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CPAT > Endocrine- pancreas (wk 6) > Flashcards

Endocrine- pancreas (wk 6) Flashcards

1
Q

What is the main function of the pancreas?

A

Accessory digestive gland

Both endocrine and exocrine

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2
Q

T/F:

Endocrine constitutes majority of the pancreas function

A

False

Exocrine

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3
Q

Where does the main pancreatic duct with the bile duct empty? What is the name of the associated sphincter?

A

Into the duodenum at the hepatopancreatic duct

Sphincter= sphincter of Oddi (hepatopancreatic sphincter)

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4
Q

Which cells produce the proenymes?

A

Acinar cells

zygomen granules fuse with the apical membrane and release the enzymes into the lumen

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5
Q

T/F:

enzymes produced by acinar cells are in the active form

A

False
inactive form
chyme in the duodenum will activate them

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6
Q

What is the role of columnar cells of the larger ducts?

A

They produce mucin

Creates a barrier so that the enzymes don’t damage the pancreas

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7
Q

What is the role of centroacinar cells?

A

Secrete bicarbonate ions to neutralize the pH of the pancreas

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8
Q

What is the role of Cholecystokinin (CKK)?

A 
(Exocrine pancreas)
Produced by I-cells in the mucosal epithelium
Secreted into the duodenum
Activates gall bladder secretion of bile
Activates secretion of digestive enzymes
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9
Q

Which proenzyme does the pancreas secrete that will go onto cleave the other enzymes and activate them?

A

Trypsinogen

Activated into trypsin which goes and cleaves the other enzymes to activate them

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10
Q

Development of the pancreas occurs in week ___ to ___ of development.

A

5 to 8

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11
Q

What is a major gene that contributes to the signalling pathways involved in the development of the pancreas?

A

PDX1

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12
Q

If signalling pathways are not controlled during pancreatic development, which gene can you assume is mutated?

A

PDX1

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13
Q

What is Pancreas Divisum?

A

When the duct system fails to fuse
Causes the main drainage to occur via accessory ducts
This elevates intraductal pressure
Increased risk of chronic pancreatitis

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14
Q

If you have mutations in PDX1 gene, what term is given?

A

Pancreatic agenesis

non-survival

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15
Q

What is ectopic pancreas?

A

When acini cells aren’t localised to the pancreas

Often found in stomach and duodenum

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16
Q

What is annular pancreas?

A

Ring of pancreatic tissue around the duodenum

Leads to increased pressure

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17
Q

What is pancreatitis?

A

Inflammation of the pancreas

Inappropriate activation of digestive enzymes

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18
Q

What are the four things the pancreas does to ensure appropriate activation of enzymes?

A

Secretes inactive form
Maintenance of the zygomen granule
Bicarbonate ions to maintain the pH environment
Chemical barrier formed by mucin

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19
Q

Acute pancreatitis is ____ inflammation of the pancreas

A

Reversible

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20
Q

What are the two most popular causes of acute pancreatitis

A

Alcoholism (increased ROS which breakdown zygomen granules)

Biliary tract disease (gall stones block the passage of juices)

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21
Q

What are the symptoms a patient will experience when suffering acute pancreatitis?

A

Acute abdominal pain in upper right quadrant
pain in upper back and left shoulder
Nausea/vomiting
Increased white blood cell count
Serum concentrations of amylase and pancreatic lipase (increased, these shouldn’t be in the blood stream)
Fluid exudates
enlargement
Small amount of bruising (enzymes are breaking down blood vessels)

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22
Q

What does acute pancreatitis look like macroscopically?

A

Destruction of pancreatic parenchyma
Microvasular leakage= edema
Necrosis of fat by lipolytic enzymes= chalky appearance
Acute inflammation= enlarged
Destruction of blood vessles= interstitial hemorrhage

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23
Q

What does acute pancreatitis look like microscopically?

A

Trypsin- activating other proenzymes
Phospholipase- degrading fat cells
Elastase- breaking down elastic fibres of vasculature

Fat necrosis
Inflammation
Focal parenchymal necrosis

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24
Q

What are the three mechanisms that cause acute pancreatitis?

A

Duct obstruction
Acinar cell injury
Defective intracellular transport

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25
Q

List some proinflammatory mediators involved in acute pancreatitis

A

TNFalpha
IL-1beta
IL-6
IL-8

(can lead to systemic inflammatory response syndrome)

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26
Q

How can you treat acute pancreatitis?

A

Fluids
Pain relief
No eating to rest exocrine function (get food via drip)
Antiemetics to reduce nausea and vomiting
Drainage of fluids

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27
Q

Chronic pancreatitis is _____ destruction of exocrine parenchyma and _____

A

irreversible destruction of exocrine parenchyma

fibrosis!!

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28
Q

T/F:

Late stage chronic pancreatitis can lead to the destruction of endocrine pancreas

A

True

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29
Q

What are some causes of chronic pancreatitis?

A

Alcoholism
Biliary tract obstruction
PRSS1, SPINK1 gene mutations
Idiopathic= up to 40%

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30
Q

T/F:

serum concentrations in patients suffering chronic pancreatitis will be high in amylase and pancreatic lipase

A

False

don’t expect there to be increased levels of this because the cells aren’t doing their job in the first place

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31
Q

T/F:

Chronic pancreatitis patients may have elevated blood glucose levels and CCK

A

True

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32
Q

T/F:

Acini are enlarged in number and size in chronic pancreatitis

A

False

reduced in size and number

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33
Q

Under the microscope, what might you observe in chronic pancreatitis?

A

Parenchymal fibrosis
Reduced number and size of acini
Relative sparing of the islets of Landerhands
Variable dilation of the pancreatic ducts
Inter and intra ducts contain protein plugs
Chronic inflammatory infiltrate observed around the ducts with atrophic epithelium

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34
Q

List the 5 suggested mechanisms that contribute to chronic pancreatitis

A 
Ductal theory
Acinar theory
Electrophilic stress
Multiple cause theory
Two-hit theory
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35
Q

What contributes to fibrosis in chronic pancreatitis?

A

Inflammatory cells release pro-inflammatory mediators- can increase collagen synthesis
They also release pro-fibrotic cytokines= promotes proliferation of periacinar myofibroblasts
Deposition of collagen and remodelling of ECM

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36
Q

What can you do to treat chronic pancreatitis?

A

Pain relief
Steroids
Some enzyme therapies
Micronutrients to stimulate exocytosis of ZG
Treatment of protein-energy malnutrition
Surgery= drainage, stent the bile duct, lateral pancreaticojejunostomy

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37
Q

T/F:

Diabetes is an exocrine disorder

A

False

Endocrine disorder

38
Q

Which cells do most of the endocrine function?

A

Islet of Langerhands cells
Controls glucose, lipid and carbohydrate metabolism
4 main cell types: (alpha, beta, delta, PP)

39
Q

T/F:

Islet of Langerhands cells have a faster turn over rate in comparison to Acinar cells

A

False
much slower
take a lot longer to regenerate

40
Q

T/F:

Alpha cells secrete insulin

A

False

beta cells secrete insulin and alpha cells secrete glucagon

41
Q

T/F:

Delta cells secrete somatostatin

A

True

42
Q

What do PP cells secrete?

A

Pacreatic Polypeptide

43
Q

Select the correct answer:

  • Glucagon granules have a rectangular crystaline matrix surrounded by a halo
  • Pancreatic polypeptides have a round closely applied membrane
  • Glucagon granules appear darker than somatostatin granules
A

Glucagon granules appear darker than somatostatin granules

44
Q

T/F:

Insulin granules have a rectangular crystalline matrix with a halo

A

True

45
Q

T/F:

Glucagon granules are round with a closely applied membrane, appear darker than somatostatin

A

True

46
Q

T/F:

Somatostatin granules are large and pale with a closely applied membrane

A

True

47
Q

T/F:

Pancreatic polypeptides are small dark granules

A

True

48
Q

Insulin is released in response to _____

A

increased blood glucose

49
Q

Glucagon is released in response to _____

A

decreased blood glucose

50
Q

What is the role of somatostatin?

