Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology > Obesity > Flashcards

Obesity Flashcards

1
Q

Where does our energy intake come from?

A

Food specifically proteins, carbs, fats and alcohol

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

What are the three main health conditions associated with being overweight or obese?

A

Diabetes
Cancer
Cardiovascular disease

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

What is the role of the hypothalamus in energy homeostasis?

A

The hypothalamus is essential in control of energy homeostasis and it exerts is effects via neuronal or humoral mechanisms.

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

Which system controls energy homeostasis?

A

Central Nervous System

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

What are the three divisions of energy expenditure?

A

Thermogenesis
Digestion and absorption
ATP (often used for physical exercise)

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

When does obesity occur?

A

When the energy intake is greater than the energy expenditure

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

What are the three neurotransmitters released from the hypothalamus during energy homeostasis?

A

5-HT
Norepinephrine
Neuropeptide Y

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the role of leptin in energy homeostasis in application to obesity.

A

In obesity there are increased deposition within adipose tissue, therefore an increased number of fat cells. Leptin is expressed on fat cells therefore there is an increased expression of Leptin and insulin.
This decreases expression of two neurons Neuropeptide and Agouti-related peptide. In addition to increasing expression of pro-opiomelanocortin which increases activation of a-melanocyte stimulating hormone. This increases activation of the anorexigenic pathways which reduces food intake and increases the energy expenditure resulting in a reduction of the number and size of the fat cells resulting in weight loss.

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

When is it appropriate and not appropriate to administer recombinant leptin?

A

If there are Leptin deficiencies, administrating Leptin can then trigger the cascade in energy homeostasis, reducing the number and size of fat cells and therefore causing weight loss.
However if there are in mutations in the Leptin receptor recombinant therapies are not appropriate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some examples of how Leptin resistance can occur?

A

Defect in synthesis
Carriage in circulation
Transport into CNS
Defects in leptin receptors or postreceptor signalling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Does Leptin deficiency, mutations in the receptor or Leptin resistance contribute to the most cases of obesity?

A

Leptin resistance where the brain no longer responds to leptin so patients keep eating despite the fat stores, almost becomes desensitised.

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

Describe the basal metabolic rate.

A

The basal metabolic rate is the total amount of energy expended by the body to maintain basic physiological functions over a 24 hour period.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Who has a higher basal metabolic rate males or females?

A

Males

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

How is basal metabolic rate measured?

A

The subject lies at rest in a warm environment and it is typically measured 12 hours after having a meal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does basal metabolic rate change with age?

A

Usually peaks around puberty but then decreases with age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe meal induced thermogenesis?

A

It is the change in metabolic rate following a meal due to digestion. Normally this occurs over five hours and accounts for 10% of energy intake.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How much of the energy intake is left for physical exercise expenditure?

A

20-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the inheritability rate of obesity?

A

30-40%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the main gene disorders that links to obesity?

A

B3-adrenoreceptors and glucocorticoid receptor mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What BMI are you considered overweight?

A

25-29.9

21
Q

What BMI are you considered obese?

A

Above 30

22
Q

What BMI are you considered underweight?

A

Below 18.5

23
Q

What are the three main health concerns that arises due to obesity?

A

Sex hormone imbalance
Increased free fatty acids
Mechanical stress

24
Q

What are some complications of the sex hormone imbalance?

A

Hormone dependent tumours such as breast cancer

25
Q

What are some complications of increased fatty acids?

A

Leads to metabolic syndrome
Hypertension
Dyslipidemia
Type 2 diabetes melluitis

26
Q

What are some complications of mechanical stress?

A

Sleep opnea (struggling to breathe when asleep)
Osteoarthritis
Lower back pain
Shortness of breath

27
Q

What are the three main drug targets to tackle obesity? Provide an example for each.

A

Appetite suppression- methylcellulose
Decreasing absorption- Orlistat
Increasing metabolism

28
Q

Describe the process of triglyceride absorption.

