the pancreas Flashcards

(59 cards)

1
Q

2 main functions of the pancreas

A
  • exocrine

- endocrine

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2
Q

exocrine pancreas

A
  • CCK is released from duodenum and stimulates acinar cells
  • acinar cells secrete proenzymes for digestion
  • after secretion carried to duodenum to be activated
  • neutralizes acids
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3
Q

endocrine pancreas

A
  • islet of langerhans

- secrete insulin, glucagon, somatostatin, pancreatic polypeptide

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4
Q

what cells secrete insulin

A

beta cells

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5
Q

what cells secrete glucagon

A

alpha cells

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6
Q

what cells secrete somatostatin

A

gamma cells

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7
Q

causes of hyperglycemia in diabetes

A
  • defects in insulin secretion
  • defects insulin action
  • usually both
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8
Q

normal glucose homeostasis

A
  • glucose produced in liver
  • glucose uptake and utilized mainly in skel muscle
  • insulin and glucagon regulate glucose
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9
Q

what determines fasting plasma glucose levels

A

hepatic glucose output

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10
Q

GLUT2

A
  • located on beta cells and liver

- allows for glucose to be taken into beta cells -> insulin released

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11
Q

GLUT4

A
  • located on skel muscle and fat cells
  • found in cytoplasm
  • cascade of events causes translocation to p membrane
  • uptake of glucose
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12
Q

where are GLUT3 receptors found

A
  • all tissues

- CNS

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13
Q

how do you measure glycemic control

A
  • HbA1c
  • is the average glucose over last 2-3 months
  • shows amount of glucose that sticks to RBC which is proportional to amount of glucose in blood
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14
Q

metabolic action of insulin on adipose tissue

A
  • increased glucose uptake
  • increased lipogenesis
  • decreased lipolysis
  • decreased FFA
  • stim FA and TG synthesis in fat and liver
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15
Q

metabolic action of insulin on liver

A
  • decreased gluconeogenesis
  • increased glycogen
  • increased lipogenesis
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16
Q

metabolic action of insulin skeletal muscle

A
  • increased glucose uptake
  • increased glycogen synthesis
  • increased protein synthesis
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17
Q

where is glucose obtained from

A
  • intestinal absorption of food
  • glycogenolysis
  • gluconeogenesis
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18
Q

metabolic action of insulin on protein metabolism

A
  • increased transport of AA into muscle, adipose, liver

- increased rate of protein synthesis in muscle, adipose, liver

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19
Q

factors that stimulate insulin release

A
  • glucose

- vagal stimulation

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20
Q

factors that amplify glucose-induced insulin release

A

beta-adrenergic stimulation

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21
Q

factors that inhibit insulin release

A

alpha-adrenergic effect

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22
Q

type 1 diabetes

A
  • autoimmune
  • destruction of beta cells
  • absolute deficiency in insulin
  • can also be idiopathic
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23
Q

type 2 diabetes

A
  • combo of peripheral resistance to insulin and inadequate secretory response
  • relative insulin deficiency
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24
Q

