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CRRAB II- FINAL > Renal Phys- Muster > Flashcards

Renal Phys- Muster Flashcards

1
Q

What are the 3 primary signaling pathways that stimulate renin release?

A
  1. sympathetic imput (increased NE)
  2. Decreased stretch in the afferent arteriole
  3. Decreased chloride (Na+) delivery to the Macula Densa
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2
Q

What are the primary actions of angiotensin II?

A
  1. Stimulates ALDOSTERONE
  2. Systemic Vasoconstrictor
  3. Stimulates Proximal Tubule Reabsorption of Na+
  4. Increases sympathetic activity
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3
Q

Where is aldosterone secreted from?

A

Cortex glomerulosa of adrenal gland

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4
Q

What does aldosterone do once it leaves the cortex glomerulosa of the adrenal gland?

A

Lipophillic
Crosses membrane, and binds steroid response element
Increases transcription of:

  1. Na/K ATPase on basolateral side
  2. ENac channel on luminal side (Na gets reabsorbed)
  3. ROMK channel (K+ leaves cell)
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5
Q

What is Liddle Syndrome?

A

Gain of function mutation
Increases ENaC channels
Increased Na+ reabsorption in collecting tubules

Autosomal dominant
Results in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone

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6
Q

What is Gitelman Syndrome?

A

Reabsorptive defect of NaCl in DCT
Autosomal recessive
Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

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7
Q

Bartter Syndrome

A

Reabsorptive defect in thick ascending loop of Henle
Autosomal recessive
Affects NKCC cotransporter
Results in hypokalemia and metabolic alkalosis with hypercalciuria

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8
Q

What symptoms would you expect with a low serum concentration of Na+

A 
Nausea
Malaise
Stupor
Coma 
Seizures
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9
Q

What usually causes hyponatremia with low urinary osmolarity

A

Almost always due to excessive water intake (primary polydipsia) - typically a psych disorder

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10
Q

What is normal serum sodium concentration?

A

135-145 meq/L

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11
Q

What equation can you use to estimate the plasma/serum osmolarity? What should it be at?

A

Serum osmolarity = 2[Na] + BUN/2.8+ Glucose/18

Should be 285-300

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12
Q

Where does ADH bind? Then what happens?

A

V2 receptor in collecting tubules

  • activates a protein kinase
  • causes Aquaporin 2 to move from cytoplasm to luminal membrane
  • forms water channels
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13
Q

ADH is released in response to?

A

Serum hyperosmolarity

Hypovolemia

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14
Q

What should you do if patient has hyponatremia and the urinary osmolarity is > 100? (Concentrated urine)

A

Looks at urinary Na+ concentration and volume status (on physical exam)

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15
Q

How do you treat hyponatremia if patient is also volume depleted?

A

Give normal saline to replenish volume and turn off ADH

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16
Q

How do you treat hyponatremia when neutral volume or volume expanded?

A

Restrict fluid intake!! or treat states of poor perfusion

May also give ADH antagonist

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17
Q

MOA of Tolvaptan and Conivaptan?

A

ADH antagonists –> target ADH receptors

Indicated in volume expanded hyponatremia

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18
Q

At what rate should you correct hyponatremia out of the “danger range”?

A

0.5 meq/L/hour

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19
Q

What is the “danger range” of hyponatremia?

A

115-120

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20
Q

What treatment should you use if hyponatremia and serum sodium is 115-120?

A

3% NaCl solution

If siezures - 100 cc over 10 mins IV

If just other neuro symptoms- 30-50 cc/hr for several hours

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21
Q

In what circumstances would you see hypernatremia?

A

due to excessive water losses and inadequate intake

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22
Q

What is the difference between Central diabetes insipidus and nephrogenic diabetes insipidus?

A

central = hypothalamus/pituitary axis not releasing ADH so kidney can’t reabsorb free water

nephrogenic = collecting tubules don’t respond to ADH so kidney can’t reabsorb free water

*can be partial or complete!

