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GIGU Exam 1 > Endocrine Pancreas - Dr. Rogers > Flashcards

Endocrine Pancreas - Dr. Rogers Flashcards

1
Q

CASE 1: 58yo m, BMI 31= Android -> midsection, (not hips and butt-> Gynoid)
rash under arm —-> Acanthosis Nigricans
Weakness, fatigue, irritable, foot ulcer not healing
Blurred vision at times
Elevated Fasting glucose and A1C
Elevated insulin and C-Peptide
Elevated BP, FAs

A

Metabolic Syndrome

Increased risk for = kidney, eye, liver NAFLD, vascular, heart problems, skin ulcers and wound healing

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2
Q

Major anabolic H

A

Insulin and secreted in response to CHO- and protein ingestion (glucose)

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3
Q

Endocrine Pancreas secretes

A

Insulin, Glucagon, Somatostatin
Lipid, carb, protein metabolism
In Islet of Langerhans
Innervation by adrenergic, cholinergic, and peptidergic neurons

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4
Q

What does B cells secrete

A

Insulin and C peptide

Destroyed in Type 1 diabetes

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5
Q

What does alpha cell secrete

A

Glucagon in the periphery of the islet of langerhans

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6
Q

What does g cells and F cells secrete

A

Somatostatin (looks like a neuron)

PP cells, pancreatic peptide, satiety signal = neuropeptide Y)

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7
Q

How are cells in the pancreas communicate

A

Tight junctions and depolarization
Blood supply comes into the middle of the islet so B cells get the most - release insulin, and later the insulin goes to the periphery of a cells to inhibit glucagon release

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8
Q

Steps to make insulin

A
  1. 2 chains peptide H. (Preproinsulin) = signal peptide A + B and C Peptide
  2. Proinsulin= C peptide and insulin in granules
  3. Insulin and C peptide
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9
Q

Insulin Resistance person

What is role of insulin

A

Type 2
Insulin tells adipose and muscle to take up glucose and store it
Insulin tells liver to stop making free glucose

This person has very high insulin and high glucose in blood

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10
Q

How is insulin released

A
  1. Glucose enters B-cell by GLUT2
  2. Glucokinase phosphorylates glucose
  3. G-6-P is oxidized = ATP made
  4. ATP closes K+ channels (prevent K+ to leak out= depolarization)
  5. voltage CA+2 channels open (Ca+2 enter cell)
  6. AP, insulin and C peptide inside viscose are released
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11
Q

What does Sulfonylurea receptors drugs do

A

Bind to the ATP-dependent K+ channel

Keeps K+ channel closed longer, to keep cell depolarized longer for Type 2 diabetics to release more insulin

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12
Q

For is Insulin Released on a graph

A

It is biphasic so there is a quick initial peak followed by a slow rise for 30-60min
Type 2 : no first peak

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13
Q

Insulin resistance happens first where

A

In the periphery, liver, muscle, fat

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14
Q

How does insulin cause glucose uptake

A
  1. Insulin binds to insulin receptor
  2. Phosphorylates, P13K,Akt,mTOR, MAP kinase
  3. GLUT 4 transporter is moved to plasma membrane of the cell
  4. GLUT 4 brings glucose into the cell (facilitated diffusion)
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15
Q

What happens in the cell during insulin resistance

A

MITOCHONRIAL OVERLOADING
Inhibits these chemical reactions to happen when insulin binds
= GLUT 4 does not move to the plasma membrane

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16
Q

What stimulates insulin release

A 
Glucose, ACh, CCK
Glucagon (just to modulate not too much glucose released), GIP, GLP-1
Cortisol, K, Vagal stimulation 
Sulfonylurea drugs
Obesity
17
Q

What inhibits the relates of insulin

A

Somatostatin, Exercise, NE, Hypoglycemia drugs

18
Q

Incretin Effect

A

HEALTHY: eat sugar and high increases in insulin

TYPE 2 progressively: eat sugar, GI does not absorb all and not a lot of insulin is released

