Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

T/F:

Endocrine constitutes majority of the pancreas function

A

False

Exocrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which cells produce the proenymes?

A

Acinar cells

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the role of centroacinar cells?

A

Secrete bicarbonate ions to neutralize the pH of the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

5 to 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

PDX1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

PDX1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

Pancreatic agenesis

non-survival

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is ectopic pancreas?

A

When acini cells aren’t localised to the pancreas

Often found in stomach and duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is annular pancreas?

A

Ring of pancreatic tissue around the duodenum

Leads to increased pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is pancreatitis?

A

Inflammation of the pancreas

Inappropriate activation of digestive enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Acute pancreatitis is ____ inflammation of the pancreas

A

Reversible

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the three mechanisms that cause acute pancreatitis?

A

Duct obstruction
Acinar cell injury
Defective intracellular transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
List some proinflammatory mediators involved in acute pancreatitis
TNFalpha IL-1beta IL-6 IL-8 (can lead to systemic inflammatory response syndrome)
26
How can you treat acute pancreatitis?
Fluids Pain relief No eating to rest exocrine function (get food via drip) Antiemetics to reduce nausea and vomiting Drainage of fluids
27
Chronic pancreatitis is _____ destruction of exocrine parenchyma and _____
irreversible destruction of exocrine parenchyma | fibrosis!!
28
T/F: | Late stage chronic pancreatitis can lead to the destruction of endocrine pancreas
True
29
What are some causes of chronic pancreatitis?
Alcoholism Biliary tract obstruction PRSS1, SPINK1 gene mutations Idiopathic= up to 40%
30
T/F: | serum concentrations in patients suffering chronic pancreatitis will be high in amylase and pancreatic lipase
False | don't expect there to be increased levels of this because the cells aren't doing their job in the first place
31
T/F: | Chronic pancreatitis patients may have elevated blood glucose levels and CCK
True
32
T/F: | Acini are enlarged in number and size in chronic pancreatitis
False | reduced in size and number
33
Under the microscope, what might you observe in chronic pancreatitis?
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
34
List the 5 suggested mechanisms that contribute to chronic pancreatitis
``` Ductal theory Acinar theory Electrophilic stress Multiple cause theory Two-hit theory ```
35
What contributes to fibrosis in chronic pancreatitis?
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
36
What can you do to treat chronic pancreatitis?
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
37
T/F: | Diabetes is an exocrine disorder
False | Endocrine disorder
38
Which cells do most of the endocrine function?
Islet of Langerhands cells Controls glucose, lipid and carbohydrate metabolism 4 main cell types: (alpha, beta, delta, PP)
39
T/F: | Islet of Langerhands cells have a faster turn over rate in comparison to Acinar cells
False much slower take a lot longer to regenerate
40
T/F: | Alpha cells secrete insulin
False | beta cells secrete insulin and alpha cells secrete glucagon
41
T/F: | Delta cells secrete somatostatin
True
42
What do PP cells secrete?
Pacreatic Polypeptide
43
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
Glucagon granules appear darker than somatostatin granules
44
T/F: | Insulin granules have a rectangular crystalline matrix with a halo
True
45
T/F: | Glucagon granules are round with a closely applied membrane, appear darker than somatostatin
True
46
T/F: | Somatostatin granules are large and pale with a closely applied membrane
True
47
T/F: | Pancreatic polypeptides are small dark granules
True
48
Insulin is released in response to _____
increased blood glucose
49
Glucagon is released in response to _____
decreased blood glucose
50
What is the role of somatostatin?
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
T/F: | Pancreatic polypeptide is released when blood glucose levels are high
``` False released when they are low Stimulates gastric juice secretion regulates endocrine and exocrine pancreas Limits intestinal motility ```
52
T/F: | Exocrine pancreas is regulating the whole body blood glucose homeostasis
False | endocrine pancreas
53
What happens after you eat a meal?
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
What happens when you are hungry?
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
