Endocrinology Flashcards
Decreased FSH and LH
Anosmia
Renal agenesis
Kallmann Syndrome
Failure of the hypothalamus to release GnRH
Central obesity
Increased LDL and cholesterol
Reduced lean muscle mass
Subtle findings for GH deficiency in adults
Causes of Nephrogenic DI?
Chronic pyelo
Amyloidosis
Myeloma
SCD
Lithium
Hypercalcemia and hypokalemia
The difference between central and nephrogenic DI is determined by…
the response to vasopressin
Treatment of central vs nephrogenic DI
central = long-term vasopressin (desmopressin)
nephrogenic = correct the underlying cause, HCTZ, amiloride, NSAIDs
Overproduction of growth hormone (pituitary adenoma) leading to soft tissue overgrowth throughout the body
Acromegaly
What else should you look for when a patient is diagnosed with acromegaly?
Parathyroid and Pancreatic disorders (i.e., MEN1)
Increased hat size
Body odor
Coarse facial features
Colonic polyps
HTN
Acromegaly
(Abuse of GH can also give the same presentation)
Best initial test for acromegaly
IGF-1
Most accurate test = glucose suppression test (unsuppressed GH levels)
Treatment for acromegaly
- Surgery: transphenoidal resection (70% effective)
- Medications: Pegvisomant is a GH receptor antagonist that inhibits IGF release from the liver
- Radiotherapy
What are two endocrine disorders that would cause elevated prolactin without there being an adenoma?
Acromegaly: prolactin is cosecreted with GH
Hypothyroidism: extremely high TRH levels will stimulate prolactin secretion
What is the only CCB to raise prolactin level?
Verapamil
After prolactin level is found to be high, which diagnostic tests should be performed?
Thyroid function tests
Pregnancy test
BUN/creatinine
LFTs
Treatment for hyperprolactinemia
- DA agonists: cabergoline is better tolerated than bromocriptine
- Transphenoidal surgery
- Radiation (rarely needed)
Patient is having symptoms of hypothyroidism, but their T4 is normal and TSH is only slightly elevated. How do you determine if they need thyroid replacement?
Antithyroid peroxidase antibodies
Positive = replace thyroid hormone
If TSH was double the upper limit of normal, you can replace without ordering antibodies
All forms of hyperthyroidism have an elevated…
T4 level
Only pituitary adenomas will have a high TSH level (low in all others)
What is the most appropriate next step if a patient presents with a palpable mass on her thyroid (i.e., a nodule)?
Get T4 and TSH levels
If the patient has a hyperfunctioning gland (i.e., T4 is elevated or the TSH is decreased), the patient does not need immediate biopsy because malignancy is not hyperfunctioning
The most common cause of hypercalcemia
Primary hyperparathyroidism
Primary hyperparathyroidism and cancer account for 90% of hypercalcemia patients
Treatment for hypercalcemia
- Saline hydration
- Bisphosphonates: pamidronate, zoledronic acid
If calcium levels remain elevated, give calcitonin (inhibits osteoclasts). Prednisone controls hypercalcemia when it is from sarcoidosis or any other granulomatous disease.
Primary hyperparathyroidism is from:
- Solitary adenoma (80-85%)
- Hyperplasia of all 4 glands (15-20%)
- Parathyroid malignancy (1%)
What study is best for determining the bone effects from high PTH?
DEXA
NOT bone x-ray
When surgery is not possible for hyperparathyroidism, what is another option?
Cinacalcet (inhibitor of PTH release)
Facial nerve hyperexcitability
Perioral numbness
Seizures
Tetany
Long QT
Signs of hypocalcemia
Confusion
Lethargy
Short QT
Signs of hypercalcemia
Causes of hypocalcemia
Primary hypoparathyroidism (from prior neck surgery)
Hypomagnesemia (necessary for PTH release and decreases urinary loss of Ca)
Renal failure (decreased 1,25 hydroxy-D)
For every point decrease in albumin, the calcium level decreases by 0.8
Cushing syndrome vs Cushing disease
Cushing syndrome = hypercortisolism
Cushing disease = pituitary overproduction of ACTH
Moon face/Buffalo hump
Striae
HTN
Erectile dysfunction
Polyuria
Signs of hypercortisolism
The best initial test for the presence of hypercortisolism
24-hour urine cortisol
1 mg overnight dexamethasone suppression test is the best next choice
What causes false positives to the 1 mg overnight dexamethasone suppression test (i.e., cortisol is still elevated in the morning)?
Depression
Alcoholism
Obesity
After hypercortisolism is confirmed, what is the best test to determine the cause (source) or location?
ACTH
Low ACTH = adrenal source (aka ACTH-independent)
High ACTH = pituitary (suppresses with high dose dexamethasone) or ectopic
Hyperglycemia
Hyperlipidemia
Hypokalemia
Metabolic alkalosis
Leukocytosis
Effects of hypercortisolism
How far should you go in the evaluation of an unexpected, asymptomatic adrenal lesion on CT?
4% of the population has adrenal “incidentalomas”
Metanephrines of blood or urine to exclude pheochromocytoma
Renin and aldosterone to exclude hyperaldosteronism
1 mg overnight dexamethasone suppression test
What is the next step when high-dose dexamethasone suppresses the cortisol level, but a pituitary mass is not seen on MRI?
Petrosal sinus sampling for ACTH
Chronic hypoadrenalism is called
Addison disease
Difference between Addison disease and acute adrenal crisis
Addison disease is caused by autoimmune destruction of the gland (rarely caused by TB, adrenoleukodystrophy, or metastatic cancer) and is a chronic condition with slow progression
Acute adrenal cirisis is caused by hemorrhage, surgery, hypotension, or trauma that rapidly destroys the gland (sudden removal of chronic high-dose prednisone can precipitate adrenal crisis)
Common lab findings in hypoadrenalism:
Glucose
K
Na
BUN
Metabolic
Hypoglycemia
Hyperkalemia
Hyponatremia
High BUN
Metabolic acidosis
Eosinophilia is also common
The most specific test of adrenal function is
cosyntropin test (synthetic ACTH)
However, treatment is more important than testing in acute adrenal crisis
Treatment for acute adrenal crisis
Hydrocortisone
Fludrocortisone can be useful if the patient still has evidence of postural instability (high mineralocorticoid/aldosterone-like effect)
High BP + hypokalemia
Primary hyperaldosteronism
80% from solitary adenoma (most of the rest are from bilateral hyperplasia; it is rarely malignant)
Best initial test for primary hyperaldosteronism?
Plasma aldosterone to plasma renin ratio (an elevated plasma renin excludes the diagnosis)
The most accurate test to confirm the presence of a unilateral adenoma is a sample of venous blood draining the adrenal (DO NOT start with CT scan d/t high prevalence of incidental lesions)
Treatment of primary hyperaldosteronism
Unilateral adenoma = resection via laparoscopy
Bilateral adenoma = eplerenone or spironolactone
Episodic HTN
Headache
Sweating
Palpitations/tremor
Pheochromocytoma
Nonmalignant lesion of the adrenal medulla autonomously overproducing catecholamines despite a high BP
Diagnostic tests for pheochromocytoma
Best initial test = free metanephrines in plasma (confirmed with a 24-hour urine collection)
Followed by CT/MRI
MIBG scanning detects the location of pheochromocytoma that originates outside the adrenal gland
Treatment for pheochromocytoma
Phenoxybenzamine (alpha blocker)
CCB and beta blockers can be used afterwards
Remove surgically
Diabetes is defined/diagnosed by:
2 fasting blood glucose > 125
1 blood glucose > 200 with symptoms
Hemoglobin A1C > 6.5%
When is metformin contraindicated?
In patients with renal dysfunction (can accumulate and cause metabolic acidosis)
Sitagliptin
Saxagliptin
Linagliptin
Alogliptin
DPP-IV Inhibitors (block the metabolism of the incretins)
GIP
GLP
“The incretins”
GIP = glucose insulinotropic peptide
GLP = glucagon-like peptide
Both increase insulin release and decrease glucagon release from the pancreas
Exenatide
Liraglutide
Albiglutide
Incretin mimetics
Nateglinide
Repaglinide
Stimulators of insulin release in a similar manner to sulfonylureas (but do not contain sulfa)
Acarbose
Miglitol
Alpha glucosidase inhibitors
Block glucose absorption in the bowel
Treatment for DKA
Large-volume saline and insulin
Replace potassium after the level comes down to a level approaching normal
What is the best test to determine the severity of DKA?
Serum bicarbonate
(Hyperglycemia and ketones are NOT)
If the bicarbonate level is low, the anion gap is increased, and the patient is at risk of death
When should patients with DM start on an ACE-i/ARB
If their BP is > 140/90
or
If urine tests positive for microalbuminuria
Treatment for gastroparesis caused by DM
Metoclopromide and erythromycin
Management of diabetic retinopathy
Tighter control of glucose
When neovascularization and vitreous hemorrhages are present (proliferative retinopathy), it can be treated with laser photocoagulation
