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Nephrology > Week 1 > Flashcards

Week 1 Flashcards

1
Q

Where are aquaporin 1 channels?

A

Proximal tubule

thin descending limb of loop of Henle

aquaporins allow for reabsorption of water

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2
Q

Where does nephron first become impermeable to water?

A

ascending thin limb of loop of Henle

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3
Q

Is the DCT permeable to water?

A

no

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4
Q

Is the collecting tubule permeable to water?

A

only if ADH is present

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5
Q

Where do efferent arteries flow into?

A

vasa recta / peritubular capillaries

these capillaries supply the nephron

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6
Q

What is only part of nephron with brush border?

A

proximal tubule

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7
Q

What is the thin descending tubule epithelium ?

A

simple squamous, no microvilli

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8
Q

What is the thick ascending tubule epithelium ?

A

cuboidal epithelium

lots of tight junctions

low water permeability

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9
Q

What structure of nephron has no villi?

A

distal convolute tubule

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10
Q

What are 2 types of epithelia cells in collecting tubule?

A

principle cells (few microvilli)

intercalated cells (no cilia! surface micoplicae)

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11
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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12
Q

When are the peritubular capillaries called a vasa recta?

A

in a juxtamedullarly glomerulus

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13
Q

juxtamedullarly glomerulus

A

located deep within the cortex

loop of henle dips into the medulla

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14
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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15
Q

Is reabsorption of solute in proximal tubule active or passive?

A

mostly active

Na/K/ATPase pump

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16
Q

What happens when afferent arteriole is constricted?

A

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

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17
Q

What happens when efferent arteriole is constricted?

A

GFR stays the same

RPF decreases

increased filtration fraction (GFR/RPF)

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18
Q

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

A

afferent arteriole dilates and efferent arteriole constricts

want to maximize RPF/GFR

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19
Q

Myogenic response

A

responding to BP / stretch

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20
Q

When is RAAS activated?

A

in period of massive volume loss

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21
Q

What does RAAS do to arterioles in volume loss?

A

AT2 causes efferent arteriolar constriction

afferent arteriole doesn’t constrict due to counteracting prostaglandin influence

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22
Q

Increase NaCl causes macula densa to do what?

A

vasoconstrict afferent arteriole

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23
Q

What is tubuloglomerular feedback?

A

macula densa sensing NaCl

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24
Q

When are prostaglandins more important?

A

severe volume depletion

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25
Q

Where is ADH released from?

A

the pituitary gland

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26
Q

What is primary effect of ADH?

A

decreased water secretion

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27
Q

How much Na+ do we secrete daily?

A

0.4%

most Na+ is reabsorbed

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28
Q

Where does ENAC work?

A

principal cells of collecting duct

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29
Q

What does sodium reabsorption from ENaC cause?

A

negative potential that leads to secretion of potassium and hydrogen ions (from intercalated cells)

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30
Q

What happens to bicarbonate with excess aldosterone production?

A

increased H+ ion secretion leads to more bicarbonate being added to body

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31
Q

Where does aldosterone primarily act?

A

principal cells of collecting duct

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32
Q

When does ANP release increase?

A

if there is an increase in extracellular fluid volume

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33
Q

Where is 2/3 of sodium reabsorbed?

A

proximal tubule

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34
Q

Where is sodium not reabsorbed?

A

descending thin limb of loop of Henle

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35
Q

Where does ADH regulate water reabsorption?

A

the collecting tubule

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36
Q

Where is water flow passive?

A

in the proximal tubule

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37
Q

What is the main release factor for ADH?

A

plasma osmolarity

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38
Q

How do physicians assess extracellular fluid?

A

physical examination

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39
Q

How do physicians assess effective arterial circulating volume? When is this not helpful?

A

urine studies

not in CHF and cirrhosis

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40
Q

What is a good proxy for total body sodium?

A

Extracellular fluid volume (physical examination)

since sodium is tightly regulated, any increase in sodium will have increase in TBW

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41
Q

Angiotensin II effects

A

constricts both efferent and afferent arteriole

afferent arteriole constriction is counteracted by prostaglandins

efferent arteriole will therefore constrict more

angiotensin ALSO increases sodium reabsorption in the proximal tubule

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42
Q

What indicates activation of RAAS?

