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Renal > Renal Midterm > Flashcards

Renal Midterm Flashcards

0
Q

angiotensin II works in _____ to increase ____

A

Ang II works on proximal tubule to ↑ Na⁺ reabsorption

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1
Q

How much does interstitial fluid volume have to rise to become detectable as edema? What is the general increase in extracellular volume?

A

interstitial fluid increase = 2.5-3 liters ECV increase = 4-5 liters

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2
Q

What conditions lead to increased capillary wall permeability (and thus edema)?

A
  • pregnancy - local inflammation (IL2, TNF, histamine, free radicals) - sepsis - ARDS
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3
Q

Where are high pressure baroreceptors located?

A

left ventricle, carotid sinus, aortic arch

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4
Q

What is the underfill mechanism of Na and H20 retention in liver disease?

A

Increased pooling of blood and hypoalbuminemia → ↑ascites → ↓effective arterial pressure → ↑ RAAS, sympathetic nervous system, ADH → ↑ edema, ascites

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5
Q

What is the overfill mechanism of Na and H20 retention in liver disease?

A

.

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6
Q

What is nephrotic syndrome?

A

An increase in the permeability of the glomerular capillary wall to proteins, leading to urinary protein excretion > 3.5 g in 24 hours, hypoalbuminemia, edema, lipiduria, dyslipidemia

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7
Q

What are salt-retaining states?

A

CHF, liver disease, nephrotic syndrome

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8
Q

How do high/low cardiac output states lead to Na/H20 retention and edema/ascites?

A

perception of decreased effective arterial blood volume

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9
Q

What is the diagnostic approach to hyponatremia?

A

First evaluate tonicity. If normal or elevate, could be pseudohyponatremia or hyperglycemia. If hypotonic, refer to diagram.

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10
Q

How do you calculate effective osmolality/tonicity? What about total osmolality/tonicity?

A

effective = 2(Na) + glucose/18 (normal is 280-290) total = 2(Na) + glucose/18 +BUN/2.8 +EtOH/3.7

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11
Q

What is the osmotic stimulus for ADH release?

A

↑ pOsm

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12
Q

What are non-osmotic stimuli for ADH release?

A

↓ ECFV ↓ blood pressure drugs, vomiting, stress, SIADH

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13
Q

How do loop diuretics work? What would happen to the Na serum concentration of someone with SIADH if they’re on one?

A

Loop diuretics like furosemide inhibit generation of the medullary osmotic gradient. Thus, urine osmolality will decrease (even if ADH is the same) and serum Na level.

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14
Q

What are the ADH receptors and where are they located?

A

Aquaporin 2s on the apical surface of principle cells

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15
Q

What are 5 major causes of SIADH?

A

1) Drugs (SSRIs, opioids, NSAIDs, ecstasy) 2) Pulmonary disorders (pneumonia, positive pressure ventilation) 3) CNS disorders (mass lesions/hemorrhages) 4) Post-operative state 5) Tumors (small cell lung cancer, renal cell carcinoma and lymphomas)

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16
Q

What does ANP do?

A

decreases Na reabsorption in the collecting duct

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17
Q

A patient is started on a diuretic and loses 280 mEq of Na over 5 days. How much weight did they lose?

A

280 mEq x 1L/140 mEq = 2L = 2kg

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18
Q

What does total body sodium correlate with? What is an exception?

A

Total body sodium normally correlates well with ECF. An exception is SIADH which leads to decreased total body sodium.

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19
Q

What clinical data support ADH being released?

A

urine osmolality > 100 mOsm/kg despite ECF hypotonicity

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20
Q

Why is “aldosterone escape” attenuated in patients with decreased effective arterial blood volume (say, as a result of heart failure)?

A

Patients with low EABV continue to retain Na, leading to ↑ ECF volume, total body sodium and eventually edema. This happens in these ways: 1) decreased renal perfusion → ↑ proximal tubule Na/H20 reabsorption. similarly, Na/Cl cotransporter activity in the distal tubule is increased. 2) cannot generate pressure natriuresis 3) ANP is blunted because less Na makes it to the medullary collecting duct where ANP does its magic

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21
Q

How do you manage hyponatremia in a patient with CHF?

