Pancreatic Hormones Flashcards

(46 cards)

1
Q

Where does pancreatic hormones secrete into?

What type of gland is the pacreas?

A

Exocrine and endocrine gland

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2
Q

What are the 3 types of cells in the pancreas?

What does each cell secrete?

A

Islets of Langerhan
Acinar cells
alpha, beta, delta cells

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3
Q

What do alpha cells produce?
Which cell is in

A

Glucagon

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4
Q

What do beta cells secrete?
Is this in abundance?
Which cell is in most abundance?

A

Insulin

Yes, more beta than delta

Delta cells in most abundance?

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5
Q

What do acinar cells produce?

A

Various enzymes

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6
Q

What is insulin known as?

How is it structured?

A

The hormone of abundance because it used for future energy

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7
Q

How is proinsulin stuctured?

A
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8
Q

What is the purpose of the C-peptide?

A

Folding of A chain and B chain to ensure proper folding

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9
Q

How is insulin released?
What is the most important factor?
What does ATP do?

A
  • Via beta cells
  • Glucose influences insulin secretion
  • Inhibits K channel and closes it, thus depolarization ensues
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10
Q

What does an increase in calcium cause?

What is the #1 trigger?

A

More cells with insulin which goes to the membrane and then there’s an increase in insulin secretion

Depolarization

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11
Q

What are factors that influence more insulin secretion?

A
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12
Q

What is an insulin receptor?

Where is the binding site?

Which type of phosphorylation occurs?

What is the overall net effect?

A

2 major chains (a & B) that are connected via disulfide bridge- Tyrosine Kinase receptor

Binding site on alpha chain this causes confirmational change in beta chain then

Autophosphorylation occurs

Glucose uptake

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13
Q

What is autophosphorylation?

Where does this occur?

A
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14
Q

What are the actions of insulin?

A
  1. Decreases blood glucose levels by increasing glucose transport into muscle and adipose cells
  2. Promotes
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15
Q

How does insulin promote glucose uptake in muscle and adipose tissue?

What is needed for this mechanism to occur?

A

Via GLUT 4 transporters on the membrane thus glucose transport into the cell is increased

Insulin

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16
Q

What is insulin resistance?

A

Not enough GLUT 4 into the membrane thus there is no transport and you have excess glucose -> hyperglycemia

ie: Diabetes

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17
Q

Why are amino acids taken into the liver?

A
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18
Q

What are ketoacids?

What is the overall mechanism?

A

Metabolites which are produced from the fatty acids by the liver. Replaces glucose as the primary fuel of the brain in fasting conditions

Fat -> ketone bodies -> Fuel

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19
Q

What is the 2nd action of insulin?
How does it carry out this process?

A

Decreased blood fatty acid and ketoacid concentrations

  • Triglyceride formation into adipose tissues for storage
  • Decreases ketone bodies:
  • Inhibits oxidation of fatty acids and inhibits lipolysis in adipose tissue
20
Q

What is the counter hormone of insulin?

21
Q

What is glucagon?

What secretes glucagon?

A

Hormone of starvation promotes mobilization of glucose, stimulates gluconeogenesis

Polypeptide synthesized by alpha cells

22
Q

What are the actions of glucagon?

A
  1. Promotes glycogenolysis
  2. Inhibits glycogenesis
  3. Promotes gluconeogenesis
  4. Increased blood fatty acid and ketoacid conc.
  5. Glucagon increases lipolysis and inhibits fatty acid synthesis
  6. Ketoacid (B-hydroxybutyric) and acetoacetic acid are produced from fatty acids
23
Q

What is diabetes mellitus?

A

Chronic disorder of carbohydrate, fat and protein metabolism characterized in its fully expressed for my fasting hyperglycemia, glycosuria and a tendency for development of HTN, atherosclerosis, microangiopathy, nephropathy and neuropathy

24
Q

What occurs with insulin in a normal pers on?
What occurs in DM?

