Hypoglycemia, a bG < 60 AND symptoms, in a non-diabetic is
usually factitious disorder. Two potential disease states (that are
quite rare) are insulinoma and autoimmune hypoglycemia. To
discover if the patient is doing it to themselves, obtain a Cpeptide,
Pro-Insulin, bG, and Secretagogue screen.
Endogenous insulin comes from Pro-insulin, cleaving the Cpeptide
portion to result in insulin. Thus, if there's NO rise in Cpeptide,
the insulin must be exogenous (self-injecting). Your job
is done if the C-peptide is normal.
Endogenous insulin secretion may be induced by secretagogues
(like sulfonylureas) or produced by insulinomas. The only way
to tell the two apart is to obtain a secretagogue screen. If positive,
they're ingesting secretagogues - tell them to stop.
Only evaluate for insulinoma if the C-peptide is elevated AND
the secretagogue screen is negative. Perform a 72-hour fast,
retest for all the same things above, and if positive perform the
CT scan or MRI of the abdomen to find + resect the tumor.
If all else fails, consider the option of looking at insulin
Etiology: Acute: Infection, infarction, surgery, and radiation. Chronic: Tumor, infiltration, and autoimmune.
Presentation: Acute (Lethargy, coma, death, hypotension, coma, death). Chronic: More stable.
Work up: Carryout insulin stimulation tests. Insulin will cause hypoglycemia, which with result in increased GH (cortisol and glucagon). If positive, progress to MRI.
Treatment: Replace missing hormones
Pathophys: A disease of excess cortisol, it's caused by one of four conditions: 1) Iatrogenic (most common, taper off to fix), 2) Pituitary tumor
(Cushing's disease), 3) Adrenal Tumor, or 4) Ectopic ACTH.
Presentation: "Cushingoid appearance": central
obesity, moon facies, extremity wasting, a buffalo hump, glucose intolerance or diabetes, and hypertension.
Work up: 24hr free cortisol level and confirm with a 1mg low dose dexamethasone suppression test.If cortisol is ↑ it's Cushing's. Follow that with an ACTH level to distinguish adrenal
(↓ ACTH) from extra-adrenal (↑ ACTH).
If extra-adrenal, perform a high dose
dexamethasone suppression test to determine pituitary (suppresses) vs ectopic (Ø suppression). Confirm pituitary Cushings with an MRI followed by transsphenoidal resection. If
ectopic, find it with CT/MRI of 1) Chest (Lung Ca), 2) And (Pancreatic ca), then 3) Pelvis (adrenals). Remember "Low-Dose
Treatment: (1) Iatrogenic Cushing Syndrome: tapering of glucocorticoid; (2) Pituitary Cushing Syndrome: surgery (transsphenoidal ablation of pituitary adenoma) - usually safe and effective); Adrenal adenoma or carcinoma: adrenalectomy.
Pathophys: Over production of aldosterone. Can be primary (renin independent - timor or adenoma called Conn's Syndrome) or secondary (renin dependent - CHF, cirrhosis, nephrotic syndrome). Mimickers include Licorice, exogenous mineral corticosteroids, CAG)
Renin --> Ang II --> Aldosterone --> HTN and Hypokalemia
Work up: When suspected, perform 8am levels for Aldosterone, Renin, and Aldo:Renin Ratio. Ensure any hypertension medication is discontinued (ACE, CCB, Diuretics confound the test). If elevated (>20 Aldo and >20 Aldo:Renin), it's likely primary. Confirm with the salt suppression test (where aldo will not decrease after a 200g - Na load via saline infusion or oral sodium load). The tumor is found by CT or MRI. If early AM levels are Ø elevated a different disease is likely provoking the aldosterone increase.
Treatment: Surgical Resection is curative for adenoma. For bilateral hyperplasia, spironolactone inhibits the action of aldosterone.
Pathophys: Overproduction of catecholamines.
refractory HTN or Paroxysmal Five P's which are 1) Pressure (HTN), 2) Pain (Headache or Chest Pain), 3) Pallor (vasoconstriction), 4) Palpitations (tachycardia, tremor), and 5) Perspiration.
Work up: Screen for this disease with
24 hr urinary metanephrines or Urinary VMA (metanephrines is better, VMA is cheaper). If , do an MRI/CT of the pelvis. They should be easy to spot. If not, a MIBG Scintigraphy can be done.
Treatment: The treatment is resection but with caution; touching one can cause
release of catecholamines. Pretreat first with α-blockade to prevent
unopposed α-action with β-blockade, then β-Blockade, then
Pathophys: The loss of adrenal function may be from a variety of etiologies,
and may be sudden/acute with multiple presentations. The most common cause in the US is autoimmune adrenalitis; it's TB worldwide. In the setting of sepsis there may be bilateral adrenal destruction from hemorrhage (Waterhouse - Friderichsen).
Presentation: In primary failure (loss of
cortisol, maintenance of ACTH) the symptoms will be hypotension, fatigue, N/V of cortisol loss, as well as the hyperpigmentation and hyperkalemia. Hyperpigmentation is a result of ACTH production trying to increase cortisol while hyperkalemia is from deficient aldosterone. In secondary failure,
no ACTH is produced so hyperpigmentation is absent. Because aldosterone production is intact there's also no hyperkalemia.
Work up: It's key to make sure it's not a primary deficiency so perform a cosyntropin test (exogenous ACTH administration). Establish a
baseline cortisol in the morning (<3ug = Dz, >18ug = ruled out). Give the ACTH then reassess in 60 minutes to determine if there's
any change in cortisol. (3, 3, 3 = Ø ACTH problem = 10 deficiency) vs (3, 3, 20 = ACTH problem, 2o deficiency).
Treatment: Treat this by giving
the steroids they don't have. Prednisone for all types and fludrocortisone for primary only (it's a synthetic aldo that has its function retained through the RAAS in secondary).
Pathophys: decreased metabolism secondary to decrease T4.
Presentation:A variety of things slow:
heart (bradycardia), mind (dementia), reflexes (↓ DTRs), bowel
function (constipation), and metabolism (weight gain).
Iatrogenic: Most common cause. Treat hyperthyroidism and cancer with ablation or surgery, leaving the patient without thyroid. Treat with levothyroxine.
Hashimoto's: Most common disease that causes hypothyroidism. It's caused by lymphocytic infiltrate secondary to antibodies (antithyroid peroxidase and andtithyroglobulin 90% specific). Treat with levothyroxine.
Subclinical Hypothyroidism: Increased TSH + normal T4/T3. If antibody +, will progress to primary hypothyroidism. If ab -, will most likely get better.There's no consensus on when to start treatment,
but generally make the patient happy by treating when symptoms start and treat everyone with overt hypothyroidism
Myxedema coma: There is usually a precipitating event, everything shuts down. Like thyroid storm this is a medical emergency. Hypothermia, hypotension, and coma. Treatment is high dose T4, but because peripheral conversion is impaired, also give straight up T3 if T4 fails or symptoms are sere from the start.
Treatment: No matter the causes of hypothyroidism, give levothyroxine.