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33 Cards in this Set
- Front
- Back
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WHAT DO HYPOTHALAMIC NUCLEI SYNTHESIZE?
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ADH (AVP) AND OXYTOCIN
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WHERE ARE ADH AND OXYTOCIN STORED?
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POSTERIOR PITUITARY GLAND
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WHAT IS ANOTHER NAME FOR THE POSTERIOR PITUITARY?
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NEUROHYPOPHYSIS
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ACTION OF ADH
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ACTS ON RENAL TUBULES TO CAUSE WATER REABSORPTION THAT RESULTS IN URINARY CONCENTRATION
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WHAT IS CENTRAL DI?
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DEFICIENCY OF ADH SECRETION FROM THE POSTERIOR PUTUITARY
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ETIOLOGIES OF CENTRAL DI
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PITUITARY SURGERY, TRAUMA TO THE PIT. STALK, INFECTIONS LIKE SYPHILIS OR TB, TUMORS OF THE PITUITARY, INFARCT OR INFLAMMATION OF THE PITUITARY
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WHAT IS THE CAUSE OF NEPHROGENIC DI?
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RENAL INSENSITIVITY TO ADH
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ETIOLOGIES OF NEPHROGENIC DI?
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MEDS AND ALCOHOL, CHRONIC RENAL DISEASE, PYELONEPHRITIS, HYPOKALEMIA, CHRONIC HYPERCALCEMIA, SICK CELL ANEMIA, MYELOMA
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WHAT TESTS DO YOU DO TO DIAGNOSE DI?
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PLASMA AND URINE OSMOLALITY; WATER DEPRIVATION TEST
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WHAT DOES A URINE VOLUME LESS THAN 2 LITERS IN 24 HRS IN AN ADULT TELL US?
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RULES OUT DI
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TREATMENT FOR CENTRAL DI
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DESMOPRESSIN ACETATE- LOWEST EFFECTIVE DOSE
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TREATMENT FOR NEPHROGENIC DI
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INDOMETHACIN- NSAIDS POTENTIATE ADH ACTION AT RENAL TUBULES
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TREATMENT FOR CHRONIC AND MILD DI
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SIMPLY MAINTAIN ADEQUATE WATER INTAKE---FOR THOSE THAT STAY ASYMPTOMATIC WITH NORMAL ELECTROLYTES
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WHAT IS SAIDH?
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INAPPROPRIATE SECRETION OF ADH IN THE ABSENCE OF OSMOTIC STIMULUS
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CLINICAL CRITERIA FOR SIADH
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DECREASED URINE OSMOLALITY AND INAPPROPRAITE CONCENTRATION OF THE URINE
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ETIOLOGIES OF SIADH
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TUMORS EXCRETING ECTOPIC ADH- SMALL CELL LUNG CANCER; SOME OTHER CANCERS; MEDICATION/DRUG INDUCED; LESIONS IN THE PATHWAY OF RECEPTORS- CNS DISORDERS, PULMONARY DISEASE, PAIN, PHYSICAL STRESS, POSTOP
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SYMPTOMS OF SIADH
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FATIGUE, HA, NAUSEA, ANOREXIA---EVENTUALLY VOMITING AND NEUROLOGIC IMPAIRMENT AS THE SODIUM LEVEL DECREASES
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WHAT IS CONSIDERED THE URGENT SODIUM LEVEL- MUST BE TREATED?
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LESS THAN 120
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COMMON CAUSES OF HYPONATREMIA
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CHF, RENAL INSUFFICIENCY, GLUCOCORTICOID INSUFFICIENCY, HYPOTHYROIDISM, USE OF THIAZIDE DIURECTICS (RULE OUT AS A CAUSE BEFORE YOU DETERMINE IT IS SIADH)
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HYPONATREMIA, LOW PLASMA OSMOLALITY, NORMAL PLASMA VOLUME INDICATE WHAT CONDITION
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SIADH
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URINE SODIUM IN SIADH WILL BE GREATER THAN _______.
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20
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TREATMENT OF SIADH DEPENDS ON WHAT FACTORS (2).
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THE DURATION AND THE SEVERITY
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IF HYPONATREMIA OCCURS _______________ AND PATIENT IS ____________, YOU TREAT THE SIADH QUICKLY.
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QUICKLY; SYMPTOMATIC
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IF HYPONATREMIA OCCURS OVER ______ AND PATIENT IS ________________, CORRECT SLOWLY AND WITH _____________ OVER TIME.
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TIME; ASYMPTOMATIC; WATER RESTRICTION
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WHAT IS THE USE FOR DEMECLOCYCLINE IN SIADH?
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USED FOR PATIENTS WHO CANNOT ADHERE TO WATER RESTRICTIONS; IT CAUSES SHORT TERM NEPHROGENIC DI WHICH INHIBITS EFFECT OF ADH ON RENAL TUBULES; HELPS MAINTAIN BALANCE IN EUVOLEMIC PATIENTS
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WHAT IS TREATMENT FOR HYPOVOLEMIC PATIENTS WITH SIADH?
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ISOTONIC FLUIDS TO SUPPRESS HYPOVOLEMIC STIMULUS FOR ADH RELEASE
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WHAT GROUP OF PATIENTS DO WE USE WATER RESTRICTION AS A TX FOR SIADH IN?
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EUVOLEMIC PATIENTS- WATER RESTRICTION SO SODIUM INTAKE DOES NOT BECOME DILUTED
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IF CNS SYMPTOMS ARE PRESENT IN A PATIENT WITH SYMPTOMATIC HYPONATREMIA (LESS THAN 120 FOR SERUM SODIUM LEVEL USUALLY BUT TREAT IF PRESENT AT ANY LEVEL), WHAT IS THE TX?
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REFER TO ENDO/NEURO ASAP; IV SALINE AND LASIX; DEMECLOCYCLINE
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NO SYNDROMES OF INCREASED SECRETION OF THIS HORMONE HAVE BEEN DEFINED.
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OXYTOCIN
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REGULATORS OF ADH SECRETION
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OSMORECEPTORS IN THE HYPOTHALAMUS (DETECT OSMOLALITY OF THE BLOOD) AND ATRIAL AND CAROTID BARORECEPTORS (DETECT CIRCULATING VOLUME)
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THIS INHIBITS SECRETION OF ADH
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ETHANOL
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STIMULI FOR SECRETION OF ADH
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HEMOCONCENTRATION, HYPOVOLEMIA, HYPOTENSION, INCREASE IN TEMP, N AND V, HORMONES, DRUGS
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CLINICAL PRESENTATION OF DI
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EXCESS URINE VOLUME (2-20 L PER DAY) AND LOW SPECIFIC GRAVITY; EXCESS POLYDIPSIA AND HYPERNATREMIA, DEHYDRATION, AND HYPOTENSION
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