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23
Q

What medication can induce nephrogenic diabetes insipidus?

A

LITHIUM!

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24
Q

What fluids would you give for hypernatremia?

A

Free water orally
D5W IV
1/4 NaCl for hypernatremia due to volume depletion (Na+ is also depleted)
NS if patient is hypotensive with fluid losses

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25
Q

What is normal serum K+ concentration?

A

4-5 meq/L

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26
Q

What are the two primary functions of potassium?

A

Cell metabolism (protein and glycogen synthesis)

The RATIO of intracellular/extracellular is primary determinate of resting membrane potentials

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27
Q

How much K+ is stored intracellularly?

A

98%

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28
Q

How does Insulin affect the activity of the Na/K+ ATPase?

A

Increases its activity!
Promotes skeletal and muscle uptake

When we eat, we stimulate insulin, which alleviates a sharp rise in concomitant K+ serum levels

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29
Q

How does catecholemines affect the Na/K ATPase?

A

B2 receptors stimulate the Na-K ATPase inducing cellular uptake

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30
Q

Immediate treatment for hyperkalemic patient

A

INSULIN! (and glucose)

Give Ca+ to stabalize cardiac membrane (lasts 45 minutes)

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31
Q

Which part of the nephron is the primary site for K+ excretion?

A

Principle cell in the collecting duct!

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32
Q

Which two channels facilitate the excretion of K? Are they always in the membrane?

A

ROMK - stored intracellularly and inserted

BK - always in membrane, but only open at HIGH [K+]

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33
Q

What symptoms would you see in hypo/hyper kalemia?

A

-symptoms relate to inability to generate action potentials in muscles

Cramps
Muscle weakness/ paralysis (starts in the legs)
EKG changes
Cardiac arrhythmias

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34
Q

List the primary solutes of the different body compartments

A

Intracellular = K+, PO4, and anions

Intravascular (plasma) = Na+

Interstitial = Na+

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35
Q

What percent of your body is water? How much is intracellular? interstitial? Plasma?

A

60% (50% in females)

2/3 of that is intracellular

Of the remain 1/3

3/4 of that is interstitial
1/4 of that is plasma

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36
Q

What compartments does normal saline distribute to?

A

Interstitial & Plasma!
Extracellular volume will increase

No effect on intracellular volume or osmolality –> cannot enter cells!*

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37
Q

If you drink water, how will it distribute in your compartments?

A

It will distribute proportionately according to the volume of the compartments

38
Q

How does 1/2 normal saline distribute to the compartments?

A

Basically half acts like normal saline and half of it acts like you drank water

Extracellular volume increases
Slight increase in intracellular volume
Osmolality slightly decreases

USE FOR SWEAT LOSSES

39
Q

How will D5 Fluid distribute among the compartments?

A

5% dextrose
will distribute just like water because glucose is taken up by cells, water follows, and then the sugar is degraded completely

If can’t drink water, then give D5

40
Q

Distinguish between volume depletion and dehydration

A

Volume depletion = extracellular volume loss for ANY CAUSE (most often loss of salt and water)

Dehydration = presence of HYPERNATREMIA due to pure water loss

41
Q

What fluids would you give for diabetetic ketoacidosis? sepsis? secretory diarrhea?

A

Normal Saline

42
Q

What fluids would you give for sweat losses? Or sick old people in the hospital?

A

1/2 normal saline (replace sweat with sweat!)

43
Q

What fluids would you give for diabetes insipidus or severe hypoglycemia?

A

D5

44
Q

How many L of water does a normal healthy young 70 kg person contain?

A

42 L of water (60% of body weight!)

45
Q

How many liters does the kidney filter in one day (normal GFR)?
What is this per minute?

A

180 L/ day

125 mL/min

46
Q

What are the three things that limit size of particle filtrated through the glomerulus?

A 
Capillary Endothelium (has fenestrations)
Basement membrane 
Podocytes (small negatively charged slits)
47
Q

Do anionic or cationic particles get filtered less? why?

