UWORLD endocrine Flashcards
(61 cards)
Clinical presentation of Hypopituitarism
- ACTH deficiency (secondary adrenal insufficiency): postural hypotension, tachycardia, fatigue, weight loss. hypoglycemia, eosinophila
- Hypothyroidism (central): fatigue, cold intolerance, constipation, dry skin, bradycardia, slowed DTRs
- Gonadotropins: Women –> Amenorrhea, infertility. Men –> Infertility, loss of libido
Describe the lab values seen in Panhypopituitarism
- Central adrenal insufficiency: Low cortisol and ACTH
- Hypogonadotropic hypogonadism: low FSH, LH, testosterone
- Central hypothyroidism: low or inappropriately normal TSH, Low free T4
Is aldosterone affected in hypopituitarism?
NO, it is regulated primarily by the RAS
Describe the lab/imaging of a prolactinoma
- Serum prolactin often >200 (normal is <15)
- Rule out renal insufficiency (creatinine) and hypothyroidism (TSH, thyroxine)
- MRI of brain/pituitary
Treatment of a prolactinoma
- Dopamine agonist (cabergoline)
- Trans-Sphenoidal surgery
What are the LH and TSH levels like in a prolactinoma
- LH: low or inappropriately normal
- TSH may be also low or normal
Describe the clinical features of Painless thyroiditis (silent thyroiditis)
- Variant of chronic autoimmune thyroiditis
- Mild, brief hyperthyroid state
- small, NONtender goiter
- Spontaneous reccover
Diagnostic testing of Painless thyroiditis (Silent thyroiditis)
- Positive TPO antibody
- Low radioiodine uptake
radioiodine uptake in Graves disease
High
Describe Stuma ovarii
a very rare cause of thyrotoxicosis and is due to production of thyroid hormone by an ovarian teratoma
- it typically present in women over age 40 with a pelvic mass, ascites, or abdominal pain
- Thyroid gland NOT enlarged
What is the effect of intensive glycemic control in type 2 diabetes on MACROvascular complications (Acute mi, stroke)?
No change
What is the effect of intensive glycemic control in type 2 diabetes on MICROvascular complications (nephropathy, retinopathy)?
decrease
What is the effect of intensive glycemic control in type 2 diabetes on all cause mortality?
-No decrease possibly because the microvascular benefits are offset by complications of hypoglycemia.
What is the pathophysiology of Milk-alkali syndrome
- Excessive intake of calcium and absorbable alkali
- Renal vasocontriction and decreased GFR
- Renal loss of sodium and water, reabsorption of bicarb
Symptoms of Milk-Alkali syndrome
- Nausea, vomiting, constipation
- Polyuria, polydipsia
- Neuropsychiatric symptoms
lab finding in milk-alkali syndrome
- Hypercalcemia
- Metabolic alkalosis
- Acute kidney injury
- suppressed PTH
- hypophosphatemia
- hypomagnesemia
Treatment of Milk-Alkali syndrome
- Discontinuation of causative agent
- Isotonic saline followed by furosemide
Milk alkali syndrome in pt with osteoporosis is likely due to ingestion of what
calcium carbonate
What medications raise the risk of milk alkali syndrome
- Thiazide diuretics
- ACEI’s/ARBs
- NSAIDs
How does thyrotoxicosis effect heart rhythm
- Sinus tachy
- Premature atrial and ventricular complexes
- Afib/flutter
How does thyrotoxicosis effect hemodynamics
- Systolic HTN and increased pulse pressure
- increase contractility and cardiac output
- decrease systemic vascular resistance
- increase myocardial oxygen demand
describe the mechanism behind HTN in HYPOthyroidism
increased systemic vascular resistance
Systolic HTN in thyrotoxicosis is caused by what
hyperdynamic circulation resulting from increased myocardial contractility and heart rate
Describe the cutaneous finding in a glucagonoma
-Necrolytic migratory erythema: Erythematous papules/plaques on face, perineum, extremities . . .Lesions enlarge and coalesce over next 7-14 days with central clearing and blistering, crusting and scaling at borders