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RC Peds Endo 2023 > Water Balance > Flashcards

Water Balance Flashcards

1
Q

what receptor does ADH bind in the kidneys
what kind of R
where

A

V2
GPCR
collecting ducts and distal tubule

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2
Q

what are the ADH receptors and where are they

A

V1a - blood vessels: vasocronstriction

V2 - principle cells in renal collecting ducts: increased AQ2 on apical membrane

V3 (=V1b) - anterior pituitary: increases ACTH secretion

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3
Q

Regulatory of ADH secretion

A

Osmolality&raquo_space;> Volume > Pressure
○ 1% increase in Osm = AVP release
○ 10-fold higher required for V/P
- Baroreceptors (carotid, aorta)
- atrial stretch receptors
- plasma tonicity
- Pain, nausea
○ Ex head injury

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4
Q

what inhibits ADH release

A
  • GABA
  • Dynorphin
  • Somatostatin
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5
Q

effect of lithium on ADH?

A

inhibits action of AQ2 going on cell membrane after ADH binding to R

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6
Q

HyperCa effect on ADH?

A

inhibits action of AQ2 going on cell membrane after ADH binding to R

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7
Q

Plasma osmolality - what is it and how to calc

A

Plasma Osmolality = Osmotically active molecules in plasma

2 x [Na+] + 2 x [K+] + Glucose

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8
Q

SNS HypoNa

A

Seizures
Coma
Confusion/disorientation
Gait instability
Tremor
Asterixis
Myoclonus
Dysarthria
Muscle weakness
Cheyne-stokes respiration

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9
Q

HypoNa -first labs to rule out

A

HyperBG
HyperTG
Hyperproteinemia

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10
Q

HypoNa - volume status normal/high DDx

A

Urine Osm <200:
- Hypothyroidism
- GC def
- Nausea
- SIADH
- Carbamazepine, cyclophosphamide, vinblastine

Urine Osm >200:
- Psychogenic polydipsia
- Water intoxication

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11
Q

HypoNa - hypovolemic DDx

A

Urine Na >30
- Diuretic
- MC def
- Kidney disease (CKD, polycystic kidney)
- CSW
- Na administration

Urine <30
- non renal loss w XS water intake
- hypovolemic dehydration
- CHF
- Nephrotic syndrome
- Cirrhosis
- PPV

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12
Q

HypoNa - look at volume status and then what?

A

If hypovolemic -> look at urine SODIUM
– because it’s a water problem and that means you look at the Na

If eu-/hypervolemia -> look at urine OSM

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13
Q

what deficiencies decrease water excretion

A

Hypothyroidism and adrenal insufficiency

when present may mask diabetes insipidus

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14
Q

HyperNa - Ddx for hypovolemia

A

XS free water loss:
- Renal
– DI (C/N)
—osmotic diuresis w nonNa solute
— tubulopathy
- GI
—Diarrhea, emesis, stromal loss
- Derm
—burns
—sweating
- Premature neonates
- Pulmonary
—tachypnea
—mech vent
- AVP antagonist (captains)

Inadequate free water intake:
- inability to BF
- inadequate IVF in very sick kids
- neurologically impaired children w inability to communicate
- adipsia

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15
Q

HyperNa - Ddx for N/hi volume status

A

Na overload (usually w impaired/immature renal fn)
- Infants concentrated formula
- Infusion hypertonic saline
- Salt poisoning (munchausen by proxy)

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16
Q

Ddx polyuria

A
  • Central DI
    –congenital, LCH, germinoma, autoimmune hypophysitis
  • Congenital nephrogenic DI
  • Pregnancy induced DI
  • Hypercalcemia
  • Diuretic use
  • Glucocorticoid use
  • Diabetes mellitus
  • Primary polydipsia
  • HyperCa
  • HypoK
  • Fluid overload (ex post op)
  • Polyuric phase of renal failure or AKI/ATN
  • Cerebral salt wasting
  • UTI
  • Mannitol
  • Infiltrative renal diseases (e.g. histiocytosis)
  • Low sodium intake (diminished tonicity of renal medullary interstitium and NDI)
  • Decreased protein intake (diminished tonicity of renal medullary interstitium and NDI)
  • Sickle cell nephropathy
  • Lithium
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17
Q

what is nephrogenic SIADH
- what is it
- gene
- labs to differentiate from other SIADH

A

extremely rare mutation of the V2 receptor producing chronic activation
AVP2R gene

would have low AVP/copeptin level

18
Q

Meds causing SIADH

A
  • Desmopressin
  • SSRI, TCA, MOA
  • Chemo (cisplatin, cyclophosphamide, vincristine, vinblastine)
  • Anti-epileptic (carbamazepine)
  • Ecstasy
19
Q

Diagnostic Criteria

A
  • Hyponatremia <134
  • Hypoosm <280
  • Euvolemia
  • High urine Na >40
  • inappropriate conc urine for hypoNa >100
  • Excluded AI
  • Excluded hypothyroid
  • Excluded diuretic use
20
Q

Tx options for SIADH

A
  • 3% saline if sx’atic
  • fluid restrict
  • Loop diuretics (furosemide) - preferentially excrete free water over sodium or potassium
  • Sodium supplementation
  • Vaptans -> ADH-R antagonist
21
Q

DI Criteria

A

Pathlogic polyuria and polydipsia >2L/m2/day
AND
(EITHER Serum osm >300 and/or Na >145 with urine Osm <300
OR water dep w serum osm >300 and/or Na >145 with urine osm <600 and NOT rising despite plasma osm rising)

22
Q

Causes of CDI

A
  • surgery
  • trauma
  • cranio
  • germinoma
  • infiltration: LCH, sarcoid, mets
  • autoimmune
  • Idiopathic
  • Drugs: Ethanol; Phenytoin; Opiate antagonists; Halothane; Alpha-adrenergic agents
  • Congenital hypopituitarism
  • Familial
    — AD mutation in ADH: magnocellular cell death by the accumulation of misfolded AVP precursors within the endoplasmic reticulum (“toxic gain of function”)
    — AR mutation in ADH: early onset polyuria and hypernatremia
    —Wolfram syndrome (DIDMOAD: CDI, DM, optic atrophy, and deafness) AR with incomplete penetrance
23
Q

Causes of NDI

A

Drugs
- Lithium
- Vaptans
- Orlistat
- Cisplatin
- tetracyclin Abx

Labs
- hyperCa
- HypoK

Sickle cell

Syndromes:
- Bartter
- Bardet Biedl

Genetics:
- AVPR2 mutation
- AQP2 mutation

24
Q

Tests for DI

A
  • Water dep
  • Hypertonic Saline infusion
  • Arginine copeptin stimulation test
25
Q

Triple phase
- phases and duration, onset

A

DI (12h-few days)
onset day 1-2
- edema, cells “stunned”
- sometimes skip this phase

SIADH (up to 2 weeks)\
onset day 5-8
- ADH released as cells die

SI (indefinite)
onset variable, by day 14

26
Q

how to test or DI in infants

A

○ No water deprivation

○ Administer DDAVP (1 µg SQ or IV over 20 min, max dose 0.4 µg/kg)

○ Measure urine osm at baseline and Q30min x2 hours

○ If urine osm doesn’t increase by >100 mosmol/kg over baseline, the diagnosis of nephrogenic DI is made and DNA should be obtained for mutation analysis

27
Q

DI test: copeptin in water dep

A
  • Ratio of stimulated copeptin (change in copeptin level over 8hrs during water dep) to plasma sodium (at the end of test)

≥0.02pmol/L = complete central DI
<0.02pmol/L = partial central DI

28
Q

DI test: Plasma copeptin stimulated by hypertonic saline infusion

A

≤4.9 pmol/L = complete or partial central DI
>4.9 pmol/L = primary polydipsia

29
Q

Advantages of using copeptin

A
  • smaller sample volume
  • copeptin assay does not require extraction step or other pre-analytical procedure
  • copeptin is stable in plasma/serum ex vivo, handling is less complicated
30
Q

how does hypertonic saline test work

A

administration of hypertonic saline to increase serum osmolality above 300 mOsm/kg, with subsequent measurement of serum vasopressin levels -> should see it rise

31
Q

Copeptin helps differentiate what, how?

A

CDI:copeptin levels are low
primary polydipsia: intermediate
NDI: elevated

32
Q

CDI tx

A

thirst intact
- DDAVP, titrate to effect

thirst not intact
- DDAVP
- fluid restrict to 1L/m2/d

33
Q

Other than DDAVP, options to tx CDI

A
  • High free water intake
  • Low solute diet
  • Thiazide diuretic
  • Chlorpropamide
  • Carbamazepine
  • NSAID
34
Q

Excess extracellular volume (edema, ascites) + urine w:
- low Na
- high Na

A
  • low Na: hyperaldo
  • high Na: SIADH
35
Q

what is the post pit

A

not a gland but only the distal axon terminals of the hypothalamic magnocellular neurons that make up the neurohypophysis

36
Q

what hormone problems decreased water excretion

A

Hypothyroidism and adrenal insufficiency

when present may mask diabetes insipidus

37
Q

Atrial Natriuretic Peptide - what does it do
- where is it releases
- stimuli

A

Inhibits Aldosterone Secretion

Atria

increased volume,
increased Na,
neurologic inputs

38
Q

where are the V2 receptors

A

collecting duct of kidneys

39
Q

what will you see with DDAVP in water dec test with nephrogenic DI vs central DI

A

i. Nephrotic DI – urine osm <300 mOsm/kg and does not increase by >50% after DDAVP
ii. Complete central DI – urine osm increase by >50% after DDAVP

40
Q

2 meds to tx NDI

A

HCTZ - causes natriuresis which produces some contraction of extracellular fluid volume, decrease GFR, decreased delivery of fluid to the collecting duct, and a decreased urine volume

ii. Indomethacin - has antidiuretic action that especially prolongs the action of vasopressin and administered DDAVP, it also decrease urine volume

RC Peds Endo 2023 (17 decks)

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