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Renal Physiology > Electrolyte Regulation > Flashcards

Electrolyte Regulation Flashcards

1
Q

What is the normal range of Potassium?

A

0.3 mEq/L - 4.5 mEq/L

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2
Q

Under normal conditions how much of filtered K+ is excreted? How little can be excreted? Maximum amount?

A

about 20% is normal, 1-2%, and greater than 100% (implying it is also secreted)

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3
Q

How much K+ is reabsorbed in the different parts of the nephron and by what mechanism?

A

65% in PCT by passive diffusion in paracellular path and some evidence of a pump, 25% in LOH via tri-transporter, in the distal tubule and collecting duct the K+ secretion is regulated (only 10% or less of filtered, this is the area that adjusts for dietary intake)

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4
Q

How is K+ secretion regulated?

A

aldosterone increases Na-K-ATPase expression and activity, increases ENaC and enhances secretion of K+, aldosterone levels respond to the plasma level of K+

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5
Q

What effect does hydrogen have on potassium secretion?

A

increase in H+ or acidosis results in a decrease in K+ excretion, believe there is a pump along the basolateral side of tubular cells transporting both K+ or H+ so when there is an increase in H+ in the plasma then there is a decrease in K+ excretion due to competition

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6
Q

How does sodium effect potassium excretion?

A

increased sodium excretion will cause an increase in potassium excretion acutely, more sodium in tubule means more can enter the luminal cell and K+ to pass out of the cell into the tubule,

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7
Q

What hormones increase cellular uptake of K+?

A

insulin, beta-adrenergic agonists (epinephrine), aldosterone (via Na/K ATPase)

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8
Q

For which ions does absorption by the gut equal excretion by the kidney?

A

Mg, Pi, and Ca

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9
Q

Where is calcium present in the body?

A

ECFV, ICF, and Bone; in the blood 50% is free and 50% bound to proteins; in ICF it is distributed btwn ER and Mitochondria

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10
Q

How is the balance of calcium between ICF and ECFV maintained?

A

action of CA ATPase and NCX

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11
Q

How is calcium concentration and balance maintained?

A

hypocalcemia detected by Ca sensing receptors CaSR in the parathyroid glands, PTH released, which increases Ca release from bone, increased reabsorption by the kidneys, increased 1-hydroxylase activity in PT, increased production of calcitriol, calcitriol facilitates PTH mediated release from bone, increased absorption in the gut, increased reabsorption by the kidneys

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12
Q

How is calcium regulation different from Na and K?

A

Na and K are almost completely absorbed in the gut, Ca absorption from food is regulated by calcitriol balance is then achieved by matching gut absorption to renal excretion

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13
Q

Under normal conditions how much is filtered, reabsorbed, and excreted?

A

50% of plasma concentration available for filtration, 99% of filtered Ca is reabsorbed: 70% in PT, LOH 20%, and DT & CD 9%, typically <1% excreted

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14
Q

By what mechanism is Ca reabsorbed in PT?

A

PT through paracellular path 80% and 20% through transcellular path uptake on apical side via ion channels and extrusion across basolateral membrane by CaATPase and NCX

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15
Q

How does PTH effect reabsorption of calcium?

A

PTH acts on the NCX and Ca ATPase

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16
Q

How is paracellular diffusion driven?

A

favorable electrochemical gradient, lumen becomes more positive in later portions of proximal tubule, more Ca reabsorption occurs here, any factor that increases Na and H20 reabsorption will increase the gradient favoring paracellular Ca diffusion, so Na and Ca reabsorb in parallel

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17
Q

By what mechanism is Ca reabsorbed in LOH?

A

transcellular mechanism, Na and Ca usually change in parallel

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18
Q

What effects do loop diuretics have on electrolytes?

A

inhibit tri-transporter in TAL which decreases Ca reabsorption by TAL because this process is coupled to Na reabsorption in that nephron segment

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19
Q

What effects do thiazide diuretics have on electrolytes?

