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148 Cards in this Set

  • Front
  • Back
In what part of the cell is the preprohormone synthed and cleaved?
Where is the prohormone cleaved?
What are thyroid, epinephrin and norepi derivatives of?
What is an example of + feedback?
surge of LH before ovulation
What is an example of down regulation of receptors? of up-regulation?
progesterone down regs it's own and estrogen
egen- upregs it's own receptor and LH
What hormones are derived from proopiomeanocortin (POMC)?
Melanocyte-stimulateing hormone
What hormone is structurally equivalent to PRL?
What icreases the pulsatile release of GH?
sleep, stres, hormones of puberty, starvation, exercise, hypoglycemia
What decreases the pulsatile release of GH?
somatostatin, somatomedins, obesity, hyperglycemia, preggs
True or false hyperglycemia stims GH release?
Where is IGF made?
What are the direct actions of GH?
decrease gcose uptake
increase lipolysis
increase protein synth
increase lean body mass
increase IGF
What are the actions of GH through IGF?
Increase protein synth in chondrocytes and linear growth
increase protein synth in muscle and increase lean body mass
increase protein synth in most organs and increase organ size
What happens in GH deficiency?
faliure to grown, shor stature, mild obesity, delayed puberty
What are the causes of GH deficiency?
lack of pit. growth hormone
hypothalamic ddysfuncion
failure of IGF in the liver
GH receptor deficiency
What are the consequences of GH excess?
before puberty- gigantism- increased linear growth
after puberty- acromegaly
A woman with diffuse goiter and hyperthyroidsim. What are the TSH and T4,3 values?
low TSH high T3,4
48 y/o w/ progressive lethargy and sensitivity to cold. WHat is the Dx?
Pt w/ elevated serum cortisol w/ 1 mg dexamethasone suppresion that doesn't decrease cortisol but 8mg does.
Pituitary tumor
50 y/o complains of diarrhea. face is plethoric and heart murmur is detected. What is teh Dx?
Carcinoid syndrome
Women with short stature and shortened 4th and 5th metacarpals. What is the diagnosis?
Albright's hereditary osteodystrophy.
nondiabetic pt. w/ hypoglycemia but low c peptide
Sureptitious insulin injection
what lab test is the best way to diagnose thyroid disease?
TSH- first to change.
What are the three regions of the adrenal cortex? What do they produce?
GFR- the deeper you go, the sweeter it gets. Salt, Sugar, Sex.

G- glomerulosa
F- fasciculata
R- reticularis

Salt- aldosterone
Sugar- glucocorticoids
Sex- androgen
How does the L and R ovary drain?
L- Renal