initial response to exercise in nondiabetics

A
  • use glucose in muscle
  • convert glycogen to glucose
  • glucose cant be transferred out of muscle to prevent hypoglycemia
  • takes up glucose from blood
  • E and NE released, cause lipolysis
25
long term response to exercise in nondiabetics
- dev of new capillaries in muscles - increased translocation of GLUT4 receptors - causes increased insulin sensitivity
26
exercise in type 1 diabetes
- exs modestly lowered blood glucose concentrations and raise blood ketone concentrations in well controlled pts - in poorly controlled pts have less of a fall of glucose and increased ketogenesis
27
exercise in type 2 diabetes
- acute exercise- increase in glucose uptake | - exs training causes increased GLUT4 protein expression
28
immunologic response in type 1 DM
- autoantibodies - T cell response to islet cells - antigen binds to MHC class II molecules on APCs - binding allows antigen to be presented to autoreactive CD4
29
imbalances in type 1 diabetes
- t reg cells have impaired function -> failing to suppress autoreactive t cells - t cells resistant to immune regulation
30
diabetic ketoacidosis
- ketone dev is normal after depletion of liver glycogen - in glucose poor environment too much oxaloacetete diverted away from gluconeogensis - prevents ACoA to enter krebs -> ketogenesis
31
effect of hyperglycemia in type 2 DM
- impair pancreatic beta cell function - magnify insulin resistance - worsens metabolic state
32
metabolic syndrome
- co-occurance of metabolic risk factors for type 2 diabetes and CVD
33
metabolic defects in type 2 DM
- insulin resistance - inadequate insulin secretion by beta cells mediated by GLUT2 - genetic alterations in GLUT2 expression - processing of proinsulin to insulin is impaired
34
disorders affected by insulin resistance
- type 2 DM - obesity - stress - infection - pregnancy - glucocorticoid excess - metabolic syndrome - HTN - hyperlipidemia - CAD
35
consequences of insulin resistance
- failure to inhibit gluconeogenesis - high fasting blood glucose - failure of glucose uptake and glycogen synthesis -> high postprandial blood glucose - failure to inhibit lipoprotein lipase -> excess FFA
36
what 3 things is obesity associated with
- increased inflammation - increased FFA - deficiency in adipokines
37
how does increased FFA affect insulin resistance
- excess FFA saturate oxidative and storage capabilities of hepatocytes - FFA intermediates accumulate and impair insulin signaling - induce expression of inflammatory genes
38
symptoms of type 1 DM
- polydipsia - polyuria - weight loss with hyperglycemia and ketonemia
39
symptoms of type 2 DM
- mostly asymptomatic and hyperglycemic - polyuria - polydipsia - nocturia - blurred vision
40
diabetic macrovascular disease
- stroke - MI - lower extremity ischemia
41
diabetic microvascular disease
- retinopathy - nephropathy - neuropathy
42
advanced glycosylation end products (AGEs)
- form due to chronic hyperglycemia - glucose form irreversible crosslinks with macromolecules like collagen - results in vascular stiffening and myocardial dysfunction
43
acute pancreatitis
- due to gallstones or alcohol abuse - abdominal pain - elevated pancreatic enzymes
44
mechanism of gallstone pancreatitis
- reflux of bile into pancreatic duct - obstruction of ampulla during gallstone passage - obstruction of ampulla secondary to stone or edma
45
alcohol induced pancreatitis
- sensitization of acinar cells to CCK -> premature activation of zymogens - generate toxic metabolites - activate stellate cells by acetaldehyde and ROS -> fibrosis
46
pathogenesis of acute pancreatitis
- intraacinar activation of proteolytic enzymes - microcirculatory injury - leukocyte chemoattraction, release of cytokines, oxidative stress
47
why is intraacinar activation of proteolytic enzymes problematic
- blockade of secretion of pancreatic enzymes - synthesis continues - causes autodigestion - cycle of active enzymes damaging cells while they release more enzymes
48
systemic inflammatory response syndrome (SIRS)
- happens due to severe acute pancreatitis - activated by pancreatic enzymes - cytokines released into circulation from inflamed pancreas
49
clinical response to SIRS
- ARDS - myocardial depression and shock - acute renal failure - metabolic complications - bacterial translocation
50
chronic pancreatitis
- progressive fibroinflammatory process | - irreversible destruction
51
causes of chronic pancreatitis
- mainly long term alcohol abuse - cigarette smoking - hereditary - ductal obstruction - systemic disease - idiopathic
52
chronic pancreatitis pathogenesis
- hypersecretion of digestive enzymes not compensated by increase in ductal bicarb - inflammation - collagen secretion - fibrosis - loss of acinar cells
53
primary clinical features of chronic pancreatitis
- abdominal pain that radiates to back | - pancreatic insufficiency
54
pancreatic insufficiency
- when 90% of pancreatic fn is lost - fat malabsorption -> steatorrhea - pancreatic diabetes due to hyperglycemia - alpha cells can be affected -> hypoglycemia
55
pain in pancreatitis
- nerve GF (NGF) produced in chronic pancreatitis - mast cells sensitize nociceptor neuron by up regulating substance P - cytokines and inflammatory mediators
56
what is the most common type of pancreatic cancer?
- pancreatic intrapeithelial neoplasias (PanIN) in small ducts
57
pathogenesis of pancreatic cancer
- multifactorial - combo of genetic mutations - strongest environmental factor is cigarette smoking
58
interactions of pancreatic cancer and adipose tissue
- causes adipose tissue inflammation - systemic cytokine response - abnormal adipokine secretin - lipolysis - peripheral insulin resistance and beta cell dysfunction
59
most common sx of pancreatic cancer
- usually silent until invade into adjacent structures - pain- usually first sx - jaundice - weight loss - head of pancreas causes obstructive jaundice