Edoncr. posterior. SIADH, polydipsia, DI 11-01 (1) Flashcards
Stimuli for ADH secretion. Osmotic?
Serum osmolality > ~ 285
Stimuli for ADH secretion. Nonosmotic?
Nausea
Pain
Physical or emotional stress
Hypotension
Hypovolemia
Hypoxia
Hypoglycemia
SIADH. CNS etiologies?
eg. stroke, hemorrhage, trauma
SIADH. Medication etiologies?
eg carbamazepines, SSRIs, NSAIDs
SIADH. Lung etiologies?
eg pneumonia
SIADH. Ectopic secretion?
eg small cell lung cancer
SIADH. also etiology - pain and nausea
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SIADH. CP?
Volume status and sodium.
Euvolemia - moist mucous membranes, no edema, no JVD
Mild/moderate hypoNa - nausea, forgetfulness
Severe hypoNa - seizures, coma
SIADH. labs?
HypoNa
Serum osmolality - hypotonic < 275
Urine osmolality > 100
Urine sodium > 40
SIADH. management?
Fluid restriction (< 800 ml/day) +/- salt tablets
For severe - hypertonic saline 3 proc.
Correction gradual (max 10mmol/l within 24 hours, or 0.5 mmol/L/hour) and under ICU observation to
prevent central pontine myelinolysis.
Reverse underlying disease.
Induce diabetes insipidus by giving demeclocycline.
Poliuria. Po situ slepiasi 3 dalykai: primary polydipsia, central and nephrogenic DI.
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Primary polydipsia - cause mechanism?
ADH independent (excessive water intake)
Central DI - cause mechanism?
ADH deficiency (CNS pathology)
Nephr DI - cause mechanism?
ADH resistance (renal disease)
Primary polydipsia - etiology?
Antipsyhotics (dry mouth)
Psychiatri conditions
Central DI - etiology?
Idiopathic
Trauma
Pituitary surgery
Ischemic encephalopathy
Nephr DI - etiology?
Chronic lithium use
HyperCALCEMIA
Hereditary mutations in aquaporins (AVPR2 - vasopressor V2 and aqua 2 mutations)
Primary polydipsia - water deprivation result?
High urine osmolality
Central DI - water deprivation result?
Low urine osmolality
Nephr DI - water deprivation result?
Low urine osmolality
Primary polydipsia - response to desmopressin?
No change
Central DI - response to desmopressin?
Increased urine osmolality
Nephr DI - response to desmopressin?
No change
Evaluation of suspected polyuria scheme. first step?
complete 24h urine collection
Evaluation of suspected
polyuria scheme. 24h urine collection –> urine output < 3l –>?
No true polyuria;
work up causes of urinary frequency
Evaluation of suspected
polyuria scheme. 24h urine collection –> urine output > 3l = polyria present –> what evaluate then?
dilute or concentrated urine
Evaluation of suspected
polyuria scheme. > 3l = polyria present –> concentrated urine - what diuresis and causes?
OSMOTIC diuresis
Increased solute excretion (glucose, urea, saline)
Evaluation of suspected
polyuria scheme. > 3l = polyria present –> dilute urine - what diuresis and causes?
WATER diuresis
Primary polydipsia, DI
Water deprivation scheme. first thing prior test?
No water 2-3h prior to test
Water deprivation scheme.
No water 2-3h prior to test –> 2 things to evalute?
Measure urine volume and osmolality every hour
Measure serum osmolality and osmolality every 2 hours
Water deprivation scheme.
No water 2-3h prior to test –> evaluate serum (Na) and urine (volume) and osmolality –> Urine osmol > 600 YES –>?
Primary polydipsia
Water deprivation scheme.
No water 2-3h prior to test –> evaluate serum (Na) and urine (volume) and osmolality –> Urine osmol > 600 NO –>? evaluate and raise 2 questions
Urine osmol stable on 2-3 consecutive hourly measurements
Plasma osmol > 295 or plasma sodium Na > 145
Water deprivation scheme.
Urine osmol stable on 2-3 consecutive hourly measurements
Plasma osmol > 295 or plasma sodium Na > 145
NO –>?
Continue testing until these endpoints are reached
Water deprivation scheme.
