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
.
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.
.
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