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Renal > Aquaretics > Flashcards

Aquaretics Flashcards

1
Q

aquaretic definition

A

agents affecting the renal conservation of water

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2
Q

aquaretic site of action

A

collecting ducts

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3
Q

ADH/AVP site of synthesis

A

paraventricular and supraoptic nuclei of hypothalamus

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4
Q

ADH/AVP stimuli

A 
increase plasma osmolarity >280mOsm/kg
decrease ECF
pain
nausea
hypoxia
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5
Q

V1R location

A

vascular smooth muscle

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6
Q

V1R binding effect

A

vasoconstriction

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7
Q

V1R mechanism

A

Gq–>PKC–>IP3 pathway releases Ca2+

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8
Q

V2R location

A

principal cells of renal CD

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9
Q

V2R binding effect

A

increase CD permeability to H2O & urea (concentrates urine)

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10
Q

V2R mechanism

A

Gs–>cAMP–>PKA, which:

  • moves aquaporin vesicles to apical membrane
  • phosphorylates aquaporin-2
  • phosphorylates VRUT (UT1)
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11
Q

aquaporin-1 location

A

proximal tubule & thin descending limb

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12
Q

aquaporin-2 location

A

collecting duct

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13
Q

central DI mechanism

A

inadequate ADH secretion

ADH-sensitive DI

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14
Q

nephrogenic DI mechanism

A

insufficient response to ADH in kidney

ADH-insensitive DI

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15
Q

central DI etiology

A

head injury, surgery, or trauma in the pituitary/hypothalamus
tumors
CNS ischemia
AD (chromosome 20) gradual loss of ADH

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16
Q

nephrogenic DI etiology

A

acquired: obstructive renal disease
drug-induced: lithium, clozapine
genetic: X-linked mutation in V2R

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17
Q

DI mechanism

A

impaired water reabsorption

AKA too much water excretion

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18
Q

DI symptoms

A

polyuria

polydipsia

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19
Q

polyuria

A

excrete large volumes of dilute urine

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20
Q

polydipsia

A

drink a lot of water b/c increased thirst

21
Q

how to distinguish (clinically) b/t types of DI

A

administer V2R agonist

  • central DI: increase urine osmolarity (concentrates urine, aka H2O reabsorbs)
  • nephrogenic DI: no change
22
Q

Tx of central DI

A

synthetic vasopressin peptides

selective V2R agonists: desmopressin

23
Q

desmopressin MOA

A

selective V2R agonist

minimal V1R effects

24
Q

desmopressin ROA

A

nasally
IV
oral tablet

25
Q

desmopressin clinical uses

A

central DI
bleeding disorders (increase factor VIII & vWF via extrarenal V2R)
nocturnal enuresis

26
Q

Tx of nephrogenic DI

A

maintain adequate H2O intake

thiazide diuretics

27
Q

thiazide diuretic MOA in DI

A

inhibit NCCT in DCT

  • mild depletion of ECF H2O&Na+
  • compensatory increase in PCT reabsorption
  • less volume delivered to DCT
28
Q

V1R agonists

A

terlipressin

29
Q

V1R agonists effect

A

GI & vascular smooth muscle contraction

30
Q

V1R agonists clinical uses

A

post operative ileus
reduce bleeding in
-esophageal varices
-acute hemorrhagic gastritis

31
Q

terlipressin ROA

A

IV (restricted use, less side effects than vasopressin)

32
Q

SIADH mechanism

A

excessive production of ADH

  • impaired H2O excretion (AKA too much reabsorption)
  • plasma hypoosmolarity (hyponatremia)
33
Q

SIADH etiology

A 
drug-induced
-psychotropics: SSRI, haloperidol, tricyclic antidepressants
-sulfonylureas: chloropropamide
-vinca alkaloids: vinblastine, vincristine
hypovolemia induced
-CHF
-liver cirrhosis
-nephrotic syndrome
34
Q

SIADH cutoffs (based on Posm)

A

Posm = 125-132mM –> asymptomatic

Posm begin treatment

35
Q

Tx for asymptomatic SIADH

A 
water restriction
(IV hypertonic saline)
36
Q

Tx for symptomatic SIADH

A 
water restriction
IV hypertonic saline
loop diuretics
demeclocycline
vaptans
37
Q

loop diuretics MOA in SIADH

A

interfere w/kidney concentrating ability

38
Q

demeclocycline MOA

A

technically an antibiotic

also antagonizes ADH at V2R

39
Q

V2R antagonists

A

tolvaptan

conivaptan

40
Q

tolvaptan clinical uses

A

hypervolemic/euvolemic hyponatremia
symptomatic hyponatremia w/CHF, cirrhosis, SIADH
only in hospital

41
Q

tolvaptan metabolism

A

CYP3

42
Q

tolvaptan ADEs

A

hyperglycemia
GI disturbances
clotting problems

43
Q

tolvaptan BBW

A

SLOWLY correct hyponatremia

  • monitor serum Na in the hospital
  • esp. for susceptible patients
  • too rapid can cause osmotic demyelination (and a crap ton of problems with it.. not including those here)
44
Q

pts susceptible to osmotic demyelination

A

severe malnutrition
alcoholics
advanced liver disease

45
Q

conivaptan ROA

A

IV

46
Q

conivaptan clinical uses

A

acute Tx of hyponatremia (in hospital setting)

47
Q

conivaptan metabolism

A

CYP3A4

48
Q

conivaptan ADE

A

infusion site reaction

probably also everything w/tolvaptan..

49
Q

conivaptan selectivity

A

V1a & V2 receptors

Renal (5 decks)

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