Urine osmol stable on 2-3 consecutive hourly measurements
Plasma osmol > 295 or plasma sodium Na > 145
YES –>? what to do and monitor
Administer desmopresin
Monitor urine osmol and volume every 30 min for 2 hours.
Water deprivation scheme.
Administer desmopresin
Monitor urine osmol and volume every 30 min for 2 hours.
When get results, diff. central and neph DI. on what changes?
Central DI: incr. urine osmolality 50-100 proc.
Nephr DI: small or no incr. in urine osmolality.
Mehl. SIADH. central causes?
follows head trauma, meningitis, brain cancer, and pain (latter on 2CK Surg)
Mehl. SIADH. ectopic causes?
small cell lung cancer secreting ADH.
Mehl. drug induced ADH causeS?
ultra-rare on USMLE, but carbamazepine can do it.
Mehl. SIADH. Na, serum osmol, serum spec. gravity
urinary osmol, urinary spec. gravity
Na - low
serum osmol - low
serum spec gravity - low
urine oslom - high
rinary spec. gravity - high
M. - You must know serum sodium is normally 135-145 mEq/L. So in SIADH, it’s <135.
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M. - Serum vs urinary osmolalities will be all over the place and you do not need to memorize values. They might say serum osmolality is 250 and urinary is 750, and then you say, “Well I can tell serum is dilute compared to urine, which sounds like SIADH.”
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M. Specific gravity will be 1.000-1.030 on USMLE. Sounds obscure, but it shows up quite a bit, particularly on 2CK Qs. It’s to my observation that values 1.000-1.006ish are “dilute”; 1.024-1.030 are “concentrated.” For 9/10 Qs, values will be what you expect.
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M. SIADH. medullary collecting duct osmolality will change in response to ADH.
M. PCT isotonic (always, no matter what) ;
Juxtaglomerular apparatus (JGA) hypotonic (alway no matter what);
MCD hypertonic = in siadh, because it takes water from urine.
M. SIADH - first line Mx? 2ck
“Fluid restriction”.
We want to see how serum/urinary values change in response.
M. SIADH - Tx? 2ck
Demeclocycline
M. SIADH - demeclocycline, what group drug?
Demeclocycine is technically a tetracycline antibiotic but isn’t used because it can cause insensitivity to ADH at the kidney (i.e., nephrogenic diabetes insipidus). So we essentially cause a 2nd problem that cancels out the 1st problem.
M. SIADH - what antagonists can be used?
Conivaptan and tolvaptan are ADH receptor antagonists that can be used for SIADH.
Conivaptan and tolvaptan are ADH receptor antagonists that can be used for ….?
SIADH
The primary cells in the brain that recognize serum osmolality and contribute to the secretion of vasopressin are hypothalamic osmoreceptor cells. These are located in the organum vasculosum of the lamina terminalis (OVLT) and the subfornical organ, which detect changes in the osmolality of the blood. serum osmolality causes these osmoreceptors to stimulate the nearby supraoptic and paraventricular nuclei.
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DI. Similar to central SIADH, central DI can be caused by ……?3
Head trauma, meningitis, and cancer.
DI. Nephrogenic DI is caused by …?4
lithium, demeclocycline, hypercalcemia, and NSAIDs.
There is an NBME Q that asks about a patient’s response to ADH who is on chronic NSAIDs, and the answer is ADH and urinary osmol changes?
no change in response to ADH” and no change urinary osmolality” (meaning no change).
no change tai tipo bruksniukas su rodyklem i sonus
2CK Q gives patient with primary hyperparathyroidism and incr. (2 arrows) serum calcium + nephrogenic DI; Q asks cause of the DI?
Hypercalcemia. High calcium can cause renal insensitivity to vasopressin.
DI. Serum vs urinary values are the opposite of ….?
SIADH
serum na high; serum osmol high; serum spec. grav high.
urine osmol decr., urine specific gravity decr.
DI. PCT isotonic; JGA hypotonic; MCD hypotonic.
The PCT is always isotonic no matter what; the JGA is always hypotonic no matter what; the MCD is clearly hypotonic in DI since we’re not pulling free water out of the urine.
DI. When we are trying to first diagnose DI, the first thing we do is ????
Fluid restriction [same as with SIADH. We want to see how serum/urinary values change first.]
DI. After we determine that the urine is staying dilute + the serum is staying concentrated, the next best step is ……????
Desmopressin (analogue of vasopressin.
If the urine gets more concentrated, (i.e., if the drug works), we know central DI is the diagnosis and we’re merely deficient in ADH.
DI. If desmopressin doesn’t work, we know we have …..
nephrogenic DI.
DI. If desmopressin doesn’t work, we know we have nephrogenic DI. I should point out that even in nephrogenic DI, desmopressin might work but only very little, whereas with central DI, administration will urinary osmolality robustly. It will be obvious on USMLE. But my point is, don’t say, “Oh well desmopressin worked like 5% so we can’t have nephrogenic DI here.”
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Treatment for central DI is …..???
desmopressin
Treatment for nephrogenic DI is ….??????2
NSAID + a thiazide.
Treatment for nephrogenic DI is NSAID + a thiazide. Sounds weird, but ̄ Na+ reabsorption induced by thiazides in the early-DCT promote compensatory Na+ reabsorption in the PCT, where water follows Na+ and our net loss of fluid is less than without the thiazide. In healthy individuals, however, they will lose more net fluid with the thiazide. The NSAID presumably ̄ renal blood flow, which will decr. GFR and decr. net fluid loss.
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DI. There is difficult 2CK NBME Q where they say patient is on lithium + has incr. urinary output, and fluid restriction is wrong answer to this question (I say hard because 9/10 times, fluid restriction is correct when it’s listed); answer = ???
NSAID + thiazide diuretic. The implication is, if it’s obvious what the patient’s diagnosis is already nephrogenic DI, going straight to Tx is acceptable.
Mehl. Psychogenic polydipsia (PP) = means the patient is simply drinking too much.
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Mehl. Psychogenic polydipsia (PP).
urine and serum osmol?
Both the urine and serum will be dilute
Mehl. Psychogenic polydipsia (PP).
serum values - same in SIADH: low Na, low serum osmol, low serum spec gravity.
urine values - as in DI: low urine osmol; low urine spec gravity.
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Mehl. Psychogenic polydipsia (PP).
I’d say 3/4 Qs on USMLE are obvious and will say some psych patient is drinking lots to “clear himself from evil spirits,” etc.
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Mehl. Psychogenic polydipsia (PP).
Probably 1/4 Qs won’t be an obvious psych vignette, but will just show you the lab values where you have to say, “The urine and serum are both dilute, so this is psychogenic polydipsia.”
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Mehl. Psychogenic polydipsia (PP). first step in Dx?
First step in diagnosis is fluid restriction in order to see how urinary/serum values change.
UW. 43 y/o woman + nausea, dizziness, and headache for a day. Her menses began 2 days ago. She has occasionally had fatigue and dizziness during her menstrual periods, but today’s symptoms feel different. The patient has a history of von Willebrand disease, causing recurrent, heavy menstrual blood loss, and is scheduled for an endometrial ablation procedure. Her only medication is intranasal desmopressin taken on the first 3 days of her menstrual period. Vitals normal. The patient appears restless. Mucous membranes are moist. Deep tendon reflexes are 2+ throughout and Babinski sign is absent. Sensory examination shows no focal deficits. The chest is clear to auscultation. The abdomen is soft and nontender. There is no peripheral edema. The remainder of the examination is unremarkable. Which of the following is the most appropriate next step in diagnosis?
SERUM ELECTROLYTES
An 8-year-old boy is brought to the office due to a 2-month history of excessive urination. He has been drinking large amounts of water and has been irritable and restless. The patient takes no medications and has had normal growth with achievement of all expected developmental milestones. Vital signs are normal. Physical examination, including neurologic examination, is normal. Laboratory results are as follows:
Serum chemistry
Sodium 142 mEq/L
Potassium 4.2 mEq/L
Chloride 100 mEq/L
Bicarbonate 24 mEq/L
Blood urea nitrogen 30 mg/dL
Creatinine 1.0 mg/dL
Calcium 9.2 mg/dL
Glucose 100 mg/dL
Urinalysis
Specific gravity 1.001
Protein none
Blood negative
Glucose negative
Ketones negative
Nitrites negative
Bacteria none
White blood cells 1-2/hpf
Urine osmolality is 120 mOsm/kg, and urine output over 24 hours is 3.7 L. Which of the following is the most appropriate next step in management?
WATER DEPRIVATION TEST
