn increasing water reabsorption in the proximal tubule.
  • elevated water reabsorption, along with sodium loss in the urine, corrects hypernatremia
40
Q

Stimulation of the sympathetic neurons to the kidney causes

A
  • vasoconstriction of the arterioles, but has a greater effect on the afferent arteriole
  • as a consequence: RPF, PGC, GFR decreases; FF increases; PPC decreases; oncotic pC increases
  • increased forces promoting reabsorption in the peritubular capillaries because of a lower peritobular capillary hydrostatic pressure and an increase in plasma oncotic pressure (FF increases)
41
Q

Angiotensin II

A
  • vasoconstrictor
  • constricts both afferent and efferent arterioles, but it has a bigger effect on efferent arteriole
  • RPF decreases; PGC, GFR, FF increase; PPC decreases; oncotic PC increases
  • increasing forces promoting reabsorption in the peritubular capillaries because of a lower peritubular capillary hydrostatic pressure and an increase in plasma oncotic pressure (FF increases)
42
Q

During a stress response, there is

A
  • increase in both sympathetic input and very high levels of circulating ang II
  • increased SNS tone to the kidneys and very high levels of ang II vasoconstrictor both afferent and efferent arterioles. There is a large drop in the RPF and only a small drop in GFR
  • increase in FF–>increase in oncotic pressure–>increase in reabsorption in proximal tubules
  • less fluid is filtered and a greater percentage of that fluid is reabsorbed in the PT, leading to preservation of volume in a volume depleted state
  • also an increase in ADH due to low volume state
  • activation of SNS also directly increases renin release
43
Q

Net effect of ang II is to

A

preserve GFR in volume-depleted state

-prevents a large decrease in GFR but allows a beneficial small decrease

44
Q

In nephrotic syndrome, there is

A
  • marked disruption of the filtering membrane, so plasma proteins now pass through the membrane and are eliminated in urine
  • typically associated with a non-inflammatory injury to the glomerular membrane system
  • marked proteinura; edema; hypoalbuminemia; lipidura; hyperlipdemia
45
Q

In nephritic syndrome, there is

A

an inflammatory disruption of the glomerular membrane system.

  • this disruption allows proteins and cells to cross filtering membrane
  • proteinuria
46
Q

Filtered load=

A

GFR x Px

47
Q

Filtered load > excretion

A

-net reabsorption

48
Q

Filtred load

A

net secretion

49
Q

Clearance of inulin

A
  • independent of plasma concentration

- inulin neither secreted nor reabsorbed

50
Q

At low plasma levels, clearance of glucose is

A

zero, because all is reabsorbed

51
Q

Glucose appears in urine when

A

filtered load exceeds TM

52
Q

Primary site of action for carbonic anhydrase inhibitors is the

A

PT

-blocking CA reduces bicarbonate reabsorption and the activity of the Na+–H+ exchanger

53
Q

Loop diuretics block

A

the Na+-K+-2Cl- transporter in the ATL, thereby reducing their reabsorption
-blocking this transporter also reduces calcium and magnesium reabsorption, all of which results in a marked diuresis

54
Q

Bartter’s syndrome

A
  • a genetic mutation resulting in diminished function of the Na/K/2Cl transporter
  • leads to a low volume state, which causes an increase in renin and aldosterone
  • patients exhibit hypokalemia, alkalosis, and elevated urine calcium
55
Q

Familial hypocalciuric hypercalcemia

A

-autosomal dominant genetic disorder resulting in hypercalcemia
-CaSR is mutated such that it does not respond to plasma calcium.
calcium reabsorption in the kidney is elevated despite hypercalcemia
-patients also have high levels of PTH because CaSR is expressed in cells of the parathyroid gland

56
Q

Potassium sparing diuretics work by

A

blocking ENaC or by blocking aldosterone receptors or the production of aldosterone
-sodium reabsorption is reduced and potassium secretion is diminished

57
Q

Liddle’s syndrome

A
  • a genetic disorder resulting in a gain of function of ENaC channels in the CD
  • results in enhanced sodium reabsorption and potassium secretion.
  • patients are hypertensive, hypokalemic, and alkalotic
58
Q

A decrease in free calcium is a signal to

A
  • increase PTH secretion and the function of PTH is to raise free calcium
  • PTH increases Ca2+ reabsorption in PT of the kidney; inhibits phosphate reabsorption in PT; stimulates 1-alpha-hydroxylase enzyme in kidney, converting inactive vitamin D to active form; causes bone resorption, releasing Ca2+ and Pi into the blood

Renal 2 Test 1 (16 decks)

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