Endocrine Flashcards
What will radioactive scan show in a toxic goiter?
“toxic”= makes T4
T4 up
TSH down
Normal thyroid will react to down TSH and not make T4 and will not take up iodine
Goiter is active despite any TSH stimulus and so will make T4 and take up iodine
SO RAIU will show increased uptake but only in nodular tissue
What will radioactive scan show in a Graves’ disease?
The entire thyroid gland will be hot with diffuse uptake because Thyroid Stimulating antibodies work throughout the thyroid equally.
Graves’ will show thyroid stimulating antibodies, proptosis, exophthalmos, pretibial myxedema, and a diffusely enlarged thyroid on exam.
What is the treatment for Follicular thyroid cancer?
Total thyroidectomy plus postoperative radioactive iodine.
What is the MEN type 1 syndrome?
MEN1 on chrom 11
Parathyroid tumors or hyperplasia
Pituitary tumors
Pancreatic endocrine tumors
What is the MEN type 2a syndrome?
RET on chrom 10
Parathyroid hyperplasia
Pheochromocytoma
Medullary thyroid carcinoma
Marfanoid habitus
What is the MEN type 2b syndrome?
RET on chrom 10
Pheochromocytoma
Medullary thyroid carcinoma
Mucosal neuromas- Intestinal/oral ganglioneuromatosis
Marfanoid habitus
What is the treatment for central diabetes insipidus?
Deficiency of ADH from the posterior pituitary
With exogenous ADH administration, the Diabetes Insipidus is reversed and the urine concentrates.
Treatment for central diabetes insipidus is DDAVP.
What is the treatment for nephrogenic diabetes insipidus?
Nephrogenic diabetes insipidus has no ADH-receptors. No matter how much ADH there is, endogenous or exogenous, the kidneys will not reabsorb water. Therefore, the urine osmolality will not change during the water deprivation test. This is treated with gentle diuresis (furosemide)
What is the best test to screen for diabetes?
A fasting blood glucose is the best test to screen for diabetes. It is cheap and effective, though it does require confirmatory testing. While a random glucose > 200 (any one time) gives you the diagnosis of diabetes, a fasting glucose measurement >125 on two occasions gives you diabetes.
When is the two-hour glucose tolerance test done?
When a patient is screened with a fasting glucose and screens positive (bg > 125). So retesting is indicated.
If the second fasting glucose is negative (bg < 125),
THEN a 2 hour glucose tolerance test is performed.
How do you screen for Cushing’s syndrome?
Low-Dose Dexamethasone Suppression test (which can be replaced by a 24-hour urinary cortisol) is the screening tool for Cushing’s syndrome.
Cushing’s presents with hypertension, diabetes, central obesity, moon facies (Acne), purple striae (stretch marks), and extremity wasting.
How is pheochromocytoma diagnosed?
1st- Biochem evidence- values of VMA, epinephrine, and norepinephrine in a 24-hour urinary collection.
With biochemical evidence of pheochromocytoma, the subsequent steps are imaging for a mass, then adrenal vein sampling to confirm, then resection.
MIBG scan is the choice when there is biochemical evidence of pheochromocytoma but the imaging is negative. It is possible to have ectopic tumors producing catecholamines. If you dont clearly have a mass on some imaging, but biochemically she is positive, get the MIBG.
What does the RAIU scan look like for Hashimoto’s, silent lymphocytic, and de Quervain’s thyroiditis?
All would show low T4, high TSH, and a cool thyroid on RAIU
How is primary hyperaldosteronism (conn’s syndrome) diagnosed?
Elevated Aldosterone WITHOUT an elevated renin, and an Aldo:Renin ratio >20.
Some form of confirmatory test (salt suppresion, captopril challenge, fludrocotisone suppression).
After biochemical confirmation, identifying an adrenal mass is the goal, and CTs are cheaper and just as good as MRIs for Conn’s syndrome.
What is the workup for acromegaly?
The first step is to check an Insulin-Like Growth Factor 1. Growth hormone unreliable as it is too variable throughout the day. ILGF-1, on the other hand, which GH stimulates the liver to make, is reliable.
Growth hormone levels are useful though. After the ILGF-1 is elevated, the next step is to get a glucose suppression test where the GH level fails to suppress, confirming the diagnosis.
After that, it is an MRI pituitary to see the lesion.
How does hyperosmolar hyperglycemic Non-ketotic coma present?
Combination of a low sodium because of a high glucose (hyperosmolar), a high sugar (hyperglycemic), and a coma
Make sure it is NOT DKA there is no acidosis or ketones
more common in Type II DM
How is primary adrenal failure diagnosed?
Failure of the cosyntropin stimulation test to produce any increase in cortisol levels.
