[6] Loop of Henle and Distal Convoluted Tube Flashcards

1
Q

What occurs in the descending loop?

A

Descending: Dry

Water diffuses out

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2
Q

What occurs int he thick ascending loop?

A

Ascending: Asin

Na+ diffuses down electrical gradient

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3
Q

Osmolarity at the top of nephron

Osmolarity at the bottom of nephron

A

300 milliosmoles

1200 milliosmoles

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4
Q

Why does the interstitium have to be concentrated?

A

Otherwise you’ll urinate to death

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5
Q

Main Function: Countercurrent Multiplier

A

Create a hyperosmotic medullary interstitium

Have an osmotic equilibrium of water in the medulllary collecting tubules and medullary interstitium

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6
Q

[Red Slide]

What clinical conditions will produce a concentrated urine?

A dilute output?

A

Do research, send me answers. =))

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7
Q

[Descending Limb of Henle]

What is it permeable to?
What is it impermeable to?

A

P: Water
I: Na and Cl

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8
Q

[Descending Limb of Henle]

How does water pass?

A

Aquaporin 1

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9
Q

[Thin Ascending Limb of Henle]

What is it permeable to?
What is it impermeable to?

A

Highly impermeable to water

Permeable to Na, Cl and Urea

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10
Q

What’ll happen to Potassium levels if the Na K 2Cl pump gets deactivated?

A

Research

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11
Q

[Red Slide]

What happens if a drug inhibits the area of the thick ascending limb of the Loop of Henle?

A

Research

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12
Q

[Major Problem of the Loop of Henle]

How does NaCl get out of the thin ascending loop?

A

Urea concentration gradient helps move sodium out of the loop

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13
Q

[Red Slide]

What happens in persons with Marasmus in terms of the concentration gradient

A

They are frequently urinating because they have no urea. Since they have Marasmus, which has a lack of protein, and urea is a byproduct of protein breakdown, they cannot create a very concentrated urine.

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14
Q

Kidney receives what % of CO?

A

20%

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15
Q

How many liters/day of glomerular filtrate?

A

180 liters

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16
Q

What keeps NaCl from leaving the medulla?

A

Vasa Recta

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17
Q

Origin of the Vasa Recta

A

Efferent Arterioles

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18
Q

[Red Slide]

How does Mannitol, an osmotic diuretic, increase urine output?

A

Increases renal blood flow in the vasa recta, allowing less time to concentrate your urine.

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19
Q

Active pumping out of NaCl occurs where?

A

Thick Ascending Loop

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20
Q

CCD: Principal Cells

Effect of Aldosterone and Vasopressin

A

Opens water and sodium channels

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21
Q

Ammonia Secretion

A

Glutamine -> NH3 + H -> NH4 + Cl -> NH4Cl

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22
Q

Where is Glutamine secreted?

A

Proximal Tubule

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23
Q

OMCD has which Aquaporins?

A

2 and 3

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24
Q

IMCD mainly Water Absorption/Secretion?

What about Urea?

A

Absorption for both

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25
Q

Intercalated cells increase/decrease in number as collecting duct descends?

A

Decrease

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26
Q

Is the collecting duct permeable/impermeable to water?

A

Impermeable

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27
Q

Function: Macula Densa

A

Na-K-Cl Reabsorption

Adenosine Secretion

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28
Q

Function: DCT1

A

Na and MG Reabsorption

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29
Q

Function: DCT2

A

H and K Secretion

CA Reabsorption

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30
Q

Function: CNT

A

Na, K, Ca reabsorption

K Secretion

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31
Q

Function: CCD

A

H AND HCO3 SECRETION

Water and Na Reabsorption

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32
Q

Function: OMCD

A

H and NH3 Secretion

Water Reabsorption

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33
Q

Function: IMCD

A

Water and UREA Reabsorption

34
Q

Gitelman Syndrome

A

NCCT

35
Q

Classic Bartter Variant

A

Cl-CK2b

36
Q

Clinical Presentation of Patient with Gitelman Syndrome

A

Hyponatremia because there is a lot of salt loss

Primarily hypovolemic then dehydration because of the salt loss

37
Q

Do you treat a dehydrated person immediately?

What about a hypovolemic person?

A

Slowly to get the system accustomed to it

Immediately

38
Q

What electrolyte problems do you foresee in patients with Gitelman Syndrome?

A

Research

39
Q

What electrolyte problems do you foresee in patients with AE1 Mutations?

A

Research

AE1: Cl-HCO3 Antiport
AE1: Distal Renal Tubular Acidosis

Hyperchloremic metabolic acidosis

40
Q

Type 1 Pseudohypoaldosteronism (PHA)
Liddle Syndrome

What symptoms do you expect in patients with Liddle Syndrome?

