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Patho II > Pancreas > Flashcards

Pancreas Flashcards

1
Q

What is the exocrine function of the pancreas?

A

Digestion of food

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2
Q

What types of cells are found in the exocrine pancreas?

A

Acinar cells

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3
Q

What is secreted by the exocrine pancreas?

A

Proenzymes:

Trypsinogen
Chymotrypsinogen
Procarboxypeptidase
Proelastase
Kaliikreinogen
Prophsopholipase
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4
Q

Where do the proenzymes/enzymes secreted by acinar cells go after being secreted?

A

Carried by ducts to the duodenum where they are activated

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5
Q

What is the endocrine pancreas composed of?

A

Islets of Langerhans cells

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6
Q

What is secreted by the Islets of Langerhans cells?

A

Insulin by beta cells

Glucagon by alpha cells

Somatostatin by gamma cells

PP cells secrete pancreatic polypeptide

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7
Q

What do ductal cells release?

A

Bicarbonate to neutralize digestive enzymes

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8
Q

Before proenzymes can become active, what must they undergo?

A

Cleavage

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9
Q

What is Diabetes Mellitus?

A

Group of metabolic disorders sharing the common feature of hyperglycemia

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10
Q

What is hyperglycemia in diabetes Mellitus caused by?

A

Defects in insulin secretion

Insulin action

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11
Q

What does the chronic hyperglycemia and associated metabolic dysregulation of diabetes Mellitus cause?

A

Secondary damage in multiple organ systems like the kidneys, eyes, nerves, and blood vessels

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12
Q

What is normal glucose homeostasis?

A

Glucose production in the liver

Glucose uptake and utilization by peripheral tissues, chiefly skeletal muscle

Actions of insulin and glucagon, on glucose uptake and metabolism

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13
Q

What are fasting plasma glucose levels determined by?

A

Hepatic glucose output

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14
Q

What occurs following a meal?

A

Insulin levels rise and glucagon levels fall in response to the large glucose load

Insulin then promotes glucose uptake and utilization in tissues

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15
Q

What is insulin produced by?

A

Beta cells in pancreatic islets

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16
Q

Where is insulin stored?

A

Secretory granules

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17
Q

What is the most important stimulus for insulin synthesis and release?

A

Glucose

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18
Q

How does glucose enter the beta cells?

A

Via GLUT 2 glucose transporter

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19
Q

How does insulin get glucose to be taken in by the cell?

A

Insulin binds to insulin receptors on cell surface and causes translocation of GLUT 4 within the cell which allows the uptake of glucose by the cell

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20
Q

What does the translocation of GLUT 4 allow to happen?

A

Uptake of glucose by the cell

Alterations in glucose, lipid, and protein metabolism

Changes in gene expression and cell growth

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21
Q

Where are GLUT 2 glucose receptors found?

A

Beta cells

Liver

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22
Q

Where are GLUT 3 glucose receptors found?

A

All tissues

Major transporter in neurons of CNS

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23
Q

Where are GLUT 4 glucose receptors found?

A

Skeletal muscle

Fat cells

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24
Q

What do we use to measure glycemic control?

A

HbA1c test

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25
Q

What is the HbA1C test?

A

Test that measures a person’s average blood glucose level over the past 2 to 3 months

Test shows the amount of glucose that sticks to the RBCs which is proportional to the amount of glucose in the blood

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26
Q

What does insulin cause to happen in adipose tissue?

A

Increased Glucose uptake

Increased lipogenesis

Decreased Lipolysis

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27
Q

What does insulin cause to happen in striated muscle cells?

A

Increased Glucose uptake

Increased GLycogen synthesis

Increased protein synthesis

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28
Q

What does insulin cause to happen in the liver?

A

Decreased Gluconeogenesis

Increased GLycogen synthesis

Increased lipogenesis

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29
Q

What three main sources is glucose obtained from?

A

Intestinal absorption of food

Glycogenolysis

Gluconeogenesis

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30
Q

What is insulin’s effects on glucose metabolism?

