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97 Cards in this Set
- Front
- Back
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___ --> stimulates zona glomerulosa --> releases ___
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renin-angiotensin; aldosterone
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___ --> stimulates zona fasciculata --> releases ___
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ACTH, CRH; cortisol, sex hormones
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___ --> stimulates zona reticularis --> releases ___
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ACTH, CRH; sex hormones
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___ --> stimulate adrenal medulla (chromaffin cells)--> releases ___
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preganglionic sympathetic fibers; catecholamines (NE, epi)
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Pheochromocytoma vs. neuroblastoma?
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Pheo - adults, episodic HTN
Neuro - kids, no episodic HTN |
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Drainage of L adrenal:
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L adrenal vein --> left RENAL vein --> IVC
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Drainage of R adrenal:
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R adrenal vein --> IVC
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What does the posterior pituitary release? Where in the hypothalamus were those products made?
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ADH - supraoptic nucleus
Oxytocin - paraventricular nucleus |
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The posterior pituitary is derived from embryonic ___.
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neuroectoderm
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The anterior pituitary is derived from embryonic ___.
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oral ectoderm
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What does the anterior pituitary make?
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FSH, LH, ACTH, TSH, prolactin, GH, MSH (melanotropin)
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What do TSH, FSH, LH, and hCG have in common?
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alpha subunit - the beta subunit is what makes each hormone specific
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Pancreatic alpha islet cells make:
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glucagon
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Pancreatic delta islet cells make:
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somatostatin (anti-growth hormone dec. insulin & glucagona secretion)
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Sheehan's syndrome =
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life threatening, postpartum pituitary infarct (must replace glucocorticoids and thyroid hormone immediately)
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Prolactin secretion is inhibited by:
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DOPAMINE! so that's why dopamine ANTagonists (neuroleptics) stimulate prolactin secretion
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In women, prolactin inhibits ___ synthesis & release, which inhibits ___. So that's why ___ is commonly seen in prolactinomas.
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GnRH, ovulation; amenorrhea
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Which hypothalamic hormone stimulates the anterior pituitary to release prolactin?
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TRH - thyroid releasing hormone
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Prolactin increases ___ synthesis & release from the hypothalamus.
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dopamine
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17-a-hydroxylase deficiency manifests with:
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Low cortisol, low sex hormones, high aldosterone! --> HTN, hypokalemia, phenotypically female but no maturation
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21-b-hydroxylase deficiency manifests with:
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Most common form. Low aldosterone, low cortisol, high sex hormones! --> masculinization, female pseudohermaphroditism, HYPOtension, hyponatremia, hyperkalemia, high renin, volume depletion (and possibly shock in newborns) due to salt wasting
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11-b-hydroxylase deficiency manifests with:
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Low aldosterone, low cortisol, high sex hormones! --> masculinization, HTN (11-deoxycorticosterone acts like weak aldosterone)
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Angiotensin II stimulates activity of which enzyme?
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aldosterone synthase
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5-a-reductase:
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converts testosterone --> DHT
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Aromatase converts testosterone to:
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estradiol
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4 functions of PTH, which is made by chief cells of parathyroid gland:
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1) inc. bone resorption of calcium and phosphate
2) inc. kidney reabsorption of calcium 3) dec. kidney reabsorption of phosphate (makes you pee out more phosphate) 4) stimulate 1-a-hydroxylase to make active Vitamin D |
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How is PTH regulated?
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Low serum free calcium stimulates PTH release.
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Which bone cells does PTH act on?
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BOTH osteoblasts & osteoclasts!!
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If your serum phosporus gets too low, how will your body fix that?
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Kidney make more active Vitamin D so you will:
1) reabsorb more calcium and phosphate from the gut 2) cause phosphate release from bone matrix |
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Vitamin D3 comes from sun exposure, Vitamin D2 comes from plants, and both are converted to active ___ in the kidney.
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1,25(OH)2
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3 functions of Vitamin D:
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1) inc. gut absorption of calcium...
2) ... and phosphate 3) inc. bone resorption of calcium & phosphate when low serum phosphate |
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What 3 situations cause increased active Vitamin D production?
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1) high PTH
2) low serum calcium 3) low serum phosphate |
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How is Vitamin D production inhibited?
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Inhibits itself.
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To review, what is it called when kids don't get enough Vitamin D? Adults?
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rickets; osteomalacia
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What are a patient's Ca/P/ALP levels like in osteoporosis?
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All normal!
