wyb
Forum Junior
Topics: 8
Posts: 43
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Please someone help me with the explanation. The question is what is the relation between SiADH and small cell carcinoma of lung. I understand that SiADH(syndrome of inappropriate ADH) presents low sodium, cerebral edema, no pitting edema and volume depletion, but why small cell carcinoma of lung is the cause of SiADH. I really dont have any idea of it. Thanks for help!
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| silver
Forum Guru
Topics: 21
Posts: 771
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this phenomenon is known as paraneoplastic syndrome. ADH is ectopically secreted by the tumor cells thus leading to SIADH (dilutional hyponatremia). ACTH can also be secreted resulting in cushing's.
if you have goljan's rapid review--check it out-->p. 323
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| wyb
Forum Junior
Topics: 8
Posts: 43
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Thanks alot for your quick reply! I see, this is one type of paraneoplastic syndrome, called endocrine metabolic syndrome.
Happy study to you
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| mediocre
Forum Elite
Topics: 37
Posts: 229
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Ah! Siadh, the more u read the more u forget! just keep revising ...
check this out from one of the web pages,
hope its useful;
CAUSES of SIADH BY PROBABLE MAJOR MECHANISM OF ACTION
Increased hypothalmic production of ADH
A. Neuropsychiatric disorders*
Infections: meningitis (tuberculous or bacterial), encephalitis, abscess, Herpes zoster
Vascular: thrombosis, subarachnoid or subdural hemorrhage, temporal arteritis, cavernous sinus thrombosis, cerebrovascular accident
Neoplasm: primary or metastatic
Skull fracture, head injury
Psychosis, delirium tremens
Other: Guillain-Barré syndrome, acute intermittent porphyria, autonomic neuropathy, hypothalamic sarcoidosis, postpituitary surgery, multiple sclerosis, epilepsy, hydrocephalus, lupus erythematosus, Shy-Drager syndrome, peripheral neuropathy, spinal cord lesions
B. Drugs
Intravenous cyclophosphamide* (increased sensitivity may also contribute)
Carbamazepine (though increased sensitivity is probably important). Hyponatremia is more common with oxcarbazepine.
Vincristine or vinblastine
Thiothixene
Thioridazine, other phenothiazines
Haloperidol
Amitriptyline, other tricyclic antidepressants or serotonin-reuptake inhibitors
Monoamine oxidase inhibitors
Bromocriptine
Lorcainide
Clofibrate
General anesthesia
Narcotics, opiate derivatives
Nicotine
C. Pulmonary disease
Pneumonia*: viral, bacterial, fungal
Tuberculosis
Lung abscess, empyema
Acute respiratory failure
Positive pressure ventilation (via inhibition of low-pressure cardiopulmonary baroreceptors)
Other: asthma, COPD, atelactasis, pneumothorax, cystic fibrosis
D. Postoperative patient*
E. Severe nausea
F. Pain
G. Infection with HIV
H. Idiopathic
Ectopic (nonhypothalamic) production of ADH:
Carcinoma: Small cell carcinoma of lung* (2/3 of patients with small cell have impaired water excretion), bronchogenic, duodenum, pancreas, thymus, olfactory neuroblastoma, bladder, prostate, uterus
Lymphosarcoma, reticulum cell sarcoma, mesothelioma, Ewing sarcoma
Hodgkin's disease, leukemia
Pulmonary tuberculosis (?)
Potentiation of ADH effect
Chlorpropamide*
Carbamazepine
Psychosis
Intravenous cyclophosphamide
Tolbutamide
Prostaglandin-synthesis inhibitors (salicylates, NSAIDS)
Exogenous administration of ADH
Vasopressin, desmopressin
Oxytocin
Possible production of another antidiuretic compound (or increased sensitivity to very low levels of ADH)
Prolactinoma
Waldenstrom's macroglobulinemia
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| mediocre
Forum Elite
Topics: 37
Posts: 229
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DIAGNOSIS & Imp D/D
Suspect SIADH in patients with concentrated urine (Uosm > 300 mOsm/kg) and hyponatremia in the absence of edema, orthostatic hypotension, or features of dehydration. Must rule out other causes of hyponatremia, particularly those causing euvolemic hyponatremia: cortisol deficiency, hypothyroidism, reset osmostat. Cardiac, renal, and hepatic function should be normal.
May be difficult to distinguish SIADH from salt wasting renal diseases (in both urine sodium > 20 mmol/L and FeNa > 1%). Fluid restriction to 600-800 mL/d for 2-3 days will result in weight loss and correction of hyponatremia and salt wasting in SIADH. Fluid restriction fails to correct hyponatremia and sodium wasting in salt-losing renal disease.
A controversial disease entity, cerebral salt wasting syndrome, thought to result from a factor secreted in cerebral disease which causes proximal tubule sodium wasting, is very similar to SIADH (both have increased Uosm, urine sodium > 20 mmol/L, hyponatremia, Uosm > Sosm, low serum urate, increased FEurate, and in both hyponatremia corrects with fluid restriction). Patients with SIADH are euvolemic while those with CSWS are hypovolemic, but this determination is problematic. The only way to distinguish may be that with fluid restriction, serum urate and FEurate correct in SIADH but fail to correct in CSWS.
Water load test: Useful to differentiate low-set osmoreceptor (excrete water normally) from other conditions with hyponatremia and concentrated urine. Must first bring serum sodium > 125 mmol/L (by water restriction or saline administration). Water load (20 mL/kg up to 1,500 mL) is taken orally (in 10-20 min) and urine is collected hourly, with patient recumbent, for 4-5 hours in the morning. At least 65% of the water load should be excreted in 4 hr, or 80% in 5 hr, and the lowest Uosm, usually reached in the second hour, should be < 100 mmol/kg. Patients who fail to excrete the water normally should not take any further water that day (to prevent water intoxication). Failure to excrete the water load may occur in adrenal insufficiency or renal insufficiency, as well as in SIADH.
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"Do not worry if you have built your castles in the air. They are where they should be. Now put the foundations under them." - Henry David Thoreau
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