19
Q

Insulin effect on K

A

Increased uptake into cells

20
Q

Exercise caused increased glucagon why

A

Becuz glucose is taken up without insulin = AMP-Kinase activated and causes GLUT 4 to move to plasma membrane
and that causes glucagon to be released to increase blood glucose
= Blood glucose stays about the same except in long distance

21
Q

Glucagon and glucose coming to the a-cell

A

The glucose comes to the a-cell
The cascade causes inhibition of Ca+2 voltage gated channels
This makes no depolarization or AP and no glucagon is released

Glucose——> g cell and causes somatostatin release

22
Q

What stimulates glucagon

A

ACh, high AA (alanine and arginine)

CCK, adrenerguc agents, Fasting

23
Q

What inhibits glucagon release

A

Somatostatin, FAs, Ketoacids

24
Q

Who is in risk of getting TYPE 2 diabetes

A

40% likely if one parent is
70% if both parents are
African Americans, Native Americans (10X higher), Hispanics

25
Q

Environmental cues that increase risk of type 2 diabetes

A

Excess calories,
Sedentary behavior
Rapid postnatal growth
Sleep deprivation
Chronic inflammation - adipose tissue recruits macrophages, that causes inflammation of the adipose and tell them to release cytokines (IL-6, TNF-a, IFN-g, CRP) + releases FAs + disrupts lepton and adipokines
Maternal disease- while baby is in the uterus

26
Q

Progression of Insulin Resistance

A
  1. Systemic resistance to insulin
  2. Reactive hyperinsulinemia = after meal you have high insulin, however normal blood glucose
  3. After eating you have high glucose , only fasting glucose is normal
  4. INCRETIN RELEASE
  5. Chronic elevated insulin
  6. Chronic elevated glucose
    =Hyperglycemia (5-30 years to go through all this)
27
Q

What happens first high insulin or high glucose in the progression of type 2 diabetes

A

High elevated insulin

28
Q

TX for T2D

A

Weight reduction, caloric restriction, PE(lower insulin)
Metformin- Biguanide drugs = make you more sensitive to insulin
Insulin Secretagogoues = makes you release more insulin
Slow CHO- absorption
Bariatric Surgery
*CONSTANT MONITORING IS REQUIRED of A1C

29
Q

T1D

A

B-cells destroyed by T-cells autoimmune = no insulin and no C-peptide
Sx: when 80% of b-cells are destroyed
Increased ketoacids, blood glucose

30
Q

Diabetic Ketoacidosis (DKA)

A

When you don’t uses ketoacids anymore

31
Q

T1D and K

A

Hyperkalemia, high K outside the cell
Low insulin = low Na/K pump
Plasma levels of K can be low due to increased thirst

32
Q

Diabetes and increased urine and thirst

A

Increased Glucose in the blood = water drawn into the kidney tubules and excreted
No reabsorption of water and electrolytes

33
Q

Development of T1D

A

Family history
30% if mom needs dad both has it
3-6% if one has it (higher if dad)

34
Q

Which gene is mutated in the T1D

A 
DQ2/DQ8 or DR3/DR4
Of HLA class 2 lack of Asp57
Most have other autoimmune problems
35
Q

Some environmental risk factors of developing autoimmune disorders that can cause T1D

A 
Early exposure to cow milk, not breast feeding 
VIT D deficiency 
Wheat gluten (Celiac Disease)
only few childhood infections
Obesity
Viral infections of mumps, rubella....
36
Q

When to take insulin for T1D

A

Depends on when you eat (you want to take before meal) and you need to consider if you exercised and if you’re going to exercise and other factors (cortisol)

37
Q

T1D Sx:

A

Ketosis (not is T2D)
Even more intensely elevated glucose
No insulin no C-peptide
More likely to have hyperkalemia

38
Q

Incretin effect

A

Food in GI causes Hs to be released that tell B-cells to release insulin, this is dysfunctional

39
Q

Initial spike of insulin in normal people causes

A

Prevents initial spike in glucose after eating

GIGU Exam 1 (19 decks)

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