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What are a patient's Ca/P/ALP levels like in Paget's disease of bone?
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Calcium may be normal or high, ALP is extremely high.
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Someone with low calcium, high phosphate, and normal ALP has:
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renal insufficiency
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Someone with high calcium, low phosphate, and high ALP has:
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hyperparathyroidism
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Someone with high calcium, high phosphate, and normal ALP has:
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vitamin D intoxication
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What are some causes of Cushing's SYNDROME? (too much cortisol)
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1) Cushing's disease - pituitary adenoma making ACTH
2) adrenal hyper/neoplasia making cortisol 3) ectopic ACTH from small cell lung CA 4) iatrogenic |
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What does Cushing's syndrome look like clinically?
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HTN, wt. gain, abnormal fat distribution, hyperglycemia, osteoporosis, amenorrhea, thin skin & easy bruising, immune suppression
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In a healthy person, giving a low dose of dexamethasone would -->
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low cortisol
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If you gave your patient with Cushing's syndrome a high dose of dexamethasone, and his cortisol level remained high, you know he has:
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cortisone-producing tumor (cannot suppress even with high dose steroid)
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In someone with ACTH-producing tumor, what would low dose dexamethasone do to his cortisol level? High dose?
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low dose --> cortisol high
high dose --> cortisol low |
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What is Conn's syndrome?
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PRIMARY hyperaldosteronism - we have an aldo secreting tumor that --> HTN, hypokalemia, metabolic alkalosis, and low renin
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How does one get hyperaldosteronism without an aldo-secreting tumor?
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renal artery stenosis, chronic renal failure, CHF, cirrhosis, nephrotic syndrome - anything that causes kidney to perceive "low intravascular volume" (this would lead to high renin-AII-aldo)
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How do you treat hyperaldosteronism?
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spironolactone - aldo antagonist
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What causes Addison's disease?
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adrenal atrophy involving all 3 cortical layers --> aldo and cortisol deficiency
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Why is one "tanned" in Addison's disease?
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low cortisol stimulates ACTH production, make a lot of MSH in the process which stimulates melanin
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What do pheochromocytomas secrete?
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- dopamine
- NE - epinephrine *see high urinary VMA, blood catecholamines |
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What is the rule of "10's" with pheochromocytomas?
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- 10% malignant
- 10% bilateral - 10% in kids - 10% outside of adrenal - 10% familial - 10% calcify |
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What are 5 episodic manifestations of pheochromocytoma?
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- pressure (HTN)
- pain (headache) - perspiration (tachycardia) - palpitations - pallor |
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MEN type 1 (Wermer) =
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- pancreas
- parathyroid - pituitary tumors (presents with kidney stones and stomach ulcers) |
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MEN type 2 (Sipple) =
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- medullary CA of thyroid
- pheochromocytoma - parathyroid tumor |
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MEN type 3 =
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- medullary CA of thyroid
- pheochromocytoma - mucosal neuromas (oral, intestinal) |
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How are MEN syndromes inherited?
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auto dominant... boo
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MEN 2 and 3 are associated with which oncogene?
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ret
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Pentagastrin-stimulated rise in calcitonin is highly suggestive of:
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medullary CA of thyroid (recall: thyroid C cells make calcitonin)
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Reidel's thyroiditis =
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hypothyroidism where gland is replaced by fibrous tissue - feels very firm, may be autoimmune, can extend to adjacent muscle and connective tissue of neck
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Wot is Grave's Disease?
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Type II, autoAb's STIMULATE TSH receptors --> hyperthyroidism with bulgy eyes, pretibial myxedema, diffuse goiter, low TSH
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Wot is Hashimoto's thyroiditis?
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autoimmune disease --> hypothyroidism (anti-thyroglobulin Ab's, anti-microsome Ab's) w/slow growing nontender goiter
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What is de Quervain's thyroiditis?
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GRANULOMATOUS focal destruction & inflammation of thyroid - follows viral infection like coxsackie or mumps, self-limited, gland is VERY TENDER, get transient hyperthyroidism
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What is the most common thyroid cancer?
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papillary CA - good Px, tend to affect middle aged women, ground glass (clear) nuclei, psammoma bodies, frond-like appearance under microscope
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Which thyroid cancer do you see uniform follicles containing colloid?
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follicular CA - good Px, well-circumscribed tumor
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Which thyroid cancer makes calcitonin?
