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Nephrology > Formatives Review > Flashcards

Formatives Review Flashcards

1
Q

What two things happen when the macula densa senses increases in Na+?

A

1) afferent constriction through adenosine

2) decreased renin (don’t want more Na+ absorption)

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2
Q

tubuloglomerular feedback

A

macula densa senses increased Na+ which leads to a decrease in RPF and decrease in GFR

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3
Q

tubuloglomerular feedback effect on K+/H+ secretion

A

tubuloglomerular feedback decreases RAAS

we also know this state has more Na+

this leads to more K/H+ secretion

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4
Q

What happens to glomerular hemodynamics when you constrict the efferent arteriole?

A

Increase pressure of GC which increases GFR

You also decrease RPF

this leads to overall increase in filtration fraction

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5
Q

Filtration fraction formula

A

FF = GFR / RPF

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6
Q

How do you calculate clearance of a substrate?

A

Cx = V * Ux / Px

(make sure you make V in mL / min)

(normally given 24 hr urine volume)

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7
Q

How do you determine ECF? If ECF is elevated, what does this indicate?

A

ECF is determined by physical exam

If ECF is elevated, TBNa and TBW are elevated as well

HOWEVER, you need to check if TBNa has increased more than TBW to determine free water state

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8
Q

What is true if TBNa has increased more than TBW?

A

there is a deficit of free water

normally occurs in hypernatremia

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9
Q

What is true of free water in hyponatremia?

A

there is normally an excess of free water

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10
Q

Do thiazides impair concentration or dilution of urine?

A

they impair urinary dilution

(this can lead to hyponatremia)

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11
Q

Do loop diuretics effect urinary concentration or dilution?

A

they effect both

since they effect both, their effects largely cancel out

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12
Q

How do thiazides increase water reabsorption?

A

prostaglandin-mediated effect in the collecting duct

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13
Q

In a steady state, what is overall true?

A

urinary excretion should equal intake

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14
Q

What is true in the short term (before steady state is reached) of secreted sodium vs. intake sodium in diuretic use?

A

when you first start diuretics, you secrete a little more sodium than you take in

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15
Q

What is true of urine osmolality and urine sodium in SIADH?

A

urine osmolality is high (ADH working)

urine sodium is high

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16
Q

What happens to BP in hyperaldosteronism?

A

BP increases due to the increase in ECF expansion from increased Na/H2O reabsorption

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17
Q

How do you calculate free water deficit?

A

0.6 * weight * (serum Na - 140 / 140)

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18
Q

Does high or low plasma tonicity increase ADH?

A

high plasma tonicity

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19
Q

What is the target rise in PNa in a patient with chronic hyponatremia?

A

4-6 mEq/L increase per 24 hrs

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20
Q

Why do we give Ca2+ if there are EKG changes with hyperkalemia?

A

to stabilize the membrane potential

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21
Q

What do carbonic anhydrase inhibitors do?

A

they prevent reabsorption of HCO3-

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22
Q

How does increased serum bicarb affect potassium?

A

more H+ secreted into blood to stabilize bicarb

this leads to more K+ intracellularly and hypokalemia

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23
Q

What does liver failure result in in regard to BUN?

A

decreased BUN as liver can not produce urea

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24
Q

What marker of GFR isn’t as affected by muscle mass?

A

cystatin C

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25
Q

Effects of NSAIDs on loop diuretics

A

they compete for the same transporter that secretes loops into the lumen

therefore, NSAIDs lead to loop diuretic resistance

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26
Q

Why should you avoid NSAIDs with ACE/ARBs?

A

they can drop the GFR too low

NSAIDs constrict afferent which decreases GFR

ACE/ARBs prevent constriction of efferent which also decreases GFR

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27
Q

What is ACE/ARB effect on potassium levels? How?

A

ACE/ARB also block aldosterone (since they block AG II)

this leads to decreased K+ secretion and hyperkalemia

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28
Q

How do thiazide / loop diuretics cause metabolic alkalosis?

A

increased Na+ delivery to the collecting duct results in increased secretion of H+

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29
Q

What is the only location in nephron that has a brush border?

A

the proximal tubule

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30
Q

What are aquaporin 1 channels?

A

proximal tubule

thin descending limb

*these areas are always permeable to water

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31
Q

What capillaries supply the nephron?

A

vasa recta / peritubular capillaries

these capillaries shoot off the efferent arteriole

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32
Q

What is the thin descending tubule epithelium ?

A

Simple squamous

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33
Q

What is the thick ascending tubule epithelium ?

