Endocrinology Flashcards
Treatment for subacute thyroiditis (de Quervain thyroiditis)
- Beta-blockers: control of thyrotoxic symptoms
- NSAIDs: pain relief
*Glucocorticoids for severe thyroid pain not responding to NSAIDs
Most accurate markers indicating resolution of diabetic ketoacidosis
- Serum anion gap
- Serum beta-hydroxybutyrate levels (not acetoacetate)
Best initial test to Dx acromegaly
Insulin-like growth factor-1 (IGF-1)→significantly ↑↑ level compared to the average for age-matched equivalents►positive screen
Confirmatory test for acromegaly
Measure GH after 100 g of glucose is given orally
- Positive if GH remains high (>5 ng/mL)
- Normally a glucose load completely suppresses levels of GH
Why don’t you have hyperkalemia and salt loss in secondary adrenal insufficiency caused by pituitary disease?
Aldosterone production is mainly dependent on the renin-angiotensin system not from ACTH
*Salt wasting, hyperkalemia, and death are associated with aldosterone deficiency
Use of Metyrapone test. How does it work?
- Assess ACTH production
- Block cortisol production→↑ACTH levels
*A failure of ACTH levels to rise→suggests pituitary insufficiency
Most common cause of panhypopituitarism
Pituitary adenomas
Most common presentation of glucagonoma
- Glucose intolerance
- Necrolytic migratory erythema→annular erythematous dermatitis, blistering and erosions
- Weight loss
- Normocytic normochromic anemia
- Diarrhea, thromboembolism
What is the differential diagnosis in a patient with polydipsia and polyuria? Initial steps in management.
- Diabetes insipidus, psychogenic polydipsia, Diabetes mellitus
- 1st step to evaluate→measure urine osmolarity
- 2nd step→Water deprivation test
Most sensitive test to diagnose pheochromocytoma
Plasma free fractionated metanephrines
Specific findings at the physical exam of Graves disease
- Ophthalmopathy-exophthalmos (proptosis)
- Periorbital edema
- Pretibial myxedema
How are the potassium deposits in DKA and why?
Excess of glucagon→hyperglycemia, ketonemia, osmotic diuresis►net renal loss of K+→depletion of total body K+ stores
*Despite reduction in K+ stores→serum [K+] may be ↑ due to acidemia and ↓insulin activity►redistribution of K+ to the extracellular fluid compartment
Which androgen can be used as a diagnostic marker of androgen-producing adrenal tumors?
Dehydroepiandrosterone sulfate (DHEAS)
*produced predominantly in the adrenal glands that
How do you differentiate hyperthyroidism due to thyroiditis and exogenous thyroid hormone use (factitious thyrotoxicosis)? What do they have in common?
- Common→Radioactive iodine uptake (RAIU) decreased
- Differentiate:
- ↑Thyroglobulin→thyroiditis (subacute or silent), iodide exposure
- ↓Thyroglobulin→Factitious thyrotoxicosis
Why are the thyroid antibodies (antithyroid peroxidase/antithyroglobulin) important to evaluate hypothyroidism?
If TSH is less than double the normal and antibodies are positive→replace thyroid hormone
How can you suspect Hypoparathyroidism induced by low magnesium?
- Low Calcium
- Low Phosphorus (different from other causes of hypoparathyroidism➡High Phosphorus)
Mechanism by which hypomagnesemia induce hypocalcemia
↓Mg→⬆resistance to PTH and ⬇PTH secretion
What potassium level do you expect in a hyperglycemic crisis (DKA or HHS)? Why?
- Normal or slightly elevated serum potassium
- Insulin deficiency→put K+ out of cells
- Osmotic diuresis→excessive urinary K+ loss
*Total body potassium deficit (3-5 mg/kg)
Which is the implication of a total body potassium loss in a Hyperglycemic Hyperosmolar State?
Insulin therapy→abruptly decrease K+ - severe hypokalemia
*K+ reposition during initial insulin therapy
Most likely secondary cause of bone loss when presented with ⬆creatinine, anemia and hypercalcemia?
Multiple myeloma
*⬆Total protein might be found
Cause of Osteitis fibrosa cystica and clinical presentation
- Primary Hyperparathyroidism➡⬆Resorption in cortical bone with subperiosteal thinning and cystic degeneration▶hypercalcemia (constipation, fatigue, etc)
- Secondary hyperparathyroidism➡chronic renal failure
*X-ray: lytic lesions with multifocal involvement
Clinical presentation of myopathy in Cushing syndrome
- Painless progressive proximal muscle weakness, atrophy, no tenderness (may interfere with daily activities)
- Lower extremity more involved
- ESR and CK normal
Cause of myopathy in Cushing syndrome
Glucocorticoid-induced myopathy: Direct catabolic effects of cortisol on skeletal muscle➡muscle atrophy
Common findings of chronic primary adrenal insufficiency
- Hyponatremia: hypovolemia-induced antidiuretic hormone secretion
- Hypoglycemia: cortisol deficiency
- Peripheral eosinophilia: normally inhibited by corticosteroids
*History of weakness, fatigue, anorexia, weight loss