Explain the physiology behind beta cells uptaking glucagon and how this ends up resulting in the release of insulin
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
T/F: | Insulin can translocate the cell membrane
False never it always stays on the outside
57
Explain how GLUT4 brings in glucose into peripheral organs
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
Distinguish between type 1 and type 2 diabetes
``` 1= beta cell destruction, can't make insulin 2= resistance of peripheral tissue to insulin ```
59
What is diabetes?
Any metabolic disorder where the underlying feature is hyperglycemia
60
T/F: | Type 2 diabetes has no inherited basis
False | although mostly correlated with obesity, there is some genetic predisposure
61
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
False | Type 1 has this description
62
What two clinical problems can develop when you suffer type 1 diabetes and don't get adequate insulin supplies?
Ketoacidosis | Coma
63
Ketoacidosis overall state is ____ insulin and ____ glucagon
decreased insulin | increased glucagon
64
Describe what happens when you suffer ketoacidosis
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
Describe patient symptoms of Type 1 Diabetes
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
T/F: | Type 1 diabetes includes presence of islet-directed antibodies
False
67
T/F: | T1DM loci has associated genetic susceptibility for type 1 diabetes
True | IDDM1 IDDM2 and IDDM12 are of particular interest
68
T/F: | Type 1 diabetes generates autoantibodies against all islet cells
False spares alpha, delta, PP cells, exocrine cells Only targets beta cells
69
What are some possible environmental factors that may trigger pre-diabetics to develop overt type 1 diabetes?
Viral- mumps, rubella, cosackie B, Environmental toxins e.g. nitrosamines Foods= cow's milk protein, gluten Gut microbiome
70
What are the three mechanisms proposed to explain the autoimmunity of beta cells?
Bystander damage Molecular mimicry Viral de ja vu
71
Explain the bystander damage theory
Infections induce islet injury and inflammation, leading to the release of sequestered beta cell antigens and the activation of auto reactive T cells
72
Explain the molecular mimicry theory
Viruses produce proteins that mimic beta cell antigens and the immune response to the viral protein cross-reacts with self tissue
73
Explain the viral de ja vu theory
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
What is insulitis? How does this contribute to the progressive loss of beta cells?
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
What are two parts of the beta cell that the immune response generally makes auto antibodies against?
Insulin | Beta cell enzyme glutamic acid decarboxylase (GAD)
76
T/F: | As soon as you start generating autoantibodies against beta cells, symptoms of type 1 diabetes will appear
False | Takes many years before the disease becomes evident
77
T/F: | When 10% of beta cell destruction has occurred, hyperglycemia and ketosis occur
False | about 90%
78
How can you improve glycaemic control in patients with type 1 diabetes?
Diet Appropriate insulin delivery Monitoring BGL
79
List some treatment options for type 1 diabetes patients
``` Insulin (recombinant insulin made in e coli) Insulin mimetics Routine insulin injections Insulin pump Smart patches ```
80
On a cellular level, how can you treat type 1 diabetes?
Stem cell therapy Pancreatic transplant Islet transplants (need two donors)
81
What are two clinical classifiers of type 2 diabetes?
Weight gain | Absence of auto-antibodies
82
What are two metabolic defects that characterise type 2 diabetes?
Peripheral resistance to insulin | Beta cell dysfunction
83
What is hyperinsulinemia?
Beta cells try to secrete heaps of insulin | This will occur before hyperglycemia
84
T/F: | T2DM is only caused by environmental factors
False | some genetic role as well
85
T/F: | T2DM genetic susceptibility is related to genes involved in immune tolerance and regulation
False | this is T1DM
86
In T2DM, polymorphisms in genes are often associated with ____ and ____
Beta cell function | Insulin secretion
87
Distribution of body ___ also influences insulin sensitivity
fat
88
In T2DM, peripheral tissues are less likely to uptake _____ and have an inability to suppress ______
glucose | hepatic gluconeogenesis
89
What three factors of obesity can influence insulin sensitivity
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
Explain how nonesterified fatty acids promote insulin resistance
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
How do beta cells respond to insulin insensitivity by peripheral tissues?
They secrete lots of insulin= hyperinsulinema Try to compensate Eventually they can't and you become hyperglycemic
92
How can you manage Type 2 diabets?
``` Diet Exercise mediation= e.g. metformin, sulfonylureas Insulin injections weight loss surgery ```

CPAT (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions