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GIR Test 3 > B5.050 Prework 1: Water Balance and Disorders of Water Metabolism > Flashcards

B5.050 Prework 1: Water Balance and Disorders of Water Metabolism Flashcards

1
Q

2 primary mechanisms that regulate ECF osmolarity

A 
mechanism of thirst (water intake)
kidney function ( water excretion)
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2
Q

proximal tubule water reabsorption

A

in a constitutive “automatic” fashion

linked to Na+

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3
Q

loop of henle water reabsorption

A

not directly involved in reabsorbing much water

fundamental for ADH dependent water balance

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4
Q

distal tubule water reabsorption

A
  1. regulated by ADH

2. secondary to NA+ reabsorption regulated by aldosterone

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5
Q

collecting duct water reabsorption

A

regulated by ADH

independent of Na+

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6
Q

what happens as a result of an increase in extracellular fluid osmolarity

A

activation of thirst center and osmoreceptors
water ingestion
ADH release
increased H2O reabsorption
increased osmolarity and decreased volume of urine produced

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7
Q

relationship between plasma ADH, urine osmolarity, and flow rate

A

min plasma ADH: max diuresis, min osmolarity

max plasma ADH: min diuresis, max osmolarity

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8
Q

loss of water > solutes

A

water reabsorption stimulated
urine volume decreases
urine concentration increases (hypertonic_

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9
Q

excess water over solutes

A

water excretion stimulated
urine volume increases
urine concentration decreases (hypotonic)

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10
Q

excess of isotonic fluid

A

water and solute excretion stimulated
increase in urine volume
isotonic urine

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11
Q

urine osmolarity

A

50-1200 mOsmole/kg H20

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12
Q

urine volume

A

0.5 to 20 L

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13
Q

stimuli that trigger ADH release

A

plasma osmolality
blood pressure
blood volume

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14
Q

summarize the mechanism of action of ADH

A

binds to V2 receptors on collecting duct to increase expression of aquaporins on apical membrane
binds to V1 receptors in vessel smooth muscles to stimulate vasoconstriction

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15
Q

2 major classes of disorders of water metabolism

A 
diabetes insipidus (low body water, polyuria)
syndrome of inappropriate ADH release (excess body water)
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16
Q

types of diabetes insipidus

A

ADH insufficiency (central)
reduced renal response to ADH (nephrogenic)
psychogenic polydipsia

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17
Q

causes of central DI

A

trauma
neurosurgery
primary or metastatic pituitary tumors
stroke (hypothalamic ischemia)

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18
Q

causes of nephrogenic DI

A

genetic (mutations in V2 receptor)
acquired (lithium)
renal tubular disease

19
Q

causes of inappropriate ADH

A

high ADH levels

presence of ADH like substances

20
Q

drugs that illicit an inappropriate ADH level

A

opioids
chlorpropamide
chlorpromazine
cytotoxins

21
Q

4 reasons for the presence of ADH like substances

A

pulm disorders (abscess, aspergillosis, tuberculosis)
CNS neurological disorders (infections, head injury, subarachnoid hemorrhage)
malignancy (pancreatic cancer, lymphoma, small cell lung cancer, prostate cancer)
endocrine (Addison disease, hypothyroidism)

22
Q

causes of solute diuresis

A

DM
Fanconi syndrome
inhibition of salt reabsorption by drugs
decreased aldosterone

23
Q

describe the process of solute diuresis

A

excess solutes in the filtrate > decreased water reabsorption in the proximal tubule > partial, but insufficient compensation by distal tubule reabsorption > urine osmolarity isotonic or close to plasma > increased urine volume

24
Q

describe the process of water diuresis

A

increased water ingested > decreased extracellular fluid osmolarity > decreased ADH secretion/ renal insensitivity to ADH > decreased nephron water permeability and reabsorption > solute reabsorption continues > increased urine dilution

25
Q

what is considered polyuria

A

> 3 L/day

26
Q

process of diagnosing polyuria

A
  1. history
  2. water restriction test (raises plasma osmolarity), monitor urine osmolarity and volume, measure plasma ADH levels, administer vasopressin
27
Q

water restriction test in central vs nephrogenic DI

A

urine osmolarity doesn’t increase and urine volume doesn’t decrease in response to water restriction
in central- responds to exogenous ADH (vasopressin)
in nephrogenic- no response to exogenous ADH

28
Q

SIADH causes…

A

hyponatremia (serum sodium < 135)

29
Q

ADH insufficiency causes…

A

hypernatremia (serum sodium > 145)

30
Q

causes of hyponatremia

A

excess water intake
hyponatremia with plasma hypertonicity (psuedohyponatremia)
hyponatremia with plasma hypotonicity

31
Q

reasons for hyponatremia with plasma hypertonicity (psuedohyponatremia)

A

severe hyperglycemia
hypertonic mannitol
hyperproteinemia (myeloma)
hyperosmolarity shifts water to the IVF

32
Q

reasons for hyponatremia with plasma hypotonicity

A

renal failure- low GFR with water retention
edematous states- CHF, cirrhosis, nephrotic syndrome
thiazides- alteration in renal water excretion
SIADH
endocrine- hypothyroidism, adrenal insufficiency

33
Q

causes of hypernatremia

A

extra-renal water loss
renal water loss
iatrogenic

34
Q

extra renal water losses

A 
insensible losses (fever, tachypnea, mechanical ventilation, sweat, burns)
GI losses
35
Q

renal water loss

A 
osmotic diuresis
central DI (head trauma, neoplastic, meningitis)
nephrogenic DI (chronic renal disease, acute renal failure, lithium)
36
Q

treatment of DI

A

ADH analogs

37
Q

treatment of SIADH

A 
control hyponatremia
fluid restriction
demeclocyclin (inhibitor of ADH V2)
tolvaptan, conivaptan (ADH V1/V2 receptor inhibitor)
correct underlying cause
38
Q

treatment of severe acute hyponatremia

A

raise plasma sodium but with 0.9% saline

39
Q

treatment of moderate acute hyponatremia

A

raise plasma sodium at lower rate and over longer period

stop if symptoms subside

40
Q

treatment of hypovolemic chronic hyponatremia

A

raise plasma sodium
control diarrhea
stop thiazides
control sodium loss

41
Q

treatment of euvolemic chronic hyponatremia

A

raise plasma sodium
water restriction
treat adrenal failure and hypothyroidism

42
Q

treatment of hypervolemic chronic hyponatremia

A

raise plasma sodium
water restriction
treat cardiac and renal failure

43
Q

treatment of hypernatremia

A

correct severe ECFV depletion with 0.9% sodium
continue with hypotonic fluid administration
calculate approximate water deficit
administer water replacement at a rate sufficient to correct hypernatremia but slowly enough to avoid cerebral edema
frequent monitor therapy checking sodium concentration

GIR Test 3 (19 decks)

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