Low sodium and high potassium, indicating that aldosterone is also not effective.
How is the treatment for primary adrenal failure?
both prednisone and fludrocortisone to support the cortisol and aldosterone deficiencies.
What is the treatment for a patient in DKA?
Diabetes (elevated sugar), Ketosis (ketones in the urine), and Acidosis (pH < 7.4)
1) vigorous hydration
2) Insulin
3) Potassium
since insulin shifts potassium into cells
if K is low Give fluids+K THEN Insulin
If K is high or normal.. its safe to give insulin then fluids
What is syndrome of inappropriate ADH (SIADH)?
- High ADH, water intoxication (too much)
- Low sodium (dilutional)
- concentrated high urine sodium
- Risk of seizures
Demeclocycline causes a nephrogenic diabetes insipidus by preventing the binding of ADH to its receptors and reverses the pathology.
What is diabetes inspidus?
- Low ADH, low water in body
- High sodium
- Polyuria, high urine output
- Treat w/ DDAVP (ADH)
What is the Dawn and Somogyi effects?
Dawn phenomena- early (3 AM) sugar reveals hyperglycemia (the Dawn Phenomena). While patients sleep, the liver produces glucose (gluconeogenesis) and an insufficient load of night time insulin may cause hyperglycemia
or Somogyi effects- there is too much insulin at night, leading to an undetected hypoglycemia with subsequent rebound in the morning. This is corrected by REDUCING the amount of qHS insulin.
These are differentiated by the early morning blood glucose.
What is psychogenic polydipsia?
“young woman with asymptomatic hyponatremia”
A low sodium (dilute blood) combined with a dilute urine indicates medullary washout, as caused by psychogenic polydipsia
Also look for the comatose or seizing young female without a seizure disorder whose sodium is critically low.
What is euthyroid sick syndrome?
changes seen in patient thyroid function tests administered in the medical ICU during episodes of critical illness
Measure reverse T3 levels and they will be very low
TSH and T4 are usually normal
TX underlying disease and thyroid will get better on its own
malingering /factitious thyroid disorder
Exogenously consuming T4 (levothyroxine). This will feedback on a normal pituitary to turn off TSH (so TSH is low). Thyroglobulin is only elevated with T4 if the T4 came from thyroid. As it is exogenous (and not from the thyroid) the thyroglobulin will be low. Since there is no TSH there is no thyroid activity, so RAIU will be decreased.
What is pheochromocytoma?
Pheochromocytoma presents with the “5 Ps”: paroxysms of pain (headache), perspiration (sweating), pressure (HTN), and palpitations (tachycardia).
24-hour urinary metanephrines and/or VMA is used as the screening for pheochromocytoma.
What do you do with a palpable thyroid nodule but euthyroid?
if a nodule is found and the TSH is normal, you should reflex to ultrasound guided biopsy
What are labs for Addison disease?
Autoimmune destruction of the adrenal gland
Low mineralocorticoid –> low aldosterone, low cortisol
Hyponatremia and hyperkalemia
Korsakoff syndrome
Vitamin B1 (thiamine) deficiency in the setting of chronic alcohol abuse
Amnesia, nystagmus, and gait impairment
Bilateral atrophy of the mammillary bodies on MRI
What kind of thyroid cancer has elevated calcitonin, hypercalcemia, and elevated PTH
Medullary thyroid cancer
Least common type of thyroid cancer
Neoplasm of the parafollicular “C” cells
Part of MEN2a
How to definitively diagnose Amyotrophic lateral sclerosis (ALS)?
degeneration of motor neurons in the corticospinal tract and ventral horn
Dx: Electromyography (EMG)
Physical exam signs
1) Murphy sign – acute cholecystitis
2) McBurney point – acute appendicitis
3) Chvostek sign – hypocalcemia
4) Homans sign – deep vein thrombosis
5) Courvoisier sign – pancreatic cancer
6) Rebound tenderness – peritonitis
7) Chandelier sign – pelvic inflammatory disease
8) Kernig sign - meningitis
9) Brudzinski sign – meningitis.
