Test 2: Wk7: 6 Water Balance - Puri Flashcards by Zane Griffith

— and — consumption decide solute excretion

salt and protein

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— controls water excretion

hydration

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if free water clearance is negative the kidney is

conserving water

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CH2O =

CH2O = V (1 - (Uosm / Posm)

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max and min free water clearance

1200 mOm/L

50 mOm/L

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function of the countercurrent mechanism

create urine with an osmolarity different from serum osmolarity

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countercurrent mechanism conserve water

generates urine osmolarity greater than plasma

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countercurrent mechanism excrete water

urine osmolarity less than plasma

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concentrated urine is produced when — is present in the plasma

ADH

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In the absence of — a dilute urine is produced.

ADH

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

The descending limb

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

The ascending limb

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Reabsorption of NaCl without water creates a

dilute urine

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— is called the “diluting segment”

The thick ascending limb

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The interstitial around Henle’s loop provides the ΔOsm for

water to cross compartments

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

hypertonic; tonicity

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— & — are required for renal water conservation

Hypertonic medullary interstitium and ADH

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Medullary Hypertonicity does what

draws water out

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ADH Provides

water permeability

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

tALH, TAL, DCT—

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urine at the end of the proximal tubule is always

isotonic

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— and — are impermeable to water

tALH and TAL

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Medullary Hypertonicity is Made By (3)

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

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Urine osmolality — and then —

along the nephron

rises; falls

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Na transport in TAL

active

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

tDLH

urea recycling

Urea that diffuses out of the MCD re-enters | the tubules in the thin limbs

ADH and urea

ADH responsible for removing urea

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

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

negative

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

positve

ADH (AVP) binds to, and activates, ---on the --- of the nephrons and increases --- This leads to

V2 receptor; collecting ducts; cAMP recycling of AQP2 & UT-A1 to the luminal membrane

Through V1 receptor AVP induces

vasoconstriction and platelet aggregation

Normal control of ADH Secretion is via the

osmoreceptors

Osmoreceptors normally control

urine water excretion

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

conserves

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

ALL, V2

Primary effect of ADH increase

increase of AQP2 channels into the cell membrane

Additional effects of ADH increase

increase ins NKCC2 activity in TAL | Increase urea permeability in collecting duct

two key stimulators of ADH release

↑Plasma osmolarity and ↓intravascular volume

if urine osmolarity > plasma osmolarity,

CH2O is NEGATIVE— | urine is concentrated

if urine osmolarity < plasma osmolarity,

CH2O is POSITIVE

if urine osmolarity ≈ plasma osmolarity

CH2O is zero (seen with | loop diuretics)

Too little ADH activity

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

Too much ADH activity

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

Central diabetes insipidus

inability of the neurohypophysis to release AVP in response to osmolality increases very low or unmeasurable levels of serum AVP, too low for Posm

Nephrogenic diabetes insipidus

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

Gestational diabetes insipidus

elevated levels or activity of placental vasopressinase during pregnancy very low or unmeasurable levels of serum AVP

Primary polydipsia

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

Osmoreceptor dysfunction

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

Diabetes Insipidus Central is

Idiopathic

Diabetes Insipidus Central Genetic defect

Dominant (AVP gene mutation) Recessive (DIDMOAD syndrome

Recessive DIDMOAD syndrome

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

Diabetes Insipidus 2 types

central and nephrogenic

Diabetes Insipidus Nephrogenic genetic defect (2)

V2 receptor mutation | Aquaporin-2 mutation

Diabetes Insipidus Nephrogenic Drug therapy

* Lithium * Demeclocycline Poisoning * Heavy metals

Diabetes Insipidus Nephrogenic associated with

Chronic kidney disease

Diabetes Insipidus Symptoms

Large volumes 3.5-20 L/d of dilute urine are produced Blood volume↓, while [Na+]↑ and osmolality↑ extreme thirst, and polydipsia

most Diabetes Insipidus patients are not

hypernatremic

Central Diabetes Insipidus tx

Hormone replacement

Central Diabetes Insipidus Hormone replacement (2)

Vasopressin - not used DESMOPRESSIN

Nephrogenic Diabetes Insipidus Results from

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

Nephrogenic Diabetes Insipidus tx

both types of diabetes insipidus can be treated with thiazide diuretics

Nephrogenic Diabetes Insipidus response to DDAVP

does not respond

Convaptan action

V1A and V2 Antagonist

Convaptan lowers blood volume, | only use in --- and --- patients

euvolemic and hypervolemic

Convaptan administration

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

Tolvaptan action

Selective V2 antagonist

Tolvaptan administration

oral tablets

Tolvaptan indication

tx of hyponatremia

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

euvolemic and hypervolemic

Tolvaptan only use if pts are

symptomatic

Tolvaptan for pts with

SIADH and CHF

Tolvaptan can produce

liver toxicity so therapy limited to 30 days

Tolvaptan can produce

liver toxicity so therapy limited to 30 days

Lithium Carbonate use

off label use tx of hyponatremia | SIADH

Lithium Carbonate indications

Antimanic drug | Significant toxicity if [Li+]plasma > 1mM

Lithium Carbonate side effects

30% patients→ diabetes insipidus | Renal handling analogous to sodium Re-absorbed by CD cells via Na+ channels

Lithium Carbonate side effects tx

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

Tetracycline antibiotic with unique property

Demeclocycline

Demeclocycline side effect

Diabetes insipidus, mechanism same as Li+

Demeclocycline use (4)

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

Demeclocycline is

Less toxic and effects more predictable than Li+