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204 Cards in this Set

  • Front
  • Back
woman presents with diffuse goiter and hyperthyroidism. What are the expected values of TSH and thyroid hormones?
low TSH & hight thyroid hormones
48y/o female presntes with progressive lethargy and extreme sensitivity to cold temperatures. What is the diagnosis
pt with elevated serum cortisol levels undergoes a dexamethasone does not decrease cortisol levels, but 8 mg does. What is the dz?
pituitary tumor
50y/o man complains of diarrhea. On physical exam his face is plethoric and a heart murmur is detected. What is the dx?
carcinoid syndrome
woman of short stature presents with shortened 4th and 5th metacarpals. What endocrine d/o comes to mind?
Albright hereditary osteodystrophy or pseudohypoparathyroidism
Nondiabetic pt presents with hypoglycemia but low levels of C pepetide. What is the dx?
Surreptitious insulin injection
cortex of the adrenal glands comes from what embryologic source?
medulla of the adrenal glands comes from what embryologic source?
neural crest
GFR corresponds to
Salt (Na+)
Sugar (glucocorticoids) and
Sex (androgens)

mneu: the deepr you go the sweeter it gets
What does GFR stand for?
zona glomerulosa
zona fasciculata
zona reticularis
what does the zona glomerulosa secrete
what is the primary regulatory control of the zona glomerulosa
what does the zona fasciculata secrete
cortisol, sex hormone
what is the primary regulatory control of the zona fasciculata
ACTH, hypothalamic CRH
what does the zona reticularis secrete
sex hormones (e.g., androgens)
what is the primary regulatory control of the zona reticularis
ACTH, hypothalamic CRH
what do the chromaffin cells cells of the medulla secrete
catecholamines (epi, NE)
what is the primary regulatory control of the medulla
preganglionic sympathetic fibers
what is the most common tumor of the adrenal medulla in adults
what is the most common tumor of the adrenal medulla in children
out of pheochromocytoma and neuroblastoma which one causes episodic hyperension
how does the left adreanal gland drain blood
left adrenal ->left adrenal vein -> left renal vv -> IVC
how does the right adreanal gland drain blood
right adrenal ->right adrenal vein -> IVC
posterior pituitary is derived from what embryological origin
posterior pituitary secretes what
vasopressen and oxytoxin
where are vasopressen and oxytoxin made
where are vasopressen and oxytoxin shipped
where is the anterior pituatary derived from
oral ectoderm
what does the anterior pituitary secrete

ACTH, Melanotropin (MSH)
alpha subunit is a common subunit to
Beta subunit determines this
hormone specificity
islet of Langerhans are collections of these three types of cells.
alpha, beta, delta cells
what part of the pancreas are the alpha, beta, & delta cells most numerous
from where do the islets of Langerhans arise
pancreatic buds
alpha cells secrete
beta cells secrete
delta cells secrete
image adrenal cortex and medulla [p.247]
prolactin regulation image p. 248
prolactin ____ dopamine synthesis and secretion from the hypothalamus.
dopamine subsequently _______ prolactin secretion
dopamine agonists (e.g., bromocriptine) ______ prolactin secretion. Dopamine antagonist (e.g., most antipsychotics) __________prolactin secretions.
in females prolactin inhibits_______ synthesis and release, which inhibits ovulation
___________ this is commonly seen in prolactinomas
adrenal steroids pathway [p. 249]
what is the congenital adrenal hyperplasia: Female that is not maturing presents with HYPERTENSION, hypokalemia, she has decreased sex hormones, decrease cortisol, increased mineralocorticoids
17 alpha hydroxylase deficiency
this congenital adreanal hyperplasia is the most common form. It results in decreased cortisol (increased ACTH), decreased mineralocorticoids, increased sex hormones. Complications include masculinization, female psuedohermaphroditism, HYPOtension, hyponatremia, hyperkalemia, increased plasma renin activity, and volume depletion. Salt wasting can need to hypovolemic shock int he newborn
21 beta hydroxylase deficiency
this congenital adreanal hyperplasia results in low cortisol, low aldosterone and corticosterone and high sex horones. Complicatons include masculinization and (HYPERtension (11-deoxycorticosterone acts as a weak mineralocorticoid)
11 beta hydroxylase deficiency
where does PTH come from (cells and tissue)
chief cells of parathyroid
what are the 4 fxs of PTH
1) increased bone resorption of Ca++ & phosphate
2) increased kidney resorption of Ca++ in the distal convoluted tubule
3) decreased kidney resoption of phosphate
4) increased 1,25 (OH)2 vitamen D (cholecalciferol) production by stimulating kidney 1 alpha hydroxilase

mneu: PTH increases serum CA, decreases serum PO, increases urine PO4, and stimulates both osteoclasts and osteblasts

PTH: phosphate trashing hormone
what causes PTH secretion
decreased serum Ca++
image p. 250 actions of PTH and 1,25 OH D in maitenence of Ca++ & phosphate homeostasis
shown are the main actions of PTH & 1,25 (OH)2 D in the maintenance of Ca++ and phosphate homeostasis
source of vit D3
sun exposure in skin
source of D2
where are D2 & D3 converted to 25 OH vit D
where is 25 OH vit D converted to 1,25 (OH)2 vit D (active form)
what is the fx of vit D
1)increased absorption of dietary Ca++
2) increased absorption of dietary phosphate
3)increased bone resorption of Ca++ & (PO4)3-
what dz do you get if you don't get enough vit D (kids and adults)
what is 24,25-(OH)2 vit D
inactive form of vit D
in the regulation of vit D, what does increased PTH cause
increase 1,25-(OH)2 vit D formation
in the regulation of vit D, what does decreased [Ca++]cause
increase 1,25-(OH)2 vit D production
in the regulation of vit D, what does increased 1,25-(OH)2 vit D cause
increase 1,25-(OH)2 vit D inhibits its own production
What dz?
Ca++: ↑
Alk Phos:↑
What dz?
Ca++: N/↑
Alk Phos:↑↑↑
paget's dz of bone
What dz?
Ca++: ↑
Alk Phos:N/↑
vit D intoxication
What dz?
Ca++: N
Alk Phos:N
What dz?
Ca++: ↓
Alk Phos:N
renal insufficiency
where does calcitonin come from
parafolicular cells (C cells) of thyroid
what is the fx of calcitonin
↓ bone resorption of calcium
calcitonin opposes the action of what hormone
what stimulates calcitonin secretion
increased serum Ca++
the need for gene transcription and protein synthesis delays the onset of action of these steroid/thyroid hormones
mneu: PET CAT

Thyroxine and T3
image p. 251 steroid/thyroid hormone mechanism
these hormones are lipophilic and insoluble in plasma; therfore, they must circulate bound to specific binding globulins, which increase solubility and allows for increased delivery of steroid to the target organ.
increased levels of sex hormone-binding globulin (SHBG) leads to lower levels of free testosterone and results in this physical exam finding
decreased SHBG raises free testosterone leading to this finding
these are iodine containing hromones taht control the body's metabolic rate
thyroid hormones (t3/t4)
source of thyroid hormones
follicles of thyroid. Most T3 formed in the blood
fx of thyroid hormones
1) bone growth (synergism w/ GH
2)CNS maturation
3) beta adrenergic effects (increased CO,HR,SV, contractility
4) increase BMR via increased Na+/K+ ATPase activity -> increased O2 consumption, RR, increased body temp
5) increased glycogenolysis, gluconeogesis, lipolysis

