Endocrine Pancreas Flashcards
exocrine cells of pancreas secrete?
-secreted into?
digestive enzymes
bicarb
***into duodenum
what digestive enxymes does pancreas secrete
trypsin
chymotrypsin
lipase
amylase
endocrine cells secrete?
insulin
glucagon
role of insulin
drive glucose into cell
role of glucagon
causes release of glucose into the blood for the tissues that need it
name the hormones that raise blood [glucose[
glucagon
cortisol
GH
norepi/epi
what cells secrete insulin
beta cells of pancreas
what organ produces glucagon
what organ stores it
liver produces as GLYCOGEN
pancreas stores
high blood gluc levels stimulates insulin to promote_____ (2)
glycolysis—b/d of glucose–ATP
AND
glyocogenesis–production of glycogen (glucose storage)
when glucose levels are low… glucagon decreases____(1) and increases _____ (2)
- decreases glycolysis (glucose b/d)
- increases gluconeogenesis (glucose formation)
- increases glycogenolysis–b/d of glycogen to release glucose
define the following:
- Glycolysis
- Gluconeogenesis
- Glycogenolysis
- glycogenesis
- b/d glucose
- making of glucose– in the LIVER
- b/d of glycogen to release glucose
- synthesis of glycogen–aka storing glucose
where does gluconeogenesis occur
the liver
what is the storage form of glucose
glycogen–liver
what is the real goal of glucagon
mobilize glucose stores from the liver so that it can be sent to the brain and heart– for energy
its goal is not directed to breaking down glucose for energy
after insulin takes up glucose into the celll– it is stored as?
glycogen
fat
protein
what cells produce glucagon
alpha cells
what cells produce insulin
beta cells
what cells produce somatostatin
delta cells
where are the endocrine cells of the pancreas located?
islets of Langerham
which cell (A B or D) composes most of the mass?
beta
arterial blood supply to pancreas
splenic artery
which organ is exposed to most of the endocrine hormones?
why
LIVER
because of the venous drainage of pancreas drains into hepatic portal vein
do pancreatic hormones go through first pass metabolism?
yes
what does vagal nerve stimulation do to pancreas>
stimulates insulin release
things that simulate insulin release: 2
- high blood glucose levels
- vagal nerve stimulation
vagal nerve stimulation activates secretion of?
insulin
glucagon
somatostatin
pancreatic polypeptide
which cells in the islets is generally spared from auto immune destruction
pancreatic poylpeptide cells
hyperglucagonemia?
hypersecretion of glucagon–>excess glucagon in blood
alpha cell dysfunction is reflected by?
hyperglucagonemia
sympathetic nerve stimualtion inhibits___ and activates secretions of?
inhibits insulin and somatostatin secretion
activates glucagon and pancreatic polypeptide secretion
insulin is what kind of homrone
polypeptide
active form of insulin is produced by modification of?
proinsulin
principle stimulus for insulin release?
glucose
how does glucose enter the Beta cells?
via GLUT 2
what happens to glucose after entering beta cells?
undergoes glycolysis–ATP production
glucose levels higher than _______ mg/dl will stimulate insulin synthesis
70
what neurotransmitter will amplify the glucose induce release of insulin
acteylcholine
*binds to cell membrane of beta cells and stimulates the insulin release
release of insulin is ___ and ___ in nature
rhythmic and pulsatile
pulsatile release of insulin is imp for?
reaching maximal physiologic effects
ex of the physiologic effects that the pulsatile release of insulin do?
