Endocrine Pancreas Flashcards
pancreas location and describe its development
posterior to the stomach
largest gland ande develops embryologically as an outgrowth from the foregut
[fore gut = coelic trunk / midgut = Superior mesenteric artery / hindgut = inferior mesenteric artery]
functions of pancreas
- exocrine ; acini 99% wc release digestive enzymes directly into duedenum (OCCUPY MOST OF THE SPACE)
- endocrine ; islets of langerhans 1% releases hormones (OCCUPY LITTLE OF THE PANCREAS)
GI 3 devisions and where is pancreas
foregut; supplies by b from coeliac trunk
midgut; supplied by b from superior mesenteric artery
hindgut ; inferior mesenteric artery -
outgrowth of a foregut structure so supplied by coeliac trunk
histology of islets of lagerhands
imge
hormones made by islets of langerhans and the cell types
what type of hormones are released?
- somatosatin : D cells (delta)
- insulin : B cells (beta)
- gluagacon A cells (alpha)
- gastrin G cells
- ghrelin e cells
- vasoactive intestinal peptide
- pancreatic polypeptide PP
peptie hormones
for insulin and glucagon whats the function
regulation of metabolism of carbs, fats and proteins
- insulin lowers - glucagon ^
where are the actions of glucagon and insulin
- I; liver,adipose,skelteal,muscle
- G; liver, adipose
normal bgl , after meal?renal threshold?
- 3.5-5mmol/L
- 7-8mmol/L
- 10mmol/L
whats glycosuria and what are changes in it?
- g in pee
- pregnant ladies d v renal threshold
- elderly have ^ threshold
insulin is a/c? what other key words is it?
- anabolic
- anti-gluconeogenic and anti-lipolytic and anti-ketogenic
how is insulin made
- preproinsulin made by ribosomes on the RER
- the single peptide then directs it into the cisternal region of RER where it is cleaved off, undergoes modification and folds where correct alignment of cysteine residues
- goes into Golgi where packaged into storage vesicles wc undergo proteolysis whereby remove connecting peptide C peptide (wc consists of 31aa joined together with 4 basic aa(3 arginine and 1 lysine) , so the proinsulin breaks into C peptide and insulin
- vesicles marginated wc means vesicle contains insulin and C peptide and they sit under cell membrane in pancreatic beta cell and wait till they are released when the correct stimulus is present wc is the Katp channels shutting as a result of ^glucose
- the vesicle then fused with membrane and release contents via exocytosis
how is insulin stored in the vesicle during margination
crystalline zinc-insulin complex
what type of receptor family is insulin
tyrosine kinase
how is insulin release
- ATP sensitive insulin channel on plasma membrane open allow efflux of k+ ion c membrane to become more
- d hyper-polarisation
- if metabolism is low, so v ATP so cant inhibit it so, they open and no insulin related
- if metabolism high, ^ ATP wc inhibits these channels c them to close and insulin released
- v gated ca2+ Channes are activated and allow movement of ca2+ to enter the cell down th eocnc gradient, and this ca2+ c exocytosis of the marginated insulin vesicles
what does insulin do then to the glucose
stimulates it being taken up in liver fat skeletal via GLUT 4 channel
what does glucagon do and how it is synthesised
synthesised in rER, same as insulin and marginate, lower plasma glucose level they are released via exo and act on target to ^ lv of - don’t need to know cell signalling of glucagon
why is glucagon useful in clinical
-glucagon is event to hypoglycaemia
what type of receptor does glucagon bind to on cell surface membrane and what happens
binds to Gcouple Protein receptor
causes the enxyem andeylate cyclase to activate wc increases cAMP intracellularly
high cAMP activates protein Kinase A wc phosphorylates and thereby activates a number of important enzymes in target cells
type 1 diabetes
autoimmune destruction of pancreatic beta cells
type 2 diabetes
resistance to insulin
defective post receptor events
or exvessive inapporitate glucagon
what happens to an insulin resistant patient thats young (12 yrs old)
first B cells copensate by ^ insulin levels
B cells then fail to maintain ^ insulin lvels so impaited glucose tolerance
finally B cell dysfunction leads to relative insulin defieceny
pateint develops overt type 2 diabetes
