Mod 4 KC Module 4 .pdf - Scenario syndrome of antidiuretic hormone(SIADH A 67 y\/o Caucasian woman was brought to the clinic by her son who sated that

Mod 4 KC Module 4 .pdf - Scenario syndrome of antidiuretic...

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Scenario: syndrome of antidiuretic hormone (SIADH) A 67 y/o Caucasian woman was brought to the clinic by her son who sated that his mother had become slightly confused over the past several days. She had been stumbling at home and had fallen once but was able to ambulate with some difficulty. She had no other obvious problems and had been eating and drinking. The son became concerned when she forgot her son’s name, so he thought he better bring her to the clinic. PMH – type 2 DM with peripheral neuropathy x 20 years. COPD. Depression after death of spouse several months ago Social/family hx – non contributory except for 30 pack/year history tobacco use Meds: metformin 500mg BID, ASA 82mg PO q AM, lexapo 5mg PO q AM (Started 2 months ago) Labs – CBC WNL, chem 7 – glucose 92 mg/dl, BUN 18mg/dl, creatinine 1.1 mg/dl, Na – 120 mmol/l, K – 4.2 mmol/L, Co2 – 37mmol/L, Cl – 97mmol/l The APRN refers the pt to the ED and called endocrinology for a consult for diagnosis and management of syndrome of inappropriate antidiuretic hormone (SIADH) Define SIADH and identify any patient characteristics that may have contributed to the development of SIADH. Inappropriate and excessive antidiuretic hormone (ADH, arginine vasopressin) secretion decreased urine production. SIADH is caused by an excessive amount of antidiuretic hormone (ADH). Signs of SIADH are hyponatremia, hypo-osmolality, and urine osmolality over 100 mosmol/kg. Normal production of ADH is stimulated by low blood pressure, increased serum osmolality, and decreased plasma volume. A common cause of SIADH is production of ADH by tumors originating throughout certain parts of the body. Patients with SIADH have fluid retention, dilutional hyponatremia, hypochloremia, concentrated urine with abnormally low urine output and normal fluid volume or edema. Fluid retention causes dilution, creating lower plasma sodium concentration. Extracellular fluid volume triggers an increase in urine sodium excretion creating normal extracellular volume and further lowering plasma sodium concentration. Patients with normal kidney and endocrine function have normal to increased blood volume, normal blood protein levels, and experience no edema. Scenario: secondary hypocortisolism A 43 y/o female presents to the clinic with a c/c of fever, chills, n/v, weakness. She has been unable to keep any food, liquids, or medications down. the sx began 3 days ago and have not responded to ibuprofen, acetaminophen or nyquil when she tried to take them. Her temp has reached as high as 102F. Allergies: nka Medications: prednisone 20mg daily, omeprazole 10mg q AM
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PHM – 20 year hx steroid dependendent RA. GERD. Social: denies alcohol, illicit drugs, vaping, tobacco use. PE: thin, ill appearing woman who is sitting in exam room as she said she was too weak to climb on exam table. VS temp 101.2F, BP 98/64, pulse 110, resp 16, SpO2 96% RA.
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