-supresses liver gluocse production
physiologic effects of insulin:
- immediate
- early (witin mins)
- moderate (hours)
- delayed (within days)
immediate: glucose and K+ transport into cells
early: regulation of metabolic enzyme activity
moderate: modulation of enzyme sythnesis
delayed: effects on growth and cell diffferentiation
insulins actions on target tissue promote sythnesis of?
carbohydrates
fat
protein
insulin and effect on carb metabolism
- stimulates
- inhibits
stimulates:
- glucose transport into adipose and muscle tissue
- glycolysis
- glycogen storage
inhibits:
- glycogen b/d
- glycogenolysis and gluconeogenesis in liver
insulin affets on lipid metabolism
- stims
- inhibs
stims
- synthesis of FAs
- uptake of trigs from blood–>tissue
- cholesterol synthesis liver
inhibs:
- lipolysis in tissue–lowering plasma FA level
- ketogenesis
insulin affects on protein metabolism
- stims
- inhibs
stims
- AA transp into tissue
- protein synthesis
inhibs
- protein b/d
- urea formation
specific effects of insulin on____ _____ is the dominant action of insulin
skeletal muscle glucose
what is one of the main target organs of insulin
skeletal muscles
insulin levels are High/Low during early DM2?
HIGH
hence the insulin resistance
high levels of insulin are called?
hyperinsulinemia
hyperinsulinemia has been linked to?
certain types of CA:
- endometrium
- breast
- colon
- kidney
list conditions that cause elevated insulin
high waist circumference excess visceral fat high waist-to-hip ratio -high BMI -sedetary lifestle -high energy intake
cells do what when exposed to hyperinsulinemia?
excessive proliferation
hyperinsulinemia and insulin resistance closely linked with what pathologic conditions
HTN
atherosclerosis
CVD
dyslipidemia
glucagon is what kind of hormone
polypeptide
antagonist homrone to insulin?
glucagon
two main products of proglucagon?
glucagon–alpha cells pancreas
glucagon-like-peptide 1 (GLP-1) in the intestinal cells
GLP-1 is produced in resonse to?
high [ ] of glucose in intestinal lumen
another name for GLP-1
incretin
what is an endocrine mediator that amplifies insulin release from beta cells in response to a glucose load?
GLP-1 or incretin
what inhibits and stimulates glucagon release
hyperglycemia–inhibits
hypoglycemia–stims
a meal high in carbs will stimulate and inhibit release of?
stim–insulin thru beta cells via release of GLP-1
inhib–glucaogn
epinephrine stims/inhibis glucagon release
stimulates
epinpehrine stims/inhibis insulin rel
inhibits
somatostain inhibs/stims glucagon release?
inhibits
vagal stimulation increase/decreasses glucagon rel?
increases
principle target tisssue for glucagon?
liver
how does glucagon increase plasma glucose concentrations
stimulates de novo hepatic glucose production through gluconeogenesis and glycogen b/d—–bc these actions counter act insulin
glucagon receptor is found where in body
liver********* pancreatic beta cells kidney adipos tissue heart vascular tissues brain stomach adrenal glands
what does pro-insulin make after proteolytic processing
c-peptide
mature insulin
how and where are C-peptide and mature insulin sotred
together
in beta cell
how are c-pep and mature insulin secreted
co-secreted from secretory granules in beta cells
which is cleared slower–c pep or mature insulin
c-peptide cleared slower in the body
which is a more useful marker of insulin secretion—c peptide or insuin
c-peptide bc it is cleard slower vs inisulin
elevated levels of ____ can be used to indicate early beta dyfsunction
pro-insulin
high levels of pro inslin help indicate early?
beta cell destruction
c peptides travel to?
portal circulation
which hormone is the best to differentiate b/w DM 1 and 2
c-peptides
whcih hormone is a better accurate reading of islet cell functions?
c peptides
DM1:
c-peptides high or low?
insulin high or low?
c-peptides: low
insulin: low
DM2:
c-peptides high or low?
insulin high or low?
normal or high level c-peptide
insulinoma?
insulin secreting tumor on pancreas
insulinoma can be assoc with?
