Obesity and diabetes Flashcards

1
Q

Explain how carbohydrates, proteins and triglycerides are absorbed.

A
  • The intestines breakdown these three macromolecules into micronutrients; proteins become amino acids, triglycerides become glycerides and fatty acids and carbohydrates become glucose
  • These nutrients are taken into liver by the portal vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Explain the process of cellular respiration

A

Glycolysis
• Glucose is a 6 carbon molecule
• This is broken down into two 3 carbon molecules called pyruvate
• ATP is produced

Oxidation
• When oxygen is present, the two pyruvate molecules enter the mitochondria
• Each pyruvate molecule is converted into acetyl- CoA by NADH (oxidised)
• H electrons from each pyruvate are transferred to NAD, reducing it to NADH
• A carbon is lost, forming Co2

Krebs cycle
• Acetyl CoA bins with a 4 carbon molecule called oxaloacetate
• A series of enzymatic reactions take place
• Many NADH/ transport carriers are formed

Electron transport chain
• High energy electron carriers (NADH) from the previous stages bring their electrons to the transport chain
• The electron carriers bind to transport proteins, releasing their electrons into the mitochondrial intermembrane space
• These ions flow back into the mitochondria through a ATP synthase enzyme
• The energy yielded from the ions flowing into the enzyme enables ADP to be phosphorylated into ATP.
• 32 - 38 ATP are created
• This is done in the presence of oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Explain how fats and proteins are able to participate in cellular respiration when glucose reserves are depleted

A

Fats as fuel:
• Triacylglycerol are stored in adipose cells
• Lipases break the glycerol head away from the fatty acids.
• Glycerol is converted to an intermediate in glycolysis called “PGAL”, and enters cellular respiration in the cytoplasm.
• The fatty acid tails are converted to Acetyl CoA and enter the Krebs cycle in the mitochondria

Proteins as fuel:
• Proteases break down proteins into amino acids
• Deaminases break the amino group from the amino acid, releasing ammonia
• The remaining amino acids molecules can be rearranged to become a pyruvate, acetyl CoA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define Metabolic Syndrome

A

Isa clustering of at least three of the five following medical conditions: central (abdominal) obesity, hypertension, high blood glucose, high serum triglycerides and low serum HDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Explain the role of adipocytes in the development and pathophysiology of MetSy

A

Adipose tissue
• Composed of adipocytes, cells that store energy as fat
• Adipocytes are regarded as endocrine organs. They synthesise and release adipokines

Proinflammatory adipokines
• Some pro-inflammatory adipokines include leptin, resistin, TNF and IL- 6. These induce chronic inflammation, promote insulin resistance and thus contribute to metabolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Explain the role of the following in MetSy:

* Obesity and hypertension

A

• Excess food intake/ genetics/ being sedentary leads to adipogenesis = overweight
• Being overweight forces the heart to work faster which wears the endothelium of vessels quicker
• This leads to hypertension
With vessel damage, the SNS is activated causing vasoconstriction and sodium retention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Explain the role of the following in MetSy:

* Insulin resistance

A
  • Being overweight leads to excess insulin production. Overtime, the body becomes desensitised to insulin
  • This places stress on the pancreas causing damage
  • When adipocytes develop insulin resistance, they can no longer take up glucose and free fatty acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Explain the role of the following in MetSy:

* Hyperlipidaemia

A

• Excess circulating free fatty acids are redirected to the liver
• The liver also makes its owns lipids through lipogenesis
• This results in elevated triglyceride levels
= Cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the health impacts of obesity

A
  • Hypertension
  • High LDL cholesterol, low HDL cholesterol
  • Type 2 diabetes
  • Coronary heart disease
  • Stroke
  • Gallbladder disease
  • Osteoarthritis
  • Sleep apnea and breathing problems
  • Low quality of life
  • Mental illness such as clinical depression and anxiety
  • Body pain and difficulty with physical functioning
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Diagnose MetSy using the most appropriate risk factor criteria

A
  • Central obesity plus any two of the following four factors: high triglycerides, high blood sugar, hypertension and reduced HDL cholesterol
  • Can use BMI or body fat distribution methods
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the ranges of BMI?

A

BMI=Weight/Height
• Normal range 18.5 – 24.9
• Overweight 25 – 29.9
• Obese >30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

List the limitations of BMI

A
  • Doesn’t factor in body fat distribution
  • Doesn’t consider ethnicity
  • Cannot accurately provide an indication of intra- abdominal adiposity
  • Does not differentiate between fat and lean body mass. For example, an athlete with a large amount of muscle mass could fall into the overweight category
  • Age and gender: women tend to have more body fat than men, older people have more fat than children
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe how body fat distribution is assessed

A
  • It focuses on the amount of central fat

* It involves measuring waist circumference and hip circumference and assessing which ranges the individual falls into

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

List the functions of the exocrine and endocrine pancreas

A
  • Exocrine pancreas: digestive enzymes released into the GIT

* Endocrine pancreas: releases hormones into the bloodstream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
List the names of the following pancreatic islelts:
• α – cell
• β – cell
• δ – cell
• γ – cell
A
  • α – cell: glucagon
  • β – cell: insulin (most abundant)
  • δ – cell: somatostatin
  • γ – cell: pancreatic polypeptide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Explain the roles of insulin, somatostatin and pancreatic polypeptide

A

Insulin
• Hormone that allows glucose can be taken up by cells

Somatostatin
• Inhibits insulin and glucose release

Pancreatic polypeptide
• Plays a role in appetite and ion transport within the intestine

17
Q

Explain the role of glucagon, and define the following:
Glycogenolysis
Gluconeogenesis

A
  • Glucagon works to increase blood sugar levels, opposing the work of insulin
  • It stimulates the liver to convert its stores of glycogen back into glucose = glycogenolysis
  • It stimulates the liver to take up amino acids from the blood and convert them into glucose = gluconeogenesis
  • It stimulates lipolysis, the breakdown of stored triglycerides into free fatty acids and glycerol.It may travel to the liver and be converted to glucose
18
Q

Understand the effects thiazides, epinephrine/ sympathetic activation and anti- covulsants have on insulin

A

They reduce the amount of insulin released

19
Q

Describe the association between stress and hyperglycaemia

A
  • Stress causes the release of adrenaline and cortisol/ growth hormone
  • Adrenaline: promotes glycogenolysis which is the breakdown of glycogen into glucose = increase of blood glucose
  • Cortisol/ growth hormone: makes fat and muscles cells resistant to the effect of insulin and enhances the production of glucose in the liver
20
Q

List the oral manifestations of diabetes

A
  • Narrowing of the blood vessels = reduce blood supply to the gums
  • Increased the risk of infection
  • High chances of periodontal disease
  • Low saliva
  • Dry mouth -> increase plaque and tartar
  • Caries and periodontal disease
  • An increase of sugars in the gingival fluid = caries
  • Impaired immune system disease, fungal infection etc
  • Delayed soft tissue healing – impairments in growth factor expression, impair angiogenesis and matrix formation, poor collagen formation, prone to infection
  • Ketoacidosis: halitosis
  • Peripheral neuropathy oral paraesthesia (burning mouth syndrome) and altered taste sensations
21
Q

List complications that can arise due to:
Type I diabetes
Type II diabetes

A

Type I diabetes
• Diabetic ketoacidosis

Type II diabetes
• Hyperosmolar coma
• Macrovascular and microvascular changes

22
Q

Describe diabetic ketoacidosis

A

• An extreme metabolic state where blood sugar is very high and acidic substance called ketones build up in the body

23
Q

Describe hyperosmolar coma

A

Characterised by high blood and dehydration

24
Q

Describe the macrovascular and microvascular changes associated with type II diabetes

A

Macrovascular:
• Heart disease
• Stroke

Microvascular :
• Nephropathy
• Retinopathy
• Neuropathy, foot ulcers

25
Q

List the effects of insulin on the:
Liver
Adipose tissue
Muscles

A

Liver
• Glycogen synthesis
• Increased protein synthesis
• Increased lipid synthesis

Adipose tissue
• When the liver is has taken up its capacity of glycogen, insulin signals fat cells to take up glucose to be stored as triglycerides.
• Decreased lipolysis

Muscles
• Increased glucose entry
• Increased glycogen synthesis
• Increased amino acid uptake
• Increased protein synthesis in ribosomes