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
, 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.
ROS negative other than GI symptoms
Based on the pt’s clinical presentation, the APRN diagnoses the pt as having secondary hypocortisolism
due to the lack of prednisone the pt was taking for her RA secondary to vomiting.
Explain why the patient exhibited these symptoms?
The patient’s symptoms were caused by adrenal insufficiency. The cause is usually related to a
trigger such as surgery, trauma, infection, or withdrawal from glucocorticoids. Primary adrenal
insufficiency is a chronic disease in which the adrenal glands do not produce enough steroid
hormones. Cortisol is the most potent glucocorticoid and is needed to maintain life. Cortisol is a
steroid hormone is responsible for carbohydrate metabolism. Cortisol also mobilizes amino acids
from skeletal muscle and enhances the liver's capacity for gluconeogenesis. Other functions
include; metabolic, neurological, anti-inflammatory, immunosuppression, and growth
suppression effects. Corticotropin-releasing hormone from the hypothalamus prompts release of
ACTH from the anterior pituitary gland then stimulates release and synthesis of cortisol from the
adrenal cortex.
Scenario: primary hyperparathyroidism
64 y/o Caucasian female presents to the clinic with vague symptoms of non-specifid abd papin, myalgias,
constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had a bout of kidney
stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy
or other interventions. She was told by the urologist to follow up with ther PCP after the kidney stones
resolved.
The APRN examining the patient orders a chem 7 which revealed a serum calcium of 13.1mg/dl. The
APRN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist,
who does a complete workup and concurs with the APRN’s diagnosis.
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
, 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.
ROS negative other than GI symptoms
Based on the pt’s clinical presentation, the APRN diagnoses the pt as having secondary hypocortisolism
due to the lack of prednisone the pt was taking for her RA secondary to vomiting.
Explain why the patient exhibited these symptoms?
The patient’s symptoms were caused by adrenal insufficiency. The cause is usually related to a
trigger such as surgery, trauma, infection, or withdrawal from glucocorticoids. Primary adrenal
insufficiency is a chronic disease in which the adrenal glands do not produce enough steroid
hormones. Cortisol is the most potent glucocorticoid and is needed to maintain life. Cortisol is a
steroid hormone is responsible for carbohydrate metabolism. Cortisol also mobilizes amino acids
from skeletal muscle and enhances the liver's capacity for gluconeogenesis. Other functions
include; metabolic, neurological, anti-inflammatory, immunosuppression, and growth
suppression effects. Corticotropin-releasing hormone from the hypothalamus prompts release of
ACTH from the anterior pituitary gland then stimulates release and synthesis of cortisol from the
adrenal cortex.
Scenario: primary hyperparathyroidism
64 y/o Caucasian female presents to the clinic with vague symptoms of non-specifid abd papin, myalgias,
constipation, polyuria, and says she feels “fuzzy headed” much of the time. She had a bout of kidney
stones a few weeks ago and she fortunately was able to pass the small stones without requiring lithotripsy
or other interventions. She was told by the urologist to follow up with ther PCP after the kidney stones
resolved.
The APRN examining the patient orders a chem 7 which revealed a serum calcium of 13.1mg/dl. The
APRN believes the patient has primary hyperparathyroidism and refers the patient to an endocrinologist,
who does a complete workup and concurs with the APRN’s diagnosis.