A

low urine sodium due to more sodium reabsorption due to activation of RAAS

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43
Q

What 2 conditions trigger ADH release?

A

1) reduced effective arterial volume

2) increased plasma osmolarity

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44
Q

Which diuretic commonly causes hyponatremia? Why?

A

thiazide diuretics

normal medullary osmotics that allows you to reabsorb lots of water without reabsorbing salt

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45
Q

Where do thiazide diuretics work?

A

Na-Cl cotransporter in DCT

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46
Q

When can loop diuretics cause hyponatremia?

A

if the patient is volume depleted

this will lead to high ADH levels being secreted and hyponatremia

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47
Q

What can happen with chronic loop diuretic use? What do you do about this?

A

distal tubule hypertrophy

use a thiazide to help

48
Q

What does blocking aldosterone do?

A

aldosterone normally secretes K+/H+ and reabsorbs Na+

by blocking aldosterone, you decrease Na+ reabsorption and K+ secretion

49
Q

What do you need to adjust for in CKD with diuretics?

A

in CKD, less blood is flowing through nephron

therefore, less drug will reach target site

need to increase the threshold dose of a drug

50
Q

What happens to risk of hyperkalemia as CKD progresses?

A

risk goes up as GFR decreases

51
Q

How can loop and thiazide diuretics cause hypokalemia?

A

there is increased Na+ flow to distal DCT due to blocking Na+ reabsorption downstream

this leads to increased ENaC reabsorption of Na+ which correspondingly pushes K+ out through ROMK channels

this will lead to more K+ excretion and hypokalemia

52
Q

How do K+ sparing diuretics actually spare potassium?

A

since they work on the ENaC channels they prevent excretion of K+ through ROMK channels and spare K+

53
Q

Diabetes insipidus

A

low ADH release leads to low volume

have dilute urine since you aren’t retaining as much water (ADH not working)

54
Q

Effects of bicarbonaturia on K+ secretion

A

Increased bicarb = increased K+ secretion

55
Q

What 2 channels secrete potassium

A

ROMK

Maxi-K

55
Q

Why do loop diuretics cause hypocalcemia?

A

by blocking Na-K-2Cl channels they prevent creation of positive gradient that normally drives calcium reabsorption

55
Q

How can carbonic anhydrase inhibitors cause increased potassium secretion?

A

carbonic anhydrase inhibitors can cause bicarbonaturia

56
Q

Where is ADH produced and secreted from?

A

produced from anterior hypothalamus

secreted from pituitary

57
Q

What does renin lead to?

A

secretion of angiotensin II

58
Q

What does angiotensin do?

A

constricts the efferent arteriole

59
Q

When do you secrete renin?

A

when there is decreased sodium or water detected by baroreceptors

60
Q

What does low urine sodium tell you?

A

RAAS is activated and blocking secretion of Na+

means that EACV is low cause RAAS is working

61
Q

What is activated when EACV is low?

A

RAAS

62
Q

What is activated when EACV is high?

A

ANA

63
Q

What is a common fluid state in CHF / cirrhosis?

A

ECV is high but EACV is low

64
Q

Where does angiotensin act on?

A

proximal tubule

65
Q

Where are aquaporin 2 channels? What puts them there?

A

principal cells in collecting duct

ADH increases these channels

66
Q

Where are H+ ATPase channels?

A

intercalculated discs of collecting ducts

secrete H+

67
Q

What does hyponatremia indicate in CHF / cirrhosis?

A

the disease is advanced

there is low EACV

68
Q

What is the filtration fraction?

A

GFR / RPF

69
Q

Effects of RAAS on filtration fraction

A

RAAS increases filtration fraction by constricting the efferent arteriole

this leads to a decrease in RPF with no change in GFR

70
Q

What does hypertonic saline infusion do to RAAS?

A

decreases RAAS since you don’t need more sodium

71
Q

How do diuretics work in theory?

A

increase secretion of Na+ which decreases ECF

72
Q

What is a risk of carbonic anhydrase inhibitors?

A

increase bicarb excretion (less bicarb) can lead to acidosis

73
Q

Differences between maxi-K and ROMK?