A

Inhibition of glycogenolysis and gluconeogenesis

Increased glucose transport into fat and muscle

Increased glycolysis in fat and muscle

Stimulation of glycogen synthesis

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31
Q

What is insulin’s effect on lipid metabolism?

A

Inhibition of lipolysis in fat

Decreased plasma fatty acid concentrations

Stimulation of fatty acid and triacylglycerol synthesis in fat and liver

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32
Q

What is insulin’s effect on protein metabolism?

A

Increased transport of some amino acids into muscle, adipose tissue, liver, and other cells

Increased rate of protein synthesis in muscle, adipose tissue, liver, and other tissues

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33
Q

What two factors stimulate insulin release?

A

Glucose

Vagal Stimulation

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34
Q

What factor amplifies glucose-induced insulin release?

A

Beta-adrenergic stimulation

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35
Q

What inhibits insulin release?

A

Alpha-adrenergic effect

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36
Q

What is Type 1 diabetes?

A

An autoimmune disease characterized by pancreatic beta cell destruction and an absolute deficiency of insulin

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37
Q

What is Type 2 diabetes?

A

Caused by a combination of peripheral resistance to insulin action and an inadequate secretory response by the pancreatic beta cells

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38
Q

What is type 2 diabetes caused by?

A

Genetic defects of Beta cell function

Genetics defects in insulin action

Exocrine pancreatic defects

Endocrinopathies

Infections

Drugs

Genetics syndromes associated with diabetes

Gestational diabetes Mellitus

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39
Q

What are the short term effects of exercising for non diabetics?

A

Muscles initially use glucose and later convert muscle glycogen to glucose to provide energy

Glucose CANNOT be transferred out of muscle to prevent hypoglycemia

Exercising muscle takes up glucose from circulation, which requires the availability of insulin

If exercise continues, NE and Epi stimulate lipolysis

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40
Q

What are the long term training effects of non-diabetics?

A

Development of new muscle capillaries

Increased translocation of insulin-responsive GLUT 4 transporters

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41
Q

What are the effects of exercise on Type 1 diabetics?

A

Exercise modestly lowered blood glucose concentration and raised blood ketone concentrations in normal and well controlled diabetics

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42
Q

What are the effects of exercise on type 2 diabetics?

A

Insulin-independent increase in glucose uptake

INcreased skeletal muscle GLUT4 protein expression

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43
Q

Who does type 1 diabetes most commonly develop in?

A

Children

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44
Q

Where are the major susceptibility genes for type 1 diabetes located?

A

HLA region

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45
Q

What genes are most commonly carried in patient with type 1 diabetes?

A

DR4

DQB*0302 and/or DR3

DQB*0201

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46
Q

What is the immunologic response happening in type 1 diabetes?

A

Relapsing remitting disease course with autoantibodies and T cellular responses to islet autoantigens

  1. Antigen binds to MHC class II molecules on APCs
  2. Binding allows antigen to be presented to antigen receptors on autoreactive CD4+ cells which initiate autoimmune injury to the pancreatic beta cells
  3. Binding of other molecules to T cells are important costimulatory pathways that further increase T cell activation
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47
Q

What is the natural history of type 1 diabetes?

A

Triggered by one or more environmental agents and usually progresses over many months or years

Most patients during that time are asymptomatic and euglycemic

Large percentage of the functioning beta cells are lost before hyperglycemia appears

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48
Q

What is prerequisite screening done for individuals who are at risk of developing type 1 diabetes?

A

Measurement of islet autoantibodies

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49
Q

What is the entry criteria for immunological response in type 1 diabetes?

A

Presence of two or more of the islet autoantibodies

50
Q

What are the confirmed targets of autoantibodies in type 1 diabetes?

A

Insulin

Glutamic acid decarboxylase

Insulinomia associated antigens 2

ZnT8 = zinc transporter

51
Q

When do the genetic markers appear for type 1 diabetes?

A

Present from birth

52
Q

When to the immune markers appear for type 1 diabetes?

A

First appear at the time of the environmental triggering events

53
Q

When does clinically evident type 1 diabetes occur?

