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BMS 615 Cardiovascular > Test 2: Wk7: 6 Water Balance - Puri > Flashcards

Test 2: Wk7: 6 Water Balance - Puri Flashcards

1
Q

— and — consumption decide solute excretion

A

salt and protein

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2
Q

— controls water excretion

A

hydration

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3
Q

if free water clearance is negative the kidney is

A

conserving water

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4
Q

CH2O =

A

CH2O = V (1 - (Uosm / Posm)

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5
Q

max and min free water clearance

A

1200 mOm/L

50 mOm/L

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6
Q

function of the countercurrent mechanism

A

create urine with an osmolarity different from serum osmolarity

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7
Q

countercurrent mechanism conserve water

A

generates urine osmolarity greater than plasma

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8
Q

countercurrent mechanism excrete water

A

urine osmolarity less than plasma

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9
Q

concentrated urine is produced when — is present in the plasma

A

ADH

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10
Q

In the absence of — a dilute urine is produced.

A

ADH

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11
Q

— is impermeable to solutes, but freely permeable to water.

A

The descending limb

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12
Q

— reabsorbs large quantities of NaCl & is impermeable to water.

A

The ascending limb

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13
Q

Reabsorption of NaCl without water creates a

A

dilute urine

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14
Q

— is called the “diluting segment”

A

The thick ascending limb

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15
Q

The interstitial around Henle’s loop provides the ΔOsm for

A

water to cross compartments

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16
Q

The medullary interstitium in the juxtaglomerular nephrons is —, with — increasing towards the hairpin loop

A

hypertonic; tonicity

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17
Q

— & — are required for renal water conservation

A

Hypertonic medullary interstitium and ADH

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18
Q

Medullary Hypertonicity does what

A

draws water out

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19
Q

ADH Provides

A

water permeability

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20
Q

Urine is progressively diluted by the —, —, and — regardless of the state of hydration

A

tALH, TAL, DCT—

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21
Q

urine at the end of the proximal tubule is always

A

isotonic

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22
Q

— and — are impermeable to water

A

tALH and TAL

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23
Q

Medullary Hypertonicity is Made By (3)

A
  1. Thin ascending limb—passive transport
    2.Thick ascending limb—NKCC2
    3.Collecting duct—urea transport by UTA1
    —stimulated by ADH
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24
Q

Urine osmolality — and then —

along the nephron

A

rises; falls

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25
Q

Na transport in TAL

A

active

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26
Q

The Presence of Urea draws water out of the —, concentrating urine with NaCl.

A

tDLH

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27
Q

urea recycling

A

Urea that diffuses out of the MCD re-enters

the tubules in the thin limbs

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28
Q

ADH and urea

A

ADH responsible for removing urea

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29
Q

if free water clearance is negative then Na excretion > < =water excretion

A

>

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30
Q

If urinary osmolality is greater than

plasma—free water clearance is said to be

A

negative

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31
Q

If urinary osmolality is less than plasma —free water clearance is said to be

A

positve

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32
Q

ADH (AVP) binds to, and activates, —on the — of the nephrons and increases —

This leads to

A

V2 receptor; collecting ducts; cAMP

recycling of AQP2 & UT-A1 to
the luminal membrane

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33
Q

Through V1 receptor AVP induces

A

vasoconstriction and platelet aggregation

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34
Q

Normal control of ADH Secretion is via the

A

osmoreceptors

35
Q

Osmoreceptors normally control

A

urine water excretion

36
Q

In response to heart failure or hypovolemic shock the kidney — NaCl and water

37
Q

ADH increases water permeability of — nephron segments after distal convoluted tubule —action of —receptors

38
Q

Primary effect of ADH increase

A

increase of AQP2 channels into the cell membrane

39
Q

Additional effects of ADH increase

A

increase ins NKCC2 activity in TAL

Increase urea permeability in collecting duct

40
Q

two key stimulators of ADH release

A

↑Plasma osmolarity and ↓intravascular volume

41
Q

if urine osmolarity > plasma osmolarity,

A

CH2O is NEGATIVE—

urine is concentrated

42
Q

if urine osmolarity < plasma osmolarity,

A

CH2O is POSITIVE

43
Q

if urine osmolarity ≈ plasma osmolarity

A

CH2O is zero (seen with

loop diuretics)

44
Q

Too little ADH activity

A

Leads to excessive water loss in urine, excessive urine volume of dilute
urine and increase in plasma sodium – Diabetes Insipidus

