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Step 1 Decks > Renal > Flashcards

Renal Flashcards

1
Q

Is the vast majority of potassium in the intracellular or extracellular space?

A

HIKIN’: HIgh K+ INtracellularly

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2
Q

The 60–40–20 rule refers to ——— for average person):
- 60% of body mass is ——— (while 40% of body mass is ———)

A
  • % of body weight
  • total body water (TBW)
  • non water mass (NWM)
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3
Q

The 60–40–20 rule refers to ——— for average person):
- 40% ———, mainly composed of what 3 things: ———

A
  • % of body weight
  • ICF (I.e., ICF 2/3 of total body water)
  • K+, Mg2+, organic phosphates (eg, ATP) ƒ
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4
Q

The 60–40–20 rule refers to ——— for average person):
- 20% ———, mainly composed of what 4 things:

A
  • % of body weight
  • ECF (I.e., ECF 1/3 of total body water)
  • Na+, Cl–, HCO3 –, albumin
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5
Q

ECF is made up of ———% plasma and ———% interstitial fluid

A
  • 25
  • 75
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6
Q

Plasma volume can be measured by:

A

radiolabeling albumin

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7
Q

Extracellular volume can be measured by:

A

inulin or mannitol

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8
Q

In Fanconi syndrome there is a ———defect in the ———, leading to decreased excretion of:

A
  • generalized reabsorption
  • PCT
  • amino acids, glucose, HCO3 –, and PO4 3–, and all substances reabsorbed by the PCT
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9
Q

List 3 key findings in Fanconi syndrome:

A
  • metabolic acidosis (proximal RTA)
  • hypophosphatemia
  • hypokalemia (most K+ reabsorbed at PCT)
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10
Q

List 4 causes of Fanconi syndrome:

A
  • Hereditary defects (eg, Wilson disease, tyrosinemia, glycogen storage disease)
  • ischemia
  • multiple myeloma
  • drugs (eg, ifosfamide, cisplatin, tenofovir, lead poisoning)
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11
Q

List 2 common associated findings in Franconia syndrome:

A
  • Growth retardation and rickets/osteopenia common due to hypophosphatemia
  • Volume depletion also common
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12
Q

Bartter syndrome is a reabsorption defect in ——— (affects ———transporter)

A
  • thick ascending loop of Henle
  • Na+/K+/2Cl– cotransporter
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13
Q

List 3 key findings in Bartter syndrome:

A
  • Metabolic alkalosis
  • hypokalemia
  • hypercalciuria
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14
Q

Mode of inheritance for Bartter syndrome:

A

Autosomal recessive

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15
Q

Bartter syndrome presents similarly to chronic ——— use

A

loop diuretic

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16
Q

Gitelman syndrome is a reabsorption defect of ——— in ———

A
  • NaCl
  • DCT
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17
Q

List 4 key findings in Gitelman syndrome:

A
  • Metabolic alkalosis
  • hypomagnesemia
  • hypokalemia
  • hypocalciuria
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18
Q

Mode of inheritance in Gitelman syndrome:

A

Autosomal recessive

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19
Q

Gitelman syndrome presents similarly to chronic ——— use

A

thiazide diuretic

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20
Q

Which is more severe Gitelman syndrome or Bartter syndrome?

A

Gitelman syndrome less severe than Bartter syndrome

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21
Q

Liddle syndrome refers to a ——— mutation leading to decreased ——— Žand increased ——— in ———

A
  • gain of function
  • Na+ channel degradation
  • Na+ reabsorption
  • collecting tubules
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22
Q

List 4 key findings in Liddle syndrome:

A
  • Metabolic alkalosis
  • hypokalemia
  • hypertension
  • decreased aldosterone
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23
Q

Mode of inheritance in Liddle syndrome:

A

Autosomal dominant

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24
Q

Liddle syndrome presents similarly to ———, but ——— is nearly undetectable

A
  • hyperaldosteronism
  • aldosterone
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25
Q

List 1 treatment for Liddle syndrome:

A

amiloride

26
Q

Normally, cortisol activates mineralocorticoid receptors, and enzyme ——— converts cortisol to ——— (inactive on these receptors); Hereditary deficiency Žof this enzyme (resulting in: ——— disease) leads to increased ———, and thus increased ——— activity

A
  • 11β-HSD (11β-hydroxysteroid dehydrogenase)
  • cortisone
  • SAME (Syndrome of Apparent Mineralocorticoid Excess)
  • cortisol
  • mineralocorticoid receptor
27
Q

List 4 key effect of SAME (Syndrome of Apparent Mineralocorticoid Excess):

A
  • Metabolic alkalosis
  • hypokalemia
  • hypertension 
  • decreased serum aldosterone level

(cortisol tries to be the SAME as aldosterone)

28
Q

Mode of inheritance for SAME is ———; also, can acquire SAME from ——— (present in ———), which blocks activity of ———

A
  • Autosomal recessive
  • glycyrrhetinic acid
  • licorice
  • 11β-hydroxysteroid dehydrogenase
29
Q

Treatment of SAME include:

  • ——— diuretics (decrease ——— effects)
  • ——— (exogenous ——— will decrease endogenous ———, and thus decrease ——— activation)
A
  • K+-sparing
  • mineralocorticoid
  • corticosteroids
  • corticosteroid
  • cortisol production
  • mineralocorticoid receptor
30
Q

Metabolic acid-base disorders cause ——— alterations; Respiratory acid-base disorders cause ——— alterations

A
  • HCO3 –
  • PCO2
31
Q

Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in metabolic acidosis:

A

pH: decreased

pCO2: decreased (compensatory)

HCO3–: decreased

Compensatory response: hypERventilation (immediate)

32
Q

Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in metabolic alkalosis:

A

pH: increased

pCO2: increased (compensatory)

HCO3–: increased

Compensatory response: hypOventilation (immediate)

33
Q

Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in repiratory acidosis:

A

pH: decreased

pCO2: increased

HCO3–: increased (compensatory)

Compensatory response: increased renal [HCO3 –] reabsorption (delayed)

34
Q

Describe the pH, pCO2, HCO3–, and compensatory response (and it’s speed) in respiratory alkalosis:

A

pH: increased

pCO2: decreased

HCO3–: decreased (compensatory)

Compensatory response: decreased renal [HCO3 –] reabsorption (delayed)

35
Q

Winters formula calculates the ——-; If measured Pco2 > predicted Pco2, there is ———; if measured Pco2 < predicted Pco2, there is ———

A
  • Predicted respiratory compensation for a simple metabolic acidosis
  • concomitant respiratory acidosis
  • concomitant respiratory alkalosis
36
Q

Acidemia is defined as pH of ———, and Alkalemia is defined as pH of ———

A

pH < 7.35

pH > 7.45

37
Q

Respiratory acidosis is caused by ———; list 5 specific causes:

A
  • Hypoventilation
  • Airway obstruction
    Acute lung disease
    Chronic lung disease
    Opioids, sedatives
    Weakening of respiratory muscles
38
Q

In order to asses the cause of metabolic acidosis, check the ———, which is:

A

Anion gap

= Na + – ((CI–) + (HCO3-))

39
Q

List 7 causes of metabolic acidosis with normal anion gap (which is ———): by

A

8-12 mEq/L

HARDASS:
Hyperchloremia/hyperalimentation
Addison disease
Renal tubular acidosis
Diarrhea
Acetazolamide
Spironolactone
Saline infusion

40
Q

List 8 causes of metabolic acidosis with increased anion gap (which is ———):

A

> 12 mEq/L

GOLDMARK:
Glycols (ethylene glycol, propylene glycol)
Oxoproline (chronic acetaminophen use)
L-lactate (lactic acidosis)
D-lactate (exogenous lactic acid) Methanol (and other alcohols)
Aspirin (late effect)
Renal failure
Ketones (diabetic, alcoholic, starvation)

41
Q

Respiratory alkalosis is caused by ———; list 6 specific causes:

A
  • hyperventilation
  • Anxiety/panic attack
    Hypoxemia (eg, high altitude) Salicylates (early)
    Tumor
    Pulmonary embolism
    Pregnancy
42
Q

In order to asses the cause of metabolic alkalosis , check the ——— in order to asses if ———

A

Check urine Cl–

Saline-resistant or Saline-responsive

43
Q

List 4 causes of Saline-resistant metabolic alkalosis:

A

Hyperaldosteronism

Bartter syndrome

Gitelman syndrome

Current loop/thiazide diuretics

44
Q

List 3 causes of Saline-responsive metabolic alkalosis:

A

Vomiting

Recent loop/thiazide diuretics

Antacids

45
Q

Presence of casts in the urine indicates that hematuria/pyuria is of ——— origin

A

glomerular or renal tubular

46
Q

In terms of nomenclature of glomerular disorders, define and give an example of Focal:

A

< 50% of glomeruli are involved

Focal segmental glomerulosclerosis

47
Q

In terms of nomenclature of glomerular disorders, define and give an example of Diffuse:

A

> 50% of glomeruli are involved

Diffuse proliferative glomerulonephritis

48
Q

In terms of nomenclature of glomerular disorders, define and give an example of Proliferative:

A

Hypercellular glomeruli

Membranoproliferative glomerulonephritis

49
Q

In terms of nomenclature of glomerular disorders, define and give an example of Membranous:

A

Thickening of glomerular basement membrane (GBM)

Membranous nephropathy

50
Q

In terms of nomenclature of glomerular disorders, define and give an example of Primary glomerular disease:

A

1° disease of the kidney specifically impacting the glomeruli

Minimal change disease

51
Q

In terms of nomenclature of glomerular disorders, define and give an example of Secondary glomerular disease:

A

Systemic disease or disease of another organ system that also impacts the glomeruli

SLE, diabetic nephropathy

52
Q

List the 4 key processes underlying Nephritic syndrome:

A

Glomerular inflammation, leading to

GBM damage, Žleading to

loss of RBCs into urine, leading to

dysmorphic RBCs and hematuria

53
Q

List the 5 key clinical presentations of Nephritic syndrome:

A

Hematuria

RBC casts in urine 

Decreased GFR Žwith oliguria and azotemia

Increased renin release leading to HTN

Proteinuria often in the subnephrotic range (< 3.5 g/day) but in severe cases may be in nephrotic range

54
Q

List the 5 key examples of Nephritic syndrome:

A

ƒ Infection-associated glomerulonephritis

Goodpasture syndrome ƒ

IgA nephropathy (Berger disease) ƒ

Alport syndrome ƒ

Membranoproliferative glomerulonephritis

55
Q

List the 3 key processes underlying Nephrotic syndrome:

A

Podocyte damage, leading to

impaired charge barrier, leading to

proteinuria

56
Q

List 4 key clinical presentations of Nephrotic syndrome:

A

Massive proteinuria (> 3.5 g/day) with edema, hypoalbuminemia leading to hepatic lipogenesis leading to hypercholesterolemia

Frothy urine with fatty casts

Associated with hypercoagulable state due to antithrombin III loss in urine

Increased risk of infection (loss of IgGs in urine and soft tissue compromise by edema)

57
Q

List the 5 key examples of Nephrotic syndrome; and list if 1° (eg, direct podocyte damage) or 2° (podocyte damage from systemic process):

A

Focal segmental glomerulosclerosis (1° or 2°) ƒ

Minimal change disease (1° or 2°) ƒ

Membranous nephropathy (1° or 2°) ƒ

Amyloidosis (2°) ƒ

Diabetic glomerulonephropathy (2°)

58
Q

List the 3 key processes underlying Nephritic-nephrotic syndrome:

A

Severe GBM damage, Žleading to

loss of RBCs into urine + impaired charge barrier, leading to

hematuria + proteinuria

59
Q

List 2 key clinical presentations of Nephritic-nephrotic syndrome:

A

Nephrotic-range proteinuria (> 3.5 g/day) and concomitant features of nephritic syndrome

60
Q

Nephritic-nephrotic syndrome can occur with any form of ——— syndrome, but is most common with: (list 2)

A

nephritic

Diffuse proliferative glomerulonephritis ƒ

Membranoproliferative glomerulonephritis

Step 1 Decks (8 decks)

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