L29 Flashcards

1
Q

what do BMI measurements mean

A

underweight < 18.5

normal = 18.5 - 24.9

overweight = 25-29.9

obese > 30

stage 1 obesity = 30-34.9

stage 2 obesity = 35 - 39.9

extremely obese > 40

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2
Q

what is the % of BMI range in NZ

A

1% underweight

33% normal weight

35% overweight

31% obese

therefore 2 in 3 adults in NZ are overweight (66%)

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3
Q

what is waist circumference a measure of

A

adiposity

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4
Q

what do you need to have to be diagnosed with metabolic syndrome

A

you need to have 3 or more of the following

elevated. ….
- adiposity
- blood pressure
- blood glucose
- triglycerides

  • decrease in HDL
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5
Q

what are the risk factors for extrinsic changes in the heat

A

volume expansion leading to increased CO and hypertension

increases cardiovascular tone from decreased NO

increased triglycerides and FFA (hypoadiponectinemia)

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6
Q

what are the risk factors risk factors

A

the main ones are altered substrate metabolism

  • increased FA oxidation
  • decreased glucose utilisation
  • reduced cardiac efficiency

lipotoxicity and altered Ca dynamics in cardiomyocytes

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7
Q

what are the mechanisms contributing to cardiac dysfunction in obesity

A
  1. Hemodynamic load (volume expansion)
  2. Heart fat - conduction system
  3. Adipocytes - Adipokines - myocardial fibrosis
  4. Microangiopathy (micro = disease of the small vessels) - endothelial dysfunction
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8
Q

hemodynamic load and size relationship

A

Someone that is taller and bigger would have a larger heart which is the same for someone with obesity

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9
Q

why does an increase in body mass cause a increase in blood flow

A

because there is more tissue to be perfused

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10
Q

per 100g of excess body fat, how much does blood flow increase

A

2–3 mL/min/100 g

theefore 100 kg of excess body fat requires an extra 3 L/min blood flow

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11
Q

describe the CO for someone weighing 70kg, 120kg and 170 kg

A

Subject of 70 kg 6.0 L/min CO

Subject of 120 kg 7.5 L/min CO

Subject of 170 kg 9.0 L/min CO

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12
Q

what happens to hemodynamic load in obesity

A

Increased mass result in increase in preload (more filling)

Cardiac output increased (HR and SV increased)

TPR will decrease! (sole effect of volume increase, more tissue to perfuse)

therefore in obesity you have a High output - low resistance state - more body mass

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13
Q

in obesity you have a High output - low resistance state

why does having more body mass cause this to happen

A

People that are obese also have more sympathetic input to the hear to get it to beat more (because you need more perfusion)

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14
Q

what kind of cardiac remodeling happens with obesity

A

dilated cardiomyopathy, heart failure

caused by volume overload (eccentric remoderling)

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15
Q

describe how remodelling in the heart happens with obesity

A

you start out with volume overload causing the left side to become bigger (eccentric remodeling)

as the body mass increases it has consequences on many body systems. one of the things it causes is hypertension

hypertension causes pressure overload concentric remoderling of the heat

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16
Q

remoderling of the heart in obesity can be broken don into 2 processes

what are these

A

Primary
Volume overload
- LA and LV eccentric hypertrophy

Secondary

  • Pressure overload
  • LV concentric hypertrophy
17
Q

what is important to note from cardiac remodelling in obesity

A

obesity is just volume overload ( primary)

it is the hypertension (that is caused by being obese) that causes pressure overload (secondary)

18
Q

when does pressure overload happen with obesity

A

Mild obese with severe systemic hypertension

19
Q

when does volume overload happen with obesity

A

Morbidly obese with mild systemic hypertension

20
Q

describe fat in a healthy heart compared to an obese heart

A

In a healthy heart there is a little bit of fat on the outside. It is good that this is there as the heart prefers FFA for energy and it is there as a store for when you need it

In the obese situation the epicardial fat becomes thicker and starts to get into the myocardium

21
Q

what is the difference between epicardial fat and pericardial fat

A

epicardial fat is good and pericardial is bad

epicardial is part of the heart and it the FFA storage

pericardial is in the pericardial sac (in between the layers) and epicardial

22
Q

what happens when you get a severe amount of epicardial fat

A

deposition (thick layer of fat on the outside of the heart)

and infiltration (when fat enters the myocardium)

23
Q

what does excess hart fat (deposition and infiltration) cause

A
  • Mechanical impairment
  • Thermoregulation (higher body core temperature)
  • Cardiac conduction
  • Endocrine effects (adipokines, cytokines)
24
Q

what is heart fats effect on the conduction system

A

LV and RV hypertrophy
eccentric and concentric remodeling

Fatty infiltration in conduction system

Prolongation of QT interval (Fat insulates for temp and for electricity therefore the conduction system is slowed down. To effect conduction it depends where the fat infiltrates the heart)

Adipokines, cytokines release

the above can cause Sleep apnea - cardiac arrhythmias - sudden death

25
Q

what is a fat cell made up of and what do they secrete

A

A fat cell is nothing more than a nucleus and lipid droplets for energy stores

The lipid droplet secrets factors called adipokines

26
Q

what are some examples of adipokines

A

Leptin, Non-Esterified Fatty Acids (NEFA), TNF-α, IL-6, C-reactive protein, angiotensinogen, adiponectin, reactive oxygen species (ROS)

27
Q

how does increased adipose tissue cause inflammation

A

Normally this release is not a lot and it is in balance with what is needed

When you increase your weight them more fat is being stored and the adipocytes will hypertrophy and become bigger. This causes them to secrete more

As they keep increasing then they will attract macrophages as they are no longer seen as a good thing therefore they causes an inflammatory response

28
Q

other than a inflammatory response what else does an increase in insulin resistance cause

A

Insulin resistance/ Hyperinsulinemia

29
Q

what is Hyperinsulinemia

A

Insulin resistance

30
Q

how do adipokines cause fibrosis

A

With hypertension you get in increase in ECM structure causing an increase in fibrosis

Adipokines has effects on most cells including cardiomyocytes and fibroblasts therefore as a response to these adipokines you get cardiac remodeling of the ECM (outside of the myocardium) which causes collagen synthesis, changes in isoform and changes in cross linking which leads to fibrosis which leads to heart failure

31
Q

what happens when you get adipocytes in the vasculature

A

When the animal is obese there is a clear difference

There is more fat cells which causes structural changes in the vasculature

the vesicle become not well arranged and they have different sizes at different parts of the vessel

32
Q

fa the soround blood vessels is called…..

A

perivascular fat

33
Q

in obesity what causes perivascular fat to become bigger

A

the more FFA they are exposed to the bigger they get

34
Q

how does perivascular fat effect the blood vessels

A

He adipokines will effect the smooth muscle cells and the vasculature of the vessels

35
Q

The effects of the adipose tissue is usually greater in the smaller vessels compared to in hypertension where it is usually greater in the larger vessels

why is this

A

adipose changes the balance between vasoconstriction (endothelin 1) and vasodilation (NO)

36
Q

what is Microangiopathy

A

disease of the small vessels

37
Q

what can Microangiopathy (disease of the small vessels) cause

A
  • Retinopathy
  • Nephropathy
  • Neuropathy
38
Q

what is the overall effect of obesity on cardiovascular pathophysiology

A

More fat = hypertrophy of adipocytes = more adipokines released which disrupts the balance which is bad