Kauflers- Pancreatic Hormone Secretion Flashcards
retroperitoneal structure; if a cancer is growing there you won’t notice until too far advanced due to no sensation of pain
pancreas
Pt will have severe pain and vomiting every time they try to eat something. Usually presents in young adults who are accused of having an eating disorder
SMA syndrome
what supplies pancreas
splenic a. and SMA
blood from pancreas drains where
into portal vein
where does pancreas come from embryologically
foregut and endoderm
when the buds don’t rotate so they don’t fuse correctly, and the pancreas is wrapped around duodenum and traps it, causing duodenal obstruction
annular pancreas
If mom has uncontrolled diabetes, all her extra blood sugar will cross the placenta and the baby will start cranking out excess insulin in response (extra insulin makes you bigger). This will make the baby really really ______, even before birth
fat
clusters of endocrine cells of pancreas
Islets of Langerhan’s
main location of Islets of langerhans
tail of pancreas
____ cells of pancreas get the most blood flow
beta cells
glucagon is made from what cells
alpha cells
insulin is made from what cells
beta cells
somatostatin is made from what cells
delta cells
pancreatic polypeptide is made from what cell
F cells
_____diabetes is caused by autoimmune destruction of the beta cells inside the islets. The B cells fill up with bad lymphocytes, then suffocate and die
type I
steps of actual insulin synthesis
Preproinsulin
proinsulin
insulin + C-peptide
mature insulin is made up what chains
alpha and beta (connected by disulphide bonds)
synthetic insulin made by drug companies does not contain what
C-peptide
how does glucose from the blood enter pancreatic beta cell
GLUT2 transporter
how insulin gets out of beta cell
glucose comes in
ATP is made
K+ channels close
Ca2+ channels open
release of insulin and C-peptide
drugs that make K+ channels close and cause insulin release
Sulfonylurea drugs
newborn w/ high blood sugar at birth due to K+ channels unable to close in beta cell and no release of insulin
monogenic (neonatal) diabetes
newborn born with low blood sugars due to excessive insulin release (K+ channels stay shut)
congenital hyperinsulinism
drug that doesn’t let K+ channels close and treats congenital hyperinsulinism
Diazoxide
marker of beta cell function
C-peptide
type I or type II diabetes how to distinguish
C-peptide low in type I and high in type II
Insulin high, C-peptide low
patient given exogenous insulin
Exogenous insulin injection will have _____ C-peptide
low
Insulin tumor (insulinoma) will have ____ C-peptide
high
most powerful stimulus for insulin release
blood glucose level
______ causes high BG, which causes insulin release
glucagon
hormone made by the gut when you eat and stimulates insulin release
GLP-1
______ nerve activation stimulates insulin release
vagal
_____-adrenergic stimulation stimulates insulin release
beta2
This medication turns off Dopamine in the brain, which turns off sympathetic nerve stimulation. When the sympathetic nerves are deactivated, they can’t inhibit insulin release, so more insulin is made by the beta cell
(antagonist for D1 and agonist for D2)
Bromocriptine
_____-adrenergic stimulation inhibits insulin release
alpha-adrenergic
Epi and NE bind _____ that inhibits insulin release
alpha adrenergic receptor
____ inhibits insulin release (also turns everything off)
somatostatin
____ hormone inhibits insulin release; why it causes elevated blood sugar levels
growth hormone
anti-inflammatory and immune suppressive drug that inhibits insulin release
glucocorticoids
what two ways to make insulin last longer in the blood
IV drip and subcutaneous injection
for type I diabetics, type of insulin shot that provides a continuous supply of low-dose insulin for 24 hours
basal dose of insulin
_______ dose of insulin, every time they eat, so that they can get a TON of insulin for the food. (lasts a couple of hours); ton of insulin at first in the first few minutes and second phase of release over about an hour or so to pick up the rest of sugar
bolus dose of insulin
the two phases of insulin release after food is messed up in type ___ diabetes
2
these patients have a lowered first phase and exaggerated second phase
(their beta cells are tired)
type 2 diabetics
low blood sugar feel the effects hours later for eating _______; body got rid of sugar by kidneys and others, and then insulin kicked in after and now low blood sugar
cake
Go LOW with ______ if you have type I diabetes, b/c basal rate keeps going on your pump, and your liver turns off!!!!!! (so no glucagon can act on it)
alcohol
Go LOW if you _____ eating, basal rate keeps going, and liver stops making sugar
stop eating
If you are making too much growth hormone because you have a growth-hormone making tumor, then you ______ the insulin receptors, which can lead to high blood sugars
down-regulate
Too much insulin (Type 2 diabetes), Obesity (eating lots of sugar which leads to too much insulin being made), and excessive growth hormone* will _____ the insulin receptors
hide (insulin resistance)
_______and ______ will increase the insulin receptors, which leads to improved “insulin sensitivity”
exercise and not eating
without ____receptors on surface of cell, glucose cannot be brought in from the blood
insulin
______ in the blood binds to the alpha parts, which causes the autophosphorylation of the tyrosine residues on the beta parts on the inside of the cell
insulin
beta parts of insulin receptor have _______ activity
tyrosine kinase
what 2 pathways are activated when tyrosine proteins get phosphorylated (insulin receptor substrates)
PI3K and MAPK
what does PI3K do
tell GLUT4 transporters
In ______, the GLUT 4 transporters never get the signal to turn on (another side effect of insulin resistance). If they don’t get turned on, then they don’t go pull any glucose out of the blood. The result is that the patient has high blood sugar, and no energy for the muscles, so they are too tired to exercise, then eat more chips, which makes insulin resistance worse
type 2 diabetes
GLUT transporter on beta cells
GLUT2
GLUT transporter on skeletal muscle cells and adipose tissue
GLUT4
anabolic hormone that will bulk you up
insulin
_____ store glucose as glycogen for their own fuel when they need it (bulks up muscle)
muscles
______ pathway also is involved in cell growth and transmits a strong anti-apoptotic signal, promoting cell survival
PI3K
acanthosis nigricans
dark velvety patches on the back of the neck, which indicates insulin resistance, or excessive amounts of insulin in the blood. Insulin increases the growth of keratinocytes on the skin and prevents their death
acanthosis nigricans
pathway responsible for the growth-promoting effects of insulin
MAPK pathway
induces storage of energy (glucose)
insulin
tells your liver, muscle, and fat cells to store glucose and don’t let it get turned into energy
insulin
insulin causes _______blood levels of:
Glucose
Free fatty acids
Ketoacids*
Amino acids
decreased
how to treat DKA
give insulin to get rid of ketones
Immediate response, within seconds of binding to the _______receptor:
Tells potassium and glucose to enter the cells, and get out of the blood
insulin
how insulin has activation effects on the liver
promotes glycogen synthesis
promotes triglyceride, fatty acid, protein synthesis
how insulin inhibits the liver
inhibits breakdown of glycogen
inhibits gluconeogenesis
inhibits breakdown of FA’s, AA’s, and ketogenesis
insulin’s activating effects on muscle
increases glucose uptake
promotes glycogen synthesis
protein synthesis
increases K+ uptake
insulin’s inhibiting effects on muscle
decreases protein degredation
inhibits breakdown of glycogen
insulin’s activating effects on fat
increases glucose uptake
promotes TG, FA synthesis
increases K+ uptake
insulin’s inhibiting effect on fat
decreased lipolysis
GLUT transporter in hepatocytes
GLUT 2
cells of nervous system mostly use GLUT _____
GLUT 3
insulin dependent glucose transporter
GLUT 4
responsible for facilitated diffusion of glucose across the cell membrane
GLUT
are responsible for the secondary active transport of glucose in the intestine and renal tubules
SGLT
stop glucose reabsorption in the kidneys; also help reduce blood pressure
SGLT2 inhibitors
GLUT transporter for brain and erythrocytes
GLUT 1
beta cells of pancreas and liver GLUT transporter
GLUT 2
most neurons have _____ GLUT transporters
GLUT 3
GLUT transporter for muscle and fat tissue
GLUT 4
GLUT transporter for sperm
GLUT 5
transporter of glucose in small intestine and renal tubules
SGLT1
transporter of glucose in renal tubules
SGLT2
In normal people, the SGLT2 will stop grabbing sugar if the blood sugar is above _____ mg/dl, and therefore the patient will spill glucose into the urine.
180
-GLIFLOZINS
SGLT2 inhibitors
synthesis of glucagon
proglucagon
glucagon
(in alpha cells)
in the GI tract, alpha cells start making Proglucagon and then processed into _____ instead of glucagon
GLP-1
_____ produced in response to a high concentration of glucose in the gut, such as after you eat a bunch of sugar
GLP-1
____goes over to the beta cells in the pancreas and increases insulin release
GLP-1
incretin – a group of gut hormones that augment insulin release after a high-sugar meal*
Feel fuller longer and eat less food
GLP-1
low blood sugar
high AA’s levels
beta2 adrenergic stimulation
vagal stimulation
stress (cortisol)
epi
(cause what)
causes release of glucagon
high blood sugar
somatostatin
insulin
alpha-adrenergic stimulators
(cause what)
causes inhibition of glucagon
what doesn’t respond to glucagon after drinking (in type I diabetes, pump is still going and liver is not on, seizure due to insulin being given with no sugar —–low blood sugar seizure )
the liver
what to do if type 1 friend is hypoglycemic after a night of drinking
give her honey or sugar on the inside of cheek
_____ has tyrosine kinase receptors
insulin
_____ has GPCR
glucagon
promotes glucose synthesis and inhibits its breakdown
glucagon
____ and ____ breakdown triglycerides and glycogen in muscle
glucagon and epinephrine
causes high blood sugar but also stimulates secretion of the things needed to bring blood sugar down so they can be on call when ready to act
glucagon
what happens in starvation
first 3 days glucagon tells liver to break down glycogen stores and make glucose
then, ketones and FA’s become main source of energy
after all fat is burned off, body breaks down muscle, using proteins for energy
causes an increase in glucagon, which increases glucose production, to keep the blood glucose level stable
exercise
ratio is ___ b/t insulin and glucagon if you eat a balanced diet
2
best diet to eat to maintain a good blood glucose level
high protein and low carbs (protein will not have as much glucose being stored so won’t gain weight as quick)
turns off everything
somatostatin
glucose, AA’s, FA’s, gastric hormones, and glucagon stimulate what release from delta cells
somatostatin
what blocks somatostatin release
insulin
Parathyroid tumors (high calcium)
Pituitary tumors (could be excess GH or prolactin)
Pancreatic tumors
multiple endocrine neoplasia type 1 (MEN1)
made by F cells and slows absorption of food; regulates hunger and absorption of food
pancreatic polypeptide
___ release is stimulated by these things
pancreatic polypeptide
what inhibits pancreatic polypeptide release
somatostatin
made by beta cells and augments insulin; helps insulin control blood sugar, turns off glucagon, and slows gastric emptying
Amylin
slowing _____ causes less sugar to get absorbed too quickly and weight gain; prevents hypoglycemia
Amylin
these 2 levels are low in type 1 diabetes
Amylin and C-peptide