A

Negative regulation of insulin, glucagon and PP
Inhibitory hormone
Reduces stomach acid secretions (directly and indirectly)
Suppresses exocrine function of the pancreas via CCK (CCK is normally involved in activating proenzymes of the pancreas)

51
Q

T/F:

Pancreatic polypeptide is released when blood glucose levels are high

A 
False
released when they are low
Stimulates gastric juice secretion
regulates endocrine and exocrine pancreas
Limits intestinal motility
52
Q

T/F:

Exocrine pancreas is regulating the whole body blood glucose homeostasis

A

False

endocrine pancreas

53
Q

What happens after you eat a meal?

A

Increased blood glucose levels
Insulin is released immediately
Insulin acts on peripheral organs which will cause them to uptake the glucose from the blood and store the excess in various founds (skeletal muscle, liver, adipocytes)

54
Q

What happens when you are hungry?

A

Blood glucose levels are low
Pancreas releases glucagon
Glucagon targets the peripheral organs and the stores will under go gluconeogenesis to make more glucose and raise blood glucose levels

55
Q

Explain the physiology behind beta cells uptaking glucagon and how this ends up resulting in the release of insulin

A

Glucose from the blood is brought into beta cells via the GLUT2 receptor
ATP produced in the beta cells will interact with a dimeric complex which will inhibit potassium channels and sulfomurea receptor
Potassium cannot be released
Membrane is now depolarized
To fix this, calcium will flux INTO the beta cell
Release of insulin from the granules is now promoted
Insulin targets insulin sensitive cells (ie cells in liver)

56
Q

T/F:

Insulin can translocate the cell membrane

A

False
never
it always stays on the outside

57
Q

Explain how GLUT4 brings in glucose into peripheral organs

A

Insulin binds to insulin receptor substrate 1
Tyrosine residues are phosphorylated
PI3K joins in with the complex
GLUT4 vesicles translocate from within the cell to the cellular membrane to bring in glucose

58
Q

Distinguish between type 1 and type 2 diabetes

A 
1= beta cell destruction, can't make insulin
2= resistance of peripheral tissue to insulin
59
Q

What is diabetes?

A

Any metabolic disorder where the underlying feature is hyperglycemia

60
Q

T/F:

Type 2 diabetes has no inherited basis

A

False

although mostly correlated with obesity, there is some genetic predisposure

61
Q

T/F:
Type 2 diabetes is an autoimmune disease in which islet destruction is caused primarily by immune effector cells reacting against endogenous beta cell antigens

A

False

Type 1 has this description

62
Q

What two clinical problems can develop when you suffer type 1 diabetes and don’t get adequate insulin supplies?

A

Ketoacidosis

Coma

63
Q

Ketoacidosis overall state is ____ insulin and ____ glucagon

A

decreased insulin

increased glucagon

64
Q

Describe what happens when you suffer ketoacidosis

A

Insulin deficiency so the peripheral organs aren’t taking in glucose from the blood and instead will try find other ways to generate energy (break down proteins, break down fats)
Increase gluconeogenesis and increase blood glucose levels
Kidneys try to filter out all this excess glucose= pee more, really thirsty, dehydrated
Excess ketones (made from breaking down fats) will increase blood pKa and create a fruity breath
Ketone levels are greatly higher

65
Q

Describe patient symptoms of Type 1 Diabetes

A

Increased thirst, dry mouth, increased urination, increased hunger, fatigue, weight losss

Definining it:
Glycated haemaglobin
sweet urine
ketones in urine and blood
presence of auto-antibodies against insulin, glutamic acid decarbozylase and islet cell cytoplasm (beta cell specific)
decrease in C peptide
66
Q

T/F:

Type 1 diabetes includes presence of islet-directed antibodies

A

False

67
Q

T/F:

T1DM loci has associated genetic susceptibility for type 1 diabetes

A

True

IDDM1 IDDM2 and IDDM12 are of particular interest

68
Q

T/F:

Type 1 diabetes generates autoantibodies against all islet cells

A

False
spares alpha, delta, PP cells, exocrine cells
Only targets beta cells

69
Q

What are some possible environmental factors that may trigger pre-diabetics to develop overt type 1 diabetes?

A

Viral- mumps, rubella, cosackie B,
Environmental toxins e.g. nitrosamines
Foods= cow’s milk protein, gluten
Gut microbiome

70
Q

What are the three mechanisms proposed to explain the autoimmunity of beta cells?

A

Bystander damage
Molecular mimicry
Viral de ja vu

71
Q

Explain the bystander damage theory

A

Infections induce islet injury and inflammation, leading to the release of sequestered beta cell antigens and the activation of auto reactive T cells

72
Q

Explain the molecular mimicry theory

A

Viruses produce proteins that mimic beta cell antigens and the immune response to the viral protein cross-reacts with self tissue

73
Q

Explain the viral de ja vu theory

A

Viral infections incurred early in life (predisposing virus) persist
Subsequent re-infection with a related virus (precipitaing virus) causes an immune response against both virus and beta cells

74
Q

What is insulitis? How does this contribute to the progressive loss of beta cells?

A

Inflammation resulting from infiltration of mononuclear lymphocytes
CD8 cells directly kill them
CD4 cells injure beta cells by secreting cytokines
B lymphocytes and macrophages also present

75
Q

What are two parts of the beta cell that the immune response generally makes auto antibodies against?

A

Insulin

Beta cell enzyme glutamic acid decarboxylase (GAD)

76
Q

T/F:

As soon as you start generating autoantibodies against beta cells, symptoms of type 1 diabetes will appear

A

False

Takes many years before the disease becomes evident

77
Q

T/F:

When 10% of beta cell destruction has occurred, hyperglycemia and ketosis occur

A

False

about 90%

78
Q

How can you improve glycaemic control in patients with type 1 diabetes?

A

Diet
Appropriate insulin delivery
Monitoring BGL

79
Q

List some treatment options for type 1 diabetes patients

A 
Insulin (recombinant insulin made in e coli)
Insulin mimetics 
Routine insulin injections
Insulin pump
Smart patches
80
Q

On a cellular level, how can you treat type 1 diabetes?

A

Stem cell therapy
Pancreatic transplant
Islet transplants (need two donors)

81
Q

What are two clinical classifiers of type 2 diabetes?

A

Weight gain

Absence of auto-antibodies

82
Q

What are two metabolic defects that characterise type 2 diabetes?

A

Peripheral resistance to insulin

Beta cell dysfunction

83
Q

What is hyperinsulinemia?

A

Beta cells try to secrete heaps of insulin

This will occur before hyperglycemia

84
Q

T/F:

T2DM is only caused by environmental factors

A

False

some genetic role as well

85
Q

T/F:

T2DM genetic susceptibility is related to genes involved in immune tolerance and regulation

A

False

this is T1DM

86
Q

In T2DM, polymorphisms in genes are often associated with ____ and ____

A

Beta cell function

Insulin secretion

87
Q

Distribution of body ___ also influences insulin sensitivity

A

fat

88
Q

In T2DM, peripheral tissues are less likely to uptake _____ and have an inability to suppress ______

A

glucose

hepatic gluconeogenesis

89
Q

What three factors of obesity can influence insulin sensitivity

A

Adipokines (reduced adiponectin secreted from adipocytes when you are obese which decreases glucose uptake and insulin sensitivity)

NEFAs and FA= toxic intermediates limit glucose uptake

Inflammation= adipose tissue and macrophages secrete pro-inflammatory cytokines

90
Q

Explain how nonesterified fatty acids promote insulin resistance

A

They undergo metabolism in the liver and stop at the DAG intermediate
DAG interacts to protein kinase C
Protein kinase C phosphoryaltes the SERINE residues of the insulin receptor
This now limits the interaction of insulin with the receptor and therefore GLUT4 can’t be translocated to go pick up glucose from the blood

91
Q

How do beta cells respond to insulin insensitivity by peripheral tissues?

A

They secrete lots of insulin= hyperinsulinema
Try to compensate
Eventually they can’t and you become hyperglycemic

92
Q

How can you manage Type 2 diabets?

A 
Diet
Exercise
mediation= e.g. metformin, sulfonylureas
Insulin injections
weight loss surgery

CPAT (9 decks)

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