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Renal > Lecture Notes > Flashcards

Lecture Notes Flashcards

1
Q

Total osmolality will change but tonicity will not with large changes in

A

BUN

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2
Q

What is the normal range of serum osmolality?

A

285-295 mOsm/kg

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3
Q

The ONLY place filtration occurs

A

Glomerulus

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4
Q

The minimum GFR we like to see is

A

60

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5
Q

In a healthy adult, steady state creatinine should be less than

A

1.5 mg/dL

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6
Q

What is the relationship between GFR and creatinine levels?

A

They are inversely related (i.e. as GFR goes up, creatinine goes down)

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7
Q

What is impeded if GFR is either too low or too high?

A

Reabsorption

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8
Q

The distal nephron can communicate with the glomerulus via the

A

Macula densa

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9
Q

An increase in NaCl tells the macula densa what?

A

That GFR is too high

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10
Q

Works in cohort with SNS to maintain BP

A

RAAS

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11
Q

What does AN-II do?

A
  1. ) Good vasoconstrictor (especially of efferent arteriole)
  2. ) Promotes aldosterone secretion
  3. ) Inhibits Renin
  4. ) promotes Na+ and H2O reabsorption
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12
Q

Upregulated by low BP or high Na+

A

AVP

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13
Q

What does AVP do?

A
  1. ) Promotes H2O reabsorption

2. ) Potent vasoconstrictor

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14
Q

What does Aldosterone do?

A
  1. ) Very active in Na+ reabsorption

2. ) Excess will cause K+ excretion

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15
Q

Extrarenal event caused by reduced renal perfusion

A

Azotemia

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16
Q

Moves K+ into forming urine to help drive NKCC

A

ROMK-2

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17
Q

What does furosemide do?

A

Blocks NKCC and promotes K+ and Ca2+ wasting

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18
Q

Which hormone is the major hormone responsible for Na+ reabsorption?

-also important for acid-base status

A

Aldosterone

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19
Q

When we see “presser” response, we are talking about

A

AVP

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20
Q

Stimulates a change in gene transcription which causes an increase in the secretion of K+ by aldosterone

A

Hyperkalemia

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21
Q

Mineralocorticoid hypertension is caused by

A

Hyperaldosteronism

22
Q

What are the possible effects of hyperaldosteronism?

A

Possible hypokalemia and metabolic alkalosis

23
Q

What are the possible symptoms of hypoaldosteronism?

A

Hyponatremia, Hyperkalemia, Metabolic acidosis, and increased HR

24
Q

If blood and urine Na+ are not following the same trend we should suspect

A

AVP problem

25
Q

Urine osmolality is

  1. ) Maximally dilute at values below
  2. ) Maximally concentrated at values above
A
  1. ) 100

2. ) 600

26
Q

Acute alcohol consumption suppresses

A

AVP

27
Q

Can cause AVP secretion

A

Nausea

28
Q

ANP is secreted in response to

A

Increased BP and RAP

29
Q

ANP inhibits

A

Renin secretion

30
Q

Characterized as an AVP insensitivity or loss of AVP

A

Diabetes Insipidus (DI)

31
Q

What are the effects of DI?

A

Mass diuresis

  • dilute urine
  • constant thirst
32
Q

A mismatch between blood osmolality and water retention can signify

A

DI

33
Q

What are the symptoms of SIADH?

A

Hyponatremia, increased SG of urine, potential hypertension

34
Q

In SIADH, patients body’s are holding too much

A

Water

35
Q

A patient presents with hypernatriemia, but is NOT antidiuresing. This suggests?

A

DI

36
Q

A patient presents with hyponatremia, but is NOT diuresing. This suggests

A

SIADH

37
Q

How can we characterize a type 2 RTA?

A

General proximal tubule defec leading to a normal AG metabolic acidosis

38
Q

Glucose in urine, PO4 wasting, and vitamin D deficiency are all symptoms of a

A

Type 2 RTA

39
Q

A UAG that is greater than 0 suggests

A

Type 1 RTA

40
Q

A patient with a kalemic and acid base disorder likely has a disorder with

A

Aldosterone

41
Q

Sulfonylureas set up gradients that favor

A

Insulin secretion

42
Q

Are patients with type 1 DM typically overweight or thin?

A

Thin

43
Q

Defects with insulin can cause problems with

A

Callular K+ uptake, FFA uptake, and peripheral glucose uptake

44
Q

DKA is very common with

A

Type 1 DM

45
Q

An autoimmune disease characterized by a destruction of B cells

A

Type 1 DM

46
Q

ST elevations and depressions suggest a problem with

A

K+

47
Q

QT elongations or shortening suggests a problem with

A

Ca2+

48
Q

Calcitriol has a negative feedback effect on

A

PTH secretion

49
Q

The point of regulation for calcitriol formation

A

1a-hydroxylase (CYP27B1)

50
Q

Under normal conditions, which effects will win, PTH or Calcitriol?

A

PTH

51
Q

In a very sick kidney, Ca2+ reabsorption will not occur and we will not be able to make calcitriol. This leads to

A

Secondary hyperparathyroidism

-eventually leads to osteoporosis

52
Q

Long QT syndrome is caused by

A

Hypocalcemia

Renal (10 decks)

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