MEN 1
PTs with insulinoma have what kind of blood gluc levels
low low low
*AMS
glucagonomas
rare
can produce s/s of DM
can produce catabolic effects on fat and muscle
type 1 DM
beta cell DESTRUCTION
5% of cases
younger people–also called juvenille DM
higher risk to develop DKA w/o insulin tx
type 2 DM
insulin resistance–part of syndrome X
loss of normal regulation of insulin secretion
accounts for more than 90% of cases
*obesity in adults
*mild hyperglycemia–rarely leads to ketoacidosis
which DM is part of syndrome x
DM 2
basic patho for DM overall
impaired entry of glucose into cells–>glucose accumulates in blood–>increase in plasma osmolarity—->urinary loss of glucose–>excess loss of water and sodium–>POLYURIA
resulting dehydration triggers compensatory thirst–>POLYDIPSIA
inability of the cells to utilize glucose resembles a state of starvation–>stimulates hunger–>POLYPHAGIA
patho for DM2
results from decr responsiveness of peripheral tissues to insulin action
also
inadequate responsvienss to B cells to glucose
so—>leads to decrease release of insulin in response to glucose
*also affects the pulsatile release of insulin–becomes sluggish, smaller bursts and erratic
do patients with type 2 DM secrete normal amounts of insulin during fasting?
YES
do patient with type 2 DM secrete normal amount of insulin in response to glucose load?
no—- they secrete less insulin (70% less)
**beta cells over time become less responsive to glucose–leads to less insulin secretion
earliest physiologic indication of B cell destruction is?
delay in acute insulin response to glucose
three main pathologic defects in DM
- excessive hepatic glucose production–seen with high fasting glucose
- defective beta cell secretory function
- peripheral insulin resistance
what is pancreas’ compensatory mechanism to insulin resistance
to release more insulin–only temporary tho
as insulin resistance increases…. ___ ___ develops
glucose tolerance
what three patholigc processes characterize DM 2
impaired insulin secretion
insulin resistance
excessive hepatic glucose production
complications of DM
- acute
- chronic
acute:
- hypoglycemia
- DKA
- hyperglycemic-hyperosmolar nonketoic coma
chronic:
- peripheral nerve damage
- skin damage
- lens damange
end state renal disease, blidness and neuropathy are MC in DM 1 or 2?
DM 1
MI and stroke are MC in DM 1 or 2? why?
DM 2
* macrovascular disease
main s/s of hypoglycemia
tachycardia
palps
sweating
tremors
gets lowr: irritability confusion blurry vision triedness HA diff speaking
super low:
LOC
seizures
main characteristics of DKA?
*patho behind DKA
characterisitcs: hyperglycemia, metabolic acidosis and incr ketone bodies
PATHO:
- gluconeogenesis continues in liver (w/o opposition of insulin
- incr [glucose]= incr osmolarity
- lack of insulin + high levels of counterregulatory hormones (gucagon, cortison, epi) cause LIPASE hormone to b/d fat for fuel and release ketones
main characerisitcs of hyperglycemic hyperosmolar coma
severe hyperglycemia
hyperosmolarity
dehydration
*ABSENCE of ketosis
underlying medication conditions (2) associ with HHC
CHF
renal insuff`
patho for DM 1
- islet cell autoantibody destruction (islets are sensitive to inflammation)
- activated lymphocytes in islets–peripancreatic lymph nodes and systemic circulation
- t lymphocytes that proliferate when stimulated with islet proteins
- release cytokines inside islets
what mediates beta cell death in DM1? and not so much?
T lymphocytes*****
not so much mediated by islet autoantibodies
explain insulin resistance *what does pancreas do as compensatory mech:?
cells in muscle, fat and liver do not respond well to insulin—- so they cannot use glucose from blood as energy
*to compensate— pancreas makes MORE INSULIN—–
a high insulin level without a correspondingly high c-peptide suggests?
exogenous insulin administration
normal or elevated levels of insulin despite hypoglycemia can indicate what pathogenic cause?
insulinoma–insulin producing tumor on pancreas
what are the corresponding levels of c-epptide with an insulinoma
elevated too because the extra insulin is endoengous
