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(Other) Qbank > Renal > Flashcards

Renal Flashcards

1
Q

How is plasm volume measured?

A

Radiolabeling albumin

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2
Q

How is extracellular volume measured?

A

Inulin or mannitol

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3
Q

Patient with Addison’s disease experiences what kind of volume shift?

A

Hypoosmotic volume contraction

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4
Q

What cells synthesize renin? Where are they located?

A

Juxtaglomerular smooth muscle cells contained in the afferent arteriole

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5
Q

How are RBCs prevented from filtration in the glomerulus?

A

Fenestrated capillaries

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6
Q

What is the equation for renal clearance?

A

Clearance of substance X = (urine concentration of X * urine flow rate)/plasma concentration of X

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7
Q

If clearance of substance is less than GFR, what does this mean?

A

Net tubular reabsorption of substance

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8
Q

If clearance of a substance is greater than GFR, what does this mean?

A

Net tubular secretion of substance X

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9
Q

What is renal clearance?

A

Volume of plasm cleared of a substance per unit of time

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10
Q

Inulin can be used to measure what?

A

GFR or extracellular volume

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11
Q

How is effective renal plasma flow estimated?

A

Para-aminohippuric acid clearance

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12
Q

How is renal blood flow calculated?

A

Renal plasma flow / (1-Hct)

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13
Q

What affect does probenecid have on penicillin?

A

It increases the half life of penicillin by inhibiting penicillin secretion in the proximal tubule via blocking the PAH transporter

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14
Q

Penicillin is secreted in the kidney by what transporter? Where?

A

Para-aminohippuric acid transporter in proximal tubule

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15
Q

What is the equation for calculating filtration fraction?

A

GFR/RPF

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16
Q

What is a normal filtration fraction?

A

20%

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17
Q

How do you calculate the filtered load?

A

GFR x plasma concentration

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18
Q

How is renal plasma flow estimated?

A

Para-aminohippuric acid

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19
Q

With an increased filtration fraction, what happens to protein concentration in peritubular capillary blood? What affect does this have on the nephron?

A

Increased protein concentration in peritubular capillary blood; which leads to increased reabsorption of water in the proximal tubule

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20
Q

What affects does decreased filtration fraction have on peritubular capillaries and the nephron?

A

Decreased protein concentration in the peritubular capillaries and decreased reabsorption of water in the proximal tubule

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21
Q

In dehydration what happens to GFR, RPF, and FF?

A

Decrease in GFR, large decrease in RPF, and therefore increase in filtration fraction

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22
Q

What affects do prostaglandins have on afferent arteriole? NSAIDs?

A

Vasodilate; NSAIDs cause vasoconstriction, could result in decreased GFR and therefore ischemia to kidney

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23
Q

How is the excretion rate calculated?

A

Urine flow rate x urine concentration of substance

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24
Q

What is the reabsorption rate?

A

Filtered - excreted

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25
Q

What is secretion rate?

A

Excreted - filtered

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26
Q

What is the equation for FENa?

A

(Plasma creatinine x Urine Na) / (Urine creatinine x Plasma Na)

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27
Q

What is seen on light microscopy from a section of the proximal convoluted tubule?

A

Simple cuboidal epithelium with brush border

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28
Q

What is seen on light microscopy from a section of the distal convoluted tubule?

A

Simple cuboidal epithelium with NO brush border

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29
Q

What type of epithelium is seen in the thin descending loop of Henle?

A

Simple squamous

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30
Q

What region of the nephron does PTH act to increase calcium reabsorption?

A

DCT

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31
Q

Where does PTH act in the kidney? What does it do?

A

Proximal to increase phosphate excretion and DCT to increase calcium reabsorption

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32
Q

What is Winter’s formula?

A

Pco2 = 1.5 [HCO3-] + 8 +/- 2

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33
Q

What is winters formula used for?

A

In simple metabolic acidosis, it can be used to calculate predicted resp compensation

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34
Q

If measured Pco2 is greater than the predicted Pco2 from winters formula, what is going on?

A

Concomitant respiratory acidosis

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35
Q

If measured PCO2 is less than predicted PCO2, what is going on?

A

Concomitant respiratory alkalosis

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36
Q

What drugs/nephrotoxins can cause Fanconi syndrome?