A

inhibit Na/Cl co-transporter in early distal tubule allows Na and H2O excretion, thereby decreasing ECF volume thereby increases proximal tubular Na reabsorption, which enhances the electrochemical driving force for paracellular Ca reabsorption in PT effect that is exploited to treat hypercalcuria, excess Ca excretion

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20
Q

How is phosphate balanced and distributed in the body?

A

Pi is in ECFV, ICF, and bone; vast majority of total Pi is in bone 86%, ICF 14%, ECF 0.03%, 10% of Pi in plasma is bound to protein

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21
Q

How much Pi is available for filtration? how much is reabsorbed and where? How much is excreted?

A

90% in plasma is free and available for filtration, PT 80%, DT 10%, Excreted 10%

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22
Q

What mechanism of transport does Pi take in the PT?

A

transcellular pathway via Na-Pi across apical side and extrusion across basolateral membrane by PiCl exchange mechanism

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23
Q

What mechanism of transport does Pi use in the distal tubule?

A

limited capacity to reabsorb Pi, mechanism unknown

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24
Q

How does PTH effect Pi excretion?

A

acts by inhibiting NaPi cotransport across apical membrane of PT, allowing increased Pi excretion

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25
Q

What other factors that increase Pi excretion?

A

increased dietary Pi intake, ECFV volume expansion, acidosis (increased [H])

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26
Q

What factors promote Pi retention?

A

decreased PTH, decreased dietary Pi intake, ECFV volume contraction, and alkalosis

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27
Q

What effect do diuretics have on Pi?

A

with exception of K sparing all diuretics acutely cause increased Pi excretion; long term therapy decreases ECF volume compensatory increase in PT Na reabsorption which is linked to Pi reabsorption via Na-Pi transporter which increases Pi reabsorption and decreases excretion

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28
Q

What is hypernatremia?

A

serum sodium above normal >144mEq/L

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29
Q

What is hyponatremia?

A

serum sodium below normal < 135 mEq/L

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30
Q

What is hyperkalemia?

A

serum potassium above normal > 5.2 mEq/L

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31
Q

What is hypokalemia?

A

serum potassium below normal < 3.5 mEq/L

32
Q

What is hypervolemia?

A

excess total body fluid often characterized by edema, ascites, pleural effusions on chest x-ray or auscultation

33
Q

What is orthostasis (orthostatic hypotension)?

A

volume depleted, decrease of blood pressure when going from lying or sitting to standing position (typically > 20mmHg

34
Q

What are the two mechanisms behind hypokalemia?

A

output exceeds intake, potassium movement into the cell occurs resulting in a lowering of serum potassium, but not total body potassium (cellular shift)

35
Q

What are common etiologies for hypokalemia?

A

GI: poor intake, diarrhea, vomiting, laxative abuse; Renal: potassium wasting- renal tubular acidosis, diuretics, hyperaldosteronism; misc: sweat, drains, periodic paralysis, non-absorbable anions; cellular shifts: alkalosis (H out K in), insulin action, catecholamines

36
Q

Most patients with mild hypokalemia >3.0 are asymptomatic, severe cases often have what neuromuscular problems?

A

muscle weakness (lower ext > upper), marked generalized weakness, paralysis including respiratory, rhabdomyolysis, constipation or ileus

37
Q

Most patients with mild hypokalemia >3.0 are asymptomatic, severe cases often have what cardiovascular problems?

A

atrial and ventricular arrhythmias (exacerbated by digoxin), cardiac arrest, refractory hypotension, U-wave on ECG

38
Q

What is the main treatment for hypokalemia? Forms? route?

A

potassium; potassium chloride, potassium citrate and potassium phosphate; oral is best, unless it is unsafe- aspiration risk, upset stomach, or an NG tube

39
Q

If oral route is unsafe how would potassium be administered for hypokalemia? What is another reason for the alternate route?

