Endocrine Anatomy & Physiology

ekadar's version from 2016-03-13 07:43


Question Answer
most common ectopic thyroid tissue sitetongue
lingual thyroidif thyroid fails to migrate, can form at any part of thyroglossal duct's usual path. It can form w/in tongue. If lingual thyroid is the only thyroid tissue in body removing can lead to significant hypothyroidism

Endocrinology Anatomy

Question Answer
Cell types in pancreasalpha (glucagon) peripheral, beta (insulin) are central, delta (somatostatin) interspersed i
Anterior/posterior pituitary derived from?anterior from oral ectoderm (Rathke's pouch), posterior from neuroectoderm
Alpha vs beta subunits in anterior pituitary hormonesalpha is the same for TSH/FSH/LH/HcG- beta determines specificity
Acidophils vs basophils of pituitary hormonesacidophils are GH and prolactin, basophils are B-FLAT- FSH/LH/ACTH/TSH
Drainage for adrenal glandsleft-->left adrenal v.-->left renal v.--> IVC
right-->right adrenal v.-->IVC
Adrenal gland derived from?cortex from mesoderm, medulla from neural crest
Arrangement of adrenal glands and hormoneszona glomerulosa (mineralocorticoids), fasciculata (glucocorticoids), reticulata (androgens), inside is medulla with catecholamines
Hormones involved in cortisol releaseCRH from hypothalamus-->ACTH from anterior pituitary-->cortisol from adrenal cortex (zona fasciculata)
Stimulants of insulin releasehyperglycemia, GH, Beta-agonists
Inhibitors of insulin releasehypoglycemia, somatostatin, alpha-2 agonists
Location of GLUT-1RBCs, Brain
Location of GLUT-2beta islet cells, kidney, liver, small intestine
Location of GLUT-4skeletal muscle & adipose tissue
insulin-dependent organsskeletal muscle & adipose tissue
where does the inferior parathyroid come frompouch 3
where does the superior parathyroid come frompouch 4

Enocrine Physiology

Question Answer
what hormone causes insulin resistanceGH
glucagon major actionsincreases serum glucose, increases serum FA, elevates urea production
insulin receptortyrosine kinase activity
beta-adrenergic stimulation and insulinpromotes insulin release
alpha-adrenergic stimulation and insulininhibits insulin release
Dopamine negatively effects?prolactin
Somatostatin inhibits?GH and TSH
Prolactin negatively inhibitsGnRH (so less FSH/LH)
HCG and TSHthere beta units look a lot alike, increased BHCG can cause hyperthyroidism
IGF-1stimulates linear growth and muscle mass
ghrelinstimulates hunger and GH release
ghrelin increaseswith sleep loss and Prader Willi
leptindecreased during starvation
leptinsatiety hormone
ADHresponds only to large increases in blood volume

Adrenal steroids

Question Answer
Think of the first 1HTN
Second 1masculinization
11 B-Hydroxylase deficiencyHTN and masculinization but still female. male will have early puberty
17 alpha-Hydroxylase deficiencyHTN
21 alpha hydroxylase deficiencymasculinization but still female. male may have early puberty
17 deficiencymake lots of aldosterone. Not making any androgens so male appears female Female would be normal but with hypertension
increased 17-hydroxyprogesterone is diagnostic21 deficiency
increased 11-deoxycortisone11 deficiency
21 deficiency versus 11 deficiency11 deficiency makes weak mineralocorticoids so no salt wasting, no hyperkalemia and no hypovolemia
cortisol is a BIG FIBincreases Blood pressure, increases Insulin resistance, increases Gluconeogenesis, decreases Fibroblast activity (causes striae), decreases Inflammatory response, decreases Bone formation


Question Answer
PTH functionsincreased bone resorption of Ca/PO4, increased renal reabsorption of Ca and decreased reabsorption of PO4, increased vit D by stimulating 1-hydroxylase
Regulation of PTHincreased when low Ca or Vit D or high PO4, decreased when there is VERY low serum Mg
If phosphate is low, mechanism to increase it?low PO4 sensed by kidneys-->more vit D made-->more PO4 absrobed in gut and more released from bone resorption
PTH effect on osteoblasts and osteoclastsPTH has a DIRECT effect on osteoblasts, an indirect effect on osteoclasts (stimulating bone resorption)
Vit D deficiency in kids vs adultskids = rickets, adults = osteomalacia
Inactive form of vit d24,25 Vit D
Vit D synthesisD3 from sun or D2 from plants --> both converted to 25 OH Vit D by liver 25-hydroxylase-->then to 1,25 OH Vit D by 1-hydroxylase in kidney (active form)
Calcitonin sourceC-cells in parafollicular cells of thyroid
Calcitonin functiondecrease bone resorption of Ca, not very important however in overall Ca homeostasis
Calcitonin regulationincreased serum Ca stimulates calcitonin


Question Answer
Hormones functioning via intrinsic tyrosine kinase pathwayinsulin, IGF-1, FGF, PDGF, EGF
Hormones functioning via receptor-associated tyrosine kinaseprolactin, immunomodulators, GH, G-CSF, erythropoietin, thrombopoietin
Hormones functioning via cAMP pathwayFSH/LH/ACTH/TSH (FLAT) CRH/HCG/ADH (V2)/MSH/PTH (CHAMP)
Hormones functioning via cGMP pathwayANP, NO...think vasodilators
Hormones functioning via IP3 pathwayGnRH, Oxytocin, ADH (V1), TRH (GOAT)
Hormones functioning via steroid receptorsreceptor is in the cytosol not on the cell membrane
increased sex hormone binding globulin in mendecreases free testosterone and leads to gynecomastia
T3 functions4 Bs- brain maturation, bone growth, beta1-adrenergic effects, increased BMR (via increase Na+/K+ ATPase)
Where is T3 formedin cytoplasm of target cell
Pregnancy and TBGincreases but serum T4 is not altered b/c of equilibrium between serum [T4] and thyroid gland T4 production
What converts T4 --> T35'-deiodinase
T3 vs T4 binding affinity to receptorsT3 has greater affinity
Thyroid hormone pathwayTRH from hypothalamus--> TSH from pituitary-->T3/T4 from thyroid (negative feedback then to anterior pituitary)
Enzyme for oxidation/organification of iodide and coupling of MIT and DITthyroid peroxidase (targeted by antithyroid drugs propylthiouracil and methimazole)
Wolf-Chaikoff effectexcess iodine inhibiting thyroid peroxidase & leads to less T3 and T4 production
PTUinhibits both peroxidase and 5' deiodinase
Methimazoleinhibits peroxidase only