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Patho II > Pancreas > Flashcards

Pancreas Flashcards

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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
What is the HbA1C test?
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
26
What does insulin cause to happen in adipose tissue?
Increased Glucose uptake Increased lipogenesis Decreased Lipolysis
27
What does insulin cause to happen in striated muscle cells?
Increased Glucose uptake Increased GLycogen synthesis Increased protein synthesis
28
What does insulin cause to happen in the liver?
Decreased Gluconeogenesis Increased GLycogen synthesis Increased lipogenesis
29
What three main sources is glucose obtained from?
Intestinal absorption of food Glycogenolysis Gluconeogenesis
30
What is insulin’s effects on glucose metabolism?
Inhibition of glycogenolysis and gluconeogenesis Increased glucose transport into fat and muscle Increased glycolysis in fat and muscle Stimulation of glycogen synthesis
31
What is insulin’s effect on lipid metabolism?
Inhibition of lipolysis in fat Decreased plasma fatty acid concentrations Stimulation of fatty acid and triacylglycerol synthesis in fat and liver
32
What is insulin’s effect on protein metabolism?
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
33
What two factors stimulate insulin release?
Glucose Vagal Stimulation
34
What factor amplifies glucose-induced insulin release?
Beta-adrenergic stimulation
35
What inhibits insulin release?
Alpha-adrenergic effect
36
What is Type 1 diabetes?
An autoimmune disease characterized by pancreatic beta cell destruction and an absolute deficiency of insulin
37
What is Type 2 diabetes?
Caused by a combination of peripheral resistance to insulin action and an inadequate secretory response by the pancreatic beta cells
38
What is type 2 diabetes caused by?
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
39
What are the short term effects of exercising for non diabetics?
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
40
What are the long term training effects of non-diabetics?
Development of new muscle capillaries Increased translocation of insulin-responsive GLUT 4 transporters
41
What are the effects of exercise on Type 1 diabetics?
Exercise modestly lowered blood glucose concentration and raised blood ketone concentrations in normal and well controlled diabetics
42
What are the effects of exercise on type 2 diabetics?
Insulin-independent increase in glucose uptake INcreased skeletal muscle GLUT4 protein expression
43
Who does type 1 diabetes most commonly develop in?
Children
44
Where are the major susceptibility genes for type 1 diabetes located?
HLA region
45
What genes are most commonly carried in patient with type 1 diabetes?
DR4 DQB*0302 and/or DR3 DQB*0201
46
What is the immunologic response happening in type 1 diabetes?
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
47
What is the natural history of type 1 diabetes?
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
48
What is prerequisite screening done for individuals who are at risk of developing type 1 diabetes?
Measurement of islet autoantibodies
49
What is the entry criteria for immunological response in type 1 diabetes?
Presence of two or more of the islet autoantibodies
50
What are the confirmed targets of autoantibodies in type 1 diabetes?
Insulin Glutamic acid decarboxylase Insulinomia associated antigens 2 ZnT8 = zinc transporter
51
When do the genetic markers appear for type 1 diabetes?
Present from birth
52
When to the immune markers appear for type 1 diabetes?
First appear at the time of the environmental triggering events
53
When does clinically evident type 1 diabetes occur?
Does NOT occur until there has been a much greater loss of functioning beta cell mass
54
At what percentage of insulin secretion do we see subclinical beta cell dysfunction?
70-80%
55
At what percentage of insulin secretion do we see critical beta cell mass and clinical type 1 diabetes Mellitus develops?
< 40%
56
What is the fundamental problem with autoimmune disease portion of the type 1 diabetes?
Autoreactive T cells Failure of self tolerance
57
What is the generation of ketone a normal response to?
Fasting
58
When does diabetic ketoacidosis occur?
Happens after depletion of liver glycogen stores
59
How is diabetic ketoacidosis produced?
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
What are ketone bodies?
