Pancreas Flashcards

1
Q

Types of Pancreatic Receptors and what they secrete

A
  1. Alpha - glucagon
  2. Beta - insulin and amylin
  3. Delta - somatostatin
  4. Grelin
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2
Q

What is special about beta cells?

A

Can regulate what other cell types do due to its central location w/in the islet

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3
Q

How is insulin synthesized and structured?

A

Preproinsulin –> proinsulin –> insulin (+C peptide)

Secreted w/ C- peptide, can measure to see how much endogenous insulin they are making, greater half life than insulin

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4
Q

How is ATP Released?

A

High Glucose stims Mito, produces TP to block K efflux channel –> depols membrane –> Ca enters –> Insulin is released

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5
Q

Effect of Insulin on Carbohydrates?

A

Increases glucose uptake into target cells
Insulin–> phos of TK
–> GLUT4 is translocated to membrane –> allows glucose to enter
GLUT 4 not found in brain or liver

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6
Q

Effect of Insulin on lipids?

A

Increase uptake of FFA into Fat
- Stims lipoprotein lipase (lipoprotein to FFA) in blood –> FFA (can cross membrane easily) to triglyceride in adipose cells

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7
Q

What stimulates Insulin Secretion?

A
Glucose
AA
FFA
ACh
GIP
GLP-1
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8
Q

What inhibits secretion of insulin?

A

EPI
NE
Somatostatin

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9
Q

Where is glucagon made and what does it do?

A

Made in the liver

Increases glycogenolysis, increased gluconeogenesis, increased lipolysis

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10
Q

Synthesis and Structure of glucagon

A
  1. Major hormone to increase blood-glucose

2. Peptide hormone

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11
Q

Receptor of Glucagon

A

couple to Adenylate Cyclase/PKA system

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12
Q

Effect of glucagon on carbohydrate receptors

A

In liver = increased plasma glucose in the post ab state

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13
Q

Effect of glucagon on proteins

A

Increased gluconeogensis (hepatic protein)

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14
Q

Effect of glucagon on lipids

A

Increased Lipolysis - maintains blood glucose levels w/ high protein meals so you don’t take up too much glucose at once

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15
Q

How is glucagon stimulated?

A
  1. Low glucose
  2. AA
  3. EPI/NE
  4. ACh
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16
Q

How is glucagon inhibited?

A
  1. Insulin
  2. Somatostatin
  3. FFA (energy source)
  4. Amylin
17
Q

What does amylin do?

A

Peptide hormone secreted w/ insulin that inhibits glucagon secretion and slows down gastic emptying, glucose in blood will go up more slowly, supports action of insulin

18
Q

What are incretins and what do they do?

A

GIP (gluc-dependent Insulinotropoic polypeptide)

GLP-1 - preemptively secreting insulin, have glucose in your mouth and it warns the intestine food is coming

19
Q

What do EPI and NE do to glucagon?

A

stim glucagon release and glycogenolysis

20
Q

What does cortisol do to glucose?

A

Increases blood glucose

21
Q

What does growth hormone to insulin and glucose?

A

Anti-insulin effect

Elevates plasma glucose

22
Q

What is the only hormone that directly decreases plasma glucose?

A

Insulin

23
Q

Diabetes Mellitus Signs and Symp

A
  1. XS thirst and frequent urination

2. TYPE 1 = weight loss

24
Q

TX for Type 1 diabetes mellitus

A

Insulin injections every day

25
Q

Etiology of T1 Diabetes

A

Autoimmune destruction of pancreatic Beta cells

50/50 gen/environment

26
Q

T2 Diabetes Etiology

A

Disorder of insulin receptor signaling
Impaired Beta cell response
Some genetic component
Obesity is an aggregative factor

27
Q

Tx of T2 Diabetes

A

Weight management, exercise, drugs to regulate Beta Cells

28
Q

What is Metabolic Syndrome (syndrome X) and what disease is it associated w/?

A
Associated w/ T2 Diabetes
Need 3 or more of the following:
1. Large Waist
2. High Serum Triglyceride Levels
3. Low HDL Cholesterol
4. High blood glucose
5. High BP
29
Q

Maturity Onset Diabetes of the Young (MODY)

A

Group of monogenic disorders causing hyperglycemia of early onset
Looks like type 2 but its a genetic disorder

30
Q

Gestational Diabetes and its TX

A

Develop diabetes during pregnancy due to hormones, goes away after birth but risk persists,
high birth weight
TX: diet and exercise

31
Q

Diabetic Complications

A

Dehydrations, frequent urination and xs thirst
Diabetic Ketoacidosis
Vascular disease (macro/micro)
Retinopathy
Neuropathy (peripheral most coommon)
Nephropathy (microvascular changes - leading cause of death)

32
Q

What is diabetic ketoacidosis

A

Can’t take up glucose into fat and muscle, so body burns fat and it will generate ketone bodies (acetone)
Blood pH goes down, can detect in breath (fruity) as acetone is breathed out

33
Q

What is the mechanism of toxicity for T2 Diabetes?

A
  1. Advanced glycation end products (AGEs) - proteins bound w/ sugar
  2. Oxidative Damage
  3. Inflammation
  4. Changes in 2nd messenger systems
  5. Changes in GF signaling (VEGF)
  6. Diversion of glucose into other metabolic pathways and xs glycolysis
34
Q

What do the mechanism of toxicity ultimately cause in T2 Diabetes?

A
  1. Capillary basement membrane thickening
  2. Inflammatory signals
  3. ROS
  4. Changes in Growth factor signaling - directly from low insulin
35
Q

What is insulin shock?

A

Plasma insulin too high
You get a decrease in plasma glucose and brain won’t get enough glucose
Symp: confusion, disorientation, impaired judgement (can be dangerous if along)
Result in coma/death
need some sugar