A

Ifosfamide, cisplatin, tenofovir, expired tetracyclines, lead poisoning

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37
Q

Expired tetracyclines can cause what syndrome?

A

Fanconi syndrome?

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38
Q

What is fanconi syndrome?

A

Generalized defect in reabsorption in PCT; cannot reabsorb glucose, aa, HCO3, and PO4

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39
Q

Fanconi syndrome can result in what acid/base disorder?

A

Metabolic acidosis - proximal tubular acidosis

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40
Q

Barter syndrome is a defect in what transporter?

A

NKCC2

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41
Q

What part of the renal tubule is affected by Bartter syndrome?

A

Thick ascending limb

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42
Q

What is the inheritance pattern of Bartter syndrome?

A

Autosome recessive

43
Q

How does bartter syndrome present?

A

Hypokalemia, metabolic alkalosis with hypercalciuria; similar to chronic loop diuretic use

44
Q

What is the inheritance pattern of Gitelman syndrome?

A

AR

45
Q

What transporter is affected by Gitelman syndrome?

A

NaCl channel in DCT

46
Q

What labs are seen in Gitelman syndrome?

A

Hypocalciuria hypomagnesemia, hypokalemia, metabolic alkalosis

47
Q

What is the inheritance pattern of Liddle syndrome?

A

AD

48
Q

What transporter/channel is affected by Liddle syndrome?

A

ENaC channel

49
Q

Liddle syndrome results in what types of labs?

A

Increased Na reabsorption - resulting in HTN; hypokalemia, metabolic alkalosis, decreased aldosterone

50
Q

What enzyme is defective in syndrome of apparent mineralocorticoid excess?

A

11 beta hydroxysteroid dehydrogenase

51
Q

What is the mechanism of the enzyme 11 beta hydroxysteroid dehydrogenase?

A

Converts cortisol (active) to cortisone (inactive)

52
Q

How does syndrome of apparent mineralocorticoid present?

A

Hypertension, hyperkalemia, metabolic alkalosis; low serum aldosterone levels

53
Q

What disorder can be acquired from glycyrrhetinic acid?

A

Syndrome of apparent mineralocorticoid excess

54
Q

Where is ACE made?

A

Kidney and lungs

55
Q

What affect does AGII have on the posterior pituitary?

A

Increases release of ADH

56
Q

What is the mechanism by which ANP vasodilates?

A

Increases cGMP, relaxing the vascular smooth muscle

57
Q

What affect does ANP have on renin and aldosterone?

A

Reduces secretion of both renin and aldosterone

58
Q

What is nesiritide?

A

Recombinant BNP; used for treatment of heart failure

59
Q

What affect does ANP and BNP have on sodium?

A

Increases its filtration without increasing reabsorption; net effect is loss of both Na and water

60
Q

What increases the secretion of renin?

A

Low Na sensed by macula densa, low BP sensed by JG cells, and sympathetics acting on beta1 receptors

61
Q

What does the macula densa do?

A

Senses NaCl; if low - it promotes the secretion of renin from the JG cells

62
Q

Angiotensin II constricts what vasculature?

A

Efferent arteriole

63
Q

Where in the kidney is dopamine secreted from?

A

PCT cells

64
Q

What affect does dopamine have on the kidney?

A

Promotes natriuresis; low doses promotes vasodilation; high doses promotes vasoconstriction

65
Q

What is fenoldopam?

A

Dopamine receptor agonist - used in hypertensive emergencies

66
Q

How is Epo regulated in the kidney?

A

Low oxygen states, HIF1alpha is not hydroxylated, and therefore is not degraded, resulting in transcription of erythropoietin

67
Q

Where in the kidney is 1,25-OH D3 formed?

A

PCT

68
Q

What is the action of 1alpha-hydroxylase?

A

Converts 25-OH D3 to 1,25-OH D3

69
Q

What is ANP, BNP’s effect on the afferent and efferent arteriole?

A

Constricts efferent arteriole while vasodilating the afferent arteriole, resulting in increased GFR

70
Q

When is PTH secreted?

A

Decreased serum calcium, increased plasm PO4, or decreased plasm 1,25-OH D3

71
Q

When is aldosterone secreted?

