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97 Cards in this Set

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