A

Does NOT occur until there has been a much greater loss of functioning beta cell mass

54
Q

At what percentage of insulin secretion do we see subclinical beta cell dysfunction?

A

70-80%

55
Q

At what percentage of insulin secretion do we see critical beta cell mass and clinical type 1 diabetes Mellitus develops?

A

< 40%

56
Q

What is the fundamental problem with autoimmune disease portion of the type 1 diabetes?

A

Autoreactive T cells

Failure of self tolerance

57
Q

What is the generation of ketone a normal response to?

A

Fasting

58
Q

When does diabetic ketoacidosis occur?

A

Happens after depletion of liver glycogen stores

59
Q

How is diabetic ketoacidosis produced?

A

In glucose poor environment, too much oxaloacetate is diverted away into gluconeogenesis

This prevents acetyl-CoA from entering the Krebs cycle which results in a buildup of acetyl CoA

60
Q

What are ketone bodies?

A

Acetate

Acetone

Beta hydroxybuterate

61
Q

What is type 2 diabetes characterized by?

A

Hyperglycemia

Insulin resistance

Relative impairment in insulin secretion

62
Q

What can occur with hyperglycemia?

A

Impair pancreatic beta cell function and magnify insulin resistance

63
Q

What is metabolic syndrome?

A

Co-occurrence of metabolic risk factors for both type 2 diabetes and CVD

64
Q

What is the first predictor of type 2 diabetes?

A

Insulin resistance

65
Q

What causes inadequate insulin secretion?

A

Insulin secretion by beta cells requires glucose transport into the cell, which is mediated by GLUT-2

Genetic alteration affecting GLUT-2 expression causes impaired insulin secretion

66
Q

What occurs in impaired insulin processing in type 2 diabetes?

A

Insulin production in normal subjects involves cleavage of insulin from proinsulin

The processing of proinsulin to insulin in the beta cells is impaired in type 2 diabetes

67
Q

What is insulin resistance?

A

Broadly defined as a subnormal biological response to normal insulin

68
Q

What disorders is insulin resistance a component of?

A 
Target cell resistance
Type 2 diabetes
Obesity
Stress
Infection
Uremia
Acromegaly
Glucocorticoid excess
Pregnancy

Metabolic syndrome
Hypertension
Hyperlipidemia
Coronary artery disease

69
Q

What are the major organs associated with insulin resistance?

A

Liver

Skeletal muscle

Adipose tissue

70
Q

What are the consequences of insulin resistance?

A

Failure to inhibit gluconeogenesis in the liver = high fasting blood glucose levels

Failure of glucose uptake and glycogen synthesis to occur in skeletal muscle following a meal = high post-prandial blood glucose level

Failure to inhibit lipoprotein lipase in adipose tissue = excess circulating free fatty acids which amplifies the state of insulin resistance

71
Q

What are the four things associated with obesity and insulin resistance?

A

Central obesity

Inflammation

Free fatty acids

Adipokines

72
Q

What is the effect of free fatty acids in association with obesity and insulin resistance?

A

Excess free fatty acids compromise beta cell function and decrease insulin release by:

Saturating the oxidative and storage capabilities of hepatocytes and myocytes

Formation of fatty acid intermediates which impair insulin signaling

Induce expression of many inflammatory genes which suppress insulin signaling

73
Q

What are adipokines?

A

Variety of proteins secreted into the systemic circulation by adipose tissue

74
Q

What is the link between inflammation and insulin resistance?

A

Obesity associated chronic low grade inflammation

75
Q

What is the state of low grade inflammation in insulin sensitivity caused by?

A

Obesity = chronic nutrient imbalance activating cellular stress signaling pathways which inhibits insulin signaling and promoting inflammation

Chronic inflammation and insulin resistance

76
Q

What are the clinical presentations of childhood type 1 diabetes?

A

New onset of Polydipsia, Polyuria, Weight loss with hyperglycemia and ketonemia

Diabetic ketoacidosis

Silent (asymptomatic) incidental discovery

77
Q

What are the clinical presentations of type 2 diabetes?

