T2 L13: Hypoglycaemia

Question 1

What is hypoglycaemia defined as?

Answer 1

Blood glucose below 4mM

Question 2

What causes sweating, tachycardia, and agitation?

Answer 2

The activation of the sympathetic nervous system and release of adrenaline and glucagon

Question 3

At what [blood glucose] does a person loose consciousness?

Answer 3

2.5 mM

Question 4

How does alcohol cause hypoglycaemia?

Answer 4

It puts stress on gluconeogenesis as metabolism of alcohol is an unregulated process

Question 5

Which enzyme matabolises ethanol?

Answer 5

Alcohol dehydrogenase but the reaction requires NAD+ as a co-enzyme

Question 6

How is a high NADH:NAD+ ratio achieved in the mitochondria of hepatocytes during alcohol metabolism?

Answer 6

The enzyme alcohol dehydrogenase used to metabolise alcohol uses NAD+ as a co-enzyme so a lot of NADH is produced as a result

Question 7

Which enzyme oxidises acetyl aldehyde into acetate?

Answer 7

Aldehyde dehydrogenase

Question 8

What is the metabolic significance of NADH being oxidised for alcohol metaolism?

Answer 8

It means there are less substrates for gluconeogenesis

Question 9

When does alcohol-induced hypoglycaemia develop?

Answer 9

When someone ingests ethanol while their body is reliant on gluconeogenesis

Question 10

What is the mechanism behind alcoholic fatty liver?

Answer 10

High levels of NADH in the liver inhibit fatty acid oxidation. The NADH signals stimulate fatty acid synthesis causing an accumulation of triglycerides

Question 11

What are the 3 stages of fatty liver disease progression?

Answer 11

1. Steatohepatitis (The liver becomes inflamed and causes damage)
2. Fibrosis occurs
3. Cirrhosis

Question 12

What are the 2 consequences of acetyl-CoA accumulation caused by alcohol consumption?

Answer 12

1. Production of ketone bodies which exacerbate acidosis

2. Processing of acetate in the liver becomes insufficient so there is a buildup of acetylaldehyde

Question 13

What is the protein mechanism behind alcoholic hepatomegaly?

Answer 13

Alcohol decreases activity of proteasomes leading to accumulation of proteins and therefore enlargement of the liver.

Question 14

What causes nutritional deficiencies in alcoholics?

Answer 14

Malnourishment, Ethanol interferes GI absorption, hepatic dysfunction

Question 15

What is the half-life of thiamine?

Answer 15

10-20 days

Question 16

What % of alcoholics will have a vitamin B1 (Thiamine) deficiency?

Answer 16

50%

Question 17

What effect do glycogen storage diseases have on glycogen?

Answer 17

Abnormal amount or abnormal type of glycogen are produced

Question 18

What is Type 1 (Von Gierke’s disease)?

Answer 18

A deficiency of glucose-6-phosphate resulting in high G-6-P in liver and kidneys and impaired export of glucose from the liver. Causes hypoglycaemia that doesn’t respond to glucagon. Symptoms will appear during fasting when the body relies on liver glucose

Question 19

What is Type 2 (Pompe’s disease)?

Answer 19

A deficiency in alpha-1,4-glucosidase activity in lysosomes. Causes death by cardiorespiratory failure

Question 20

What is Type 3 (Cori’s disease)?

Answer 20

Deficiency in amylo-1,6-glucosidase (debranching enzyme) resulting in hypoglycaemia. Symptoms often appear at puberty

Question 21

What is Type 4 (Andersen’s disease)?

Answer 21

Liver glycogen is in normal amounts but is unbranched making it not very soluble. Sufferers don’t live beyond 5 years

Question 22

What is type 5 (McArdle’s syndrome)?

Answer 22

Affects muscle glycogen phosphorylase so muscles cannot break down glycogen . Sufferers have a low tolerance for exercise and fatigue easily, with painful muscle cramps but have a normal life-span