Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CRRAB II > Sodium disorders > Flashcards

Sodium disorders Flashcards

1
Q

Normal serum Na+?

A

135-145 Meq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Normal plasma/serum osmolality?

A

285-300 Meq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Eqn to estimate plama/serum osmolality?

A

Na x 2 + BUN/2.8 + Gluc/18

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Main contributor to serum osmolality?

A

Na

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Symptoms of hypo/hypernatremia are due to effects on which orhan?

A

Brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sodium abnormalities are usually caused by ____________ NOT ___________.

A

Water problems

NOT

Salt problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Extracellular hyp-O-osmolality have what effent on neurons?

A

swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sx if Na+

A

nausea

malaise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Sx if Na+ = 115-120:

A

headache

lethargy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Sx if Na+

A

obtundation

seizures

coma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

More severe sx in fast or slow hyp-O-natremia?

A

Fast

brain has less time to adapt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Effect of hyp-ER-natremia on neurons?

A

cells shrink

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sx of hyp-ER-natremia?

A

lethargy

weakness

irritability

twitching

seizures

coma

death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Decreased brain volume due to hyp-ER-natremia can have what effect on vasculature?

A

rupture cerebral vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinically significant water shift occurs with 30-35 mosm/kg osmolar gradient between plasma and brain; what is the corresponding rise in serum Na+?

A

17 meq/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hormone responsible for maintenance of plasma osmolality:

A

ADH

arginine vasopressin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Where is ADH produced?

A

supraoptic and paraventricular nuclei of hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where is ADH stored and released?

A

secretory granules

posterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Osmotic stumuli of ADH release:

A

INCREASED plasma osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Non-osmotic stimuli of ADH release:

A

hypovolemia –> baroreceptors

pain

esophageal stimuli

medications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What receptor binds ADH to release aquaporin 2 to luminal membrane?

Where does this occur?

A

V2 (activates protein kinase)

collecting tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

With high presence of ADH:

Urine osmolality = ?

Plasma osmolality = ?

A

urine- increased

serum- decreased

**water flows out of tubule back into blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In low/absent ADH state:

Urine osmolality= ?

Blood osmolality= ?

A

urine- increased

blood- decreased

**water excreted in urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Physiologic responses to HIGH plasma osmolality:

A

thirst

ADH release

water reabsorption

concentration of urine –> high urine osmolality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Physiologic response to LOW plasma osmolality:

A

No thirst

No ADH release

Loss of free water – collecting tubules impermeable

Low urine osmolality – dilute urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Plasma osmolality maintained within __%.

A

1%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Indicator of the presence of ADH?

A

Urine osmolality

28
Q

What generally tells you what the kidney THINKS about the body’s volume status?

A

urine sodium

29
Q

Range of urine osmolality in a normal kidney?

A

50-1400 mosm/L

30
Q

Normal daily osmolar load from dietary protein/salt?

A

500-750 mosm

excreted in urine

31
Q

If you have 500 mosm/day to get rid of and your maximum urine osmolarity is 1000 mosm/L, how much urine will be excreted?

A

0.5 L

32
Q

If you have 500 mosm/day to get rid of and your minimum urine osmolarity is 50 mosm/L, how much urine will you excrete?

A

10 L

33
Q

Hormones responsible for retention of sodium in volume depleted state?

A

Ang II

Aldosterone

34
Q

What is the kidney doing of urine sodium is

A

senses low effective circulating volume, so it’s holding on to sodium

35
Q

What’s going on in the kidney if urine sodium is > 10 meq/L?

A

-sensing expanded ECV

OR

-not able to properly retain Na+

OR

-excreting Na as an obligate cation with something else

36
Q

What is pseudohyp-O-natremia?

What causes this?

A

low Na with normal or elevated Plasma osmolality.

Caused by:

Hyperlipidemia (normal Posm)

Hyperproteinemia (normal Posm)

Hyperglycemia (elevated Posm)

Hypertonic mannitol (elevated Posm)

37
Q

How does hyponatremia develop if mechanisms are in place to maintain plasma osmolality within 1%?

A

Non-osmotic stimuli override osmotic stimuli (or lack of) to secrete ADH at the expense of plasma osmolarity

**perfusion to brain is more important than perfect osmolality in plasma

38
Q

Four steps in clinical eval of hyponatremia:

A
  1. Check Posm: confirm true hypoosmolar hyponatremia
  2. Check Uosm: is ADH acting?
    - 100 – yes, despite hypoosmolar state, either appropriate for volume status or inappropriate
  3. Check UNa+: what is the kidney’s perception of ECV?
  4. Check the patient: volume status/clinical picture?
39
Q

Hyponatremia with Uosm

A

excess water intake (primary polydipsia)

**need to drink 10-15 L/day to overwhelm kidney’s ability to clear free water

40
Q

Two exceptional causes of hyponatremia with Uosm

A

beer potomania

tea and toast syndrome

**not ingesting enough(or any) protein/solutes for an extended period (low daily osmolar load)

41
Q

Treatment for primary polydypsia?

A

water restriction

42
Q

UNa+

A

Reabsorbing Na+ in an effort to reexpand vascular space

43
Q

UNa+

A

Recieving the wrong signal.

Edematous states: think CHF/cirrhosis/nephrosis

44
Q

UNa+ > 10, patient is volume depleted and hyponatremic. What is the kidney doing?

A

Salt wasting. Receiving the wrong signals. This is rare.

45
Q

UNa+ > 10, patient is volume expanded and hyponatremic. What is the kidney doing?

A

Volume is appropriate or expanded

Brain or kidney is confused

46
Q

Causes of volume depleted hyponatremia with UNa+ of

A

GI– N/V, diarrhea

Skin– burns

Diuretics– late

Pure cortisol deficiency (Addison’s???)

47
Q

Causes of hyponatremia with UNa+

A

Edematous states/poor perfusion–reduced ECV

  • CHF
  • Cirrhosis/liver failure (low albumin?)
  • nephrotic syndrome (proteinuria?)
48
Q

Causes of salt wasting (hyponatremia with volume depletion and UNa+ > 10):

A

adrenal insufficiency

salt wasting renal disease

Early diuretics

Hypokalemia with metabolic alkalosis after vomiting (lose sodium and bicarb)

hypothyroid

49
Q

Causes of hyponatremia with UNa+ > 10 and appropriate or expanded volume:

A

SIADH– Syndrome of Inappropriate ADH secretion

  • oat cell carcinoma (paraneoplastic)
  • pulmonary process (TB, PNA, asthma)
  • Drugs (chlorpropamide, oxytocin, tegretol, cytoxan)
  • esophageal process
  • pain
  • neuropsychiatric

Reset osmostat

CKD

50
Q

Fixed ADH secretion without regard to osmotic or volume status:

A

SIADH

51
Q

Tx for SIADH:

A

fluid restriction

increase osmolar load (high protein/Na diet)

52
Q

Treatment for volume depleted hyponatremia?

A

NS

**replenish volume, turn off ADH

53
Q

Tx for volume neutral or expanded hyponatremia:

A

restrict free water intake

treat state of poor perfusion

54
Q

Tx for severe hyponatremia not related to pure volume depletion OR with neurologic sx:

A

hypertonic saline

55
Q

Pharm tx for volume expanded hyponatremia:

A

ADH antagonists

Tolvaptan, Conivaptan

56
Q

Rapid correction of hyponatremia risks?

A

Central Pontine Myelinolysis (BAD)

57
Q

Brain’s own mechanism of compensation for slowly developing hyponatremia:

A

idiogenic osmoles

**more risk in rapid correction

58
Q

V1a and V1b receptors response to ADH?

A

vasoconstriction and ACTH release

59
Q

Hypothalamus/pituitary not releasing ADH?

A

Central diabetes insipidus

60
Q

Collecting tublues don’t respond to ADH:

A

nephrogenic diabetes insipidus

61
Q

How could you differentiate central vs nephrogenic DI?

A

give exogenous ADH

if UOsm increases –> central etiology

62
Q

Dx of diabetes insipidus usually made by patient complaint of?

A

polyuria (usually not hypernatremia)

63
Q

Drug to know that causes nephrogenic DI?

A

lithium

64
Q

Safe rate for correcting hypernatremia?

A

slowly

0.5 meq/hour –> 12 meq/24 hr

65
Q

What to give to replace free water deficit?

A

Free water ORALLY (NOT IV)

D5W IV

**can give 1/4 NaCl if volume depleted

CRRAB II (28 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions