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GU / GYN & Renal > B&B Renal: Electrolytes > Flashcards

B&B Renal: Electrolytes Flashcards

1
Q

Potassium

Electrolytes

A

Myocardial & skeletal muscle action potentials depend on potassium
* Imbalance:
* Heart: EKG changes. arrhythmias
* Muscle: weakness

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2
Q
  1. EKG changes: peaked T waves; QRS widening
  2. Arrhythmias: sinus arrest; AV block
  3. Muscle weakness: paralysis (LE –> trunk –> UE)

Signs & Symptoms

A

Hyperkalemia

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3
Q

Most common cause of hyperkalemia

Etiology

A

Reduced K+ excretion in urine
* Acute & chronic kidney disease

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4
Q

Hyperkalemia

Etiology

A
  • Reduced K+ excretion in urine
    * Acute & chronic kidney disease
    * Type IV RTA
  • Increased K+ release from cells
    • Acidosis: H+/K+ exchange; H+ in, K+ out
    • Insulin deficiency: inactive Na+/K+ ATPase
    • Beta-Blockers: inactive Na+/K+ ATPase
    • Digoxin: inactive Na+/K+ ATPase
    • Lysis of cells: K+ released from lytic cells
    • Hyperosmolarity: H2O w/ K+ leaves cells

HIgh intracellular concentration of K+

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5
Q

Na+/K+ ATPase

Transporter

A

Uses ATP to pump 3 Na+ out of cells & 2 K+ into cells
* Activators:
* Insulin
* Epinephrine
* Inhibitors:
* Beta-Blockers
* Digoxin

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6
Q

Hyperkalemia

Treatment

A

Aldosterone
* Stimulates renal K+ secretion

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7
Q
  1. EKG changes: flattened T waves; U waves
  2. Arrhythmias: PACs, PVCs; bradycardia
  3. Muscle weakness: paralaysis (LE –> trunk –> UE)

Signs & Symptoms

A

Hypokalemia

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8
Q

Most common causes of hypokalemia

Etiology

A
  • Diuretics: Loop
  • Vomiting / Diarrhea

Loop diuretics block NKCC in TAL

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9
Q

Hypokalemia

Etiology

A
  • Increased renal losses
    • Diuretics
    • Type I & II RTAs
  • Increased GI losses
    • Vomiting
    • Diarrhea
  • Increased K+ entry into cells
    • Hyperinsulinemia: overactive Na+/K+ ATPase
    • Beta-Agonists: overactive Na+/K+ ATPase
    • Alkalosis: H+/K+ exchange; K+ in, H+ out
  • Hypomagnesemia
    • Promotes urinary K+ excretion
    • Cannot correct K+ until Mg+ is corrected

Beta-Agonists: albuterol, terbutaline, dobutamine

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10
Q
  • Often asymptomatic
  • May cause recurrent kidney stones
  • Acute: polyuria, polydipsia

Signs & Symptoms

A

Hypercalcemia
- Acute: nephrogenic diabetes insipidus
- Loss of ability to concentrate urine
- AQP downregulation in CD principal cells
- Excessive free water excretion
- Decreased GFT –> acute renal failure
- Presentation: polyuria & polydipsia

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11
Q

Hypercalcemia

Etiology

A
  • Hyperparathyroidism: Ca2+ resorption from bone
  • Malignancy: degradation of bone releases Ca2+
  • Hypervitaminosis D: exogenous alcitriol; sarcoid
  • Milk-Alkali syndrome: excess calcium carbonate
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12
Q
  • Tetany = muscle twitches
    • Trousseau’s sign
    • Chvostek’s sign
  • Seizures

Signs & Symptoms

A

Hypocalcemia
* Ca2+ blocks Na+ channels in neurons
* Low Ca2+: spontaneous contractions
* High Ca2+: muscle weakness
* Hyperexcitability of neurons & motor endplates
* Trousseau’s sign: hand spasm with BP cuff
* Chvostek’s sign: facial muscle contraction with tapping on nerve

Tetany = classic sign of hypocalcemia

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13
Q

Hypocalcemia

Etiology

A
  • Hypoparathyroidism: no Ca2+ resorption
  • Renal failure: low 1,25-Vit D results in low Ca2+
  • Pancreatitis: Mg/Ca saponification of necrotic fat
  • Drugs: foscarnet
  • Magnesium: hypo- / hypermagnesemia
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14
Q