Acetate Acetone Beta hydroxybuterate
61
What is type 2 diabetes characterized by?
Hyperglycemia Insulin resistance Relative impairment in insulin secretion
62
What can occur with hyperglycemia?
Impair pancreatic beta cell function and magnify insulin resistance
63
What is metabolic syndrome?
Co-occurrence of metabolic risk factors for both type 2 diabetes and CVD
64
What is the first predictor of type 2 diabetes?
Insulin resistance
65
What causes inadequate insulin secretion?
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
What occurs in impaired insulin processing in type 2 diabetes?
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
What is insulin resistance?
Broadly defined as a subnormal biological response to normal insulin
68
What disorders is insulin resistance a component of?
``` Target cell resistance Type 2 diabetes Obesity Stress Infection Uremia Acromegaly Glucocorticoid excess Pregnancy ``` Metabolic syndrome Hypertension Hyperlipidemia Coronary artery disease
69
What are the major organs associated with insulin resistance?
Liver Skeletal muscle Adipose tissue
70
What are the consequences of insulin resistance?
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
What are the four things associated with obesity and insulin resistance?
Central obesity Inflammation Free fatty acids Adipokines
72
What is the effect of free fatty acids in association with obesity and insulin resistance?
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
What are adipokines?
Variety of proteins secreted into the systemic circulation by adipose tissue
74
What is the link between inflammation and insulin resistance?
Obesity associated chronic low grade inflammation
75
What is the state of low grade inflammation in insulin sensitivity caused by?
Obesity = chronic nutrient imbalance activating cellular stress signaling pathways which inhibits insulin signaling and promoting inflammation Chronic inflammation and insulin resistance
76
What are the clinical presentations of childhood type 1 diabetes?
New onset of Polydipsia, Polyuria, Weight loss with hyperglycemia and ketonemia Diabetic ketoacidosis Silent (asymptomatic) incidental discovery
77
What are the clinical presentations of type 2 diabetes?
majority of patients are asymptomatic and hyperglycemic Polyuria Polydipsia Nocturia Blurred vision
78
The morbidity associated with both types of diabetes is due to damage induced by what?
Large and medium sized muscular arteries = diabetic macrovascular disease Small vessels = diabetic microvascular disease
79
What does macrovascular disease cause in diabetics?
Accelerated atherosclerosis Increased risk of MI Stroke Lower extremity ischemia
80
Where are the effects of microvascular disease most seen in diabetics?
retina = diabetic retinoapathy Kidneys = diabetic nephropathy Peripheral nerves = diabetic neuropathy
81
What do chronic complications of diabetes depend on?
Duration and degree of hypglycemia
82
What is the pathogenesis of long-term complications of diabetes?
Inflammation
83
What are two major complications that pathophysiologically effect yoru body as a result of hyperglycemia?
Production of AGE Reduction of glutathione system
84
How is Advanced Glycosylation End Products (AGE) formed?
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
What is the significance of AGEs in diabetes?
They form irreversible cross-links with macromolecules like collagen, that contributes to vascular stiffening and myocardial dysfunction
86
What is acute pancreatitis?
an inflammatory condition of the pancreas characterized clinically by abdominal pain and elevated levels of pancreatic enzymes in the blood
87
What is the cause of acute pancreatitis?
Gallstones | Alcohol abuse
88
What is the mechanism of gallstone pancreatitis?
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
What are the mechanisms of alcohol-induced pancreatitis?
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
What is the pathogenesis of acute pancreatitis?
1. Intraacinar activation of proteolytic enzymes 2. Microcirculatory injury 3. Leukocyte chemoattraction, release of cytokines, and oxidative stress
91
What occurs in intraacinar activation of proteolytic enzymes?
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
What occurs in microcirculatory injury?
Vasoconstriction Capillary Stasis Decreased oxygen saturation Progressive ischemia Causing... Increased vascular permeability and swelling of the pancreas
93
What occurs in leukocyte chemoattraction, release of cytokines, and oxidative stress?