Right ain't renal
adrenals are teh same.
Where does the post. pituitary derive from?
Which hormones are acidophils?
What hormones have the common alpha?
TSH and the sex hormones
Where are teh islets of langerhans most numerous?
What is made in the following Islet cells:
tail of pancreas
What is the connection between Dopamine and PRL?
Dopa inhibs PRL
dopa agonists like bromocriptine inhib PRL
dopa antags (antipsychotics) stim PRL.
PRL stims Dopa release, inhibs GnRH
TRH stims PRL release
What increases PRL secretion?
Dopa antags
What decreses PRL secretion?
What is the action of 17-alpha hydroxylase?
Pregnenolone to 17-hydroxypregnenolone (step towards androgens and cortisol)
Progesterone to 17-hydroxyprogesterone
What is consequences of a 17 hydroxylase deficiency?
decreased sex hormones
decreased cortisol
increased mineralocorticoids
female pheno type, no matureation.
Where is CRH made?
paraventricular nuclei of the hypothalamus
What is cholesterol desmolase?
ACTH stims thsi to trigger converstio nof chol to pregenolone in the first step of adrenal hormone synth.
What are the mechanisms of action of ACTH?
stims chol desmolase
upregs the ACTH receptor
2nd messenger is cAMP
What are the actions of glucocorticoids
increase protein catabolism
decrease glucose utilization and insulin sensitivity
increase lipolysis
Inhibs phospholipase A3 with lipocortin
inhibs IL2
Inhibs histamine and serotonin release from mast cells
Upregulates Alpha1 receptors
What are some causes of 1ry adrenal insufficiency?
What are the Sx of 1ry adrenal insufficiency?
decreased glucocorticoids, androgen, aldosterone
increased ACTH
ECF volume contraction. hypotension, hyperkalemia adn met acidosis
What are the differences between 1ry and 2ry adrenal insufficiency in Sx.
no hyperpigmentation.
no aldosterone effects (volume contraction, hypotention, hyperkalemia, met acidosis)
What are the Sx of adrenocortical excess?
increased cortisol and androgen
increased protein catabolism and muscle wasting
Central Obesity
poor wound healing
What are the causes of excess adrenal function?
exogenous glucacorticoids
bilateral hyperplasia of the adrenal glands
Pituitary- Cushing's Disease
What is the Rx of cushings disease?
Ketoconozol- inhibs synth.
What is Conn's syndrome?
What are the symps of hyperaldosteronism?
aldosterone secreatign tumor
Met alkalosis
decreased renin.
What is 21 B hydroxylase deficiency?
common biochem abnlty of steroidogenic pathway
decreased cortisol and aldosterone
increased 17 and progesterone
increased ACTH
hyperplasia of zona fasciculata and reticularis from high levels of ACTH
Increased androgens
Virilization of women
suppression of gonadal function
When is there a + Ca balance? When is there a - Ca balance?
+ in growing kids
- in preggers, and lactation
Where is PTH made?
Chief cells of the parathyroid
What stims the secretin of PTH?
decreased Ca
Decreased Mg (mild, severe inhibit)
What is the action of PTH
icnreased resorption
decreased P reabsorption - proximal tubule(increased urinary cAMP)
increasaed Ca reabsorption- distal tubule
increased Ca absorption from gut
What is hydroxyproline?
biproduct of the reabsorption of organic matrix of bone- excreted in urine
what happens in 1ry hyperparathyroidism?
parathyroid adenoma
icreased Ca
decreased P
increased urinary P
increased urinary Ca excretion
increased urinary cAMP
increased bone resorp
What happens in humoral hypercalcemia of malginancy?
PTH-rp secreted by breast, lung tumors.
increased serum Ca
decreased P
decreased PTH
incrased urinary P
What happens with hypoparathyroid?
thyroid surgery or congenital
- decrused serum Ca
- increased serum P
decreased urniary P excretion
What is Albright's hereditary osteodystrophy?
pseudohypoparathyroidsims type Ia
defective Gs protein in kdney and bone-> resistance to PTH
elevated PTH
How does chronic renal failure affect Ca?
decreased GFR-> decreased elim of P
incrased P -> decreased ionized Ca
Decreased 1,25-dihydroxy
decreased Ca-> hyperPTH -> renal osteodystrophy
What is the role of Vit D?
Increases Ca and phosphate absorption to ECF for bone mineralization
Binds to calbindin D-28K (PTH triggers formation of Vit. D)
Increases renal absrop of Ca and P
Increases bone reasorp
What does a deficiency in Vit D cause?
How is Vit D metabbed?
Cholecalciferol, 25-hydroxycholcalciferol and 24,25-dihydroxycholcalciferol are inactive
Active form is 1,25-hydroxycholcalciferol is catalized by 1-alpha-hydroxylase
What regs 1-alpha-hydroxylase?
decreased serum Ca
increased PTH
decreased serum P
What is the source of Vit. D?
sun exposure and plants
What is the role of calcitonin?
Synthed and secreted by parafollicular cells of thyroid (C cells)
secretion stimmed w/ increased Ca
Inhibits bone resorp.
What are the Ca, P, and alk P in hyperPTH, Paget's, Vit D intox, Osteoporosis and renal insufficiency?
Ca, P, alk P
hyperPTH- up, down, up
Paget's- little up, normal, really up
Vit D intox- up, up, littl up
Osteoporosis- normal, normal, normal
Rnal insufficiency- down, up, normal
Breakdown the metab of thyroid synth.
stimmed by TSH
1. Iodid pump- follicular cells transport iodide- inhibbed by thiocyanate, perchlorate anions, high levels of I
2. Peroxidase enzyme- make I2 (inhibbed by propylthiouracil)
3. Tyrosine is incorporated on the ribosomes of the thyroid follicular cells. Packaged into secretory granules on golgi-> follicular lumen
Thyroglobulin reacts w/ I2-> DIT and MIT
4. Two DITs-> T4
1 DIT and 1 MIT-> T3
5. stored in follicular lumen
more T4 made than T3
6. When stimmed, taken back in, thyroglobulin is degraded by lysosomes-> T3,T4
Leftovers are deiodinated by thyroid deiodinase
7. T3 and T4 is bound to TBG
8. T4-> T3 or rT3
What is the role of thiocyanate and perchlorate anions?
inhib the iodide pump
What happens to TBG in hepatic failure and pregs?
hepatic failure- TBG levels decrease- decrease in total thyroid hormone levels, normal free hormone

Pregs- TBG increase-> increase in total T.
What are the actions of T3,4?
Growth- bone formation, maturation
Perinatal CNS maturation
BMR- increaes BMR and Na/K ATPase
CV- increased HR and SV
Increased Resp
Metabolic- increased glucose absorp, glycogenolysis, gluconeogenesis, glucose oxidation, lypolysis, protein synth and degradation
What are some characteristics of steroid hormones?
lipophilic, insoluble in plasma;, bind to globulins

Increased Sex hormone-binding globulin (SHBG)-> lower free Testosertone-> gynecomastia
Decreased SHBG-> hirsuitism
What organs are insulin-dependant?
skeletal muscle and adipose tissue- for gcose uptake
brain and RBCs take up gcose w/ glut-1
What aer some causes of 2ry hyperaldosteronism?
renal artery stenosis
chronic renal failure
Nephrotic syndrome
What is the Rx for hyperaldosteronism?
What is the staining of a pituitary PRLnoma?
What is the staining of a somatotropic adenoma
What is pituitary chachexia (simmonds disease)?
generalized panhypopituitarism
Caused by:
pit tumors
postpartum pit necrosis (sheehan)
Sheehan syndrome
ichemic necrosis of pituitary- hemorrhage and schock during child birth
first loss of gonadotropins then TSH and ACTH
benign childhood tumor derived from Rathke pouch
Nests and cords of squamous or columnar cells in a loose stroma, resembles embryonic tooth but enamel
Cystic; lining epithelium of flat or columnar cells often expands into papillary projections
Calcification on X-ray
chromaffin cells of the adrenal medulla
10% malignant
10% bilateral
10% extra-adrenal
10% calcify
10% kids
10% familial
incraease catecholamines

Spells of:

can be associated with NF or von Hippel-Lindau

Rx with Phenoxybenzamine
highly malignant, catecholamines of early childhood
adrenal medulla
converts into ganglioneuroma
amplification of N-myc oncogene
MEN type I
Wermer's- AD
3 Ps
Pancreas- ZE, insulinoma, VIPoma

Kidney stones and stomach ulcers
MEN type II
Sipple- AD
medullary carcinoma of the thyroid
MEN type III
medullary carcinoma of the thyroid
oral and intestinal ganglioneuromatosis
What is Riedels Thyroiditis?
thyroid replaced by fibrous tissue- hypothyroid
What is de Quervain's Thyroiditis?
self-limited hypothyroidism- follows flu-like illness
elevated ESR
jaw pain
early inflamm
tender thyroid
hyperthyroid early in course
mononuclear cell infiltrate, follicular dysruption, loss of colloid
What is the most common congenital anomaly of the thyroid?
thyroglossal duct cyst
from thyroglossal duct
no alterations in thyroid function
What HLAs is Graves' associated with?
What is plummer disease?
hyperthyroidism, nodular goiter, no exophthalmos
hot nodules- adenomas or nono-neoplastic
What is struma ovarii
ovarian teratoma made of thyroid tissue.
What HLAs is Hashimotos associated with?
DR5, B5
Papillary carcinoma of the thyroid
most common cancer
papillary projections into gland-like spaces
ground-glass nuclei.
spammoma bodies
better prognosis
prior radiotherapy is a risk factor
Follicular Carcinoma of the thyroid
histo - uniform follicles
poor prognosis
Medullary carcinoma of the thyroid
from C cells
produce calcitonin, (lowers Ca)
Undiffed carcinoma of the thyroid
old pts. poor prognosis
when is an increase in GH normal?
stress, exercise, hypoglycemia
What is Osteitis fibrosa cystica?
von Recklinghausen syndrome
cystic bone spaces filled with brown fibrous tissue (bone pain)
What is renal osteodystrophy?
bone lesions due to 2ry hyperPTH
What does Stones, Bones, and Groans refer to?
bones are depleted
Groans- constipation
What are the causes of hyperparathyroid?
Calcium injestion
Iatrogenic (thiazides)
Multiple Myeloma
Excess Vit D
Excess Vit A
What is Chvosteks sign?
tap facial nerve-> contraction of facial mucles

What is Trousseau's sign?
occlusion of brachial artery w/ BP cuff-> carpal spasm

When can you develop pseudohypoparathyroidism?
AR kidney unresponsive to PTH
What are some growth defects in HypoCa?
shortened 4th/5th digit
short stature
What MEN syndromes is hyperPTH associated with?
I and II
What is the major cause of 2ry hyperPTH?
renal disease-> hypocalcemia
what HLA is DM associated with?
DR 3,4
What are kussmaul respirations?
rapid/deep breathing
w/ ketoacidosis
What is diabetic ketoacidosis?
most important complication of DM1
increase in insulin requirements from increased stress (infection)
excess fat breakdown and increased ketogenesis from increase in FFAs used to make ketones
What are the Sx of diabetic ketoacidosis?
Kussmaul resps
abdominal pain
fruity breath
What are the labs in diabetic ketoacidosis?
increase H, decrease HCO3 *anion gap
increased blood ketone levels
What are the complications of ketoacidosis?
Rhizopus infection
cerebral edema
cardiac arrhythmias
heart failure
What is the Rx for Ketoacidosis?
glucos if necessary to prevent hypoglycemia
What is Diabetes Insipidus?
intesive thirst and polyuria
can't concentrate urine (no ADH)
no ADH, ore no response to ADH- lithium