mneu: T3 fx--4Bs
Brain maturation
Bone growth
Beta adrenergic effects
BMR incrase
what globulin binds most T3/T4 in blood
Throxine-binding globulin (TBG)
is free or bound thyroid hromone active
in what dz would you see decreased TBG
hepatic failure
in what condition would you see increase TBG
what hromone stimulates TSH secretion from the pituitary
TRH (hypothalamus
what cells does TSH stimulate to secrete thyroid hormone
follicular cells
negative feedback by this hormone to the anterior pituitary decreases sensititvity to TRH.
in Graves dz it is this TSH analog that stimulates follicular cells
image thyroid hormone p. 252--
what organs depend on insulin for glucose uptake
skeletal mm and adipose tissue
what organs take up glucose independent of insulin levels (GLUT-1)
brain and RBC
what fuel can the brain use in starbation states
ketone bodies
this syndrome refers to increased cortisol levels due to a variety of causes. The clinical picture includes hypertension, weight gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression
cushing syndrome
If you're pt presents with cushings syndrome you have to identify the source, if the pt has increased ACTH levels because of a pituitary adenoma the pt has
Cushing's dz
If you're pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to causes that are not iatrogenic, the pt has
primary adrenal hyperplasia/neoplasia
If you're pt presents with cushings syndrome you have to identify the source, if the pt has decreased ACTH levels due to iatrogenic causes, the pt may be taking
steroids (chronic)
describe the dexamethasone suppression test in a healthy person
low cortisol after low dose
describe the dexamethasone suppression test in a person with a ACTH-producing tumor
high cortosol after low dose; low cortisol after high dose
describe the dexamethasone suppression test in a person with a cortisone producing tumor
high cortisol after low and high dose
this dz is caused by an aldosterone-secreting tumor, resulting in HTN, hypokalemia, metabolic alkalosis, and LOW plasma renin
primary hyperaldosteronism (Conn's syndrome)
this dz is due to renal artery stenosis, chronic renal failure, cHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin0angiotensin system. Therefore, it is associated with HIGH plasma renin
secondary hyperaldosteronism
what is the tx for hyperaldosteronism
spironolactone (a K+ sparing diuretic that works by acting as an aldosterone antagonist)
this is a primary deficiency of aldosterone and cortisol due to adrenal atrophy, causing hypotension (hyponatremic volume contraction) and skin hyperpigmentation (due to MSH, a byproduct of increased ACTH production from POMC). It is characterized by Adrenal Atrophy and Absence of hormone production. It involves All 3 cortical divisions.
Addison's dz
How you distinguish Addison's dz (primary aldosterone/cortisol deficiency[renal problem]) from secondary aldosterone/cortisol deficiency [pituitary problem]
Secondary insufficency has no skin hyperpigmentation
this is the most common tumor of the adrenal medulla in adults. It is derived from chromaffin cells which arise from the neural crest
what can pheochromocytomas be associated with if they occur in pts whith MEN types II & III
this is the most common tumor of the adrenal medulla in children, but it can occur anywhere along the sympathetic chain
what do pheochromocytomas secrete
epi, NE, dopamine
how do you dx a pheo
urinary VMA and plasma catecholamines are elevated
what endocrine d/os are pheos assoc with
MEN types II & III
how do you tx pheos
alpha antagonists, especially phenoxybenzamine, a nonselective, IRREVERSABLE alpha blocker
symptoms of pheos occur in "spells"--meaning they often relapse and remit. What are the 5 "P"s of a pheo
Pressure (elevated BP)
Pain (headache)
Palpitations (tachycardia)
give the rule of 10s associated with pheos
10% malignant
10% bilateral
10% extraadrena
10% calcify
10% kids
10% familial
this MEN type involves the 1) PANCREAS (e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas) 2)PARATHYROID 3) PITUITARY TUMORS. It often presents with kidney stones and stomach ulcers
MEN I (Wermer's syndrome)= 3 "P" organs (Pancreas, Pituitary, and Parathyroidism)
MEN type II (Sipple's syndrome)
MEN type III ( formerly MEN type IIb )
all MEN have this type of inheritance
autosomal dominant
what gene are MEN type II & III associated with
ret gene
this d/o often manifests itself with cold intolerance, hypoactivity, weight gain, fatigue, lethargy, decreased appitite, constipation, weakness, decreased reflexes, facial/periorbital myxedema, dry, cool skin, and coarse, brittle hairr
what will the labs show in hypothyroidism
increased TSH (most sensitive test for primary hypothyroidism)
decreased total T4
decreased free T4
decreased T3 uptake
in this dz the pt presents hypothyroid. It results because thyroid is replaced by fibrous tissue
Riedel's thyroiditis
this d/o manifests itself with heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, increased reflexes, warm moist skin, and fine hair
this is an autoimmune hyperthyroidism with thyroid stimulating/TSH receptor antibodies. It often presents during stress (e.g., childbirth) with opthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter.
graves dz
what type of hypersensitivity rxn in graves dz
type II
what lab results will you see in hyperthyroidism
decreased TSH (if primary)
increased total T4
increased free T4
increased T3 uptake
this is an autoimmune d/o resulting in hypothyroidism. It has a slow course and often you will see a moderately enlarged, nontender thyroid. Microscopically you will see a lymphocytic infiltrate with germinal genters. Pt will test positive for antimicrosomal and antithyroglobulin antibodies
Hashimoto's thyroiditis
this is a self-limited hypothyroidism which often follows a flulike illness. Pt will presents with jaw pain and a very tender thyroid gland. Labs will show signs of early inflammation and elevated ESR.
Subacute thyroiditis (de Quervain's)
this is the most common thyroid cancer. It has an excellent prognosis. Microscopically you will see "ground glass" nuclei and psammoma bodies
papillary carcinoma
this thyroid cancer has a good prognosis. microscopically you will see uniform follicules
follicular carcinoma
this thyroid cancer arises from parafollicular "C cells". It produces calcitonin. Microscopicallly you may see sheets of cells in amyloid stroma. It is seen in MEN types II & III
medullary carcinoma
this thyroid cancer occurs in older pts. It carries a very poor prognosis
this occurs wherever endemic goiter is prevalent (lack of dietary iodine). It is common in china. It can also be caused by a defect in T4 formation or developmental failure in thyroid formation. You may see a pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue
adult pt presents with large tongue, deep furrows, deep voice, large hands and feet, coarse facial features, impared glucose tolerance (insulin resistance). What is the d/o and what hormone is in excess

increased growth hormone
what does increased GH in children cause
how do you tx increased GH either in acromegly or gigantism
give some natural states in which you might have increased GH
stress, exercise, and hypoglycemia
this is usually caused by an ademona. labs will show hypercalemia, hypercalciuria (RENAL STONES), hypophosphatemia, increased, PTH & cAMP in urine. While it is often asymptomatic it may present with weakness and constipation ("GROANS")
primary hyperparathyroidism
this d/o is due to decreaesed serum Ca++, most often due to chronic renal dz. Labs will show hypocalcemia, hyperphosphatemia, and increased PTH
secondary hyperparathyroidism (hyperplasia)
this complication of primary hyperparathyroidism results when cystic bone speaces are filled with brown fibrous tissue causing BONE PAIN
Osteitis fibrosa cystica (von recklinghausen's syndrome)
this complication of secondary hyperparathyroidism, results in bone lesions due to renal dz
renal osteodystrophy
give the rhyme that describes hyperparathyroidism
stones, bones, and groans
pt presents with hypocalcemia or tetany. what dz
give 2 causes of hypoparathyroidism
accidental surgical excision (thyroid sx)

DiGeorge syndrome
Chvostek's sign is a sign of hypoparathyroidism. What is it?
tap facial nn results in contraction of facial mm
trousseau's sign is a sign of hypoparathyroidism. What is it?
occlusion of brachial artery w/ BP cuff results in carpal spasm
pt presents w/ hypocalcemia, shortened stature and shortened 4th & 5th digits.
what is pseudohypoparathyroidism
kidneys are unresponsive to PTH
what is the inheritance of pseudohypoparathyroidism
give 5 causes of hypercalcemia