A

fluid restriction. hyponatremia in this setting is a bad sign. also, ACE inhibitors/ARBs can lead to ↓ ADH (non-osmotic secretion)

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22
Q

In SIADH, what is water excretion dependent on?

A

solute discretion. increasing Na intake will increase urine output.

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23
Q

At what pH is urine usually? What pH does it need to be for calcium phosphate stones to form?

A

normally ~ pH 6. stones form ~ pH 6.3.

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24
Q

What is the formula for total venous CO2?

A

= dissolved CO2+ HCO3 = 1.2 mEq/L + HCO3

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25
Q

What are causes of metabolic acidosis?

A

1) loss of bicarbonate from the GI tract (diarrhea) or kidney (proximal renal tubular acidosis) 2) decreased renal excretion of acid (distal renal tubular acidosis or kidney disease) 3) endogenous generation of excess acid (lactic acidosis or diabetic ketoacidosis) 4) ingestion of excess acid or a substance leading to the endogenous generation of excess acid (salicylate toxicity or ethylene glycol toxicity)

26
Q

How is respiratory acidosis caused?

A

ineffective alveolar ventilation leads to an increase in pCO2

27
Q

What are causes of metabolic alkalosis?

A

primary increase in serum bicarbonate through: 1) loss of acid from the GI tract (vomiting) or kidney (hyperaldosteronism) 2) retention of bicarbonate that has been administered

28
Q

How do you calculate the anion gap?

A

AG = Na - (Cl + HCO3) normally ~ 10 +/- 2 and is comprised of albumin NOTE: HCO3 can be measured as Total CO2

29
Q

What leads to an increased anion gap metabolic acidosis?

A

bicarbonate is lost due to presence of add’t unmeasured acid. NOTE: There is no equimolar rise in serum chloride.

30
Q

What leads to a normal anion gap metabolic acidosis?

A

bicarbonate is lost or H+ is retained. serum chloride rises in equimolar amounts due to retention in the gut or kidney.

31
Q

What are some causes of increased anion gap metabolic acidosis?

A

GOLDMARK Glycols Oxoproline (pyroglutamaic acidosis) L-Lactate D-Lactate Methanol poisoning Aspirin toxicity Renal failure (advanced: organic acids, SO4, PO4) Ketoacidosis

32
Q

Profound volume depletion leads to what urine pH? Why?

A

Low urine pH

33
Q

How do you calculate a normal secondary respiratory response in metabolic acidosis?

A

For every 1 mEq/L decrease in [HCO3], the PCO2 should fall by 1.2 mmHg with a normal response. So if normal is 40 and somebody with MA has a PCO2 of 17, then a normal compensated measurement would be 40-(17x1.2) = ~20.

34
Q

What substances can increase the osmolar gap?

A

Toxins like methanol, ethylene glycol and glycine can cause an increase in MEASURED serum osmolarity but not CALCULATED serum osmolarity, thus increasing the osmolar gap. A value more than 10 mOsm/kg is considered abnormal.

35
Q

What are laboratory signs of diabetic ketoacidosis?

A

ketones in the blood and severe hyperglycemia

36
Q

In diabetic ketoacidosis, is tonicity increased or decreased? What about cell volume?

A

Tonicity is increased because of increased glucose levels, which pulls water out of cells and dilution of sodium levels.

37
Q

What is a common initial presentation of type I diabetes mellitus?

A

diabetic ketoacidosis. Insulin deficiency prevents glucose metabolization, so body breaks down proteins and lipids. The resulting ketoacids cannot metabolized in the absence of insulin and accumulate in the serum causing an increased anion gap metabolic acidosis.

38
Q

How does glycosuria produce an osmotic diuresis?

A

increased glucose in the tubular lumen leads to increased H2O levels and decreased Na concentration, which hinders Na reabsorption in the proximal tubule. The increased delivery of Na and H20 to the distal nephron increases flow and leads to increased Na, K and water excretion. The increased flow also “washes out” the medullary concentration gradient, which further dilutes the urine and perpetuates the diuresis.

