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Human Bioscience II > Pancreatic Hormones > Flashcards

Pancreatic Hormones Flashcards

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?

A

Glucagon

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
Q

Which type of diabetes is most common?
How is it treated?

A

Type 2 diabetes: 90-95%
Decreased insulin secretion and increased insulin resistance to insulin action in tissues

26
Q

What occurs in type 1 diabetes?
What happens if it is untreated?

A

Autoimmune condition from lack of insulin
It is fatal

27
Q

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?

A

38 million Americans are affected 12% of population

Type 1

Type 2

28
Q

Which type of diabetes is increasing in children?
Why?
Is this an epidememic?

A

Type 2

Because childhood obesity
Yes!

29
Q

What is the diagnosis of DM? What are the measurements in each?

A

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
Q

What does it mean to be pre-diabetic?

What is risk of progressing to DM?

A

Fasting plasma glucose >100 and <125 mg/dL OGTT >140 <200 mg

Significant risk of progressing to DM (5-10%/year)

31
Q

What is HbA1c?

How far back does it track?

A

% of glycated hemoglobin

It’s important because

Tracks blood glucose back to 3 months ago

32
Q

What is type 1 DM?

At what age does it ocur?

A

Occurs anytime before 30 years old

33
Q

What is the clinical course of DM 1?

What is the urine associated with?

What are the 3 classic p symptoms?

A

Loss of insulin (major anabolic hormone)

Urine would be sweet and cause polyuria

34
Q

What is polydipsia?

A

Increased thirst

35
Q

What is Diabetic Ketoacidosis?

What is fatty acid converted into?

A

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
Q

What is systemic metabolic ketoacidosis?
What are the symptoms?

A

Dehydration + Ketonemia which decreases the pH (more acidic)
Breath contains a fruity odor

37
Q

What is Type 2 DM associated with?

A

Obesity, environmental factors ie: diet, sedentary lifestyle, increased risk in identical twins, increased risk if parents have it

38
Q

What causes type 2 DM?

A

Increased resistance of peripheral tissues to insulin

Inadequate insulin secretion in response to hyperglycemia in the long term

39
Q

What is gestational diabetes?

A

Human placental lactogen tends to elevate blood glucose
Hyperglycemia is common during pregnancy in women who are predisposed to DM2

40
Q

What are the 4 important DM compliations?

A
  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
Q

What happens if capillaries occluded?

A

Hypoxia which causes angiogenesis

42
Q

Where are the microvascular complications in DM?

A
  1. Eye
  2. Kidney
  3. Neuropathy
43
Q

Where are the macrovascular complications in DM?

A
  1. Brain
  2. Heart
  3. Extremities
    - Ischemia of lower extremity arteries (Foot ulceration)
44
Q

What is the effect of Glomerular lesions?

A

Pyelonephritis and necrotizing papillitis

45
Q

What are the long term complications of DM?

What occurs early?
What occurs in moderate?

A

Non proliferative diabetic retinopathy (NPDR)

Early: Microaneurysms
Moderate: Microaneurysms, hemorrhages *dot, blood or flame shaped)

46
Q

What happens in proliferative diabetic retionpathy?

Is the safest retinopathy to occur?

A

Neovascular growth and fibrous tissue formation triggered by hypoxia and VEGF

  • Tractional retina detachment <- Fix with anti VEGF drugs
  • No, most dangerous

Human Bioscience II (8 decks)

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