Diabetes

Question 1

WHat is neuroglycopenia?

Answer 1

Symptom of extremely low blood sugar in which the patient will present with:

• headache
• confusion
• slurred speech
• seizures
• coma
• death

Question 2

What role do cortisol, norepi/Epi, and glucagon play in glycogenolysis? Gluconeogenesis?

Answer 2

Glycogenolysis — cortisol plays no role

• – norepi/Epi plays a huge role
• – glucagon plays a moderate role

Gluconeogenesis — cortisol plays a moderate role

• – norepi/Epi plays no role
• – glucagon plays a moderate role

Question 3

Wh should you do in a case of insulin induced hypoglycemia?

Answer 3

If mild, eat carbs (high glycemic index carbs)

If severe, administer glucagon subcutaneously or intramuscularly

Question 4

At what times points is your body getting glucose from where?

Answer 4

The first few hours, the glucose you have in you is from your diet.

After a little while of not eating, your glycogen stores begin to get used up and can last you about 18 hours.

Then gluconeogenesis will take over in the liver where it gets what it needs from AAs, glycerol, and lactate.

Question 5

How does the body’s metabolism change after the first 24 hours into fasting?

Answer 5

1) we already said that gluconeogenesis will increase in the liver and kidneys in order to generate glucose for the brain and erythrocytes
2) most of the energy will come from fatty acids as the primary fuel source. This way all the glucose that is Left will go to the brain and erythrocytes.
- – we know that FAs can’t get made into glucose. However, they can be broken down to makes energy AND they can be made into ketone bodies. This becomes increasingly important the longer you are starving. .

Question 6

What is the difference in blood glucose when glucagon, Epi, and cortisol are released?

Answer 6

When all three are released it is more than just an additive affect but rather when they are all secreted together it is an exponential increase in the blood glucose levels.

Question 7

WHy is visceral fat so much worse for you?

Answer 7

They have inflammatory markers
Release FFAs
Secrete adipokines

• these three will lead to dyslipidemias, insulin resistance, and inflammation

Question 8

Why will FFAs released from the pancreas cause metabolic issues?

Answer 8

It will not allow insulin to be secreted from the pancreas, which will decrease glucose uptake in the muscle. It will increase gluconeogenesis because the glucagon:insulin ratio will be high. Also, the fat cells won’t take in glucose if there is insulin insensitivity.

Question 9

Anti-hyperglycemic hormones

Answer 9

Leptin

Adiponectin

Question 10

Pro-hyperglycemia

Answer 10

Resistin

Question 11

How do the three adipocyte hormones affect glucose homeostasis?

Answer 11

If you have decreased secretion of Leptin and Adiponectin you will have increased glucose levels. As is for increased Resistin secretion.

• Leptin and Adiponectin will activate AMPK, which increase glucose uptake, glycolysis, beta oxidation, lipolysis, and it will inhibit Free fatty synthesis.
• Resistin inhibits this pathway.

Question 12

What else Can Leptin do ?

Answer 12

We learned that it goes to the brain and causes satiety and reduced food intake.

Question 13

Incretins

Answer 13

Molecules that cause a release of insulin even before blood sugar rises.

• CCK
• GLP-1
• GIP

Question 14

What blood sugar do you consider diabetic?

Answer 14

Greater than 126

Question 15

Why is HbA1c a good indicator of blood glucose?

Answer 15

Because RBCs last 120 days.

Question 16

How does HbA1c occur?

Answer 16

Non-enzymatic glycosylation of Hb.

Question 17

What is sorbitol?

Answer 17

It is actually responsible for most of the symptoms of diabetes.
The organs that don’t have insulin dependent transporters get a lot of glucose if they are hyperglycemic. The glucose will get converted by aldose reductase to sorbitol. Sorbitol is osmotically active so it will bring a lot of water into the organs and make then swell.
- causes nephropathy, neuropathy, and lens of the eye issues.

Question 18

Type 1 diabetes

Answer 18

• Autoimmune attack of pancreatic beta cells.
• Sudden onset of an absence of pancreatic production and secretion of insulin.
• Sudden weight loss
• hyperglycemia
• hypertriglyceridemia
• ketoacidosis
• polydipsia (thirst), polyuria, polyphagia (hunger)
• overproduction of glucagon
• glucose in urine

Question 19

Why does Type I diabetes cause hypertriglyceridemia ?

Answer 19

Because insulin regulates LPL levels. If you don’t have insulin you won’t have enough LPL.

Question 20

Why do you pee so much if you have Type I diabetes?

Answer 20

Ketoacids are osmotically active so the increase will cause you too pee

Question 21

What is responsible for most of the initial weight loss?

Answer 21

Loss of water weight due to excessive peeing.

Question 22

What is the difference with regards to ketoacidosis in Type I and Type II

Answer 22

You will only really see ketoacids in Type I if they are not taking. Their insulin You will never see it in Type II

Question 23

In what situation would you put your patient in standard insulin therapy instead of intensive?

Answer 23

If your patient is a growing child because the risk of having low blood sugar can have detrimental affects on a growing child so they only do standard and err on the side of having higher blood glucose levels.

Question 24

standard insulin therapy vs. intensive

Answer 24

8-9% target HbA1c for standard
7% target HbA1c for intensive

Intensive - 3 or 4 injections daily

• reduces risk of many long term diabetic complications
• but hypoglycemic events are much more likely, which is why we don’t use intensive therapy on children

Question 25

Type 2 diabetes

Answer 25

Plenty of insulin but target organs are not responding

No ketoacidosis
Hyperglycemia
Hypertriglyceridemia
Gradual onset

Treatment: diet and exercise

Question 26

Why is obesity a risk factor for Type II diabetes?

Answer 26

A normal person and obese person will start off with the same blood glucose levels. However, in order to maintain this level the obese person will have to secrete a whole lot more insulin than the normal person. Over time their insulin receptor no longer react to the insulin and blood glucose will climb.

Question 27

Abarcose

Answer 27

Inhibits absorption of glucose by intestinal cells.

Question 28

Sulfonylureas

Answer 28

Bind to ATP -sensitive K channel and therefore causes depolarization of the beta-cell membrane to be longer. This then causes Calcium channels to open and insulin to be released.
- bottom line is that it causes more insulin to be released.

Question 29

Metformin

Answer 29

Inhibits gluconeogenesis. Inhibits OxPhos at complete 1. No ATP = no gluconeogenesis.

Question 30

DPP-4 inhibitor

Answer 30

Enhances Incretins levels, which stimulate the release of insulin from beta cells.

Question 31

SGLT2 inhibitors

Answer 31

Block the reabsorption of glucose In the kidney, which can increases glucose excretion and lowers blood glucose levels.