Endocrine Flashcards
(20 cards)
What are the most common causes of hypothyroidism?
Hashimoto’s thyroiditis (autoimmune), iodine deficiency, post-thyroidectomy, radiation, and medications like lithium or amiodarone.
How does primary hypothyroidism differ from central (secondary) hypothyroidism?
Primary hypothyroidism is due to thyroid gland dysfunction (elevated TSH, low T3/T4), whereas central hypothyroidism results from pituitary or hypothalamic failure (low TSH and low T3/T4).
What are common findings on exam that may indicate a diagnosis of hypothyroidism?
Bradycardia (prolonged PR on EKG), weight gain, cold intolerance, weakness, hair loss, depression, menstrual irregularities, enlargement of thyroid.
What is the management of hypothyroidism, and how is treatment monitored?
Levothyroxine (T4) replacement, with monitoring of TSH levels every 6-8 weeks until stable, then annually.
What are the most common causes of hyperthyroidism?
Graves’ disease (autoimmune), toxic multinodular goiter, thyroiditis, and excessive exogenous thyroid hormone intake.
What are the key clinical signs that differentiate Graves’ disease from other causes of hyperthyroidism?
Graves’ disease has exophthalmos, pretibial myxedema, and diffuse goiter with bruit, whereas toxic multinodular goiter and thyroiditis lack these findings.
What are the treatment options for hyperthyroidism?
Beta-blockers for symptomatic relief, antithyroid medications (methimazole or propylthiouracil), radioactive iodine therapy, or surgical thyroidectomy for refractory cases.
What is the underlying pathophysiology of type 1 diabetes?
Autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency.
What are the key differences between type 1 and type 2 diabetes in presentation?
Type 1 diabetes presents in younger patients with sudden onset, weight loss, and ketonuria, while type 2 diabetes is gradual, associated with obesity, and lacks ketonuria in early stages.
How is type 1 diabetes managed long-term?
Basal-bolus insulin therapy (long-acting + rapid-acting), carbohydrate counting, glucose monitoring, and lifestyle modifications.
What are the primary risk factors for developing type 2 diabetes?
Obesity, sedentary lifestyle, family history, metabolic syndrome, and polycystic ovary syndrome (PCOS).
What laboratory findings differentiate type 1 from type 2 diabetes?
Type 1 diabetes has low C-peptide and positive autoimmune markers (GAD antibodies, islet cell antibodies), while type 2 diabetes has high/normal C-peptide and insulin resistance.
What is the stepwise treatment approach for type 2 diabetes?
First-line: Lifestyle modifications & metformin. Second-line: GLP-1 receptor agonists (e.g., semaglutide), SGLT-2 inhibitors, or insulin for refractory cases.
What are the hallmark clinical and laboratory findings of DKA?
Polyuria, polydipsia, abdominal pain, nausea, fruity breath, Kussmaul respirations; lab findings include glucose >250 mg/dL, pH <7.3, low bicarbonate, ketonemia.
What are the key principles in DKA management?
IV fluids (NS, then switch to D5-1/2NS when glucose <250), IV insulin, potassium replacement, and treating the underlying cause (e.g., infection).
What is the difference between Cushing’s syndrome and Cushing’s disease?
Cushing’s syndrome refers to excess cortisol from any cause (e.g., steroids, adrenal tumor), while Cushing’s disease is due to an ACTH-secreting pituitary tumor.
What are the hallmark signs of Cushing’s syndrome?
Central obesity, moon facies, buffalo hump, purple striae, hypertension, glucose intolerance, muscle weakness, and osteopenia.
What diagnostic tests are used for Cushing’s syndrome?
24-hour urine cortisol, late-night salivary cortisol, and dexamethasone suppression test; ACTH levels differentiate ACTH-dependent (pituitary, ectopic tumor) vs. ACTH-independent (adrenal tumor, exogenous steroids).
How does Cushing’s disease differ from adrenal Cushing’s syndrome in hormone levels?
Cushing’s disease has high ACTH, while adrenal tumors or exogenous steroid use have low ACTH due to negative feedback.
What is the first-line treatment for Cushing’s disease?
Transsphenoidal surgery to remove the ACTH-secreting pituitary adenoma.