Hyperphosphatemia

Etiology

A
  • Reduced phosphate excretion into urine
    * Acute & chronic kidney disease
  • Hypoparathyroidism: increased PO4- resorption
  • Huge phosphate load due to lysis of cells
    * Tumor lysis syndrome
    * Rhabdomyolysis
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15
Q

Calcium-Phosphate in Renal Failure

A
  • Impaired phosphate excretion
    • High serum phosphate levels
    • Increased precipitation of serum Ca2+
  • Impaired Vitamin D activation
    • Low serum 1,25-(OH)2 Vitamin D levels
    • Reduced absorption of Ca2+ in GI tract
  • Both contribute to hypocalcemia
    • Hyperphosphatemia + hypocalcemia = characteristic of renal failure

Hypocalcemia induces PTH secretion; PTH increases Ca2+ & decreases PO4-

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16
Q

Hyperphosphatemia

Symptoms

A
  • Most patients are symptomatic
  • Symptomatic patients present with symptoms of hypocalcemia
    • Phosphate precipitates serum Ca2+
    • Hyperphosphatemia –> hypocalcemia
  • Metastatic calcifiations (calciphylaxis)
    • Seen in CKD with chronic hyperphosatemia
    • Excess phosphate is taken up by VSM
      • VSM osteogenesis –> calcification
    • Presentation:
      • Increased SBP: less vascular compliance
      • Small vessel thrombosis: painful nodules, skin necrosis
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17
Q
  • Main acute symptom: weakness
    • Often presents as respiratory muscle weakness
  • Chronic: bone loss, osteomalacia

Signs & Symptoms

A

Hypophosphatemia
* Due to ATP depletion

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18
Q

Hypophosphatemia

Etiology

A
  • Primary hyperparathyroidism
    • High PTH: PO4 excretion
  • Diabetic ketoacidosis (DKA): glycosuria
    • Osmotic diuresis: PO4 excretion
  • Refeeding syndrome in alcholics
    • Low phosphate due to malnutrition
    • Food intake –> metabolism –> lower PO4
  • Antacids: ammonium hydroxide
  • Fanconi syndrome: impaired PO4 resorption
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19
Q
  • Neuromuscular toxicity:
    • Decreased reflexes
    • Paralysis
  • Bradycardia, hypotension, cardiac arrest
  • Hypocalcemia

Signs & Symptoms

A

Hypermagnesemia
* Mg blocks Ca & K+ channels
* Neuromuscular toxicity
* Cardiac dysfunction
* Mg inhibits PTH secretion
* Hypocalcemia

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20
Q

Cause of hypermagnesemia

Etiology

A

Renal insufficiency
* Impaired Mg2+ excretion

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21
Q
  • Neuromuscular excitability
    • Tetany
    • Tremor
  • Cardiac arrhythmias
  • Hypocalcemia
  • Hypokalemia

Signs & Symptoms

A

Hypomagnesemia

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22
Q

Hypomagnesemia & Ca2+

Hypomagnesemia

A
  • Low Mg2+ –> stimulates PTH release like Ca2+
    • Increased GI absorption & renal reabsorption of Mg2+ along with Ca2+
  • Very low Mg2+ –> inhibits PTH release
    • Some Mg2+ is needed for normal Ca2+ receptor function in parathyroid gland
    • Dysfunction –> suppressed PTH release
    • Hypocalcemia seen in severe hypomagnesemia
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23
Q

Hypomagnesemia & K+

Hypomagnesemia

A

Mg2+ inhibits K+ excretion
* ROMK: apical membrane of CD cells
* Facilitates K+ secretion into urine
* Channel is inhibited by Mg2+
* Hypomagnesemia –> excess K+ excretion
* Results in hypokalemia
* K cannot be corrected until Mg is corrected
* Need Mg2+ to close ROMK

ROMK: renal outer medullary K channel

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24
Q

Hypomagnesemia

Etiology

A
  • GI losses (secretions contain Mg): diarrhea
  • Renal losses: loop & TZ diuretics; alcohol abuse
  • Pancreatitis: Mg/Ca saponification of necrotic fat
  • Drugs: omeprazole; foscarnet

Omeprazole –> impairs GI absorption of Mg2+

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25
Q

Hypomagnesemia

Etiology

A
  • GI losses (secretions contain Mg): diarrhea
  • Renal losses: loop & TZ diuretics; alcohol abuse
  • Pancreatitis: Mg/Ca saponification of necrotic fat
  • Drugs: omeprazole; foscarnet