A

IV replacement either peripheral or central, in addition to oral in severe hypokalemia

40
Q

What are the three general circumstances that hyperkalemia occurs under?

A

intake exceeds output, potassium shifts out of cells and into serum (acidemia, hypo-insulinemia); cellular injury or destruction resulting in release of potassium from cells

41
Q

Most patients with mild hyperkalemia <5.5 are asymptomatic, patients with severe hyperkalemia may present with what neuromuscular problems?

A

muscle weakness lower>upper, marked generalized weakness, paralysis-including respiratory muscles

42
Q

Most patients with mild hyperkalemia <5.5 are asymptomatic, patients with severe hyperkalemia may present with what cardiovascular problems?

A

peaked T waves, flattened p wave, prolonged PR interval, depressed ST segment, peaked T wave, atrial standstill, prolonged QRS duration, further peaking T waves, sine wave pattern

43
Q

What is the initial approach to hyperkalemia?

A

order EKG, repeat labs to ensure real value (hemolysis, wrong patient, above IVF), begin treatment if EKG changes, or if profoundly elevated K+ while awaiting repeat values

44
Q

What are the different treatment options for hyperkalemia?

A

calcium gluconate, insulin & glucose, sodium bicarbonate, Beta agonists, Kayexalate, hemodialysis, peritoneal dialysis

45
Q

When would you use calcium gluconate?

A

for hyperkalemia with EKG changes, it stabilizes the myocardium, works quickly but does not lower serum potassium

46
Q

When would you use insulin and glucose?

A

facilitates cellular shift of K+ as insulin drives K+ into cells, after several hours K+ will return to serum if measures to remove have not been initiated

47
Q

When would you use sodium bicarbonate?

A

onset of action= minutes, duration 30 min, cellular shift of K+ into cells, more effective with acidosis, dialysis patients respond poorly, after several hours, K+ will return to serum if measures to remove have not been initiated

48
Q

When would you use beta agonists?

A

albuterol 10 mg via nebulizer; after several hours K+ will return to serum if measures to remove have not been initiated (10-20x normal asthma Trx)

49
Q

When would you use kayexalate?

A

primary site of action is in colon, hence not useful in patient colectomy; actually lowers total body K+

50
Q

When would you use hemodialysis?

A

most effective means of removal, reserved for patients on hemodialysis, or those who have ARF or CRF, if patients have normal renal function it can usually be treated medically

51
Q

When would you use peritoneal dialysis?

A

reserved for patients already on PD, can effectively remove K+ if needed

52
Q

Where do you look for the potassium source?

A

place on 70 mEq/day in diet; Ace-I, ARBs, NSAIDs, Spironolactone, Calcineurin inhibitors, trimethoprim, pentamidine, IV fluids containing potassium, tissue necrosis

53
Q

What is the difference between dehydration and volume depletion?

A

dehydration is loss of H2O or loss of water in excess of Na which causes hypernatremia; volume depletion is hypovolemia- loss of sodium and water in equal amounts resulting in a decrease in ECV

54
Q

What are the physical exam findings for hypovolemia?

A

dry mucus membranes/skin, tachycardia, hypotension, and orthostasis

55
Q

What are the physical exam findings for hypervolemia?

A

edema, ascites, pulmonary crackles

56
Q

How does the renin-angiotensin aldosterone system effect urine sodium? describe how.

A

decreased renal perfusion pressure sensed by juxtaglomerular apparatus results in release of renin, initiates the cascade resulting in angiotensin II and aldosterone release; end result is avid renal sodium retention and low urine sodium; angiotensin II also stimulates thirst, in absence of volume depletion system will not be activated and urine sodium will essentially equal input; hence urine sodium will be much lower when it is activated

57
Q

How does vasopressin act in hypovolemia?