Conn Syndrome (Primary aldosteronism)
Overproduction of aldosterone (adenomas)
Hypokalemia (polyuria, polydipsia, and muscle weakness) → metabolic alkalosis
Hypernatremia (water retention) → Hypertension → Decreased serum renin
low renin: aldosterone ratio
Hypomagnesemia
Albuminuria
Congenital Adrenal Hyperplasia
Congenital Cortisol deficiency
↑ androgens → ambiguous genitalia, virilization, precocious puberty
Hyponatremia
Hyperkalemia → metabolic acidosis
Addison Disease (Adrenal insufficiency)
Hypotension
Hyperpigmentation (due to increased ACTH)
Hypoglycemia
Diarrhea
Somatostatinoma
Delta cells in head of pancreas
Somatostatin inhibits the release of many hormones including thyroid stimulating hormone, growth hormone, glucagon, insulin, gastrin, and cholecystokinin
Primary polydipsia
Causes: Psychiatric disease Hypothalamic infiltration (sarcoidosis)
Diagnosis: Low serum sodium (< 137 mEq/L) with dilute urine (less than 1/2 the plasma osmolality)
Treatment: Restrict drugs that cause dry mouth, water restriction
Central DI
Causes: Pituitary gland fails to make antidiuretic hormone
Diagnosis: A high-normal plasma sodium concentration (> 142 mEq/L)
DDAVP challenge: Uosm increases by at least 50%
Treatment: (Desmopressin) DDAVP
Nephrogenic DI
Causes: Kidneys are unresponsive to antidiuretic hormone
Diagnosis: A high-normal plasma sodium concentration (> 142 mEq/L)
DDAVP challenge: Uosm does not increase
Treatment: Low-sodium diet and thiazide diuretics
congenital adrenal hyperplasia
Classic CAH require treatment with glucocorticoids, such as prednisone, to replace insufficient cortisol levels.
Oral contraceptives (OCs) are the current first-line treatment of nonclassical, late-onset congenital adrenal hyperplasia
Long-term sequelae of bacterial meningitis
Most common hearing loss (High-dose steroids (ie, dexamethasone) administered prior to antibiotics have been shown to reduce this risk.)
Less common- blindness, paralysis, seizures, hydrocephalus, ataxia etc
DKA fluid Management
Treat DKA with isotonic fluid (normal saline) and Potassium replacement will depend on levels:
K level >5.2= IV insulin + normal saline
K level 3.3-5.2= IV insulin+IV normal saline with added K
K level <3.3= IV normal saline+ K, HOLD insulin until levels greater than 3.3
CA-125
ovarian cancer
Diagnosis of Non-classical congenital adrenal hyperplasia (CAH)
presents later in life with menstrual irregularity, hirsutism, and acne
Early morning elevated 17-hydroxyprogesterone levels are useful for the diagnosis
How can you lower gout flares with diet?
low-fat dairy products
Avoid thiazide diuretics, high-fructose beverages, Alcohol, meat, and seafood
Fractures that are more suggestive of abuse
- Posterior or lateral rib fractures
- Metaphyseal chip fractures (type II Salter-Harris fracture)
- Scapular fractures
- Ends of long bones and result from a twisting mechanism
Diagnosis of Acromegaly
1st step is to get Insulin-like growth factor 1 (IGF-1)
Alcoholic ketoacidosis (AKA)
AKA presents as an elevated anion gap metabolic acidosis, normal to low glucose levels, fruity breath odor and physical signs of volume depletion secondary to nausea and vomiting.
Development of hyperthyroid symptoms in the setting of recent infection is most likely
Subacute thyroiditis/ subacute granulomatous thyroiditis/ De Quervain thyroiditis
Thyroid may be enlarged and is tender to palpation
Labs of Subacute thyroiditis/ De Quervain thyroiditis
High Free T3/T4, Low TSH
Radioactive iodine thyroid scan shows decreased uptake because of damage to thyroid follicular cells
Tx: Anti-inflammatory therapy and monitor thyroid levels
Toxic multinodular goiter/ Plummer Disease
Focal and/or diffuse hyperplasia of thyroid follicular cells
Radioactive iodine thyroid scan and uptake test shows patchy or localized uptake
Tx: Surgery or radioidone
Which thyroid dysfunction is seen 2-6 months postpartum?
Thyrotoxicosis
Refers to a hypermetabolic state from elevated thyroid hormones
Postpartum thyroiditis is transient. Most patients develop permanent hypothyroidism
Riedel’s thyroiditis
Caused by the replacement of thyroid tissue with fibrosis. The gland becomes a rock-hard painless mass. It is completely benign
Pancreatic adenocarcinoma
Migratory thrombophlebitis (Trousseau sign) due to hypercoagulable nature
Mid-epigastric pain, weight loss, anorexia, and a palpable, nontender gallbladder (Courvoisier sign)
Insulin mangement
Most type 1 diabetics should receive 0.5 to 1.0 unit/kg per day to achieve acceptable glycemic control. Half of the total is given as long-acting insulin (Basal). The remaining half is divided by the short-acting insulin (bolus) into three meals.
If the preprandial sugars are high, then the long-acting insulin needs to be increased. If the postprandial glucose is high, then the short acting insulin needs to be increased.
Goal for preprandial glucose
90-130 mg/dL
Goal for post prandial glucose
Less than 180 mg/dL
The long-term goal of therapy in a diabetic is a hemoglobin A1c of
Less than 7%