Omeprazole –> impairs GI absorption of Mg2+

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26
Q

Foscarnet

A

Antiviral pyrophosphate analog
* Binds & inhibits viral DNA pol
* Adverse effects –> all electrolyte imbalances:
* Nephrotoxicity (limiting side effect)
* Seizures (due to electrolyte imbalances)
* Hypocalcemia (chelates calcium)
* Hypomagnesemia (increases renal losses)
* Hypokalemia
* Hypophosphatemia
* Hypercalcemia
* Hyperphosphatemia

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27
Q
A
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28
Q

Major regulators of Na+ & H20 Balance

Na+ / H2O Balance

A
  1. ADH
  2. SNS
  3. RAAS
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29
Q

Low ECV

Na+ / H2O Balance

A
  • Low ECV can lead to low BP
    • Can cause orthostatic hypotension
    • Dizziness / fainting when standing up
  • Low ECV activates:
    • SNS
    • RAAS
    • Result: Na+ / H2O retention
  • Some disease states have chronically low ECV
    • Chronic activation of SNS & RAAS
    • Chronic Na+/H2O retention by kidneys

Orthostatic hypotension = classic sign of any cause low ECV

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30
Q

Antidiuretic Hormone (ADH)

Na+ / H2O Balance

A

Promotes retention of free water
* Stimuli for release
* Hyperosmolarity
* Volume loss
* Plasma osmolality: major physiological stimulus
* Hyperosmolarity detected by hypothalamus
* ADH released by posterior pituitary gland
* ADH increases renal H2O resorption
* Responds to H2O intake to maintain [Na]
* Volume loss: 2nd trigger; non-osmotic release
* Activated with very low ECV

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31
Q

Water Balance

Na+ / H2O Balance

A
  • Water balance is maintained by ADH
    • ADH –> retention of excess free water
    • Levels modified to adjust H2O retention
  • Water balance is reflected by serum Na+
    • Serum Na+ is maintained at 140 mEq / L
    • Normal Na+: H2O in = H2O out (balance)
    • Hyponatremia: H2O in > H2O out
    • Hypernatremia: H2O in < H2O out
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32
Q

Excess Water

Regulation

A

H2O retention decreased to maintain normal [Na]
* High ECV = low osmolality
* Inhibits release of ADH
* Decreased H2O reabsorption
* Increased H2O excretion

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33
Q

Restricted Water

Regulation

A

H2O retention increased to maintain normal [Na]
* Low ECV = high osmolality
* Stimulates release of ADH
* Increased H2O reabsorption
* Decreased H2O excretion

34
Q

Na+ Balance

Na+ / H2O Balance

A
  • Serum Na+ is maintained at 140 mEq/L
  • Excess Na+ –> high osmolality
  • High osmolality –> H2O retention –> normal Na+
  • H2O retention –> increased ECV
  • Sodium intake expands ECV
35
Q

Excess Na+

Na+ Balance

A

H2O retention increased to maintain normal [Na]
* Excess Na+ –> high osmolality
* Stimulates release of ADH
* Increased H2O reabsorption
* Decreased H2O excretion
* Increased ECV

36
Q

Restricted Na+

Na+ Balance

A

H2O retention decreased to maintain normal [Na]
* Restricted Na+ –> low osmolality
* Inhibits release of ADH
* Decreased H2O reabsorption
* Increased H2O excretion
* Decreased ECV

37
Q

ECV

Regulation

A

ECV is controlled by SNS & RAAS
* Low ECV: active SNS & RAAS
* High ECV: inactive SNS & RAAS
* Na+ alters ECV –> alters SNS & RAAS activation

38
Q

Na+ Balance

Regulation

A
  • Excess intake –> expanded ECV; weight gain
    • High ECV: inactive SNS & RAAS
    • Result: increased Na+ excretion
      • Na+ out = Na+ in
      • Balance restored
  • Restricted intake –> contracted ECV; weight loss
    • Low ECV: active SNS & RAAS
    • Result: increased Na+ retention
      • Na+ out = Na+ in
      • Balance restored
39
Q

Na+ / H2O Imbalance

Effects

A
  • H2O imbalance
    • Alters serum [Na]
    • Results in hyponatremia / hypernatremia
  • Na+ imbalance
    • Alters TBW / ECV
    • Results in hypovolemia / hypervolemia
40
Q

