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Summary ITM Block 1.6 Case 1-6

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This summary has case 1-6 of block 1.6, ITM, Maastricht University. These are the cases as given in 2015/2016. Topics include determinants for obesity and lifestyle, type 2 diabetes mellitus (including pathophysiology and treatment), glucose, fat metabolism, atherosclerosis, retinopathy, nephropath...

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  • June 26, 2016
  • 21
  • 2015/2016
  • Summary

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CASES BLOCK 1.6
Diabetes, Obesity and Lifestyle




26 JUNI 2016
MARIEKE DE JONG
ITM

,Case 1: Lazy, Greedy, Undisciplined and Obese.....................................................................................3
What is Obesity? ..................................................................................................................................3
Factors Involved in Obesity..................................................................................................................3
Biological ..........................................................................................................................................3
Psychological ....................................................................................................................................4
Cultural and Socioeconomic ............................................................................................................4
Determinants for Health and Behaviour .............................................................................................4
Views on Health ...................................................................................................................................4
Case 2: Death by Sugar? ..........................................................................................................................5
Type 2 Diabetes ...................................................................................................................................5
Metabolism and Calories .....................................................................................................................6
Blood Glucose ......................................................................................................................................6
Insulin ...............................................................................................................................................6
Glucagon ..........................................................................................................................................7
Case 3: Bubbling Brown Sugar? ..............................................................................................................8
Pathophysiology of Type 2 Diabetes ...................................................................................................8
Pathogenesis ....................................................................................................................................8
Pathophysiology ..............................................................................................................................9
High Blood Sugar..............................................................................................................................9
Treatment ..........................................................................................................................................10
Lifestyle ..........................................................................................................................................10
Drugs ..............................................................................................................................................10
Case 4: Inflamed Fat? ............................................................................................................................11
Metabolism of Fat ..............................................................................................................................11
Triglycerides ...................................................................................................................................11
Cholesterol .....................................................................................................................................11
Tissues ............................................................................................................................................12
Anabolism and Catabolism ............................................................................................................12
Disturbance of Fat Metabolism in Diabetes ......................................................................................13
Consequences of Fat Accumulation and Inflammation ....................................................................14
Case 5: How to Prevent Large Blood Vessel Disease ...........................................................................15
Cholesterol .........................................................................................................................................15
Atherosclerosis ..................................................................................................................................16
Types of Diabetes...............................................................................................................................17
Case 6: Organ Damage: How Do You Get It? .......................................................................................18
Microvascular complications .............................................................................................................18

1

, Retinopathy ...................................................................................................................................18
Nephropathy ..................................................................................................................................18
Neuropathy ....................................................................................................................................18
NASH ..............................................................................................................................................19
Bibliography ..........................................................................................................................................20




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, Case 1: Lazy, Greedy, Undisciplined and
Obese
What is Obesity?
WHO definitions:
- BMI ≥ 25: overweight
- BMI ≥ 30: obese
The definition of central obesity according to the International Diabetes Federation is a waist
circumference of over 80 cm for women and over 90 for men (94 in European men).
Obesity can be divided into different classes:
- Pre-obese: 25-29.9
- Obese Class I: 30-34.9
- Obese Class II: 35-39.9
- Obese Class III: ≥40
Asians have a higher percentage of body fat than Caucasians. This leads to an increase of obesity-
related illnesses in this group at a lower BMI than in Caucasians. For Chinese men and women, a BMI
cut-off for overweight of 23 is more accurate, with 25 for obesity. This is because the main risk-
factor for obesity-related disease is intra-abdominal fat. This develops earlier in Asians, even with
the same BMI and waistline as their Caucasian counterparts.
Some studies suggest that dark-skinned people have less body fat and more muscle than Caucasians.
This would mean a higher BMI is needed for the same risk increase for obesity-related illnesses.
In 2014, 1.9 billion adults were overweight, with 600 million of them obese. This makes 39% of the
adult population overweight, and 13% obese. Men are relatively more overweight while women are
more obese in the developed world. One important thing to remember is that two people with the
same BMI can easily have a different percentage of body fat.
In 2015 in the Netherlands, 43% of people were overweight, and 11.6% obese.
In developing countries, obesity is rising 30% faster than in the developed world.
High BMI is a risk factor for cardiovascular disease, diabetes, musculoskeletal disorders and
endometrial, breast and colon cancer.

Factors Involved in Obesity
Biological
Genetic predisposition plays a role in obesity. Currently identified genes only cause a 5% variance in
body weight.
Obesity arises from a persistent positive energy balance. The body has compensation mechanisms,
but they generally only buffer small energy surpluses and deficits that are present for a short time. In
addition, they are more capable of handling deficits than surpluses.
Physical activity is also very important for prevention of obesity. As our food intake has increased
and our physical activity went down, this caused issues.
Intrauterine imprinting happens when a mother is malnutritioned, has diabetes, or smokes. This
increases the chance of obesity later in life.
Increased dopamine or dopamine receptors lead to a greater feeling of satiety. This leads to less
overeating and a smaller risk of obesity.
Leptin deficiency can be congenital. It leads to extreme hunger and, due to overeating, obesity.




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