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Pathophysiology > pancreas disorders > Flashcards

pancreas disorders Flashcards

1
Q

digestive functions of the pancreas

A

produce digestive enzymes

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2
Q

hormonal functions of the pancreas

A

islets of langerhans produce insulin that controls blood sugar levels

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3
Q

what is the endocrine pancreas made of

A

islets of langerhans

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4
Q

what is the exoocrine pancreas made of

A

acini cells

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5
Q

what do acini cells do

A

secrete pancreatic juice in the duodenum through pancreatic ducts

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6
Q

what is pancreatic juice important for

A

digestion absorption; pancreatic insufficiency and fatty stools

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7
Q

what does dysfunction of the pancreas cause

A

DM

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8
Q

what is islets of langerhan cells produce

A

insulin

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9
Q

4 parts of pancreas?

A

head, neck, body, tail

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10
Q

where is the ucinate process/curvature of the duodenum located?

A

head of pancreas

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11
Q

what is the exocrine pancreas drained by?

A

duct of wirsung

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12
Q

tell me about the duct of wirsung

A

main pancreatic duct that runs the length of the gland and is 3-4mm in diameter

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13
Q

where does the main pancreatic duct enter the duodenum

A

duodenal papilla

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14
Q

where does the main pancreatic duct end?

A

ampulla of vater

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15
Q

what does the sphincter of oddi surround

A

common bile duct and main pancreatic duct

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16
Q

what 2 ducts join together to form a common channel before ending at the ampulla of vater

A

main pancreatic duct and common bile duct

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17
Q

what is the duct of santorini?

A

separate accessory pancreatic duct pany ppl have

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18
Q

what are acinar cells

A

pyramidal epithelial cells arranged in rows; their apexes join to form the lumen of the acinus

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19
Q

where are zymogen granules found? what are they?

A

acinar cells; inactive enzymes

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20
Q

how are zymogens released

A

exocytosis from apexes of the acinar cells into the lumen

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21
Q

when are there more zymogen granules in the acinar cells? less?

A

more: fasting
less: after a meal

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22
Q

what enzymes are secreted by the acinar cells in their active form?

A

lipase, amylase, deoxyribonuclease, ribinuclease

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23
Q

what enzymes are secreted by the acinar cells as zymogens?

A

trypsinogen, chymotrypsin, prolastase, procarboxypeptidase, phospholipase 2A

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24
Q

where are zymogens activated?

A

lumen of proximal intestine

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25
Q

what does activation of zymogens in acinar cells lead to

A

acute pancreatitis and pancreatic autodigestion

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26
Q

what happens when pancreatic juice enters the duodenum

A

trypsinogen is converted to trypsin

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27
Q

what facilitates the conversion of trypsinogen to trypsin? where is this found?

A

enteropeptidase/ enterokinase; on intestinal brush border

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28
Q

why is trypsin important?

A

converts remaining zymogens to active enzymes (like a cascade)

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29
Q

if trypsinogen is activated in the pancreas, what are the two protective mechanisms?

A

pancreatic secretory trypsin inhibitor (PSTI) and trypsin autolysis

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30
Q

acute pancreatitis is a clinical syndrome resulting from what?

A

acute inflammation and autodigestion of pancreas and peripancreatic tissues

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31
Q

what are the clinical manifestations of acute pancreatitis?

A

acute upper abdominal pain, nausea, vomiting, fever

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32
Q

what are the 2 most common causes of acute pancreatitis?

A

biliary tract disease and alcohol trauma

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33
Q

what is common in all cases of acute pancreatitis?

A

activated proteolytic enzymes escape from ducts which cause local tissue injury, inflammation, necrosis, and infection in some cases

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34
Q

when does alcohol induced pancreatitis occur?

A

after a heavy episode of drinking

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35
Q

what is the mechanism of alcohol induced pancreatitis?

A

unclear how alcohol damages the gland

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36
Q

what is the metabolite of alcohol

A

acetaldehyde

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37
Q

what disease may have a direct toxic effect on the pancreatic acinar cells

A

alcohol induced pancreatitis

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38
Q

what may alcohol induced pancreatitis lead do?

A

intracellular trypsin activation and inflammation of the sphincter of oddi

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39
Q

what disease is associated with deficiences in zinc or selenium

A

alcohol induced pancreatitis and chronic pancreatitis

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40
Q

what occurs in biliary tract disease

A

gallstones or biliary sludges become lodged at ampulla of vater

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41
Q

what do gallstones or biliary sludges becomming lodged at ampulla of vater cause

A

obstruction of common bile duct and main pancreatic duct

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42
Q

is biliary tract disease more common in men or women? what about gallstones?