GI Losses

Na+ / H2O Imbalance

A

Nausea, vomiting, diarrhea
* Results in activation of SNS & RAAS
* Volume loss (low ECV) –> ADH release
* Driven by volume sensors
* No longer controlled by serum [Na]
* Non-osmotic release of ADH
* Water balance control by ADH lost
* Free water always retained by kidneys
* [Na] determined by relative intake / losses
* Often results in hyponatremia
* Drinking free water –> H2O intake
* Not eating –> no Na+ intake

41
Q

Heart Failure

Na+ Imbalance

A

Low CO –> chronically low ECV
* Chronic activation of SNS & RAAS
* Na+ balance is disrupted
* Chronic Na+ retention by kidneys
* Na+ excretion is always reduced
* High Na+ intake: Na+ in > Na+ out
* Often results in hypervolemia
* Free H2O is retained to balance [Na]
* ECV does not increase w/ fluid retention
* Failing heart unable to increase CO
* HF pts always have low ECV
* Result: congestion
* Pulmonary edema
* Elevated JVP
* Pitting edema

42
Q

Heart Failure

H2O Imbalance

A

Low CO –> chronically low ECV
* Chronic non-osmotic release of ADH
* ADH levels always high
* Release driven by volume sensors
* No longer controlled by serum [Na]
* Water balance control by ADH lost
* Free H2O always retained by kidneys
* [Na] determined by relative intake / losses
* Often results in hyponatremia

43
Q

SIADH

Syndrome of Inappropriate ADH Secretion

A

Excess ADH release
* Excess H2O retention –> hyponatremia
* Normal total body water
* H2O retention –> expanded ECV
* Inactive SNS & RAAS
* Na+ excretion –> reduces ECV
* Na+ balance restored
* Key findings:
* Hyponatremia
* Normal volume status
* Concentrated urine

44
Q

Sodium Disorders

Water Balance

A

Disorders involving water balance
* Hyponatremia = too much water
* Hypernatremia = too little water

45
Q

Sodium Symptoms

A
  • Hypo- & hypernatremia affect braim
  • Low Na+ = low plasma osmotic pressure
    • Fluid into tissues
    • Brain swells
  • High Na+ = high plasma oncotic pressure
    • Fluid out of tissues
    • Brain shrinks
46
Q
  • Malaise, stupor, coma
  • Nausea

Symptoms

A

Hyponatremia

47
Q

Hyponatremia

Diagnostic Tests

A
  1. Plasma osmolality
  2. Urinary Na+
  3. Urinary osmolality
48
Q

Plasma Osmolality (pOsm)

Hyponatremia

A

Amount of osmotically active solutes present in plasma
* Key solute: Na+
* Normal pOsm: 285 mOsm/kg
* Osmolality should be low in hyponatremia

49
Q

Hyponatremia with High Osmolality

Plasma Osmolality

A

Hyperglycemia or mannitol
* Glucose / mannitol = osmoles
* Raises plasma osmolality
* Draws water out of cells into plasma
* Increases blood volume & dilutes [Na]
* Results in hyponatremia

50
Q

Hyponatremia with Normal Osmolality

Plasma Osmolality

A

Artifact in serum Na+ measurement
* Solutes in plasma interfere with measurement
* Hyperlipidemia
* Hyperproteinemia

51
Q

Urine Osmolality

Urine Studies

A

Concentrations of all osmoles in urine
* Osmoles: Na, Cl, K, Urea
* Varies with H2O intake & urinary concentration
* Low uOsm: dilute urine; H2O excretion
* High uOsm: concentrated; H2O retention

52
Q

Urinary Sodium

Urine Studies

A
  • Normal: >20 mEq/L
  • Varies with dietary Na+ & free H2O in urine
  • Usually high when urine osmolarity is high
  • Exceptions: involve SNS & RAAS activation
    • Increased Na+ & H2O resorption
    • Low urinary Na+, high uOsm
    • Examples: hemorrhage, HF, cirrhosis
53
Q

Hyponatremia

General Principles

A
  • Urine should be dilute
    • Free H2O > solutes
    • Low urine osmolality (< 100 uOsm/kg)
    • Low urine Na+ (< 30 mEq/L)
  • If urine is dilute:
    • Kidneys responding appropriately
    • ADH is appropriately low
    • Problem is outside kidneys
  • If urine is not diluted:
    • Kidneys are not responding appropriately
    • Too much ADH or impaired kidney function
54
Q