45
Q

Too much ADH activity

A

Leads to too much water reabsorption, hyponatremia and potential
hypervolemia – patients with brain injuries (SIADH) and patients on loop diuretics

46
Q

Central diabetes insipidus

A

inability of the neurohypophysis to release AVP in response to osmolality increases

very low or unmeasurable levels of serum AVP, too low for Posm

47
Q

Nephrogenic diabetes insipidus

A

caused by the inability of an otherwise normal kidney to respond to AVP

elevated serum AVP

48
Q

Gestational diabetes insipidus

A

elevated levels or activity of placental vasopressinase during pregnancy

very low or unmeasurable levels of serum AVP

49
Q

Primary polydipsia

A

disorder of excess fluid ingestion rather than of vasopressin secretion or activity—usually psychogenic

very low or unmeasurable levels of serum
AVP, but appropriate to low Posm

50
Q

Osmoreceptor dysfunction

A

polyuria, but no polydipsia—very low or unmeasurable levels of serum AVP—Only DI with hypernatremia

51
Q

Diabetes Insipidus Central is

A

Idiopathic

52
Q

Diabetes Insipidus Central Genetic defect

A

Dominant (AVP gene mutation)

Recessive (DIDMOAD syndrome

53
Q

Recessive DIDMOAD syndrome

A

association of diabetes insipidus with diabetes mellitus, optic atrophy,
deafness

54
Q

Diabetes Insipidus 2 types

A

central and nephrogenic

55
Q

Diabetes Insipidus Nephrogenic genetic defect (2)

A

V2 receptor mutation

Aquaporin-2 mutation

56
Q

Diabetes Insipidus Nephrogenic Drug therapy

A
  • Lithium
  • Demeclocycline Poisoning
  • Heavy metals
57
Q

Diabetes Insipidus Nephrogenic associated with

A

Chronic kidney disease

58
Q

Diabetes Insipidus Symptoms

A

Large volumes 3.5-20 L/d of dilute urine are produced

Blood volume↓, while [Na+]↑ and osmolality↑

extreme thirst, and polydipsia

59
Q

most Diabetes Insipidus patients are not

A

hypernatremic

60
Q

Central Diabetes Insipidus tx

A

Hormone replacement

61
Q

Central Diabetes Insipidus Hormone replacement (2)

A

Vasopressin - not used

DESMOPRESSIN

62
Q

Nephrogenic Diabetes Insipidus Results from

A

Genetic defects in ADH receptor (X-linked) or aquaporin-2 (Autosomal)

drug side effect

63
Q

Nephrogenic Diabetes Insipidus tx

A

both types of diabetes insipidus can be treated with thiazide diuretics

64
Q

Nephrogenic Diabetes Insipidus response to DDAVP

A

does not respond

65
Q

Convaptan action

A

V1A and V2 Antagonist

66
Q

Convaptan lowers blood volume,

only use in — and — patients

A

euvolemic and hypervolemic

67
Q

Convaptan administration

A

Continuous IV infusion for maximum of 4 days, hence only used in hospitalized patients

68
Q

Tolvaptan action

A

Selective V2 antagonist

69
Q

Tolvaptan administration

A

oral tablets

70
Q

Tolvaptan indication

A

tx of hyponatremia

71
Q

Since Tolvaptan can produce hypovolemia/dehydration, only use in — and
— patients

A

euvolemic and hypervolemic

72
Q

Tolvaptan only use if pts are

A

symptomatic

73
Q

Tolvaptan for pts with

A

SIADH and CHF

74
Q

Tolvaptan can produce

A

liver toxicity so therapy limited to 30 days

75
Q

Tolvaptan can produce

A

liver toxicity so therapy limited to 30 days

76
Q

Lithium Carbonate use

A

off label use tx of hyponatremia

SIADH

77
Q

Lithium Carbonate indications

A

Antimanic drug

Significant toxicity if [Li+]plasma > 1mM

78
Q

Lithium Carbonate side effects

A

30% patients→ diabetes insipidus

Renal handling analogous to sodium Re-absorbed by CD cells via Na+ channels

79
Q

Lithium Carbonate side effects tx

A

thiazides, but lower Li+ dose, as reuptake in PT↑

80
Q

Tetracycline antibiotic with unique property

A

Demeclocycline

81
Q

Demeclocycline side effect

A

Diabetes insipidus, mechanism same as Li+

82
Q

Demeclocycline use (4)

A

off-label use for tx of hyponatremia
SIADH
Heart failure
liver disease

83
Q

Demeclocycline is

A

Less toxic and effects more predictable than Li+

BMS 615 Cardiovascular (49 decks)

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