Dx- water deprivation test
Labs- low specific gravity, high osms
Rx- adequate fluid intake; intranasal desmopressin- central
hzt, indomethacin, or amiloride- nephrogenic
What is SIADH?
inappropriate ADH secretion
water retention
urin osm>serm osm
can cause seizure (treat slowly)
Rx- demeclocycline, H2O restriction
What are the causes of SIADH?
ectopic- lung cancer
head trauma
pulm disease
drugs- cyclophosphamide
What is carcinoid syndrome?
rare syndrome caused by carcinoid tumores, especially metastatic small bowel tumors, secreete Serotonin. Not seen if tumor is limited to GI tract.-> diarrhea, cutaneous flushing, asthmatic wheezing, Rsided vasc disease

33% mets
33% 2nd malig
33% multiple

Rx- octreotide
What is the Rx for Carcinoid syndrome?
What are some 2ry causes of DM?
pancreatic disease
- hereditary hemochromatosis
- Pancreatitis
- Carcinoma of the pancreas
Other endocrine
- cushings
- acromegaly
- glucagon hypersecretion
- pheo
- hyperthyroid
What anatomic changes occur to the pancreas in type 2 diabetes?
amylin deposis, fibrosis, hyalinization
not specific
interferes w/ insulin sensing by B cells
What are the anatomic kidney changes seen in diabetes?
increased width of glomerular BM earlies and most common renal change
diffuse glomerulosclerosis, nodular, arteriolar lesions, exudative lesions, fibrin cap, capsular drop
armanni-ebstein lesioin- tubular deposition of glycogen
What changes occur in the capillaries in DM?
nonenzymatic glycosylation of membrane protein
most common
benign or malignant
increased insulin. circulating C-peptide is increased in insulinoma

Whiple triad: episodic hyperinsulin, hypoglycemia; CNS dysfunction temporally to hypoglycemia; dramatic reversal of CNS issues.
What is the Rx strategy for type 1 DM
- low-surgar diet, insulin replacement
What is the Rx strategy for DM type 2.
dietary modification adn exercise for weight loss.
What is the mechanism of action for Insulin?
increase glucose stored as glycogen
increase glycogen and protein synth, K uptake
aids TG storage
What is the mechanism of action for sulfonylureas?
Close K channel in B-cell membrane. cell depolarizes-> trigger of insulin release via increased Ca flux.
What are the SEs of Insulin?
What are the SEs of sulfonylurea?
disulfiram-like effects
2nd generation: hypoglycemia
What is the effect of biguanides?
decreased gluconeogenesis
increased glycolysis
decreased serum glucose
What are the SEs of biguanides?
lactic acidosis
What is the mechanism of Glitazones?
increase target cell response to insulin
What are the SEs of Glitazones?
weight gain
What is the mechanism of action of alpha-glucosidase inhibitors?
Inhibit brush border alpha-glucosidases.
Delayed sugar hydrolysis and glucose absorption
lead to decreased postprandial hyperglycemia
What are the SEs of alpha-glucosidase inhibitors?
GI disturbances.
What is Orlistat?
alters fat metab by inhibiting pancreatic lipases

for long term obesity management
What are the SEs of Orlistat?
Steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache
What is Sibutramine?
Sympathomimetic serotonin and NE reuptake inhibitor
Short-term and long-term obesity management.
What are the SEs of Sibutramine?
Hypertension and tachycardia
What is the mechanism of action of propylthiouracil adn methimazole?
Inhibit thyroid hormone synth.
inhibit conversion of T4 to T3
What are the SEs of propylthiouracil?
skin rash, agranulocytosis, aplastic anemia
When is GH used clinically?
GH deficiency
When is Octreotide used clinically?
When is Oxytocin used clinically?
Stims labor
uterine contractions
milk let-down
controls uterine hemorrhage
When is desmopressin used clinically?
Pituitary Diabetes Insipidous
What is the mechanism of action of Levothyroxine and triiodothyronine
Thyroxine replacement
What are the SEs of thyroid hormone replacement?
Tachycardia, heat intolerance,
What is the mechanism of action of glucocorticoids?
decrease the production of leukotrienes and prostaglandins by inhibiting Phospholipase A2 and expression of COX-2
What is the clinical use of glucocorticoids?
Addisons, inflam, immune suppression, asthma
What is the toxicity of glucocorticoids?
chushings- buffalo hump, moon facies, truncal obesity, muscle wasting, think skin, easy bruisability, osteoporosis