A

cuboidal epithelium

lots of tight junctions

low water permeability

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34
Q

List the glomerular capillary filtration barrier from inside out:

A

fenestrate capillary endothelium

glomerular basement membrane

podocyte (visceral epithelial cell)

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35
Q

What are proximal tubular cells closely associated with? Why?

A

Closely associated with peritubular capillaries so that reabsorbed solute/water can easily go back into bloodstream

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36
Q

What happens when afferent arteriole is constricted to FF?

A

GFR and RPF both proportionally decrease so there is no change in filtration fraction

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37
Q

What happens to afferent/efferent arterioles in massive fluid loss?

A

afferent dilates and efferent constricts

want to maximize GFR

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38
Q

Myogenic response

A

renal afferent arterioles contract in response to increased stretch (BP)

Ca2+ is released which triggers contraction

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39
Q

Where is ADH released from?

A

posterior pituitary

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40
Q

Hyperaldosterism has what effect on bicarb?

A

more H+ secreted = more bicarb reabsorbed into body

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41
Q

Where is sodium not reabsorbed?

A

descending limb of loop of Henle

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42
Q

2 effects of AG II

A

1) constrict the efferent arteriole to increase GFR

2) increase Na+ reabsorption in proximal tubule

43
Q

What urine finding indicates activation of RAAS?

A

RAAS is activated when urine sodium is low

more sodium reabsorption

44
Q

Which diuretic is associated with hyponatremia?

A

thiazide diuretics

45
Q

What can happen with chronic loop diuretic use? What can you do to help?

A

distal tubule hypertrophy

use a thiazide to help

46
Q

If someone has CKD, should you increase or decrease dose of CKD?

A

increase dose of CKD

less drug is going to reach target site since RPF is decreased

47
Q

What happens to risk of hyperkalemia as CKD progresses?

A

risk goes up as GFR decreases

48
Q

Difference in calcium excretion between thiazide and loop diuretics

A

loop: prevent calcium reabsoprtion which leads to serum hypocalemia

thiazide: increase calcium reabsorption at proximal tubule which leads to serum hypercalcemia (good for kidney stones)

49
Q

Carbonic anhydrase inhibitors effects on potassium

A

increased bicarb leads to increased Na+ secretion

more Na+ reaching distal tubule which results in increased K+ secretion

therefore, carbonic anhydrase inhibitors can cause hypokalemia

50
Q

What is an example of a carbonic anhydrase inhibitor?

A

Acetazolamide

51
Q

Carbonic anhydrase acid-base effects

A

leads to metabolic acidosis due to decreased HCO3- reabsoption

52
Q

What does low urine sodium tell you?

A

RAAS is activated which is leading to increased Na+ reabsorption

this also means that EACV is low since RAAS is activated

53
Q

What is a common fluid states in CHF / cirrhosis?

A

ECV is high

BUT EACV is low

water is in the wrong, interstitial spaces

54
Q

What does hypertonic saline infusion do to RAAS?

A

decrease RAAS since you don’t need more sodium

55
Q

How do diuretics work in theory?

A

increased secretion of Na+ which water follows and decreases ECF

56
Q

What happens to ICF and ECF with hypotonic solution?

A

both volume increase

some ECF water moves intracellularly

57
Q

What happens to ICF if isotonic solution is given?

A

there is no change

no water movement

58
Q

If isotonic solution is given, does this affect ADH? How about RAAS?

A

no

ADH mostly responds to changes in osmolarity

RAAS will decrease since you have more EACV

59
Q

What does hypertonic solution do to ADH?

A

increases ADH secretion

want to keep free water to balance the increase in solute

60
Q

What does high urine osmolality indicate? What does high urine sodium indicate?

A

High urine osmolality = ADH active (stopping excretion of water)

High urine sodium = RAAS active (water is being reabsorbed)

61
Q

How do we define hyponatremia with lab values?

A

PNa < 135 mEq/L

62
Q

What drugs can often cause SIADH?

A

SSRIs

63
Q

When do you worry about hyponatremia?

A

When PaNa < 125

this will lead to intracranial swelling and CNS symptoms

64
Q

When do we worry about osmotic demyelination syndrome?

A

when correcting hyponatremia too quickly

65
Q

What 4 medications can you use to treat hyperkalemia?

A

albuterol

insulin / glucose

bicarbonate

potassium binding resins

66
Q

Why do we use urea to treat SIADH?

A

urea acts as an osmotic diuretic and will increase water secretion

67
Q

Why do we use vaptans to treat SIADH? What is one of their downsides?

A

block V2 receptors for ADH

*they are expensive and hepatotoxic

68
Q

Do you use loops or thiazides with SIADH?

