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Kaplan Physio: Renal > Regional Transport > Flashcards

Regional Transport Flashcards

1
Q

Canagliflozin MOA.

A

SGLT2 blocker that inhibits proximal tubule reabsorption of glucose and is used to treat T2DM

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2
Q

Describe the formation of uric acid kidney stones.

A

If the FL (filtered load) of urate is high enough and luminal pH is low, then more of the urate exists as uric acid which can precipitate form a kidney stone.

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3
Q

Label the substances on this graph.

A

A: PAH
B: inulin
C: substance reabsorbed somewhat less rapidly than water e.g. chloride
D: major electrolytes such as sodium, potassium
E: substance reabsorbed somewhat more rapidly than water
F: substance completely reabsorbed in proximal tubule e.g glucose

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4
Q

The concentration of inulin along nephron is an index of water reabsorption. Why?

A

inulin is freely filtered; thus, its concentration in Bowman’s space is same as it is in the plasma

because water is reabsobed but inulin is not, the concentration of inulin increases throughout the nephron. The greater the water reabsorption the greater the increase in inulin concentration

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5
Q

What are 3 factors that contribute to the maintenance of concentrated medullary interstitium?

A
  • slow flow in vasa recta
  • activity of Na+ K + 2 Cl- transporter
  • urea permeability in collecting duct
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6
Q

Compare and contrast water and solute reabsorption in the descending limb and ascending limb of the loop of Henle.

A

Descending limb is impermeable to water and relatively impermeable to solute

Ascending limb is impermeable to water and solutes are transported out

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7
Q

Where are Ca2+ sensing receptors?

A

CaSR found in basolateral membrane of TAL and the parathyroid

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8
Q

How does CaSR regulate Ca2+ at the TAL

A

CaSR couples to at least 2 G proteins

  1. Gi/o which inhibits AC thereby reducing intracellular cAMP
  2. Gq which activates protein kinase C (PKC)

This inhibits of Na+/K+/2Cl- channel

This then reduces its activity reducing Ca2+ reabsorption

Thus high plasma concentrations of calcium can directly reduce calcium reabsorption in TAL

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9
Q

What is Bartter syndrome?

A

a genetic mutation resulting in diminished function of Na+ K+ 2Cl- transporter in TAL.

This leads to a low volume state, which causes an increase in renin and aldosterone (known as secondary hyperaldosteronism. Patients exhibit hypokalmeia, alkalosis, and elevated urine Ca2+

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10
Q

What is familial hypocalciuric hypercalcemia?

A

FHH is an autosomal dominant genetic disorder resulting in hypercalcemia.

CaSR is mutated such that it does not respond to plasma Ca2+; the CaSR is inactive and “fooled” into thinking that the plasma calcium is low when it is in fact elevated.

Thus, Ca2+ reabsorption in kidney is elevated despite the hypercalcemia

Patients also have high levels PTH because CaSR is expressed on parathyroid gland

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11
Q

What is Gitelman syndrome?

A

A genetic disorder resulting in a mutated (reduced function) NaCl transporter. Patients are hypokalemic, alkalotic, and have a low urine Ca2+

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12
Q

How is Ca2+ regulated at the distal tubule?

A

Calcium is actively extruded into peritubular fluid via Ca2+ ATPase or a 3 Na+ Ca2+ antiporter

These cells also express the Ca2+ binding protein, calbindin, which facilitates calcium reabsorption. Calbindin synthesis is increase by active form of vit. D, and thus vit. D enhances PTHs action of DCT.

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13
Q

What is Liddle syndrome?

A

A genetic disorder resulting in a gain of function of ENac channels in the CD

Results in enhance sodium reabsorption and potassium secretion

Patients are hypertensive and alkalotic

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14
Q

Ammonia synthesis increases or decreases in response to an acidosis?

A

increases

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15
Q

Ammonia synthesis increases or decreases in response to an alkalosis?

A

decreases

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16
Q

What is proximal renal tubular acidosis?

A

Type II acidosis

result of diminished capacity of PCT to reabsorb bicarbonate

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17
Q

What is an example of a Type II RTA?

A

Fanconi syndrome which involves a genetic defect in the PCT transport processes and CAI

18
Q

What is distal renal tubular acidosis?

A

Type I RTA

result of inability of the distal nephron to secrete and excrete fixed acid, thus an inability to form an acidic urine

Urine pH > 5.5 - 6.0

Result is a metabolic acidosis with an inappropriately high urine pH

serum K+ is also low

19
Q

What are some conditions that could lead to distal RTA?

A

autoimmune disorders (e.g. lupus, sarcoidosis, Sjogren); lithium and hypercalciuric conditions (calcium-damaging cells)

20
Q

What is Renal Tubular Acidosis Type IV?

A

hypoaldosterone states

result of inability to secrete potassium leading to hyperkalemia. There is decreased secretion of protons leading to metabolic acidosis

21
Q

Correct.

