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Endocrine
First Aid: Endocrine
| Question | Answer |
|---|---|
| What are the three layers of the adrenal cortex and what do they produce? | Zona glomerulosa (Aldosterone); Zona fasciculata (glucocorticoids); Zona reticulares (androgens) |
| What embryological layers do the adrenals derive from? | Cortex is from mesoderm; medulla is from neural crest (consider chromaffin cells postganglionic sympathetic neurons, helps you remember ACh acts on nicotinic receptors here as well) |
| Tumor of the adrenal medulla, most common in adults. | Pheochromocytoma |
| Tumor of the adrenal medulla, most common in children, doesn't always produce catecholamines. | Neuroblastoma |
| What are the two hormones produced by the posterior pituitary? | ADH (vasopressin) and oxytocin |
| What are the hormones secreted by the anterior pituitary and from what cells are they secreted? | "FLAT PiG"; Basophils "B-FLAT", FSH, LH, ACTH, TSH; Acidophils Prolactin and GH |
| What are the cell types within the islets of Langerhans and what do they secrete? | alpha (glucagon); beta (insulin); delta (somatostatin) |
| How is prolactin regulated? | Prolactin release is stimulated by TRH and inhibited by dopamine. This is a negative feedback loop because prolactin increases dopamine synthesis and secretion from the hypothalamus. |
| What inhibits release of both growth hormone and TSH? | Somatostatin |
| What enzyme in adrenal steroid synthesis is activated by ACTH? What drug inhibits this enzyme? | Desmolase, it is inhibited by ketoconazole |
| What enzyme deficiency will result in decreased sex hormones, decreased glucocorticoids, and increased mineralocorticoids? | 17alpha hydroxylase deficiency; results in phenotypic female w/out maturation, hypertension, and hypokalemia |
| What enzyme deficiency will result in increased sex hormones, decreased glucocorticoids, decreased mineralocorticoids and hypotension? | 21beta hydroxylase deficiency; results in masculinization, pseudohermaphroditism, hyponatremia, increased plasma renin activity, and volume depletion. |
| What enzyme deficiency results in increased sex hormones, decreased glucocorticoids, decreased mineralocorticoids and hypertension? | 11beta hydroxylase deficiency; results in masculinization and hypertensions because 11-deoxycorticosterone acts as a weak mineralocorticoid |
| What would lead to decreased sex hormone, decreased glucocorticoids, and decreased mineralocorticoids? | Addisons disease (low ACTH) or ketoconazole toxicity |
| What cells secrete parathyroid hormone? | Chief cells of parathyroid |
| What are the four primary functions of PTH? | 1. Increase bone resorption (both osteoclasts and osteoblasts) 2. Activate kidney 1alpha hydroxylase 3. Increase kidney reabsorption of calcium 4. Decrease kidney reabsorption of phosphorus |
| What are the 3 primary actions of vitamin D? | 1. Increased bone resorption 2. Increased absorption of dietary calcium 3. Increased absorption of dietary phosphorus |
| In Paget's disease of bone, what would you expect to be elevated, calcium, phosphorus, or alkaline phosphatase? | Alkaline phosphatase |
| In hyperparathyroidism, what would you expect to be elevated, calcium, phosphorus, or alkaline phosphatase? | Calcium and alkaline phosphatase, phosphorus should be decreased |
| In renal insufficiency, what would you expect to be elevated, calcium, phosphorus, or alkaline phosphatase? | Phosphorus would be elevated, calcium would be decreased due to insufficient vitamin D activation |
| What cells secrete calcitonin and what is its function? | Parafollicular C cells of thyroid; calcitonin functions to decrease bone resorption. It is activated by elevated serum calcium |
| What are the primary functions of T3 and T4? | The 4 B's; Bone growth, Brain maturation, Beta adrenergic effects, increased BMR |
| Through what mechanism do T3 and T4 increase BMR? | Increase activity of Na/K ATPase leading to increased Oxygen consumption, increased RR rate, and increased body temperature |
| What is the mechanism of thyroid hormone regulation? | TSH stimulates thyroid hormone release and T3 inhibits TRH release from the hypothalamus |
| What is the function of cortisol? | It is an anti-inflammatory, increases gluconeogenesis (secondary diabetes), lipolysis, proteolysis, decreases immune function, maintains blood pressure |
| How would you distinguish Cushing's disease from primary adrenal hyperplasia/neoplasia? | Both would present as Cushing's syndrome (excess cortisol); Cushing's disease would have elevated ACTH whereas adrenal hyper/neoplasia would have low ACTH; Clinically only Cushing's disease would have hyperpigmentation |
| What is the treatment for Cushing's disease? | Ketoconazole |
| How would you distinguish between Conn syndrome and secondary hyperaldosteronism? | Conn syndrome would result in low plasma renin; secondary hyperaldosteronism would have elevated plasma renin |