39
Q

Low pH, pCO2 and serum bicarbonate are consistent with what?

A

metabolic acidosis

40
Q

Low arterial pH and high arterial pCO2 are consistent with what?

A

respiratory acidosis

41
Q

How do you assess whether a secondary metabolic response to respiratory acidosis is present?

A

Serum bicarbonate levels should rise above normal (24) by 1-3.5 mEq/L for every 10 mmHG rise in PCO2. Acute is the lower end of the scale and chronic would be the upper end of the scale.

42
Q

What is the likely cause of the anion gap in somebody with respiratory acidosis and hypoxemia?

A

lactate

43
Q

Increased arterial pH, serum bicarbonate and pCO2 are most consistent with what?

A

metabolic alkalosis

44
Q

How do you assess whether a secondary respiratory response to metabolic alkalosis is present?

A

For each increase of 1 meq/l in HCO3, the PCO2 should increase by 0.7 mmHg

45
Q

What maintains metabolic alkalosis in a patient that’s been vomiting?

A

Hypovolemia leads to increased proximal reabsorption of bicarbonate and bicarbonate generation in the distal nephron under the influence of increased aldosterone

46
Q

Postural hypotension is associated with what?

A

decreased total body Na and ECF

47
Q

ICF will change in what conditions?

A

greater or lesser tonicity (effective osmolality)

48
Q

Hypokalemia generally presents as a result of what?

A

urinary losses

49
Q

What therapy can lead to prompt reversal of metabolic acidosis?

A

administration of isotonic saline and KCl to correct hypovolemia. excess bicarbonate will be excreted in the urine.

50
Q

How can urine pH be low in a patient with metabolic alkalosis?

A

The pH of the urine falls below 5.5 once the degree of hypovolemia is sufficient to cause reabsorption of all of the filtered bicarbonate in the more proximal segments of the nephron. Hypovolemia also leads to activation of the renin-angiotensin-aldosterone system. Aldosterone causes increased reabsorption of the sodium in the collecting duct via ENaC, generating a negative potential in the lumen. The lumen negative potential stimulates the secretion of both hydrogen and potassium. The secretion of hydrogen in the collecting duct further acidifies the urine and results in equimolar generation of bicarbonate on the basolateral surface of alpha-intercalated cells. Bicarbonate generated at this site is then release into the extracellular fluid, thus exacerbating the alkalosis.

51
Q

What equation do most clinical laboratories use to estimate GFR when GFR

A

* the Modification of Diet and Renal Disease equation * higher levels of GFR are reported as >60 ml/min/1.73 m2

52
Q

What serum measurement can indicate significant changes in GFR?

A

small changes in serum creatinine in the low range

53
Q

When should you use a 24-hour creatinine clearance?

A

with near normal GFR, pregnancy, amputees, severe liver disease, extremes of age and weight Clearance = Ucr * V/Pcr and convert to ml/min (1440 min/day)

54
Q

What is the most accurate way of measuring GFR?

A

radionuclide kidney clearance scanning. the complexity and cost of the test is prohibitive.

55
Q

What 4 steps do you take to analyze fluid and electrolyte disorders?

A

1) Assess ECF status 2) Assess plasma tonicity 3) Evaluate electrolyte abnormalities 4) Evaluate acid-base disturbances

56
Q

Thiazides lead to what?

A

metabolic alkalosis

57
Q

Ethylene glycol poisoning leads to what?

A

increased anion gap metabolic acidosis

58
Q

Heroin overdose leads to what?

A

acute respiratory acidosis

59
Q

Renal tubular acidosis presents with what?

A

normal anion gap metabolic acidosis

60
Q

An anxiety attack leads to what?

A

a simple primary acute respiratory alkalosis

61
Q

How much sodium is equal to about 1 kg of water?

A

140 mEq

62
Q

What laboratory results would be consistent with vomiting?

A

low urine chloride and urine sodium level above 15 mEq/L. A urine potassium:creatinine ratio of 30 would also be consistent with renal potassium wasting that occurs during vomiting.

Renal (14 decks)

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