A

both women

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43
Q

key pathologic finding in acute pancreatitis?

A

fat necrosis

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44
Q

what is chronic pancreatitis?

A

relapsing disorder with severe abdominal pain, exocrine or endocrine pancreatic insufficiency, duct abnormalities, pancreatic calcifications

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45
Q

what is the major cause of chronic pancreatitis?

A

chronic alcoholism

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46
Q

what do deficiencies in zinc and selenium inhibit in chronic pancreatitis

A

quenching of O2 free radicals

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47
Q

what can long term obstruction of the pancreatic duct cause

A

chronic pancreatitis

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48
Q

what is the key panthological finding in chronic and acute pancreatitis

A

peripancreatic and intrapancreatic fat necrosis

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49
Q

what is chronic pancreatitis characterized by?

A

scarring and shrinkage of the pancreas

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50
Q

what does scarring and shrinkage of the pancreas result from

A

fibrosis, atrophy of acini, and stenosis/dilation of ductules

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51
Q

what part of the pancreas is involved in chronic pancreatitis?

A

usually the whole gland, but it’s localized to the head and body in 1/3 of cases

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52
Q

what are ductules and ducts often filled with in chronic pancreatitis?

A

calculi (ductal stones)

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53
Q

why is the pancreas hard in chronic pancreatitis?

A

sclerosis and calcification

54
Q

why might someone need a biopsy of the pancreas

A

differentiate chronic pancreatitis from pancreatic carcinoma

55
Q

what does chronic pancreatitis look like microscopically?

A

loss of acini, dilation of ductules, fibrosis, lymphocytes

56
Q

what is preserved in chronic pancreatitis?

A

islets of langerhans

57
Q

what are the clinical manifestations of chronic pancreatitis?

A

maldigestion and impaired fat digestion

58
Q

what enzyme is essential for fat digestion

A

pancreatic lipase

59
Q

what can absence of pancreatic lipase lead to?

A

steatorrhea which is a greasy, bulky, lightly colored stool

60
Q

why do ppl with pancreatic insufficiency rarely present with carb and protein maldigestion?

A

other enzymes in gastric and intestinal juice compensate for loss of amylase and trypsin

61
Q

what is pancreatic insufficiency?

A

syndrome of maldigestion which results from disorders interfering with effective pancreatic enzyme activity

62
Q

where are islets of langerhan located?

A

embedded in pancreatic exocrine tissues

63
Q

are islets of langerhan cells vascularized

A

yes

64
Q

what are the 4 major islet cell types

A

beta, alpha, delta, and PP

65
Q

what is the predominant cell in the islet

A

beta

66
Q

what do beta islet cells secrete?

A

insulin

67
Q

what are alpha islet cells?

A

glucagon secreting cells

68
Q

what are delta islet cells?

A

somatostatin secreting cells

69
Q

what are PP islet cells?

A

pancreatic polyeptide secreting cells

70
Q

where are PP cells located?

A

posterior lobe of the head of the pancreas

71
Q

more the 70% of the insulin secreting cells must be lost/damaged before dysfunction occurs in what?

A

endocrine pancreas

72
Q

what supplies each islet with nutrients

A

one major arteriole

73
Q

where does blood from the islets drain into?

A

hepatic portal vein

74
Q

what is the major site of action of glucagon and insulin

A

liver

75
Q

what are islets innervated directly by?

A

parasympathetic and sympathetic NS

76
Q

what are islets innervated indirectly by?

A

stimulation of catecholamine release by the adrenal medulla

77
Q

what plays a key role in glucose homeostasis during stress

A

catecholamine release by the adrenal medulla

78
Q

circulator half life of insulin?

A

3-5 min

79
Q

where is insulin catabolized

A

liver and kidney

80
Q

what is the most potent stimulator of insulin

A

glucose

81
Q

what is glucose enhanced by?

A

several enteric proteins such as glucagon like peptide 1 (GLP-1)

82
Q

what is glucose inhibited by?

A

catecholamines and somatostatins

83
Q

what is the mechanism of insulin?

A

it exerts its effects by binding to insulin receptors on the surface of target cells

84
Q

what are the target cells of insulin

A

liver, muscle, fat and ovaries

85
Q

what is the role of insulin in metabolism

A

fuel homeostasis, promote fuel storage, promote formation of precursors for fatty acid synthesis, stimulate lipogenesis, inhibit hepatic glucose output

86
Q

what is anabolism

A

fuel storage

87
Q

catabolism?

A

breakdown and release of fuel

88
Q

how does insulin promote fuel storage in liver?

A

stimulating glycogen synthesis and storage

89
Q

how does insulin promote formation of precursors for fatty acid synthesis?

A

stimulating glycolysis

90
Q

how does insulin stimulate lipogenesis?

A

VLDL synthesis is increased

91
Q

how does insulin inhibit hepatic glucose output?

A

inhiting gluconeogenesis and glycogenolysis

92
Q

what inhibits fatty acid oxidation and production of ketone bodies

A

insulin

93
Q

where are ketones made

A

liver

94
Q

where and when are ketones used as fuel

A

in the brain when glucose isnt available

95
Q

what s DM

A

heterogeneous disorder defined by presence of hyperglycemia

96
Q

what can hyperglycemia be due to

A

dec in insulin secretion by pancreatic cells, dec response to insulin by target tissues, or increase in counterregulatory hormones that oppose effects of insulin

97
Q

what was formerly known asIDDM and juvelile diabetes

A

DM type 1

98
Q

what is DM type 1 characterized by

A

autoimmune destruction of pancreatic islet cells that results in severe insulin deficiency

99
Q

why does DM type 1 mainly affect

A

ppl younger than 30

100
Q

where is there a bimodal incidence peak in DM type 1

A

5-7 y/o and puberty

101
Q

who is DM type 1 more common in

A

males

102
Q

what do patients with DM type 1 present with

A

polyuria, polydipsia, and weight loss with high serum glucose levels

103
Q

what is diabetic ketoacidosis

A

when ketone bodies are increased because of lack of insulin in DM type 1

104
Q

is DM type 1 autoimmune

A

yes

105
Q

what isDM type 1 caused by

A

destruction of pancreatic beta cells which makes autoreactive T lymphocytes

106
Q

what is the early disease of DM type 1 marked by

A

lymphocytic infiltrates

107
Q

what surrounds the necrotic beta cells in DM type 1

A

CD4 T cells and cytotoxic CD8 T cells

108
Q

what is an important diagnostic criteria of DM type 1 ?

A

autoantibodies are present but are not responsible for destruction

109
Q

50% of newly diagnosed DM type 1 patients have increased…

A

islet cell autoantibodies (ICA) and insulin autoantibody (IAA)

110
Q

can screening be used to identify majority of DM type 1 ppl?

A

no

111
Q

what alleles have the strongest influence for DM type 1 risk?

A

class II HLA-DR and HLA-DQ loci

112
Q

what environmental factors may lead to DM type 1 ?

A

viral infections such as exposure to rubella

113
Q

molecular mimicry is associated with the etiology of what disease

A

DM type 1

114
Q

who does DM type 2 occur most commonly in

A

adults, native americans, mexican americans, and african americans

115
Q

is there a stronger genetic component for DM type 1 or 2

A

2

116
Q

this disorder is associated with an increased resistance to the effects of insulin at its sites of action and decreased insulin secretion by the pancreas

A

DM type 2

117
Q

what can ameliorate or even terminate DM type 2

A

weight loss in obese or overweight ppl

118
Q

what 2 metabolic defects are responsible for hyperglycemia in DM type 2

A
  1. target tissue resistance to insulin

2. inadequate pancreatic cell insulin secretion

119
Q

can a genetic test identify ppl at risk for type 2 diabetes

A

no

120
Q

what is the debate about in DM type 2

A

whether the primary lesion is insulin resistance or defective cell insulin secretion

121
Q

what is a key factor in the link btwn obesity and DM type 2

A

insulin resistance

122
Q

what is the primary source of mediators of insulin resistance

A

central/abdomoinal adiposity

123
Q

how does central/abdomoinal adiposity increase insulin resistance

A

lipotoxicity, adipokines, and hormones

124
Q

what are adipokines

A

dysregulated secretion of cytokines made in fat tissue

125
Q

what are the toxic effects of excess free fatty acids

A

dec skeletal muscle insulin sensitivity

126
Q

what does leptin do

A

controls satiety and enhances insulin sensitivity

127
Q

do most ppl with type 2 DM develop diabetes

A

no

128
Q

what kinda of disorders is DM a secondary disease?

A

pancreatitis, cushings syndrome, genetic beta cell defects, drugs like HIV protease inhibitors

129
Q

who does gestational DM occur in?

A

pregnant women in their 2nd or 3rd trimester

130
Q

what is gestational DM caused by

A

increasing levels of the hormones progesterone, cortisol, and prolactin

131
Q

how is gestational DM diagnosed

A

oral glucose tests

132
Q

when is gestational DM resolved

A

parturition, but 50% of these ppl develop type 2 DM later in life

Pathophysiology (17 decks)

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