| What are some causes of secondary hyperaldosteronism? | renal artery stenosis, chronic renal failure, decreased renal perfusion (CHF), nephrotic syndrome, etc. |
| What is primary Addison's disease? | primary deficiency of aldosterone and cortisol due to adrenal atrophy leading ot hypotension and skin hyperpigmentation (due to elevated ACTH). |
| What is secondary Addison's disease? | Decreased cortisol due to decrease in pituitary ACTH production. No skin hyperpigmentation |
| What would be expected in the urine of a patient suffering from pheochromocytoma? | Vanillyl mandelic acid (VMA), a metabolite of norepinephrine |
| What would be expected in the urine of a patient suffering from neuroblastoma? | Homovanillic acid (HVA), a metabolite of norepinephrine |
| What is Sheehan's syndrome? | Pituitary insufficiency caused by infarction following severe bleeding and hypoperfusion during delivery. |
| What is Wermer's syndrome? | MEN type I; associated w/ 3 P's (pancreas, pituitary, and parathyroid) |
| What is Sipple's syndrome? | MEN type II; associated with pheochromocytoma, medullary carcinoma of the thyroid, and parathyroid tumor |
| What is MEN type III? | Similar to type II with medullary carcinoma of the thyroid and pheochromocytoma, but with oral and intestinal ganglioneuromatosis (mucosal neuromas) instead of parathyroid tumor |
| What are the symptoms of pheochromocytoma? | 5 P's; pressure, pain (headache), palpitations, perspiration, and pallor |
| What is the treatment of pheochromocytoma? | Phenoxybenzamine; a nonselective, irreversible, alpha blocker |
| Cold intolerance, weight gain, fatigue, lethargy, and decreased reflexes. Diagnosis? | Hypothyroidism |
| Heat intolerance, weight loss, chest pain, arrhythmias. Diagnosis? | Hyperthyroidism |
| Autoantibodies which stimulate the TSH receptor. Diagnosis? | Grave's disease |
| Antimicrosomal and antithyroglobulin antibodies. Diagnosis? | Hashimoto's thyroiditis |
| What are Hurthle cells? | Enlarged epithelial with abundant eosinophilic granules in the cytoplasm. Associated with Hashimoto's and follicular thyroid cancer. |
| Hypothyroidism often following a flulike illness with elevated ESR, jaw pain, and inflamed, tender thyroid gland. | Subacute thyroiditis (de Quervain's); hypothyroid may be preceded by hyperthyroid period. |
| Thyroid cancer associated with ground glass nuclei, psammoma bodies, and irradiation exposure. | Papillary carcinoma; most common |
| Thyroid cancer of parafollicular C-cells which produce calcitonin and sheets of cells in amyloid stroma. | Medullary carcinoma |
| Thyroid carcinoma with enlarged uniform follicles. | Follicular carcinoma |
| Thyroid cancer with worst prognosis. | Undifferentiated/anaplastic |
| What causes cretinism? | a defect in T4 formation or failure in thyroid formation |
| Pot-bellied, puffy faced child with protruding umbilicus and protuberant tongue. Diagnosis? | Cretinism |
| 47 yro male diabetic w/ a large tongue with deep furrows, deep voice, large hands and feet and coarse facial features. Diagnosis? | Acromegaly; Remember GH is diabetogenic |
| Where are the cell bodies of the nerve cells in the posterior pituitary? | In the hypothalamic nuclei |
| Patient presents with renal stones, bone pain, constipation, memory problems and lethargy. Diagnosis? | Classic "stones, bones, groans(constipation), and psychiatric overtones"; hyperparathyroidism |
| What is the mechanism of renal osteodystrophy? | Renal disease leads to decreased production of activated vitamin D, decreased secretion of phosphorus, and decreased reabsorption of calcium. Leads to high PTH, low serum calcium, elevated serum phosphorus. |
| What is pseudohypoparathyroidism? | Kidney unresponsive to PTH |
| What are the causes of hypercalcemia? | My favorite pnemonic "CHIMPANZEES"; Calcium ingestion, Hyperparathyroidism/thyroidism, Iatrogenic(thiazides), Multiple myeloma, Paget's disease, Addison's disease, Neoplasms, Zollinger-Ellison syndrome, Excess vitamin D, Excess vitamin A, Sarcoidosis |
| What are the symptoms of the most common pituitary adenoma? | Prolactinoma; ammenorrhea, galactorrhea, low libidio, infertility |
| What is the treatment for prolactinoma? | Bromocriptine (dopamine agonist) |
| Patient presents with anion gap metabolic acidosis, rapid/deep breathing, vomiting, and altered mental state. Diagnosis? | DKA |
| Patient with intense thirst and polyuria and dilute urine. Diagnosis? | Diabetes insipidus |
| Patient presents with new onset seizures, found to be extremely hyponatremic but urine osmolarity is markedly elevated. Diagnosis? | SIADH; low serum sodium can lead to seizures, hyponatremia from fluid retention |
| Patient presents with diarrhea, cutaneous flushing, and asthmatic wheezing. Right sided valvular disease is found. Diagnosis? | Carcinoid syndrome; neuroendocrine cells secrete high levels of serotonin |
| What is the treatment for carcinoid syndrome? | octreotide; somatostatin analog used primarily to treat diarrhea and flushing |
Created by:
rahjohnson
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