Endo 21 Pancreas and Adrenal Morphology Pancreas has head

Endo 21 Pancreas and Adrenal Morphology
Pancreas has head, neck, body, and tail. Tail is only part that is NOT retroperitoneal
 Epithelial derived (gland)
 Islets derived from endoderm, 1 million islets in pancreas, more numerous in tail
o Most is exocrine units w/ islets scattered throughout
 Reticular fibers are support framework
 Rich capillary network and ANS fibers
% of total
Scattered throughout,
but concentrated in
the center
Decreases blood
glucose levels
Scattered throughout
Scattered throughout
PP (F)
Scattered throughout
Scattered in islets
and exocrine
Scattered in islets
and exocrine
Secretin, motilin,
substance P,
Increases blood
glucose levels
Inhibits hormone
release and inhibits
contractions of the
GI tract and the
Stimulates HCl
production by
parietal cells
Inhibits exocrine
secretions of the
hyperglycemia and
stimulates GI fluid
Secretin: stimulates
secretion from
exocrine pancreas
Motilin: promotes
gastric and intestinal
Substance P:
Insulinoma (most
common), usually
Glucose < 45 mg/ml
Glucagonoma (rare)
Secretory diarrhea
Carcinoid syndrome
90% of Insulinomas are benign, 10% are malignant
Glucagonoma causes high blood sugar
EC cells = enterochromaffin cells, carcinoid syndrome  ↑ serotonin  ↑ GI motility = diarrhea
Pancreatic Islets: alpha and beta cells secrete peptides so have: hypochromatic nucleus, Golgi
complex, high RER, mitochondria to make ATP for hormone prod
 Secretory granules packed w/ hormone and released from cell
 Vascular structures are near to pick up hormones to transport throughout the body
Insulin secretion: produced by beta cells, GLUT-2 embedded in membrane is independent of
insulin and doesn’t change based on glucose conc.
 Transports glucose from blood  beta cell  insulin secretion from vesicles, picked up
by capillaries  target cells
 DM type 2 have less effective GLUT-2 transporters so less responsive to glu challenge
Target cell response to insulin: must have a receptor, GLUT-4 transporters are dependent on
insulin, in presence of insulin GLUT-4 upregulated on plasma membrane to ↑ glucose uptake,
when insulin levels drop some GLUT-4 receptors internalized
 DM pts have defective signaling, GLUT-4 doesn’t get incorporated into membrane
 Could be defect in insulin receptor
Counter insulin hormones: glucagon, cortisol, growth hormone, and epinephrine
Complications of DM: pt compliance is #1 factor  neuropathy, loss of autonomic control
(bowel and bladder), eye problems (retinopathies, glaucoma), kidney failure, gangrene/infection,
lower limb amputation is common, atherosclerosis common @ early age, MI @ early age
Suprarenal arteries: IPAR: IP = Inferior Phrenic, parent for superior suprarenal arteries
 A = aorta, parent vessels for middle suprarenal arteries
 R = renal, parent vessels for inferior suprarenal arteries
Veins: left suprarenal vein empties into left renal vein (longer than right)
 Only 1 vein drains each adrenal gland
o Right suprarenal vein  inf vena cava, much shorter, more easily torn
In adrenal gland, delicate arteries penetrate capsule (subcapsular arterial plexus)
 One set will form cortical sinusoidal capillaries – bathe cortical cells
 Medullary arteries travels thru cortex  medullary area
o Also supplied by sinusoidal capillaries after passing thru cortex
 Functional cells are chromaffin cells
Nerves of Suprarenal glands: segmental levels are variable
 Medulla w/ modified postganglionic nerve cells
 Need to be supplied by preganglionic nerve cells
 T8-T12 and L1 are common segments supplying these cells
On MRI left adrenal gland looks like “Y” and right looks like Mercedes Benz sign
Adrenal gland is 5 grams, same as nickel
90% cortex 10% medulla
Cortex from mesoderm, medulla from neuroectoderm
Chromaffin cells (in medulla) have neuroectoderm source and neural crest cells move from
sympathetic ganglia to become chromaffin cells
 Move from ganglia  adrenal glands
 2 signaling molecules for development of chromaffin cells – cortisol and NGF
Extra adrenal tissue occurs when cells travel to other parts of body, possible areas of ectopic
medullary tissue along path of aorta
 Btw bifurcation of aorta and inferior mesenteric artery is Organ of Zuckerkandl – no
cortical tissue, medullary only
 Tumor of ectopic tissue is pheochromocytoma
 Cortical tissue or medullary tissue can develop by ovaries or male genitalia
Adrenal Cortex: 3 zones: Superficial to deep: Glomerulosa, fasiculata, and reticularis
 Fasiculata is thickest, 78% of cortex, glomerulosa 15%, reticularis 7%
 Glomerulosa = aldosterone, Fasciculata = glucoocorticoids and small amts androgens,
Reticularis = androgens and small amts glucocorticoids
 Medulla produces and secretes NE and epi
Steroid-secreting cells of zona fasciculate has lots of smooth ER, mitochondria has
tubular cristae, nucleus has euchromatin, lipid droplets contain precursor for steroid synth
o Steroid hormones diffuse across membrane, not stored, body systems signal
steroid production
 Factors affecting cortex: Angiotensin and K ions have greatest influence on aldosterone
o ACTH influences the production of aldosterone but NOT the release
o Fasciculata and reticularis, ACTH influences synthesis of cortisol and
o Too much ACTH most effect on inner 2 zones  hypertrophy and thicken
o Glomerulosa is basically unaffected
o ACTH is low, fasciculata and reticularis will shrink
 Feedback control of ACTH and cortisol secretion: too much cortisol inhibits ant pit and
hypothalamus  ↓ amts of ACTH and CRH released
Aldosterone regulates extracellular fluid volume, fluid ↓ aldosterone release ↑
Effect of cortisol of metabolic fuel flow: shift metabolic to use free fatty acids to conserve carbs
 Uses fat and protein as fuel
 Liver mainly unaffected by cortisol to maintain gluconeogenesis
 Excessive amts  fat deposition, can dvlp striae
 ↑ appetite  ↑ caloric intake
 ↑ blood volume  red face
Synthetic pathway for DA, NE, and Epi; Cortisol required by enzyme to convert NE  epi
 Tyrosine  DA  NE and Epi in cytosol  concentrated & stored in secretory granule
 Blood carries cortisol from adrenal cortex to medulla to act on enzyme
 Tumor of Organ of Zuckerkandl expected to ↑ NE release bc low levels of cortisol d/t
no cortical tissue in tumor, therefore epi prod will not ↑
 Catecholamines are released bound to chromogranin A
 Pheochromocytoma (tumor of chromaffin cells) will ↑ synthesis and release of
catecholamines and ↑ prod of catecholamine binding proteins
Congenital Adrenal Hyperplasia: occurs during development affecting fetus
 Precursor steroids  cortisol or androgens
 W/ disease can’t make cortisol so get ↑ androgens
o Body senses lack of cortisol and ↑ ACTH release from adenohypophysis 
hypertrophy and hyperplasia of androgen-producing areas  too much androgens
o Too much androgens  ambiguous genitalia, male if testes in scrotum