A

it is released during hypovolemia or perceived volume depletion such as CHF, cirrhosis and nephrotic syndrome, carotid body sensors perceive the decrease pressure and via sympathetic nervous system stimulate ADH release even in hyponatremia

58
Q

How does ADH act with plasma osmolality?

A

plasma osmolality is dependent on the action of ADH to act on the kidney to limit free water excretion and stimulation of thirst in response to changes in tonicity based on serum osmolality; w/ increase in serum osm ADH promotes H2O reabsorption in the CD, concentrated urine- urine osm > plasma osm; thirst is stimulated

59
Q

How is serum osmolality calculated?

A

= (2 x serum) + BUN/2.8 + glucose/18

60
Q

What is osmotic demyelination? What causes it?

A

initially decrease extracellular osm. will promote movement of water into cells resulting in cerebral edema, if severe it can result in increased intracranial pressure leading to severe neurologic signs/symptoms, brain adapts by movement of ECF from tissues do cerebrospinal fluid and then to circulation, movement of Na, K and osmolytes out of cells which lowers intracellular osmolality and promotes water movement out of cells

61
Q

Why do patients become hyponatremic?

A

ADH will be released if volume depleted, it replace losses with H2O causing hyponatremia, if too much H2O drank despite ADH being turned off and dilute urine, can overwhelm system, resulting in hyponatremia

62
Q

What is SIADH?

A

ADH released inappropriately causing water retention despite lowering sodium (SIADH)

63
Q

What are the three states Hyponatremia can occur in?

A

hypovolemia, euvolemia, hypervolemia

64
Q

What are the causes of hypovolemic hyponatremia?

A

GI losses, skin losses, renal losses (diuretics), and subclinical hypovolemia

65
Q

What are the causes of euvolemic hyponatremia?

A

SIADH, adrenal insufficiency (cortisol deficiency), hypothyroidism, primary polydipsia (ADH is appropriately suppressed resulting in dilute urine), subclinical hypovolemia

66
Q

What are the causes of hypervolemic hyponatremia?

A

CHF, cirrhosis, nephrotic syndrome

67
Q

How do you treat hypervolemic hyponatremia?

A

treat underlying disorder, fluid restriction, treat CHF nephrotic syndrome or cirrhosis

68
Q

How do you treat hypervolemic hyponatremia?

A

treat underlying disorder, administer normal saline 0.9%

69
Q

How do you diagnose psychogenic polydipsia euvolemic hypernatremia?

A

intake of enough H2O to overwhelm the kidneys ability to excrete, ADH is inappropriately suppressed resulting in a maximally dilute urine (<100mOsm) stop if its below 100mOsm

70
Q

How do you diagnose cortisol and thyroid euvolemic hypernatremia?

A

do not follow usual rules and are assessed by measurement of adrenal and thyroid function tests

71
Q

How do you diagnose subclinical hypovolemia euvolemic hypernatremia?

A

patients may have volume depletion that is not detectable by physical exam; patients will have a volume mediated ADH release; if its euvolemia but not SIADH, psychogenic polydipsia, cortisol or thyroid

72
Q

How is SIADH diagnosed?

A

results in decreased urinary water excretion and inappropriately elevated urine osmolality despite ongoing hyponatremia (> 100 mOsm)

73
Q

If the patient is clearly hypovolemic how is it treated?

A

require volume in the form of normal saline

74
Q

If the patient is clearly hypervolemic how is it treated?

A

need to treat underlying condition, likely includes fluid restriction and possibly diuretics

75
Q

If the patient has euvolemic hypernatremia how is it treated?

A

psychogenic polydipsia: fluid restriction

SIADH: fluid restriction, vasopressin antagonists

76
Q

When should a patient be treated with hypertonic saline? What happens if it is too rapid?

A

if a hyponatremic patient is symptomatic, if it is too rapid there is a risk for central pontine myelinolysis, a demyelinating disorder that results in severe debilitation and often death

Renal Physiology (5 decks)

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