A

Correct.

22
Q

How can insulin and epinephrine be used to reduce plasma potassium?

A

Insulin and epi stimulate Na/K ATP ase and can thus reduce plasma K+

23
Q

What is potassium secretion in the kidney determined by?

A

filtrate flow and sodium reabsorption (creates negative potential for the lumen)

  • increased flow and/or aldosterone increases potassium secretion and excretion
  • decreased flow and/or aldosterone decreases potassium secretion and excretion
24
Q

How does acidosis affect shift of K+?

A

Acidosis shift potassium from ICF to ECF

25
Q

How does alkalosis affect shift of potassium?

A

shifts potassium from ECF to ICF; increased intracellular potassium increases potassium secretion (both promote hypokalemia)

26
Q

Name some promoters of hyperkalemia.

A
  1. Transcellular shifts: metabolic acidosis, hypergylcemia, insulin deficiency, or resistance, muscle trauma
  2. GI: excessive intake (on rare occasions)
  3. Kidney: acute oliguric kidney disease, chronic kidney disease where GFR decreases dramatically from normal, hypoaldosteronism
27
Q

What are 2 ways to fix elevated potassium channels in a patient with a history of end-stage renal failure who presents with confusion after missing a dialysis session?

A

giving bicarb give patient an alkalosis.

This causes protons to leave the intracellular space down it concentration gradient. To maintain electroneutrality, potassium shifts into cells. This decreases the extracellular potassium concentration. Insulin activates the sodium/potassium ATPase and that increases the shift of potassium into the cell also

28
Q

What are some important promoters of hypokalemia to remember?

A

Transcellular shifts: metabolic alkalosis, sudden increases in insulin and catecholamines

GI: diarrhea, vomiting, low potassium diet (rarely has an effect on its own)

Kidney: diuretics, due to increased flow, hyperaldosteronism (adrenal adenoma, renal arterial stenosis) increased excretion of negative ions (bicarbonate, ketone bodies) RTA types I and II

29
Q

Characteristic finding on EKG for those with hypokalemia?

A

low T wave, high U wave

30
Q

What are some metabolic consequences of hypokalemia?

A

decreased insulin response to carbohydrate load, decreased growth rate in chidren, nephrogenic diabetes insipidus, metabolic alkalosis

31
Q

What is acute renal failure?

A

rapid loss of renal function that is often reversible. Loss of renal function results in the accumulation of waste products that kidney excretes, e.g BUN and creatinine.

32
Q

What are other names for acute renal failure?

A

acute kidney injury/ failure

33
Q

What are the pre-renal causes of ARF?

A

decreased renal perfusion as would occur with a decreased renal perfusion pressure, e.g hypovolemia of hemorrhage, diarrhea, vomiting; CHF

34
Q

What are some signs some characteristic signs of prerenal renal failure?

A

reduced GFR

Reduced FeNa+: tubular function is intact, and low GFR (reduced filtered load) allows for significant reabsorption

Elevated plasma BUN: Cr
due to high reabsorption of urea (so water can be reabsorbed) (both elevated just that BUN elevated more)

Na+ reabsorption: Ang II and catecholamines are often elevated, both of which increase Na+ reabsorption

35
Q

How can you tell if the patient has an intrarenally caused tubular damage?

A

Increased FeNa+: tubules are damaged and thus unable to reabsorb Na+

Casts/cells in the urine: damaged cells are sloughed off into the tubule

Low plasma BUN:Cr: tubular damage prevents reabsorption of urea

36
Q

What is the cause of intrarenal ARF?

A

tubular damage occurs resulting in tubular dysfunction:

toxins, interstial nephritis, ischemia, rhabdomyolysis, and sepsis are factors

37
Q

What is postrenal ARF?

A

Condition caused by obstruction of fluid outflow from the kidney renal calculi, enlarged prostate

38
Q

Early signs of postrenal ARF? Late sign?

A

early: similar to prerenal i.e reduce FeNa+ with elevated plasma BUN: Cr

late: build up of pressure results in tubular damage, resulting in characteristic of intrarenal failure i.e marked increase in FeNa+ low plasma BUN:Cr

39
Q

Difference between ARF and Chronic renal failure?

A

although nephrons often recover from the sloughing of the tubular epithelial cells, in ARF, in CRF there is an irreversible loss of nephrons

40
Q

How is renal osteodystrophy caused by chronic renal failure?

A

because there is a reduced ability to excrete phosphate leading to hyperphosphatemia, which reduces plasma calcium and increases PTH (seocondary hyperparathyroidism); result is increased bone resorption

41
Q

What is the most common cause of chronic renal failure?

A

nephropathy produced by diabetes

42
Q

What is the second most common cause of chronic renal failure?

A

hypertension

Kaplan Physio: Renal (5 decks)

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