A

anionic particles get filtered less because the GBM and the slit diaphragms of podocytes are negatively charged

48
Q

What equation describes the fluid/solute movement from the capillary lumen into bowman’s space?

A

GFR = K [Hydrostatic P in capillary + Oncotic P in BS) - (hydrostatic P in BS - oncotic P in capillary)

GFR = (forces favoring filtration) - (forces favoring reabsorption)

49
Q

What happens to RPF, GFR, and FF when there is constriction of the efferent arteriole?

A

Decreased RPF
Increased GFR (capillary hydrostatic pressure increases due to fluid “backing up” into the glomerulus)
Increased FF

50
Q

What is filtration fraction?

A

FF = GFR/RPF

51
Q

What happens to RPF, GFR, and FF when there is constriction of the afferent arteriole?

A

Decreased RPF
Decreased GFR
No change in FF (since both RPF and GFR are decreased)

52
Q

What happens to RPF, GFR, and FF when there is dilation of the efferent arteriole?

A

Dilation of efferent arteriole causes a drop in glomerular hydrostatic pressure decreasing GFR

RPF is increased

Filtration Fraction is decreased

53
Q

Does plasma protein concentration affect GFR or RPF? FF?

A

Increased [plasma proteins] = increased capillary oncotic pressure –> decreased GFR –> decreased FF

Decreased [plasma proteins] = decreased capillary oncotic pressure –> increased GFR –> increased FF

NEITHER affect the renal plasma flow

54
Q

How does angiotensin II affect the arterioles of the glomerulus?

A

Preferentially constricts the EFFERENT arteriole

55
Q

How does NE affect the arterioles of the glomerulus?

A

Constricts EFFERENT and AFFERENT arterioles

Decreased RPF
Decreased hydrostatic pressure and greatly decreased GFR

56
Q

Describe glucose reabsorption in the proximal tubule….. what kind of transporter is it? Can it be saturated?

A

SLGT = sodium linked glucose transporter

CAN be saturated = Tm (transport maximum)

Will start to see glucose in the urine at 200 mg/dL (threshold)

All transporters are fully saturated at 375 mg/dL

NOTE* pregnancy will decrease threshold!

57
Q

In the absence of ADH, which part of the tubule will the lumen have the highest osmolarity? How concentrated can the urine become?

A

Medullary segment of the loop of Henle

Will reach 600 osms

**will be most dilute at collecting ducts in absence of ADH!

58
Q

What part of the nephron does ADH act on?

A

The collecting ducts!!!! Increases permeability to water, and concentrates urine

59
Q

Loop diuretics such as furosemide and bumetanide inhibit the NKCC pumps, but to compound their diuretic effect, what else do they do?

A

Stimulate PGE release, this vasodilates the afferent arteriole

This increases the RPF and increases the GFR complementing the diuretic effect

60
Q

What is the equation for determining clearance?

A

Clr = [x in urine]*[urine flow rate]/[x in plasma]

61
Q

How do prostaglandins effect GFR?

A

They vasodilate
Decreased glomerulus hydrostatic pressure
Decreased GFR

62
Q

What % of fluid is intracellular and extracellular when you give 1/2 NS?

A

66 % is extracellular and 33 % is intracellular.

63
Q

How much blood do the kidneys take in per minute?

A

1000 mL/min

64
Q

Vasoconstricting agents constricts what 2 vessels?

It has a greater effect on which one? Why?

A

Afferent and Efferent Arterioles

Has a greater effect on the efferent arteriole because it is smaller!

65
Q

How do you determine Filtered Load?

A

[x serum] x GFR

66
Q

Equation for excretion rate?

A

[urine concentration of x] x urine flow rate

67
Q

What are the properties of the ideal solute you’d want to use to measure GFR?

A

Filtered load = excretion rate

Solute is completely filtered, not secreted, or reabsorbed

68
Q

Describe the formate recycling process. Location, direction of ion travel, etc.

A

Most of the formate anti-porters are in the LATE proximal tubule.
Chloride accumulates and by the time it reaches the late proximal tubule, there is a gradient for it to move inward through the antiporter that moves formate outward.

69
Q

What are the directions of the ions flowing in the Na+/H+ pump?

A

Sodium into the cell

H+ into the lumen

70
Q

2 places where there are no aquaporins?

A

Thick ascending limb of loop

Distal tubule

71
Q

Why do we see metabolic alkalosis in Bartter and Gitleman’s syndromes?

A

Because there is a huge drive to pull Na+ in in the proximal tubule since it is not being reabsorbed later on. This occurs via the Na+/H+ antiporter, so we are losing H+ in the process!

72
Q

In what situation would your FeNa look high and be un-interpretable?

A

After you give a diuretic!

73
Q

What are the 3 active transporters in the alpha-intercalated cell?

A

Na+/K+ ATPase on the basolateral membrane
K+/H+ antiporter on the lumenal side (K+ in, H+ out)
H+ ATPase lumenal side (H+ out)

74
Q

What antiporter is also present on the basolateral membrane of alpha-intercalated cells?

A

Bicarbonate/Chloride antiporter

bicarbonate to interstitium/chloride into cell

75
Q

What are the effects of PTH on the kidney?

What part of the kidney?

A

Increased Vitamin D production (increases gut absorption of calcium)

Increased calcium reabsorption

Decreases renal phorphorous absorption

-Distal Convoluted Tubule

76
Q

Where does glutamine uptake occur?

A

Proximal Tubule

77
Q

1/3 of urinary H+ is buffered by what?

A

Phosphorous

78
Q

What 2 major things are getting reabsorbed in the alpha-intercalated cell?

A

K+

Bicarbonate

79
Q

What effect could an opioid have as far as acid/base problems go?

A

Respiratory acidosis because they decrease respirations–build up of CO2

80
Q

What 2 renal enzymes would be upregulated in the case of a respiratory acidosis?

A

Glutaminase

Carbonic anhydrase

81
Q

Describe what would happen during a panic attack.

What does the kidney do?

A

Too much breathing–>CO2 given off–>Respiratory Alkalosis

Beta-intercalated cells will appear in the kidney to excrete bicarbonate

82
Q

Hypokalemia can induce what sort of acid/base imbalance?

A

Metabolic Alkalosis

Lose H+ ions if hypokalemic.
Alpha-intercalated cells are going to try to Reabsorb more K+, in which case H+ is excreted
(K+ in, H+ out into lumen)

83
Q

Is osmolality in the interstitium usually the same, hypo, or hyperosmolar to the tubule?

A

Hyperosmolar

84
Q

Where is 50 % of urea reabsorbed?

A

Proximal Tubule

85
Q

How is urea absorbed in the proximal tubule?

A

PARACELLULARLY! (through tight junctions…. NOT transporters on the membrane!)

86
Q

Which urea transporter is stimulated by ADH production and helps reabsorb urea?

A

UT1

87
Q

Which urea transporter contributes to urea recycling by secreting urea back in to the thin segments of loop of henle?

A

UT2

88
Q

Where would you find the UT1 transporter along the nephron? (in response to ADH of course!)

A

in the MEDULLARY collecting duct!! (the distal 1/3 of the collecting duct)

89
Q

What is glutamine split into? Why is its uptake up-regulated in acidosis?

A

Glutaminase splits glutamine into NH4 and 2 bicarbs.

Up-regulated in acidosis to increase bicarb levels in blood

(bicarb gets sent out the backside with Na+ with a 3:1 ratio)

90
Q

Why would you see proteinuria in DKA?

A

Patient becomes hyponatremic.
Sodium/AA transporters in PROXIMAL TUBULE cannot function properly.
AA stays in the lumen and is excreted in urine

91
Q

Where is K+ reabsorbed?

A

Alpha-intercalated cell

92
Q

Where is calcium reabsorbed?

A

Distal convoluted tubule!

CRRAB II- FINAL (20 decks)

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