MetS Flashcards

1
Q

What is MetS

A

“… a constellation of metabolic abnormalities that confer increased risk of
cardiovascular disease and diabetes mellitus.”
Major features: central (visceral) obesity, hypertriglyceridaemia, low high- density lipoprotein (HDL), hyperglycaemia and hypertension.

Broadly speaking a disruption of energy metabolism.

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2
Q

What is its importance

A
  • Diabetes and its complications
  • Vascular disease: cardiac and cerebral
  • Non-alcoholic fatty liver disease -> Non-Alcoholic steatohepatitis
    and cirrhosis
  • Hyperuricaemia and gout, and its complications
  • Polycystic Ovary Syndrome (PCOS) and infertility
  • Obesity associations: stigma, obstructive sleep apnoea,
    musculoskeletal damage, etc..

Note that the doctor’s attitude towards the patient will have a profound effect on success on intervention.

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3
Q

What is its prevalence and relationship to NCDs

A

Our conceptual understanding of MetS is evolving.

The prevalence varies across different populations and depends on the criteria used in different definitions.
- in some studies there is a marked gender difference
- some highlight key regions eg EasternMed and Ams
- some indicate wealth of nation is correlated (in studies of children, not so much)
MetS is an outcome of risk factor clustering, but MetS itself is also an exposure/risk factor for NCDs.

Note: clustering provides an oppportunity for intervention

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4
Q

Describe the evolution of the definition

A
  • The underlying diagnostic controversy is mainly between the role/association of ‘insulin resistance’ and ‘central obesity’ in increased CVD and
    type 2 risk.
  • Giving rise to two viewpoints explaining Mets as either being ‘Obesogenic’ or ‘Glucogenic’ in nature
    From an early recognition of clustering risk factors to syndrome ‘x’ and finally MetS, itself shifting from a glucogenic to obesogenic model.

Evolution also stems from assessing whether the definition
- works when applied at the population level
- is it explaining the observed trends?

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5
Q

Describe the harmonised METS definiton and its value

A

**
- requires a minimum of 3 of 5
- elevated waist circumference: population specific i.e. accounts for gender and race
- elevated triglyceride levels or drug treatment for elevated TGs: >1.7
- reduced HDL-C or drug treatment: <1 in men, <1.3 women
- elevated BP (“): >130 sys, >85 dias
- elevated fasting glucose (“): >5.5
- more clinically useful due to accounting for population variation AND cut-offs
- also helps patient assess risk for CVD etc

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6
Q

Discuss the role of fat in MetS aetiology

A

Adiposity location is key in MetS aetiology
Two key adiposity locations/distributions in the body.

  1. Subcutaneous
  2. Visceral - behaves differently
    Others-bone marrow/musculature/breast
    etc

Pathogenic adipose tissue
- an indicator of a whole body maldistribution/deposition issue
- fat cells increase in size and change their behaviour e.g. releasing inflammatory cytokines
- overall effect on glucose metabolism , hypertension, dyslipidemia
- ultimately culminating in atherosclerosis and vascular damage
### Visceral fat to metabolic syndrome
- a dynamic system with inter-individual variation
- the mix of consequences results in insulin resistance and other outcomes

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7
Q

Describe broadly how appetite is control

A
  • mainly coordinated by nerves, metabolites, hormones, neurotransmitters to regulate feelings of hunger and satiety
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8
Q

Describe how some internal factors contribute to obesity

A

Internal
- 30% genetic
- 70% other: psychological state, informing behaviour
- in total influencing appetite and metabolic rate to a lesser extent, in turn determining fat stores and body weight set point

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9
Q

Describe how external factors contribute to obesity

A
  • environmental triggers for genes
  • diet (high caloric, nutrient poor)
  • habits e,g what to eat and how much
  • physical activity
  • culture and family
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10
Q

Describe the social and commercial determinants of metabolic risk factors

A

Social determinants
- medicines influencing weight gain and appetite regulation
- prenatal exposures
- environmental chemicals and endocrine dysruption
- food marketing and advertising
- trauma
Commercial determinants
- ads, lobbying, social media etc
- defined as the systems practices and pathways through which commercial actors contribute to health and equity, either positively or negatively
- contribute to GBD: 36% of total death, 45% NCDs
Colonisation
- infleunces family trauma and reach of industry in turn influencing SDH and CDH

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11
Q

Provide examples of preventioon

A

Prevention model: levels of prevention
- primordial
- aims to prevent exposure
- acts to prevent obsesogenic environment
- e.g. better government regulation of commercial entities
- primary
- aims to minimise exposure
- acts to reduce unhealthy food choices and promote physical activity
- e.g. general mental and social well-being interventions, promote more active lifestyles and healthy eating, good antenatal care
- secondary
- aims to reduce impact from exposure
- acts to screen, early diagnosis, treatment for MetS
- e.g. annual or regular health checks including BP and waist circumference, child growth monitoring, assist to prevent further weight gain and encouraging a little weight loss, use of meds and surgery to support weight loss, treatment for identified conditions
- tertiary
- aims to reduce effects from impact
- acts to detect complications early and treat earlt
- e.g. treatment guidelines for NCDs, close clinical monitoring

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