Brainscape's Knowledge GenomeTM

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


See full index

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

proximal tubule water reabsorption

A

in a constitutive “automatic” fashion

linked to Na+

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

loop of henle water reabsorption

A

not directly involved in reabsorbing much water

fundamental for ADH dependent water balance

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

distal tubule water reabsorption

A
  1. regulated by ADH

2. secondary to NA+ reabsorption regulated by aldosterone

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

collecting duct water reabsorption

A

regulated by ADH

independent of Na+

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

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

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

loss of water > solutes

A

water reabsorption stimulated
urine volume decreases
urine concentration increases (hypertonic_

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

excess water over solutes

A

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

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

excess of isotonic fluid

A

water and solute excretion stimulated
increase in urine volume
isotonic urine

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

urine osmolarity

A

50-1200 mOsmole/kg H20

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

urine volume

A

0.5 to 20 L

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

stimuli that trigger ADH release

A

plasma osmolality
blood pressure
blood volume

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

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

types of diabetes insipidus

A

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

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

causes of central DI

A

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

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions