Brainscape's Knowledge GenomeTM

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


See full index

CPR > Pharmacology: Hypernatremia, Hyponatremia > Flashcards

Pharmacology: Hypernatremia, Hyponatremia Flashcards

1
Q

describe the effects of IV solutions:

isotonic (0.9%) NaCl

A

increases ECF volume

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

describe the effects of IV solutions:

0.45% NaCl

A

expands ECF > ICF, but both do expand

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

describe the effects of IV solutions:

3% or 5% NaCl

A

expand ECF, shrink ICF

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

describe the effects of IV solutions:

5% albumin

A

expand plasma volume

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

describe the effects of IV solutions:

5% dextrose (D5W)

A

expands total body water, equivalent to infusing distilled H2O

dextrose is rapidly metabolized to CO2 leaving behind H2O

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

describe the effects of renal sympathetic nerves

A

increase activity: decrease NaCl excretion

  • decrease GFR (vasoconstriction of afferent art.)
  • increase renin secretion
  • increase proximal tubule, TAL, and CD NaCl reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

describe the effects of renin-angiotensin-aldosterone

A

increase secretion: decrease NaCl excretion

  • increased angiotensin II levels stimulate proximal tubule NaCl reabsorption
  • increased aldosterone levels stimulate TAL and CD NaCl reabsorption
  • increase ADH secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

describe the effects of atrial natriuretic peptide

A

increase secretion: increase NaCl excretion

  • increase GFR (vasoconstriction efferent art.)
  • decrease renin secretion
  • decrease aldosterone secretion
  • decrease NaCl and H2O reabsorption by the CD
  • decrease ADH secretion and inhibition of ADH action on the CD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

describe the effects of ADH

A

increase secretion: decrease H2O excretion

  • increase H2O absorption by the CD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hypovolemia independently stimulates…

A

ADH secretion

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

what is the most common carcinoma leading to ectopic production of vasopressin and SIADH?

A

oat-cell carcinoma

will need indefinite treatment, at high risk of chronic SIADH

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

describe level 1 treatment for patients with hyponatremia

A

fluid restriction

symptoms are minimal: HA, irritability, inability to concentrated, altered mood, depression, falls or unstable gait

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

describe level 2 treatment for patients with hyponatremia

A

vaptan or hypertonic NaCl, followed by fluid restriction

moderate symptoms: N, confusion, disorientation, altered mental status

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

describe level 3 treatment for patients with hyponatremia

A

hypertonic NaCl, followed by fluid restriction or vaptan

severe symptoms: V, seizures, obtundation, respiratory distress, coma

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

this drug class blocks the ADH receptor (AVPR2) in the CD

A

vaptans

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

conivaptan MOA

comment on affinity

A

non-peptide arginine vasopressin receptor agonist (prevent ADH-mediated insertion of aquaporin channels in principal cell of CD)

affinity for AVP receptor subtypes V1A and V2

17
Q

conivaptan effects

A

promotes excretion of free water

18
Q

conivaptan applications

A

euvolemic and hypervolemic hyponatremia (hospitalized, symptomatic, not responsive to fluid restriction)

19
Q

conivaptan pharmacokinetics

A

IV administration

substrate of CYP3A4; eliminated in feces as metabolites
t1/2: 5.3-8.1 hrs

20
Q

conivaptan toxicities

A
  • orthostatic hypotension
  • fatigue
  • thirst
  • polyuria, bedwetting
21
Q

selective V2 receptor agonist administered orally

describe limitations of use

A

tolvaptan

  • only initiated in hospital (monitor plasma Na carefully) - must use <30 days for hyponatremia otherwise fatal hepatoxicity
  • has been used to slow progression of adult polycystic kidney disease (AD)
  • t1/2: peak at 4 hrs, effects last 4-8 hrs
22
Q

hypovolemic hypernatremia is treated with

A

isotonic saline

23
Q

euvolemic and hypervolemic hypernatremia is treated with

A

hypotonic IV solutions (D5W, half-normal saline, quarter-normal saline)

24
Q

formula for water deficit

A

= 0.6% body mass (kg) x (1 - [140/Na])

25
Q

desmopressin (DDAVP) MOA

comment on affinity

A

synthetic analogue of arginine vasopressin (antidiuretic)

V2 selective agonist

26
Q

DDAVP effects

A
  • increase cAMP in CD principal cells –> increase H2O permeability
  • decrease urine volume and increase urine osmolality
  • increase plasma levels vWF, factor VIII, and tPA –> decreased aPTT
27
Q

DDAVP applications

A
  • central diabetes insipidus
  • primary nocturnal enuresis
  • hemophilia A and von Willebrand (type 1)
28
Q

DDAVP pharmacokinetics

A
  • IV, intranasal, SL, oral
  • intranasal is greatest bioavailability
  • t1/2: 75 minutes (longer than vasopressin)
29
Q

DDAVP toxicities

A
  • hyponatremia (can be life threatening)
  • hypotension
  • acute cerebrovascular thrombosis
  • acute MI
30
Q

what therapy is the MCC of nephrogenic DI?

A

Li

  • thiazide diuretics contraindicated here, use amiloride because it will block influx of Li into CCD

CPR (3 decks)

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