Week 7 & 8: Met Syndrome

Question 1

What is Metabolic Syndrome?

Answer 1

Is a cluster of the most dangerous heart attack risk factors

• Twice as likely to die and 3 times as likely to have a heart attack or stroke.
• 5 times greater risk of developing T2D

Slide 8 of Week 7

Question 2

How do you Define Metabolic Syndrome?

The IDF definition

Answer 2

Person MUST HAVE Central Obesity (based on waist circumference with ethnicity specific values)

Plus any TWO of the following
1. Raised Triglycerides: <1.7mmol/L
2. Reduced HDL: < 1.03 males, <1.29 females
3. Raised Blood Pressure
4. Raised fasting plasma Glucose

Why do we care? Remember –> they have 5x risk of developing diabetes

Slide 10 in Week 7

Question 3

What are the Ethnic Waist Circumference Values?

Answer 3

Europids
Male: ≥ 94cm
Female: ≥ 80cm

Non European
Male: ≥ 90cm
Female: ≥ 80cm

Question 4

What is the best way to measure insulin resistance?

Answer 4

OGTT
This test looks overtime, what is the insulin doing to get the BGL below the cutoff

If the Insulin levels are getting really high to maintain the BGL –> is a sign of insulin resistance

Fasting glucose shouldnt be used to measure insulin levels

Slide 10 of Week 6 (Lizz explains it verbally)

Question 5

What is Atherogenic Dislipidemia?

Answer 5

Is the lipid profile that leads to atherosclerosis

Combination of:
- Raised TG
- Low HDL
- Elevated Apolipoprotiein B
- Small Dense LDL
- Small HDL particles

All of which are independently atherogenic

Slide 14 of Week 7

Question 6

Prevalence & Incidence of Metabolic Syndrome

Answer 6

Nearly 1/3 of populations have Met Syndrome in 2011-2012

almost 1/4 of Aus has been diagnosed with Met Syn

As we age these rates increase (particularly around 55-65 Years old)

rates higher in men

Waist circumference is higher –> greater risk of developing met syndrome

Slide 16 - 19 of Week 7

Question 7

Why do we care about metabolic syndrome?

very very important

Answer 7

If we know people are going to have disability, cognitive impairment OR depression
→ all of which are likely to lead to parkinsons or dementia
→ this will have an impact or burden on the society at a greater scale

increased components of Met Syn = increased risd of CV mortality rate

before blood glucose levels are high enough for a diabetes diagnosis, hyperglycaesmia and increased triglycerides, decreased HDLc, all increase risk of CVD

Slide 20 and 24 in Week 7

Question 8

Can a patient be diagnosed with Met syndrome if they dont have insulin resistance?

Fran expressed belief on 2/06/2024

VERY VERY IMPORTANT

Answer 8

Yes; a patient does NOT have to have insulin resistance to be diagnosed with met syn, according to the International Diabetes Federation (IDF) definition

insulin resistance is a causative factor that can lead to met syn

Question 9

Relate how physical inactivity and Excess energy intake can lead to metabolic Syndrome

NOTE: ITS COMPLEX!!!!

Answer 9

Sarcopenia
As you begin to lose muscle there is a subsequent increase in insulin resistance (No GLUT4 Translocation to the membrane)

Visceral Obesity (VO)
Ageing can cause increase in VO –> increase in VO can drive an inflammatory state (refer week 6 lecture) which contributes to insulin resistance

Insulin resistance means the tissues are subsequently impacted causing:
1. Impaired muslce glucose uptake
2. No inhibition of hepatic Gluconeogenesis
3. Impaired smooth muscle relaxation
4. Increase plasma Triglycerides

~**All this leads to Metabolic Syndrome!!**~

Refer slide 27 of Week 7

Question 10

What are the 3 ways our body’s cholesterol can be changed?

Think of relation to dyslipidemia

Answer 10

HDL (scavanger molecule) [diet]
- Picks up cholesterol sitting in tissues and redelivers to places that need it
- Is important for maintaining cell membrane in ALL CELLS
- Exercise increases HDL activity and therefore reduces poor cholesterol

Endogenous Pathway [internal to body]
- Excess LDL –> the body says we have too much and breaks it down
- Causes the foaming up and resulting in plaque
- Genetic can result in less reuptake of LDL in the liver and go down a destorying pathway and putting more in the blood stream and contribute to plaque build up

Exogenous [diet]
- Food is consumed and absorped into the bowl and taken up by chylomicrons
- This then allows for reuptake into the liver
HOWEVER!
- in genetic disorders the chylomicrons are not reuptaken into the liver
- meaning its floating around in the blood and sticks to things (e.g. blood vessel wall)

Slide 44 of Week 7

Question 11

What is the primary treatment intervention for Metabolic Syndrome?

IDF Guidelines

Answer 11

Primary intervention
Moderate Calorie restriction - To achieve 5-10% body weight loss in first year
- (500 cal reduction per day to produce half kilo weight loss/wk)

Moderate increase in PA

Change in dietary composition
e.g. processed foods, reduce sugar intake, saturated fats (due to immediately being in the body as cholesterol

Slide 48 of Week 7

Question 12

What is the Secondary Treatment for Metabolic Syndrome?

IDF guidelines

Answer 12

If lifestyle changes (PRIMARY) arnt enough –> move to secondary interventions

While there is no medication to prevent met syndrome directly, treat each individual component that are symptoms for the client
these individual components are …
- elevated BP
- atherogenic dyslipidemia
- insulin resistance and hyperglycaemia

For those considered high risk of CVD
- Drug therapy to treat hypertension or cholesterol

Slide 50 of Week 7

Question 13

What is the categorical level for hypertension?