Atrivated pancreatic enzymes Microcirculatory impairment Release of inflammatory mediators Causing... Rapid worsening of pancreatic damage and necrosis
94
What are the two diagnostic tests for acute pancreatitis?
Increased amylase and lipase in blood
95
What does the systemic inflammatory response syndrome that occurs in acute pancreatitis consist of?
``` ARDS Myocardial depression and shock Acute renal failure Metabolic complications Bacterial translocation ```
96
What is the systemic inflammatory response syndrome in acute pancreatitis mediated by?
Activated pancreatic enzymes Cytokines released into the circulation from the inflamed pancreas
97
What is ARDS?
Secondary to microvascular thrombosis and may be induced by lecithinase
98
What is Myocardial depression and shock in association with SIRS?
Secondary to vasoactive peptides an da myocardial depressant factor
99
What is acute renal failure in SIRS due to?
Hypovolemia | Hypotension
100
What are the metabolic complications included in SIRS?
``` Hypocalcemia Hyperlipidemia Hyperglycemia Hypoglycemia Diabetic ketoacidosis ```
101
What is the bacterial translocation that occurs in SIRS?
Gut barrier is comprised causing translocation of common bacteria found there to go to blood which in turn causes local and systemic infection
102
What is chronic pancreatitis?
A progressive fibroinflammatory process of the pancreas that results in irreversible destruction of exocrine parenchyma, fibrosis, and the destruction of endocrine parenchyma
103
What is the most common cause of chronic pancreatitis?
Long-term alcohol abuse
104
What are other common causes of chronic pancreatitis?
``` Cigarette smoking Hereditary pancreatitis Ductal obstruction Systemic disease Idiopathic pancreatitis ```
105
What is the pathogenesis of Chronic pancreatitis?
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
What are the two primary clinical features of chronic pancreatitis?
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
What two clinical features occur with pancreatic insufficiency in chronic pancreatitis?
Fat Malabsorption Pancreatic Diabetes
108
What occurs in fat malabsorption in chronic pancreatitis?
Steatorrhea usually occurs prior to protein deficiencies since lipolytic activity decreases faster than proteolysis
109
What occurs with pancreatic diabetes in chronic pancreatitis?
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
What is the pathogenesis of pain in pancreatitis?
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
What is the difference between acute vs. chronic pancreatitis?
Chronic = asymptomatic, fibrotic mass, normal amylase and lipase Acute = symptomatic, non-progressive, reversible, amylase and lipase are high
112
What is the most common type of pancreatic cancer?
Infiltrating ductal adenocarcinoma
113
Where do invasive pancreatic cancers arise from?
Well-defined noninvasive precursor lesions in pancreatic intraepithelial neoplasia (PanIN)
114
What is the cancer progression of the pancreas?
Nonneoplastic epithelium --> PanIN --> Invasive carcinoma
115
What mutations can cause pancreatic adenocarcinomas?
Mutational activation of oncogenes = KRAS Inactivation of tumor suppresor genes = TP53, p16/CDKN2A, and SMAD4 Inactivation of genome maintenance genes
116
What is the strongest environmental factor that causes pancreatic cancer?
Cigarette Smoking
117
What causes adipose tissue inflammation?
interaction between pancreatic cancer and adipose tissue
118
What does the adipose tissue inflammation occuring in pancreatic cancer cause?
Systemic cytokine response Abnormal adipokine secretion Lipolysis Causing... peripheral insulin resistance and Beta cell dysfunction
119
What are the most common presenting symptoms in patients with exocrine pancreatic cancer?
Pain Jaundice Weight Loss
120
What is associated most with carcinoma of the HEAD of the pancreas?
Obstructive jaundice
121
What are advanced symptoms of pancreatic cancer?
Weight loss Anorexia Generalized malaise Weakness

Patho II (16 decks)

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