A

loops

69
Q

What 2 factors does ADH effect?

A

1) water reabsorption

2) urea reabsorption

the water follows the urea

70
Q

Does hypokalemia or hyperkalemia cause a decreased response to ADH?

A

hypokalemia

71
Q

What can raise BUN?

A

high protein intake

bleeding

glucocorticoids

72
Q

What approximates GFR? What approximates RPF?

A

Inulin approximates GFR

PAH approximates RPF

73
Q

What does bicarbonuria do to potassium secretion?

A

increases potassium secretion at the collecting duct

74
Q

Higher urine concentration = *** urine osmolarity

A

higher urine osmolarity

75
Q

In what setting are osmotic diuretics, such as mannitol, commonly prescribed?

A

intracranial pressure

76
Q

How do osmotic diuretics work?

A

work in PCT to create hyperosmolar urine

hyperosmolar urine leads to increased water secretion

77
Q

What is another name for DCT? Why?

A

diluting tubule

no aquaporin to move water

dilute through pulling solutes out!

78
Q

What does membranous nephropathy show on light microscopy?

A

spike and dome pattern

(train-tracking)

79
Q

Why does ADH constrict vessels through V1?

A

in states of low volume and shock, you want to constrict to raise BP

80
Q

What type of antibiotics can cause AKI? What is associated with this class of drugs?

A

aminoglycosides

hearing loss

81
Q

What is a sign of rhabdomyalysis in urine?

A

positive dipstick but negative for RBCs

this indicates that myoglobin is present

82
Q

What drug can cause rhabdomyalysis?

A

statins

83
Q

If you have a high anion gap with normal pH, what do you know is present?

A

know that metabolic acidosis is present

need to look for a mixed alkalosis to balance pH

84
Q

Where does IgA nephropathy deposit?

A

mesangium

85
Q

If an XR does not show a kidney stone, but patient has signs of kidney stone, what is most likely diagnosis?

A

uric acid stones

they are radiolucent

85
Q

What are signs of uremia which indicate you may need to start dialysis?

A

pericardial friction rub

asterixis

somnolence / alteration of consciousness slower

uremic fetor (ammonia breath)

also: malnourished, brusing, etc.

86
Q

How can you determine ATN vs. prerenal azotemia?

A

prerenal has an elevated BUN ratio and normally signs of hypoperfusion (low BP)

ATN has a normal BUN

87
Q

What are the stages of aspirin overdose?

A

early: respiratory alkalosis

late: mixed disorder (respiratory alkalosis with metabolic acidosis)

88
Q

Where does PTH facilitate Na-Ca2+ exchange / calcium reabsorption?

A

in the DCT

89
Q

If you are volume overloaded, what is true of TBNa?

A

increased

90
Q

If aldo is high, what is true of renin?

A

if aldo is high, renin is low

negative feedback loop

91
Q

When more H+ is secreted through collecting duct, what happens to serum bicarb?

A

serum bicarb levels increase

92
Q

What hormones affect sodium reabsorption in the proximal tubule?

A

Angiotensin 2 will increase sodium reabsorption by increasing the activity of Na-K-ATPase and NHE

ANP and Dopamine will decrease sodium reabsorption by decreasing Na-K-ATPase activity

93
Q

What effect does increased serum potassium have on sodium reabsorption in the DCT?

A

increased serum K+ decreases the action of the Na-Cl transporter

decreases Na reabsorption (almost acts as a mild diuretic)

94
Q

How in general does ANP work?

A

decreases activity of Na/K ATPase which then decreases sodium reabsorption

leads to increased secretion of Na+ and H2O

95
Q

Where are ROMK channels

A

thick ascending tubule (backflow)

principal cells

96
Q

Where are BK channels

A

principle and intercalated cells

97
Q

What 2 factors prevent concentration gradient from being washed out by plasma?

A

low medulla blood flow

blood flow in the hairpin shape which matches

98
Q

Where is carbonic anhydrase found besides the PCT?

A

found in intercalated cells

works to breakdown H2Co2 to drive the H+ ATPase on intercalated cells (produces a HCO3- molecule)

99
Q

What 2 values are associated with pre-renal azotemia?

A

increased BUN: Cr ratio

decreased BP (lack of perfusion)

100
Q

If a patient has proteinuria but normal serum albumin what does this indicate?

A

this is NOT a glomerular disease!

(could be a tubular or interstitial disease)

101
Q

When do you use winter’s formula?

A

in metabolic acidosis

will tell you if their is appropriate CO2 response

(just because CO2 went down it might not have went down the appropriate amount)

102
Q
A

Nephrology (6 decks)

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