A

ROMK is only on principal cells; maxi-K on both types of cells

Maxi-K is flow mediated; ROMK is charge mediated

74
Q

Aldosterone effects on potassium secretion

A

Increases potassium secretion through increased ENaC

75
Q

Where specifically is carbonic anhydrase found?

A

on the brush border of PCT

76
Q

What type of diuretic are you more likely to get kidney stones with?

A

loop diuretics

they decrease Ca2+ cotransport and increase calcium in urine which can cause kidney stones

77
Q

Which type of diuretics can cause hypocalcemia?

A

loop diuretics

78
Q

When should you give calcium for hyperkalemia?

A

only if there are associated ECG changes

79
Q

what happens to ICF and ECF with hyptotonic solution?

A

both volumes increase

80
Q

what happens to ICF volume if isotonic solution is given?

A

there is no change

no water movement since isotonic

81
Q

what happens to ADH if isotonic solution is given?

A

ADH responds to changes in osmolarity primarily so there is no change here

82
Q

what happens to RAAS if isotonic solution is given?

A

RAAS will decrease since you have more EACV

83
Q

What does hypertonic solution do to ADH?

A

increases ADH since we want to keep more water to balance the increase in solute

84
Q

What are the 3 barriers that regulate flow through the glomerulus?

A

1) Podocytes

2) Basement membrane

3) Fenestrations in capillaries

85
Q

Where the the juxtaglomerular apparatus? What does it include?

A

along the distal tubule at vascular pole

includes macula densa, JG cells and extraglomerular mesangial cells

86
Q

How can you determine proximal vs. distal tubules?

A

Proximal have brush border and are thicker

87
Q

What can thiazide and loop diuretics cause in terms of acid/base ?

A

alkalosis

88
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)

89
Q

How do we calculate V when given a single volume?

A

you normally assume this is a daily urine volume and divide by 1440 minutes in a day

90
Q

How do we define hyponatremia with lab values?

A

PNa < 135 mEq/L

91
Q

Where can SIADH anatomically arise from?

A

posterior pituitary or lung problem

92
Q

What drugs can often cause SIADH?

A

SSRI

93
Q

When do we worry about hyponatremia?

A

when PNa < 125

at this level, you are going to start seeing intracranial swelling and CNS symptoms

94
Q

What do we worry about when treating hyponatremia?

A

that we could potentially cause osmotic demyelination syndrome

95
Q

When muscle mass is low, what happens to eGFR if we use creatinine?

A

overestimated GFR

96
Q

What does estimate of ECF largely come from?

A

physical exam!

97
Q

What is treatment for hyponatremia caused by polydipsia?

A

fluid restriction

98
Q

What is treatment for heart failure / cirrhosis hyponatremia?

A

fluid restriction, loop diuretics, V2 receptor antagonists (-vaptans), urea

*do not use vaptans / urea in cirrhosis

99
Q

What medications can you use for hyerkalemia?

A

albuterol

insulin / glucose

bicarbonate

potassium binding resins

100
Q

Why do we use urea to treat SIADH?

A

urea acts as an osmotic diuretic and will increase water secretion

101
Q

Why do we use vaptans in SIADH?

A

block V2 receptors for ADH

they are expensive and hepatotoxic

102
Q

Why do we use loop diuretics in SIADH?

A

loop diuretics secrete diluted urine which leads to more water than Na+ loss

103
Q

Where is potassium primarily secreted NOT reabsorbed?

A

cortical collecting duct

104
Q

What 2 factors does ADH primarily EFFECT?

A

water and urea reabsorption

105
Q

peaked T-wave indicates …

A

hyperkalemia

106
Q

prominent U-wave indicates …

A

hypokalemia

107
Q

does hypokalemia or hyperkalemia cause a decreased response to ADH?

A

hypokalemia

108
Q

What are RBC casts in urine associated with?

A

glomerular basement membrane damage

109
Q

What can raise BUN?

A

high protein intake

glucocorticoids

110
Q

Is urea clearance more or less than true GFR?

A

less than true GFR since some is reabsorped

111
Q

What is PAH’s relation to GFR? PAH?

A

approximates RPF

overestimates GFR

112
Q

In a steady state what is true of a solute?

A

excretion = secretion

113
Q
A

Nephrology (6 decks)

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