Endocrine Flashcards
most common ectopic thyroid tissue site
tongue
foamen cecum
normal remnant of thyroglossal duct
alpha subunit of AP hormones
hormone subunit common to TSH, LH, FSH, hCG
beta subunit of AP hormones
determines hormone specificity
GLUT 1
RBC, brain, cornea Insulin independent glucose transporter
GLUT 2
bidirectional insulin independent glucose transporter on beta islet cells, liver, kidney, small intestine
GLUT 3
insulin independent glucose transporter in brain
GLUT 5
insulin independent fructose transporter in spermatocytes, GI tract
what cell type always uses glucose for energy even in starvation
RBCs-lack mitochondria so cannot use ketone bodies
why should beta blockers be avoided in diabetics?
if theyre nonselective they can stop hepatic gluconeogenesis leading to hypoglycemia
what does TRH do?
secreted by hypothalamus and increases TSH and Prolactin secretion from the AP
GH induces its effects via
JAK STAT receptor tyrosine kinase, increases IGF transcription and production in the liver
when is growth hormone secretion highest
during sleep and exercise
what causes a decrease in GH release
glucose and somatostatin
laron dwarfism
defective GH receptor leading to diminished linear growth, increase GH and decreased IGF1
ghrelin
stimulates hunger and GH release, increased in Prader Willi and with sleep loss
leptin
produced by adipose tissue and send satiety signal, decreased with decreased sleep, decreased during starvation
endocannabinoids
stimulate cortical reward centers and increase desire for high fat food
antidiuretic hormone
monitors BP (V1 receptors) and serum osmolarity (V2 receptors)-osmolarity via aquaporin channel insertion in principal cells of the renal collecting duct -regulated primarily by osmoreceptor in the hypothalamus and secondarily by hypovolemia
Cortisol effects
BIG FIB
increase in blood pressure, insulin resistance, gluconeogenesis
decrease in fibroblast activity, inflammatory and immune response, bone formation
how does increase pH effect Ca
increases negative charge of albumin, increasing its affinity to bind to calcium leading to decreased free ionized calicium and symptoms of hypocalcemia including bone cramps, pain, paresthesia and carpopedal spasms
how does PTH increase Ca via bone breakdown
increases production of macrophage stimulating factor and RANK ligand (by osteoblast) which binds RANK receptor on osteoclasts and increases their activity
intermittent PTH causes
bone formation
what stimulates PTH secretion
decrease ca, increased phos, increased Mg (diarrhea, aminoglycosides, alcohol abuse, diuretics) ***although really low levels of Mg decrease PTH
endocrine hormones that use cAMP
FLAT ChAMP
FSH LH ACTH TSH CRH hCG ACTH MSH PTH + calcitonin, GHRH, glucagon
IP3 endocrine hormones
GOAT HAG
GnRH Oxytocin ADH TRH Histamine (H1) Angiotensin II Gastrin
endocrine hormones with intracellular receptors
VETTT CAP
Vitamin D Estrogen Testosterone T3/T4 Cortisol Aldosterone Progesterone
Endo hormones with intrinsic tyrosine kinase
Insulin, IGF 1, FGF, PDGF, EGF
MAP kinase pathway
receptor associated tyrosine kinase
PIGGlET
Prolactin Immunomodulators (cytokines, interleukins, IFN) GH, G CSF, Erythropoietin, Thrombopoietin
JAK STAT pathway
systemic effects of T3
bone growth
CNS maturation
increase beta1 in heart=increase CO, HR, SV, Contractility
increase basal metabolic rate via Na/K atpase activity=increase O2 consumption, RR, body temp
increase glycogenolysis, gluconeogenesis, lipolysis
hepatic failure effect on TBG
decrease
TBG in pregnancy/OCP/hormone replacement therapy
increase
5 deiodinase
converts T4-T3 in peripheral tissues
wolff chaikoff effect
excess iodine temporaroly inhibits peroxidase activity–> decrease idonine organification and therefore decrease T3/T4
conn syndrome
aldosterone hyperactivity 2/2 adrenal hyperplasia
hypokalemia, hypertension, muscle weakness, paresthesia and hypokalemic paresis
metyrapone stimulation test
last step of cortisol synthesis is blocked, in normal person will result in decrease in cortisol and increase in ACTH, in adrenal insufficiency ACTH will not raise
primary chronic adrenal insufficiency
Addison disease
-adrenal atrophy or destruciton by a disease-autoimmune, TB, metastasis
shock, hyponatremia, hyperkalemia, hypoglycemia, with nuchal rigidity, petechial rash
Waterhouse friderichsen syndrome secondary to Neisseria menigitidis
-hemmorhage assocaited with speticemia, DIC, or endotoxic shock
tertiary adrenal insufficiency
caused by abrupt exogenous steroid withdrawal, aldosterone synthesis unaffected
abd distension with firm irregular mass that crosses midline in child
neuroblastoma-neural crest cell derivative
as opposed to wilms tumor (smooth and unilateral)
opsoclonus myoclonus syndrome
dancing eyes dancing feet-neuroblastoma
assocaited with n myc overexpression
bombesin and neuron specific enolase +
neuroblastoma
what common pain relief medication should be avoided in hyperthyroidism
NSAID/ibuprofen-can displace t3/t4 form TBP and increase thyrotoxic state
-acetominophen is preferred instead
hashimoto thyroiditis increased risk of what canecer