A

Decreased blood volume (in response to AGII) and increased serum K+

72
Q

Patient with high serum digitalis presents to the ER. What will you see on EKG? Why?

A

Peaked T waves and wide QRS due to hyperkalemia

73
Q

Patient used way too much of his beta-adrenergic agonist. What effect does this have on K+? What will you likely see on ECG?

A

Results in hypokalemia (shifts K into cells); U waves and flattened T wave on ECG

74
Q

What affect does low serum calcium have on the ECG?

A

QT prolongation

75
Q

What are signs and symptoms of low serum calcium?

A

Prolonged QT interval on ECG, tetany, Chvostek sign (twitching), spasm (Trousseau sign)

76
Q

Patient presents with increased urine frequency, abdominal pain, back pain and anxiety. Additionally, patient states she think she passed a renal stone. What is the likely cause?

A

Hypercalcemia

77
Q

What are signs and symptoms of high serum calcium?

A

Abdominal pain, bone pain, renal stones, increased urine frequency, anxiety/altered mental status

78
Q

What is seen on ECG in low serum magnesium states?

A

Torsades de pointes

79
Q

What additional lab findings do you see with low serum magnesium?

A

Low serum calcium, low serum potassium

80
Q

What are the signs and symptoms of hypermagnesemia?

A

Low DTR, lethargy, bradycardia, hypotension, cardiac arrest, hypocalemia

81
Q

What are the signs of increased PO4 in serum?

A

Renal stones, metastatic calcifications, hypocalcemia

82
Q

What are the results of low serum PO4?

A

Bone loss, osteomalacia (adults) and rickets (children)

83
Q

What is Conn syndrome?

A

Primary hyperaldosteronism

84
Q

What affect does salicylates have on acid/base status?

A

Early - respiratory alkalosis; late - anion gap metabolic acidosis

85
Q

What does HARDASS stand for in acid/base status?

A

Non-anion gap metabolic acidosis; hyperalimentation, addison disease, RTA, diarrhea, acetazolamide, spironolactone, saline infusion

86
Q

What is type I RTA?

A

Distal renal tubular acidosis - defect in ability of alpha intercalated cells to secrete H+ and therefore no new HCO3 production, resulting in metabolic acidosis

87
Q

How does renal tubular acidosis present?

A

Symptoms of volume depletion; normal anion gap (hyperchloremic) metabolic acidosis

88
Q

What drugs cause distal renal tubular acidosis?

A

(Type I); amphotericin B and lithium

89
Q

What is the urine pH in distal renal tubular acidosis?

A

> 5.5 (because distal tubule is unable to secrete fixed acid)

90
Q

Other than drugs, what else can cause distal renal tubular acidosis?

A

Congenital - obstruction; autoimmune (Sjogrens), analgesic nephropathy, sickle cell anemia

91
Q

What drugs cause proximal renal tubular acidosis?

A

(Type 2) - acetazolamide and aminoglycosides

92
Q

What is proximal renal tubular acidosis?

A

Defect in PCT HCO3 reabsorption

93
Q

What is the urine pH in proximal renal tubular acidosis?

A

<5.5

94
Q

Distal renal tubular acidosis is associated what electrolyte imbalance?

A

Hypokalemia

95
Q

Distal renal tubular acidosis results in increased risk for what?

A

Calcium phosphate kidney stones

96
Q

Proximal renal tubular acidosis is associated with what electrolyte imbalance?

A

Hypokalemia

97
Q

Proximal renal tubular acidosis increases risk for what?

A

Hypophosphatemic rickets

98
Q

What is a distinguishing feature of type 4 RTA?

A

Hyperkalemia (both type I and type II have hypokalemia)

99
Q

What is the cause of type 4 RTA?

A

Hyperkalemic states - hypoaldosteronism, aldosterone resistance, K+ sparing diuretics, ACE inhibitors and ARBs are examples

100
Q

What drugs can cause type 4 RTA?

A

Spironolactone, ACEi, ARBs

101
Q

What serotypes of S pyogenes cause PSGN?

A

M12, M4, M1

102
Q

PSGN is what type of HSR?

A

Type III

103
Q

Goodpasture syndrome results in rapidly progressive glomerulonephritis. What type of HSR is this?

A

Type II

(Other) Qbank (33 decks)

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