Hyponatremia

Etiology

A
  1. Heart failure & cirrhosis
  2. Impaired renal function
  3. High ADH
  4. Psychogenic polydipsia / dietary causes
55
Q

Heart Failure & Cirrhosis

Etiology

A
  • Perceived hypovolemia
    • HF: low CO –> low ECV
    • Cirrhosis: vasodilation –> low SVR
  • Non-osmotic release of ADH
    • Chronic production of ADH
    • Chronic H2O retention
    • Urine is not diluted (uOsm > 100)
    • Clinical signs of hypervolemia
    • Excess H2O intake will result in hyponatremia
56
Q

Advanced Renal Failure

Impaired Renal Dysfunction

A

Impaired H2O excretion –> increased H2O retention
* Urine cannot be diluted –> min uOsm rises
* Min uOsm is minimum urine osmolarity (i.e., max dilution) that kidneys can achieve in setting of low ADH
* Normally with low ADH: uOsm < 100
* Renal failure: uOsm = 200-250
* Key point: increased uOsm in setting of hyponatremia indicates abnormal response to low serum [Na]
* Urine should be diluted (low uOsm) during hyponatremia to eliminate excess H2O
* May present with euvolemia or hypervolemia

57
Q

Diuretics

Impaired Renal Function

A

Promote Na+ & H2O excretion
* Can disrupt Na+ / H2O balance and cause hyponatremia
* Most common with TZ diuretics

58
Q

Loop Diuretics

Diuretics

A

Block Na+ reabsorption by NKCC in TAL of Henle
* NKCC creates medullary osmotic gradients
* TAL is impermeable to H2O
* Na+ reabsorption increases interstitial Osm & decreases urinary Osm
* Osmotic gradients are driving force for H2O resorption
* NKCC inhibition diminishes medullary gradients
* Results in inability to resorb free H2O
* Low likelihood of excess H2O resorption resulting in hyponatremia
* Diuretic effects: decrease Na+ reabsorption & decrease ability to reabsorb H2O

NKCC: Na-K-Cl channel

59
Q

Thiazide (TZ) Diuretics

Diuretics

A

Block Na+ reabsorption by NCC in distal tubule
* NCC inhibition decreases Na+ reabsorption
* Increases urinary Na+ & uOsm
* Medullary osmotic gradients remain intact
* Ability to resorb free H2O is intact
* Higher likelihood of excess H2O retention resorption resulting in hyponatremia
* Diuretic effect: decrease Na+ reabsorption

NCC: Na+/Cl- cotransporter

60
Q

High ADH

Hyponatremia

A

Dehydration results in high ADH
* Any cause of dehydration
* Vomiting, diarrhea
* Diaphoresis
* Serum [Na] depends on H2O intake
* Excess free H2O intake –> hyponatremia

61
Q

High ADH

Etiology

A
  • Adrenal insufficiency –> increases ADH
    • Loss of cortisol: ADH release is uninhibited
    • Loss of aldosterone: loss of Na+ / H2O loss
  • Hypothyroidism
  • SIADH
    • Inappropriate ADH release
    • Must exclude other causes: HF, cirrhosis, dehydration, thyroid / adrenal disease
62
Q

SIADH

Etiology

A
  1. Drug-induced: carbamazepine, cyclophosphamide
  2. Paraneoplastic syndrome: SCLC
  3. CNS diseases
  4. Pulmonary disease
63
Q

SIADH

Diagnostic Criteria

A
  • Hypotonic hyponatremia: low pOsm, low serum [Na]
  • Normal liver, renal, cardiac function
  • Cinical euvolemia
  • Nornal thyroid, adrenal function
  • Concentrated urine: uOsm >100 mOsm/kg
64
Q

SIADH

Treatments

A
  • Most common: fluid restriction
  • Special treatment: demeclocycline
    * Tetracycline antibiotic
    * ADH antagonist
65
Q

Psychogenic Polydipsia

Hyponatremia

A
  • Occurs in psychiatric patients
    • Compulsive water drinkers
  • Hyponatremia –> need to drink >18 L/day
  • Low uOsm (<100)
    • Kidneys respond appropriately
    • Water intake is just too high
  • Water restriction resolves hyponatremia
66
Q