non hodgkin lymphoma
hurthle cells with lymphoid aggregates and germinal centers on thyroid histo
Hashimoto thyroiditis (on exam enlarged nontender thyroid)
increase ESR, jaw pain, very tender thyroid
deQuervain thyroiditis (subacute thyroiditis) self limited usually following flu like illness and
histo: granulomatous infiltration
- iodine uptake would show diffuse decrease in iodine uptake
treatment: NSAIDs
fixed hard painless goiter with sx of hypothyroid
Riedel thyroiditis
- thyroid replaced by fibrous tissues-fibrosis can extend to local structures and mimic anaplastic carcinoma
- a manifestation of IgG disease-autoimmune pancreatitis, retroperitoneal fibrosis, noninfectious aortitis
jod basedow phenomenon
thyrotoxicosis if a patient with iodine deficiency goiter is made iodine replete
empty appearing nuceli with central clearing, psamomma bodies, nuclear grooves
papillary carcinoma-lyphatic invasion is common
history of radiation as a child, RET BRAF mutations
uniform follicle with capsular invasion
follicular carcinoma
sheets of cells in an amyloid stroma/uniform polyglonal or spindle shaped cells
medullary carcinoma
hematogenous spread
produces calcitonin
MEN 2A, 2B RET gene
markes pleomorphism, irregular giant cells, biphasic spindle cells
anaplastic/undifferentiated carcinoma
hypocalcemia, sortened 4th/5th digits, short stature
Albright hereditary osteodystrophy
-unresponsiveness of kidney to PTH
familial hypocalciuric hypercalcemia
defective ca receptor on parathyroid cells
-PTH cannot be suppressed by increase in ca2+
miild hypercalcemia with nml to high PTH, hypocalciuria
cystic bone spaces filled with brown fibrous tissue consisting of hemosiderin from hemorrhages
osteitis fibrosa cystica
atrophy or compression of pituitary
empty sella syndrome often idiopathic, common in obese women
Kimmelstiel-Wilson nodules
chronic complication of Diabetes, Nodular glomerulosclerosis
increased beta hydroxybutyrate
a ketone body intermediate and a sign of insulin deficiecncy
dermatitis, DVT, depression, diabetes
glucagonoma, tumor of pancreatic alpha cells causing excess of glucagon
low blood glucose, symptoms of hypoglycemia, resolution of symptoms after normalization of glucose levels
insulinoma
-decreaed blood glucose and increase C peptide
recurrent diarrhea, cutaneous flushin, asthmatic wheezing, right sided valvular disease
Carcinoid syndrome-increase 5 hydroxyindoleactic acid in urine, niacin deficiency (pellagra)
tx: surgical resection and somatostatin, octreotide
secretin stimulation test
used to diagnose zollinger ellison syndrome-gastrinoma, give pts secretin and see if gastrin levels remain elevated
MEN 1
parathyroid
pituitary (prolactin or GH)
pancreatic (gastrinoma, insulinoma, VIPomas, glucagonomas)
MEN 1 gene
MEN2a
parathyroid, pheochromocytoma, medullaruy thyroid cancer
RET gene
MEN 2b
pheochromocytoma, medullary thyroid carcinoma, oral/intestinal ganglioneuromatosis RET gene
rapid actin insulin
aspart, glulisine, lispro-monomeric form so work faster than regular insulin (hexamer)
se: hypersensitivity, hypoglycemia rare
intermediating acting insulin
NPH
long acting insulin
detemir and glargine (no peak)
once a day dosing
metformin
biguanide, mech not known
decreased gluconeogenesis, increases glycolysis, increase peripheral glucose uptake (increase inculin sensitivity)
SE: GI upset, lactic acidosis (not used in renal or liver insufficieny)
causes weight loss
chlorpropamide tolbutamine glimepiride glipizide glyburide
sulfonylureas
- close K channel in beta cells, causing membrane depolarization and increase insulin release with ca influx
- stimuelat the release of insulin used in T2DM (need some islet fuction)
se: risk of hypoglycemia in renal failure, first generation: disulfiram like effects, second generation hypoglycemia
pioglizatone, rosiglitazone
bind PPARgamma an dincrease insulin sensitivity via adipnoectin, T2DM se: weight gain, hepatotoxicity, HF increased risk of fractures
exenatide
GLP1 analog
increse insulin and decrease glucagon release used in T2DM se: nausea, vomitting, pancreatitis
linagliptin, saxagliptin, sitagliptin
DPP4 inhibitors
increase insulin, decrease glucagon release
used in T2DM
se: mild urinary or respiratory infections
pramlintide
amylin analog
-decreases gastric emptying
used in T2DM
se: glucosuria, UTIs, vaginal yeast infections
acarbose, miglitol
alpha glucosidase inhibitors
-acarbose, miglitol
inhibit brush border alpha glucosidass causing delayed carbohydrate hydrolysis and glucose absorption
decrease postprandial hyperglycemia
se: GI disturbances, not used in IBD, colonic ulceration, intestinal obstruction
cinacalcet
sensitizes Ca sensing receptors in parathyroid gland to circulating Ca2+ and decreased PTH, used in hypercalcemia due to primary or secondary hyperparathyroidism
toxicity: hypocalcemia
demeclocycline
ADH antagonist
SIADH
toxicity: nephrogenic DI, photosensitivity, abnormalities of the bone and teeth
somatostatin used for
acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices
conivaptan, tolvaptan
ADH antagonists used for SIADH, block the action of ADH at the V2 receptor