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medullary CA - from parafollicular C cells, see sheets of cells in amyloid stroma (stain Congo red), associated with MEN 2 & 3
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Patient is a young child with pot-belly, mentally retarded, protuberant tongue. He has:
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cretinism - either lack of dietary Iodine, or defect in T4 formation, or defect in thyroid formation
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Primary hyperparathyroid is usually due to:
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adenoma > hyperplasia > carcinoma
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Blast from the past! Osteitis fibrosa cystica (von Recklinghausen's) is due to:
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primary hyperparathyroidism!! recall: brown tumor which is cystic bone space filled with fibrous tissue
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Renal osteodystrophy is:
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kidney disease --> Calcium loss --> secondary hyperparathyroidism
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Chvostek's sign =
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tap facial nerve, get facial muscle contraction (sign of hypocalcemia)
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Trousseau's sign =
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occlude brachial artery and get carpal spasm (sign of hypocalcemia)
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Female patient with short stature presents with shortened 4th and 5th metacarpals. She has:
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Albright's osteodystrophy, or pseudohypothyroidism (AR disorder of hypocalcemia where kidneys don't respond to PTH --> don't reabsorb Ca)
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What are causes of hypercalcemia?
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- drink too much milk
- hyperparathyroid - hyperthyroid - thiazide diuretic use - multiple myeloma - Paget's bone disease - Addison's - neoplasm - Zollinger Ellison - too much vitD - too much vitA - SARCOIDOSIS |
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A type 1 diabetic presents:
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young < 30 yrs, thin, polydipsia/polyuria, ketoacidotic, severe glucose intolerance
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A type 2 diabetic presents:
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older > 40 yrs, obese, genetic predisposition, rarely ketoacidotic, not necessarily have polyuria/polydipsia
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In a chronic diabetic, what would you see in small vessels?
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thickened basement membrane, retinopathy (hemorrhage, exudate, aneurysm), glaucoma, nephropathy (leading to HTN)
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In a chronic diabetic what would you see in the large vessels?
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atherosclerosis!! CAD, peripheral occlusive disease, gangrene, cerebrovascular disease
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In a chronic diabetic, the hyperosmolarity of blood can cause what damage?
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- neuropathy (motor/sensory/autonomic)
- cataracts |
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How you do you measure long-term diabetic glucose control?
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Hemoglobin A1C
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In type 1 diabetes, the cause is:
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viral, or autoimmune destruction of beta islets
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Type 1 diabetes is HLA...
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HLA-DR3, DR4
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When might a type 1 diabetic go into ketoacidosis?
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under stress (like infection) --> excess fat breakdown --> ketone bodies
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What does someone in diabetic ketoacidosis present with?
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Kussmaul respirations (deep and fast), hyperthermia, n/v, abdominal pain, psychosis/dementia, dehydration, fruity breath
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What are complications of diabetic ketoacidosis?
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- mucormycosis, Rhizopus infections
- cerebral edema - arrhythmias - heart failure |
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How do you Tx diabetic ketoacidosis?
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- insulin + potassium
- fluid - glucose if necessary to prevent hypoglycemia |
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Causes of central diabetes insipidus =
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- pituitary tumor
- trauma - surgery - histiocytosis X *all cause lack of ADH |
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Causes of nephrogenic diabetes insipidus =
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- hereditary
- hypercalcemia - lithium (recall: LMNOP) - demeclocycline (tetracycline that antagonizes ADH) |
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Blast from the past: which mood stabilizer can cause hypothyroidism?
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LITHIUM!! recall: LMNOP
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In a person with diabetes insipidus, what does their urine specific gravity look like?
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< 1.006 (and serum osmolality > 290)
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How do you Tx central DI?
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desmopressin, ADH analog
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How do you Tx nephrogenic DI?
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hydrochlorothiazide, indomethacin, amiloride
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What is the clinical triad for SIADH?
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1) excess water retention
2) hyponatremia 3) urine osmolarity > serum osmolarity |
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Causes of SIADH:
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1) small cell lung CA
2) CNS disorder, head trauma 3) pulmonary disease 4) drugs (cyclophosphamide) |
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Tx of SIADH:
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demeclocycline (tetracycline, ADH antagonist), water restriction
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What is the most common tumor of the appendix?
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Carcinoid - secrete lots of serotonin, recurrent diarrhea, flushing, wheezing, right sided valve disease, elevated 5-HIAA in urine!
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Carcinoid tumor cells are derived from:
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GI neuroendocrine cells
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Do you remember what we give for carcinoid tumor?
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octreotide (somatostatin)
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