Answer 13

Blood pressure
≥ 140 / ≥ 90 mmHG

In patients with diabetes
≥ 130 / ≥ 80

(JNC7)
Lower cut off if they have diabetes due to the increased risk factors

Question 14

Medications for Hypertension

Answer 14

Thiazides - reduce blood volume
- Reduce water reabsorption in kidney

ACE inhibitor - Vasodilator
- Blocks action of ACE
- Drug end in ‘Pril’

ARB - Vasodilator
- Blocks action of Angtiotensin II by blocking the receptor

Calcium Channel Blocker
- Vasodilator & Reduces contractility of the Heart

Beta Blocker - Reduces HR
- be mindful during exercise because it changes the contractility of the heart
- Drugs end in ‘OLOL’

52 - 53 of Week 7

Question 15

Medications for Dyslipidemia

Answer 15

Statins
- Focuses on decreases LDL

Fibrates
Focus on increasing HDL and reducing TG (doesnt do much for LDL

Bilce Acid Sequestrants
Focus on decreasing LDL

Niacin / Nicotinic Acid
Focus on increasing HDL and reducing TG
May cause decreased HR

Most have no effect on HR, BP or ECG –> main side effet is Myalgia

57 of Week 7

Question 16

Goal levels of TG & Cholesterol for people with no CVD, Diabetes or Kidney Disease

Answer 16

Total Cholesterol
Below 4.5

LDL
Below 2.5

HDL
Above 1

TG
Below 2

Question 17

What is the role of exercise in the management of metabolic syndrome?

Answer 17

Combination of increase in PA and dietary modifications are the most optimal for to achieve weight loss of 5-10%

We dont want the client coming off medication and relying solely on lifestyle modifications (e.g. diet) –> causing CVD risk profile to still be high as the lifestyle modification only isnt enough

Question 18

What did the Diabetes Prevention Program Results indicate?

Answer 18

Adults that were randomly assigned to the lifestyle group had:
- 39% reduction in T2D compared to metformin group
- 58% reduction in T2D compared to placebogroup

TLDR
Reduction in likelihood of developing T2D if you are physically active

Slide 24 of Week 8

Question 19

What is the rationale for Progressive Resistance training for Metabolic Syndrome?

Answer 19

PRT leads to improved metabolic fitness aswell as increased Anabolic activity (AA)

AA
- Leads to an increase in body compositional change driven by an increase in muscle mass and fat loss
- Client may have an increased weight gain –> but this would be as a result from increased muscle mass NOT fat

Slide 25 of Week 8

Question 20

Summary of Exercise in management of Metabolic Syndrome

Answer 20

• Exercise is effective at managing hypertension
• Inclusion of aerobic, dynamic RT and isometric RT leads to a greater reduction in SBP than other interventions
• Exercise has minimal effect on lipoproteins but small evidence for increasing HDL and reducing LDL
• Exercise with or without dietary co-intervention can reduce risk of developing T2D by 51% (more effective than meds)

Slide 31 - 32 in Week 8

Question 21

Considerations for Exercise and Hypertension

Answer 21

Absolute Contraindications
Resting SBP ≥ 180 OR DBP ≥110

Beta Blockers
Blunten the exercise HR –> HR not a good predictor of intensity

Diuretics
Can impair exercise tolerance / performance but normalises after afew weeks

Abrupt termination of exercise
Sudden termination can cause venus pooling –> large drop in BP
Greater risk with medications
Greater risk with aerobic exercise

Slide 40 - 41 of Week 8

Question 22

consequence of no inhibition of hepatic Gluconeogenesis

Answer 22

• insulin and glucagon work together in a feedback loop
  insulin resistance –> gluconeogensis not turned off –> abudance of glucose pumped out endogenously into the blood –> long term hyperglycaemia

slide 27 week 7 lecture 42:07 what lizzie said

Question 23

what are the consequences of impaired fibrinolysis? (factor that leads to accelerated atherosclerosis)

Answer 23

impaired fibrinolysis = lack of breakdown of connecting parts of blood –> increased likelihood of blood clots –> more viscous, thicker, stickier blood –> increased BP

refer to slide 28 of week 7 lecture

Question 24

what do studies say about the consequences of metabolic syndrome?

Answer 24

riskof chronic kidney disease increases with every additional MetS component

3x more likely to develop T2D and 1.7x more likely to develop CVD (Ford, 2005 )

those with Met Syn 2.71 hazard ratio for CVD morality

those with met syn AND T2D 3.63 hazard ratio for CVD morality

CVD + T2D 7.88 hazard ratio for CVD mortality

patients with both met syn and depression had 6.6x higher risk for diabetes –> interaction of the comorbidities magnifies the risk (molecular psychiatry, 2016)

refer to slides 30, 31,32, 33, 35 of week 7 lecture

Question 25

provide an overview of the renin-angiotensin-system

Answer 25

Overall Effect: RAS helps raise blood pressure by increasing blood volume and constricting blood vessels

Process:
1. secretion of renin by kidneys in response to lower BP
2. angiotensin produced by liver is converted by renin to angiotensin I
3. angiotensin I converted by angiotensin converting enzyme (ACE) in lungs and kidneys to angiotensin II
4. end result is vasoconstriction and secretion of aldosterone –> causes sodium retention and maintence of blood volume

BP is a factor of CO and PR; anything that changes either of these factors will affect BP
BP = Q x TPR

Question 26

management reccomendations for high risk patients

Answer 26

• stay on meds –> dont want them to solely on lifestyle changes imediately coming off meds, and cardiac risk profile is still high –> behaviour change inadequate

exercise will enhnace benefits of meds

slide 60 of week 7 lecture