A

Firstly triglycerides are emulsified into micelles by bile salts (large lipid globules are broken into small lipid globules).
Pancreatic lipase hydrolyses the ester linkeage within the triglyceride forming fatty acids and glycerol.
Small chained fatty acid are absorbed into the blood via capillaries however long chain fatty acids and monoglycerides form back into triglycerides in the cell.

29
Q

Why are pancreatic lipase inhibitors a good drug target?

A

Prevents the hydrolysis of triglycerides preventing absorption of fats into the cell.

30
Q

By what mechanism does pancreatic lipase act?

A

Pancreatic lipase contains a serine residue in its active site and acts through the same mechanism as other serine proteases and serine esterases.

31
Q

How is the serine residue activated in the active site of lipase?

A

Deprotonation of neighbouring amino acid residues

32
Q

What makes a good serine protease inhibitor?

A

Placing an electrophilic group in close proximity to the nucleophile.

33
Q

Why is lipstatin a irreversible inhibitor?

A

Forms a stable acylserine intermediate, hydrolysis requires 24hrs for water to release the fatty acid.

34
Q

What was one of the problems with lipstatin?

A

It was prone to oxidation on storage due to the unsaturated fatty acid chain. Hydrogenation removed this problem- becomes saturated.

35
Q

Why is orlistat’s poor bioavailability actually beneficial?

A

The drug does not need to be absorbed systemically as it acts on lipase active site. If it absorbed systemically it would cause unwanted side effects.

36
Q

What are the two methods of Orlistat synthesis?

A

Semi-synthetic: fermentation of lipstatin and then hydrogenation
Totally synthetic: Roche process starting from simple starting materials- gives higher purity.

37
Q

Which patients are eligible for Orlistat?

A

Those with a BMI greater than or equal to 30 or greater than or equal to 28 with health risks.
It is endorsed by NICE to be given free to patients who lose 2.5kg by dieting and exercise a month prior to start of the prescription.

38
Q

What is the daily dose of Orlistat?

A

120mg three times a day, to be taken before meals.

39
Q

What are some of the side effects of Orlistat?

A

GI side effects including wind, faecal incontinence and steatorrhea due to bacterium consumed lipids when absorption is reduced.

40
Q

Describe the signalling mechanism for melanocortin.

A

Serotonin binds to 5-HT2c receptor on the GPCR pituitary gland. This stimulates POMC which is subsequently cleaved to form a-melanocyte stimulating hormone which binds to a GPCR.

41
Q

What is an example of a 5-HT2c agonist?

A

Lorcaserin but was withdrawn due to increased risk of cancer.

42
Q

Describe the mechanism of rimonabant.

A

It is an inverse agonist for the CB1 GPCR receptors in the brain. Withdrawn due to side effects.

43
Q

Why was Fen/Phen combination therapy withdrawn?

A

Fenfluramine is linked to hypertension and causes heart valve disease due to activating the 5-HT2c receptor.

44
Q

How does the phentermine/topiramate combination work?

A

Topiramate is an anti-convuslant so has multiple CNS mechanisms.
Phentermine is amphetamine-like, agonist of the trace amine-associated receptor 1 (TAAR1).

45
Q

How does the Bupropion/naltrexone combination work?

A

Bupropion is a norepinephrine-dopamine
reuptake inhibitor whereas naltrexone is an opioid receptor antagonist.

46
Q

Which antidiabetic drugs are considerations for anti-obesity?

A

GLP-1 agonists analogues semaglutide and liraglutide which retain activity but with fatty acid conjugation that promotes binding to serum albumin.

47
Q

What is the mechanism of setmelanotide?

A

Acts on the melanocortin receptor as mutations in this receptor are the most common link to obesity.

48
Q

What are some of the other anti-obesity drug developments?

A

Neutral CB1 antagonists (not inverse agonists)
Increasing cGMP signalling in the adipose tissue by PDE5 inhibitors
Combinations of peptide hormone and CNS active drug
Influence of drug microbiome on morbidity

Endocrinology (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions