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Patho 2 > the pancreas > Flashcards

the pancreas Flashcards

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
Q

long term response to exercise in nondiabetics

A
  • dev of new capillaries in muscles
  • increased translocation of GLUT4 receptors
  • causes increased insulin sensitivity
26
Q

exercise in type 1 diabetes

A
  • 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
Q

exercise in type 2 diabetes

A
  • acute exercise- increase in glucose uptake

- exs training causes increased GLUT4 protein expression

28
Q

immunologic response in type 1 DM

A
  • 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
Q

imbalances in type 1 diabetes

A
  • t reg cells have impaired function -> failing to suppress autoreactive t cells
  • t cells resistant to immune regulation
30
Q

diabetic ketoacidosis

A
  • 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
Q

effect of hyperglycemia in type 2 DM

A
  • impair pancreatic beta cell function
  • magnify insulin resistance
  • worsens metabolic state
32
Q

metabolic syndrome

A
  • co-occurance of metabolic risk factors for type 2 diabetes and CVD
33
Q

metabolic defects in type 2 DM

A
  • insulin resistance
  • inadequate insulin secretion by beta cells mediated by GLUT2
  • genetic alterations in GLUT2 expression
  • processing of proinsulin to insulin is impaired
34
Q

disorders affected by insulin resistance

A
  • type 2 DM
  • obesity
  • stress
  • infection
  • pregnancy
  • glucocorticoid excess
  • metabolic syndrome
  • HTN
  • hyperlipidemia
  • CAD
35
Q

consequences of insulin resistance

A
  • 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
Q

what 3 things is obesity associated with

A
  • increased inflammation
  • increased FFA
  • deficiency in adipokines
37
Q

how does increased FFA affect insulin resistance

A
  • excess FFA saturate oxidative and storage capabilities of hepatocytes
  • FFA intermediates accumulate and impair insulin signaling
  • induce expression of inflammatory genes
38
Q

symptoms of type 1 DM

A
  • polydipsia
  • polyuria
  • weight loss with hyperglycemia and ketonemia
39
Q

symptoms of type 2 DM

A
  • mostly asymptomatic and hyperglycemic
  • polyuria
  • polydipsia
  • nocturia
  • blurred vision
40
Q

diabetic macrovascular disease

A
  • stroke
  • MI
  • lower extremity ischemia
41
Q

diabetic microvascular disease

A
  • retinopathy
  • nephropathy
  • neuropathy
42
Q

advanced glycosylation end products (AGEs)

A
  • form due to chronic hyperglycemia
  • glucose form irreversible crosslinks with macromolecules like collagen
  • results in vascular stiffening and myocardial dysfunction
43
Q

acute pancreatitis

A
  • due to gallstones or alcohol abuse
  • abdominal pain
  • elevated pancreatic enzymes
44
Q

mechanism of gallstone pancreatitis

A
  • reflux of bile into pancreatic duct
  • obstruction of ampulla during gallstone passage
  • obstruction of ampulla secondary to stone or edma
45
Q

alcohol induced pancreatitis

A
  • sensitization of acinar cells to CCK -> premature activation of zymogens
  • generate toxic metabolites
  • activate stellate cells by acetaldehyde and ROS -> fibrosis
46
Q

pathogenesis of acute pancreatitis

A
  • intraacinar activation of proteolytic enzymes
  • microcirculatory injury
  • leukocyte chemoattraction, release of cytokines, oxidative stress
47
Q

why is intraacinar activation of proteolytic enzymes problematic

A
  • blockade of secretion of pancreatic enzymes
  • synthesis continues
  • causes autodigestion
  • cycle of active enzymes damaging cells while they release more enzymes
48
Q

systemic inflammatory response syndrome (SIRS)

A
  • happens due to severe acute pancreatitis
  • activated by pancreatic enzymes
  • cytokines released into circulation from inflamed pancreas
49
Q

clinical response to SIRS

A
  • ARDS
  • myocardial depression and shock
  • acute renal failure
  • metabolic complications
  • bacterial translocation
50
Q

chronic pancreatitis

A
  • progressive fibroinflammatory process

- irreversible destruction

51
Q

causes of chronic pancreatitis

A
  • mainly long term alcohol abuse
  • cigarette smoking
  • hereditary
  • ductal obstruction
  • systemic disease
  • idiopathic
52
Q

chronic pancreatitis pathogenesis

A
  • hypersecretion of digestive enzymes not compensated by increase in ductal bicarb
  • inflammation
  • collagen secretion
  • fibrosis
  • loss of acinar cells
53
Q

primary clinical features of chronic pancreatitis

A
  • abdominal pain that radiates to back

- pancreatic insufficiency

54
Q

pancreatic insufficiency

A
  • when 90% of pancreatic fn is lost
  • fat malabsorption -> steatorrhea
  • pancreatic diabetes due to hyperglycemia
  • alpha cells can be affected -> hypoglycemia
55
Q

pain in pancreatitis

A
  • nerve GF (NGF) produced in chronic pancreatitis
  • mast cells sensitize nociceptor neuron by up regulating substance P
  • cytokines and inflammatory mediators
56
Q

what is the most common type of pancreatic cancer?

A
  • pancreatic intrapeithelial neoplasias (PanIN) in small ducts
57
Q

pathogenesis of pancreatic cancer

A
  • multifactorial
  • combo of genetic mutations
  • strongest environmental factor is cigarette smoking
58
Q

interactions of pancreatic cancer and adipose tissue

A
  • causes adipose tissue inflammation
  • systemic cytokine response
  • abnormal adipokine secretin
  • lipolysis
  • peripheral insulin resistance and beta cell dysfunction
59
Q

most common sx of pancreatic cancer

A
  • usually silent until invade into adjacent structures
  • pain- usually first sx
  • jaundice
  • weight loss
  • head of pancreas causes obstructive jaundice

Patho 2 (15 decks)

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