Calcium ingestion, Hyperparathyroid, Hyperthyroid,, Iatrogenic (thiazides, Multiple myeloma, Paget's dz, Addison's dz, Neoplasms, Zollinger-Ellison syndrome, Excess vit D, Excess vit A, Sarcoidosis
give some acute manifestations of diabetes mellitus
polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia)
image p. 256 --Diabetes mellitis
Give some chronic manifestations of Diabetes Mellitus
small vessel dz (diffuse thickening of basement membrane) ->retinopathy (hemorrhage, exudates, microaneurysms, vessel proliferation), claucoma, nephropathy (nodular sclerosis, progressive protinuria, chronic renal failure, arteriosclerosis leading to HTN)
2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive dz and gangrene, cerebrovascular dz
Neuropathy (motor, sensory, and autonomic degeneration)
Cataracts (sorbitol accumulation
what tests should you run in dbts
fasting serum glucose
glucose tolerance test
what does HbA1c meausre
long term diabetic control
what is the primary defect in type 1--juvenile onset (IDDM)
viral or immune destruction of beta cells
what is the primary defect in type 2--adult onset (NIDDM)
increased resistance to insulin
is insulin necessary for tx in type 1--juvenile onset (IDDM)
is insulin necessary for tx in type 2--adult onset (NIDDM)
at what age does type 1--juvenile onset (IDDM)usually strike [many exceptions]
at what age does type 2--adult onset (NIDDM)usually strike [many exceptions]
is type 1--juvenile onset (IDDM)associated with obesity
is type 2--adult onset (NIDDM)associated with obesity
is there a genetic predisposition to type 1--juvenile onset (IDDM)
weak, polygenic
is there a genetic predisposition to type 2--adult onset (NIDDM)
strong, polygenic
is there an HLA association to type 1--juvenile onset (IDDM)
yes (HLA-DR3 &4)
is there an HLA association to type 2--adult onset (IDDM)
describe the glucose intolerance associated with type 1--juvenile onset (IDDM)
describe the glucose intolerance associated with type 2--adult onset (NIDDM)
Is ketoacidosis associated with type 1--juvenile onset (IDDM)
Is ketoacidosis associated with type 2--adult onset (NIDDM)
describe the beta cell numbers in the islets associated with type 1--juvenile onset (IDDM)
describe the beta cell numbers in the islets associated with type 2--adult onset (NIDDM)
describe the serum insulin associated with type 1--juvenile onset (IDDM)
describe the serum insulin associated with type 2--adult onset (NIDDM)
are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 1--juvenile onset (IDDM)
are the classic symptoms of polyuria, polydipsia, thirst, and weight loss associated with type 2--adult onset (NIDDM)
diabetic ketoacidosis is one of the most important complications of type 1 dbts describe its pathology
excess fat breakdown and increased ketogenesis from increase in free fataty acids, which are then made into ketone bodies.
what is ketoacidosis usually due to
an increase in insulin requirements due to an increase in stress (e.g., infection)
give some signs and symptoms of diabetic ketoacidosis
kussmaul respirations (rapid/deep breathing), hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration. Fruity breath odor (due to exhaled acetone)
what will the labs of a pt in diabetic ketoacidosis show
hyperglycemia, increase H+, decreased HCO3-, (anion gap metabolic acidosis, increased blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+
what are some complications of diabetic ketoacidosis
life-threatening mucormycosis, rhizopus infxn, cerebral edema, cardiac arrhythmias, heart failure
how do you tx a pt in diabetic ketoacidosis
fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia
this d/o is characterized by intensive thirst and polyuria together with aninability to concentrate urine owing to lack of ADH
diabetes insipidus
this type of diabetes insipidus may be caused by a pituitary tumor, trauma, surgery, histiocytosis
central DI
this type of diabetes insipidus may be caused by hereditary factors, hypercalcemia, lithium, demeclocycline
nephrogenic DI (lack of renal response to ADH)
how do you dx DI
water deprivation test --urine specific gravity <1.006
serum osmo >290mOsm/L
how do you tx central DI
intranasal despopressin (ADH analog
how do you tx central DI
hydrochlorothiazide, indomethacin, or amiloride
this d/o results in
1)excessive water retention
3)urine osmolarity>serum osmolarity
syndrome of inappropriate antiduiuretic hormone secretion
how do you tx SIADH
demeclocycline or H2O restriction

note: tx slowly
in SIADH very low serum sodium levels can lead to this
give some causes of SIADH
1) ectopic ADH (small cell lung CA)
2) CNS disorders/head trauma
3) pulmonary dz
4) Drugs (e.g., cyclophosphamide)
this is a rare syndrome that results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right sided valvular dz.
carcinoid syndrome
what will you find in the urine of a pt with carcinoid syndrome
increased 5-HIAA in urine
carcinoid tumor is the most common tumor in this part of large intestine
carcinoid tumors result from this type of cell
neuroendocrine cells
carcinoid tumor secretes high levels of this
5-HT (seratonin)
if carcinoid tumor is limited to here you wont see symptoms
GI tract
5-HT undergoes 1st pass metabolism in liver
give the rule of 1/3 for carcinoid tumors
1/3 metastasize
1/3 present w/ 2nd malignancy
1/3 multiple
where to carcinoid tumors derive from
neuroendocrine cells of GI tract
how do you tx carcinoid tumors
this is a gastrin secreting tumor of pancreas or duodenum. It causes recurrent ulcrs
Zollinger-Ellison syndrome
what MEN syndrome is ZE syndorme associated with
MEN type I
what is the tx strategy for type 1 DM
low sugar diet, insulin replacement
what is the tx strategy for type 2 DM
dietary modification, exercise for weight loss, and oral hypoglycemics