Volume Status in Hyponatremias

A
  • Hypervolemic
    • Cirrhosis
    • CHF
    • Renal failure
  • Euvolemic
    * SIADH
    * Hypothyroidism
    * Secondary adrenal insufficiency
    * Renal failure
    * Polydipsia
    * Dietary
  • Hypovolemic
    * Dehydration
    * Diuretics
    * Primary adrenal insufficiency
67
Q

Euvolemic Hyponatremia

Diagnosis

A

Measure urinary Osm
* uOsm <100: kidneys responding appropriately
* Psychogenic polydipsia
* Diet (tea, beer)
* uOsm >100: kidneys not responding
* SIADH
* Hypothyroidism
* Renal failure

68
Q

Hypovolemic Hyponatreamia

Diagnosis

A

Measure urinary [Na]
* u[Na] <30 mEq/L: extra-renal etiology
* Vomiting
* Diarrhea
* Sweating
* u[Na] >30 mEq/L: renal etiology
* Diuretics
* Primary adrenal disease (low aldosterone)

69
Q

Increased ADH & uOsm

Hyponatremia

A
  • Hypervolemic: low ECV –> H2O retention
    • Cirrhosis
    • CHF
  • Euvolemic
    * SIADH
    * Hypothyroidism
    * Secondary adrenal insufficiency
  • Hypovolemic: low ECV –> H2O retention
    * Dehydration
    * Diuretics
    * Primary adrenal insufficiency
70
Q

Decreased ADH & uOsm

Hyponatremia

A

Euvolemic: polydipisa, dietary
* Kidneys responding appropriately but unable to excrete adequate amount of free H2O

71
Q

Decreased ADH, Increased uOsm

A

Renal failure: hypervolemic or euvolemic
* Kidneys unable to dilute urine despite low ADH

72
Q

Hyponatremia

Treatment

A
  • Fluid restriction
  • 3% saline infusion
  • Vaptan-drugs: block ADH
    * Main use: severe hyponatremia in HF
73
Q

Central Pontine Myelinolysis

Osmotic Demyelination Syndrome

A
  • Associated w/ overly rapid correction of low [Na]
    • > 10 mEq/L increase in [Na] per 24 hours
  • Causes demyelination of central pontine axons
    • Lesion at base of pons
    • Loss of corticospinal & corticobulbar tracts
  • Results in quadriplegia
74
Q
  • Irritability
  • Stupor
  • Coma

Symptoms

A

Hypernatremia

75
Q

Hypernatremia

Etiology

A
  • Water loss
    • Skin & lungs: loss of H2O&raquo_space; Na+
    • Kidneys respond by concentrating urine & retaining free H2O
    • High ADH
    • High uOsm
  • Diabetes insipidus (DI)
    • Loss of ADH activity
    • Central: loss of ADH release from pituitary
    • Nephrogenic: ADH insensitivity
      * Congenital (rare
      * Acquired: many causes
76
Q

Acquired DI

Etiology

A

Acquired ADH insensitivity
1. Hypercalcemia
2. Hypokalemia
3. Drugs: lithium, amphotericin B

77
Q

Diabetes Insipidus

Diagnosis

A
  • Suspected with polyuria & polydipsia
  • Serum [Na]: typically normal
    • Water loss stimulates thirst
    • Hypernatremia occurs if not enough H2O intake
    • Central lesion (DI) can impair thirst
  • uOsm: low (50-200 mOsm/kg)
  • Fluid restriction
    • After 8 hours of no fluid, urine should be concentrated
    • If urine is dilute –> absent/ineffective ADH
  • Administration of vasopressin / desmopressin
    • Should concentrate urine if kidneys are functional
    • Concentrated urine = central DI
    • Dilute urine = nephrogenic DI
78
Q

Hypernatremia

Treatment

A
  • Water (ideally PO)
  • IV fluids (D5W, isotonic but no Na+)
79
Q

Central DI

Treatment

A

Desmopressin
* ADH analog
* No vasopressor effect (unlike vasopressin)

80
Q

Nephrogenic DI

Treatment

A

TZ diuretics & NSAIDs
* TZ diuretics
* Mild state of volume depletion causes increased Na+ / H2O resorption in proximal tubule
* Less H2O delivery to collecting ducts
* Paradoxical antidiuretic effects
* NSAIDs
* Inhibit renal synthesis of prostaglandins
* Prostaglandins = ADH antagonists

GU / GYN & Renal (23 decks)

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