A

Insulin spike which causes blood glucose levels to immediately decrease

  1. Decreased insulin from beta cells
  2. Decreased action of insulin -> glucose not taken up by adipose or skeletal tissue
25
Which type of diabetes is most common? How is it treated?
Type 2 diabetes: 90-95% Decreased insulin secretion and increased insulin resistance to insulin action in tissues
26
What occurs in type 1 diabetes? What happens if it is untreated?
Autoimmune condition from lack of insulin It is fatal
27
What is the prevalence of diabetes? Why type is most common in white people? Which type is most common in African Americans, Hispanics, and Native Americans?
38 million Americans are affected 12% of population Type 1 Type 2
28
Which type of diabetes is increasing in children? Why? Is this an epidememic?
Type 2 Because childhood obesity Yes!
29
What is the diagnosis of DM? What are the measurements in each?
Symptoms plus plasma glucose concentration >200mg/dL Fasting plasma glucose <126mg/dL Abnormal oral glucose tolerance >200mg/dL after 2 hours of 1gm/kg glucose
30
What does it mean to be pre-diabetic? What is risk of progressing to DM?
Fasting plasma glucose >100 and <125 mg/dL OGTT >140 <200 mg Significant risk of progressing to DM (5-10%/year)
31
What is HbA1c? How far back does it track?
% of glycated hemoglobin It's important because Tracks blood glucose back to 3 months ago
32
What is type 1 DM? At what age does it ocur?
Occurs anytime before 30 years old
33
What is the clinical course of DM 1? What is the urine associated with? What are the 3 classic p symptoms?
Loss of insulin (major anabolic hormone) Urine would be sweet and cause polyuria
34
What is polydipsia?
Increased thirst
35
What is Diabetic Ketoacidosis? What is fatty acid converted into?
Increased glucagon breaks down triglycerides into fatty acids and glycerol It is then converted to glucose via gluconeogenesis Fatty acid converted into ketone bodies
36
What is systemic metabolic ketoacidosis? What are the symptoms?
Dehydration + Ketonemia which decreases the pH (more acidic) Breath contains a fruity odor
37
What is Type 2 DM associated with?
Obesity, environmental factors ie: diet, sedentary lifestyle, increased risk in identical twins, increased risk if parents have it
38
What causes type 2 DM?
Increased resistance of peripheral tissues to insulin Inadequate insulin secretion in response to hyperglycemia in the long term
39
What is gestational diabetes?
Human placental lactogen tends to elevate blood glucose Hyperglycemia is common during pregnancy in women who are predisposed to DM2
40
What are the 4 important DM compliations?
1. With hyperglycemia, AGE floats around with binds to RAGE -> ROS - Excess oxidative stress in endothelial cells Defense: Glutathione 2. increase in proinflammatory release from macrophages and endothelial cells 3. Increase in TGF-B -> Fibrosis of vascularture -> Capillary occlusion 4. NG-kB- multiple inflammatory gene expression
41
What happens if capillaries occluded?
Hypoxia which causes angiogenesis
42
Where are the microvascular complications in DM?
1. Eye 2. Kidney 3. Neuropathy
43
Where are the macrovascular complications in DM?
1. Brain 2. Heart 3. Extremities - Ischemia of lower extremity arteries (Foot ulceration)
44
What is the effect of Glomerular lesions?
Pyelonephritis and necrotizing papillitis
45
What are the long term complications of DM? What occurs early? What occurs in moderate?
Non proliferative diabetic retinopathy (NPDR) Early: Microaneurysms Moderate: Microaneurysms, hemorrhages *dot, blood or flame shaped)
46
What happens in proliferative diabetic retionpathy? Is the safest retinopathy to occur?
Neovascular growth and fibrous tissue formation triggered by hypoxia and VEGF - Tractional retina detachment <- Fix with anti VEGF drugs - No, most dangerous