A

majority of patients are asymptomatic and hyperglycemic

Polyuria
Polydipsia
Nocturia
Blurred vision

78
Q

The morbidity associated with both types of diabetes is due to damage induced by what?

A

Large and medium sized muscular arteries = diabetic macrovascular disease

Small vessels = diabetic microvascular disease

79
Q

What does macrovascular disease cause in diabetics?

A

Accelerated atherosclerosis

Increased risk of MI

Stroke

Lower extremity ischemia

80
Q

Where are the effects of microvascular disease most seen in diabetics?

A

retina = diabetic retinoapathy

Kidneys = diabetic nephropathy

Peripheral nerves = diabetic neuropathy

81
Q

What do chronic complications of diabetes depend on?

A

Duration and degree of hypglycemia

82
Q

What is the pathogenesis of long-term complications of diabetes?

A

Inflammation

83
Q

What are two major complications that pathophysiologically effect yoru body as a result of hyperglycemia?

A

Production of AGE

Reduction of glutathione system

84
Q

How is Advanced Glycosylation End Products (AGE) formed?

A

Reversible reaction leads to the formation of an aldimine (Schiff base)

Aldimine is then followed by an Amadori rearrangement to form a ketoamine which is an intermediate in formation of AGEs

85
Q

What is the significance of AGEs in diabetes?

A

They form irreversible cross-links with macromolecules like collagen, that contributes to vascular stiffening and myocardial dysfunction

86
Q

What is acute pancreatitis?

A

an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood

87
Q

What is the cause of acute pancreatitis?

A

Gallstones

Alcohol abuse

88
Q

What is the mechanism of gallstone pancreatitis?

A

Reflux of bile into the pancreatic duct due to transient obstruction of the ampulla during passage of gallstones OR obstruction at the ampulla secondary to stone(s) of edema caused by the passage of a stone

89
Q

What are the mechanisms of alcohol-induced pancreatitis?

A
  1. Sensitization of acinar cells to cholecystokinin (CCK) induced premature activation of zymogens
  2. Generation of toxic metabolites such as acetaldehyde and fatty acid ethyl esters
  3. Activation of pancreatic stellate cells by acetaldehyde and oxidative stress causing increased production of collagen and other matrix proteins
90
Q

What is the pathogenesis of acute pancreatitis?

A
  1. Intraacinar activation of proteolytic enzymes
  2. Microcirculatory injury
  3. Leukocyte chemoattraction, release of cytokines, and oxidative stress
91
Q

What occurs in intraacinar activation of proteolytic enzymes?

A

Blockade of secretion of pancreatic enzymes while synthesis continues

This causes pancreatic autodigestion which sets up a vicious cycle of active enzymes damaging cells, which then release more active enzymes

92
Q

What occurs in microcirculatory injury?

A

Vasoconstriction
Capillary Stasis
Decreased oxygen saturation
Progressive ischemia

Causing…

Increased vascular permeability and swelling of the pancreas

93
Q

What occurs in leukocyte chemoattraction, release of cytokines, and oxidative stress?

A

Atrivated pancreatic enzymes
Microcirculatory impairment
Release of inflammatory mediators

Causing…

Rapid worsening of pancreatic damage and necrosis

94
Q

What are the two diagnostic tests for acute pancreatitis?

A

Increased amylase and lipase in blood

95
Q

What does the systemic inflammatory response syndrome that occurs in acute pancreatitis consist of?

A 
ARDS
Myocardial depression and shock
Acute renal failure
Metabolic complications 
Bacterial translocation
96
Q

What is the systemic inflammatory response syndrome in acute pancreatitis mediated by?

A

Activated pancreatic enzymes

Cytokines released into the circulation from the inflamed pancreas

97
Q

What is ARDS?

A

Secondary to microvascular thrombosis and may be induced by lecithinase

98
Q

What is Myocardial depression and shock in association with SIRS?

A

Secondary to vasoactive peptides an da myocardial depressant factor

99
Q

What is acute renal failure in SIRS due to?

A

Hypovolemia

Hypotension

100
Q

What are the metabolic complications included in SIRS?

A 
Hypocalcemia
Hyperlipidemia
Hyperglycemia
Hypoglycemia
Diabetic ketoacidosis
101
Q

What is the bacterial translocation that occurs in SIRS?

A

Gut barrier is comprised causing translocation of common bacteria found there to go to blood which in turn causes local and systemic infection

102
Q

What is chronic pancreatitis?

A

A progressive fibroinflammatory process of the pancreas that results in irreversible destruction of exocrine parenchyma, fibrosis, and the destruction of endocrine parenchyma

103
Q

What is the most common cause of chronic pancreatitis?

A

Long-term alcohol abuse

104
Q

What are other common causes of chronic pancreatitis?

A 
Cigarette smoking
Hereditary pancreatitis 
Ductal obstruction
Systemic disease 
Idiopathic pancreatitis
105
Q

What is the pathogenesis of Chronic pancreatitis?

A

Hypersecretion of digestive enzymes which is NOT compensated for by an increase in ductal bicarbonate secretion

Inflammatory changes

Collagen secretion

Pancreatic fibrosis and acinar cell loss

106
Q

What are the two primary clinical features of chronic pancreatitis?

A

Abdominal pain that is epigastric and radiated to the back

Pancreatic insufficiency = protein and fat deficiencies which occur after 90% of pancreatic function is lost

107
Q

What two clinical features occur with pancreatic insufficiency in chronic pancreatitis?

A

Fat Malabsorption

Pancreatic Diabetes

108
Q

What occurs in fat malabsorption in chronic pancreatitis?

A

Steatorrhea usually occurs prior to protein deficiencies since lipolytic activity decreases faster than proteolysis

109
Q

What occurs with pancreatic diabetes in chronic pancreatitis?

A

Hyperglycemia and overt diabetes mellitus usually occurs late in course of disease

Pancreatic alpha cells are also affected and increase the risk of hypoglycemia

110
Q

What is the pathogenesis of pain in pancreatitis?

A

Nerve growth factor (NGF) are produced in chronic pancreatitis and mast cells can sensitize the nociceptor neuron by upregulating molecules such as substance P

Inflammatory milieu produces cytokines and inflammatory mediators that act on the neurons and sensitize and/or activate them

111
Q

What is the difference between acute vs. chronic pancreatitis?

A

Chronic = asymptomatic, fibrotic mass, normal amylase and lipase

Acute = symptomatic, non-progressive, reversible, amylase and lipase are high

112
Q

What is the most common type of pancreatic cancer?

A

Infiltrating ductal adenocarcinoma

113
Q

Where do invasive pancreatic cancers arise from?

A

Well-defined noninvasive precursor lesions in pancreatic intraepithelial neoplasia (PanIN)

114
Q

What is the cancer progression of the pancreas?

A

Nonneoplastic epithelium –>
PanIN –>
Invasive carcinoma

115
Q

What mutations can cause pancreatic adenocarcinomas?

A

Mutational activation of oncogenes = KRAS

Inactivation of tumor suppresor genes = TP53, p16/CDKN2A, and SMAD4

Inactivation of genome maintenance genes

116
Q

What is the strongest environmental factor that causes pancreatic cancer?

A

Cigarette Smoking

117
Q

What causes adipose tissue inflammation?

A

interaction between pancreatic cancer and adipose tissue

118
Q

What does the adipose tissue inflammation occuring in pancreatic cancer cause?

A

Systemic cytokine response
Abnormal adipokine secretion
Lipolysis

Causing…
peripheral insulin resistance and Beta cell dysfunction

119
Q

What are the most common presenting symptoms in patients with exocrine pancreatic cancer?

A

Pain
Jaundice
Weight Loss

120
Q

What is associated most with carcinoma of the HEAD of the pancreas?

A

Obstructive jaundice

121
Q

What are advanced symptoms of pancreatic cancer?

A

Weight loss
Anorexia
Generalized malaise
Weakness

Patho II (16 decks)

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