A

WNK1

4-Type II PHA

41
Q

Nephrogenic Diabetes Insipidus

AQP2- Autosomal Nephrogenic Diabetes Insipidus

What electrolyte problems do you foresee in patients with AQP2 defects?

A

Hypernatremia due to the closed aquaporins that are a result from the lack of ADH

42
Q

What does Thiazide block?

A

Na-Cl Symporter

43
Q

What do Lactones Block?

A

Aldosterone Receptors

44
Q

[Red Slide]

How do thiazides prevent kidney stone formation?

A

Research

45
Q

[Red Slide]

How do K-sparing diuretics help in patients with Gitelman syndrome?

A

Research

46
Q

Memorize that Chart with Values of Substances Related to Loop Areas

A

Go look for it =))

47
Q

Potassium is primarily taken up by the

A. H-K ATPase
B. K-Cl Co-Transporter
C. Na-K-ATPase Pump
D. ROMK Channels

A

Don’t know yet, wanna tell me?

48
Q

What is the major intracellular ion?

A

Potassium

49
Q

How does K exit cells?

A

Mostly via K Channels

Some via K-H Exchange

50
Q

Majority of Potassium is found in?

A

Muscles

51
Q

Least Potassium found in which organs?

A

Plasma

52
Q

Which of the following conditions causes more hypokalemia?

A. Anuria
B. Polyuria
C. Constipation
D. Diarrhea

A

B

Because more potassium is excreted via urine

53
Q

Majority of K is excreted via?

A

Urine 90meq/day

Feces 10meq/day

54
Q

Aldosterone affects which pumps?

A

Na-K Pump

55
Q

Changes in K concentration have marked effects on?

A

Cell Excitability

56
Q

Potassium is a major intracellular?

A

Osmotically Active Cation

57
Q

Potassium is critical for what activities?

A

Enzyme
Cell Division
Growth

58
Q

Intracellular K participates in?

A

Acid Base regulation

59
Q

Which phase of the propagation of the action potential permits potassium ions to exit the cell?

A. Resting Potential
B. Action Potential
C. Repolarization
D. Hyperpolarization

A

C

60
Q

Action Potential

A

Na moves inside the membrane

61
Q

Repolarization

A

K move outside and sodium stays inside the cell

62
Q

Hyperpolarization

A

More K on the outside than Na on the inside

63
Q

Refractory

A

K returns inside

Na returns outside

64
Q

Buffering of ECF K through cell K uptake is impaired in the absence of?

A

Aldosterone
Insulin
Catecholamines

65
Q

Characteristics: Renal Outer Medulla K, SK/ROMK

A

Low Conductance

pH Sensitive

66
Q

Characteristics: Ca++-Acitvated (BK/Maxi-K)

A

High Conductance

Flow Stimulated

67
Q

Characteristics: H-HK ATPase

A

Colonic: Resorption
Gastric: Secretion

68
Q

Majority of K Secretion Occurs in:

A. PCT
B. TAL
C. DCT
D. CD

A

Don’t know, wanna tell me?

69
Q

Fate of Potassium

A

65% in PCT: Passive Diffusion
25% in TAL: Na-K-2Cl Pump

3% DCT
10% OMCD
1% IMCD

70
Q

Secretion of Potassium

A

10-50% DCT
5-30% CCD
15-80% IMCD

71
Q

What factors are needed to facilitate renal K secretion

A. ANP
B. Distal delivery of NA
C. ECFV Contraction
D. All of the Above

A

TIP: Usually not All of the Above for Dr. Anacleto

Don’t know, wanna tell me?

72
Q

What is the most important regulation for management of potassium problems?

A

Dietary K

73
Q

What happens in Hyperkalemia

A

Stimulates secretion of K via principal cells in DT/CCD

74
Q

High K Intake

A

Stimulates Aldosterone and SK/ROMK, BK/maxi-K channels

75
Q

Low K Intake

A

Enhance colonic H-K-ATPase

76
Q

Effect on Exercise on K Levels

A

Release of K from muscles

Opening of K channels

77
Q

What counterbalances the increase of K from exercise?

A

Catecholamines which decrease extracellular K

78
Q

Luminal Flow Rate

A

High Flow Rate -> High K Secretion in DT/CCD

79
Q

If you urinate too much what kind of potassium problems will you have?

If you don’t urinate at all what kind of potassium problems will you have?

A

Hypokalemia

Hyperkalemia

80
Q

Alkalosis leads to?

Acidosis leads to?

A

Alk: Hypokalemic, increased K secretion
Aci: Hyperkalemic, decreased K secretion

81
Q

Effect of Acidosis on Na pump

A

Lowers cellular potassium levels

82
Q

Effect: Increased luminal bicarbonate levels?

A

Increased potassium secretion