Week 4 Flashcards
how to detect AS?
assess risk factor prediction based off 5 virtues
- healthy BW
- physically active
- no smoking
- alcohol in moderation
- healthy diet
decreased risk aroud 79%
detecting symptoms of AS
- angina
- heart attack
dysfunctional arteries percentage
<50% stenosis = 68% heart attack events
50-70% stenosis = 18% heart attack events
>70% stenosis = 14% heart attack events
stenotic lesions
how to treat
- few
- fibrous and thick cap
- less compensatory
- enlargement
ischaemia detection and treated by PTCA, stent and CABG
Non-Stenotic Lesions
- many
- lipid richand thin cap
- compensatory enlargement
- infarction detection
- can rupture and create plaque
treated by lifestyle modification and drug therapy
modifiable risk factors for CVD
- high blood lipids
- smoking
- hypertension
- obesity
- diabetes
- physical inactivity
syndrome X (symptoms related to adiposity)
7 countries study link
cholesterol mg/dl of serum and coronary death rates
framingham study links
serum level increases with higher rates of coronary heart disease development
cholesterol
lipid both made by body and consumed and in animal products
cholesterol functions
- transport of fats in bloodstream (cannot transport fat in water mediums)
- plasma membrane structure
- production of vitamin D, steroid hormones and bile salts
total cholesterol equation
LDL + HDL + VLDL
oxidative modification hypothesis of AS
endothelial injury or dysfunction can exacerbate outcomes
ox-LDL can lead to…
- injury and dysfunction
- adhesion and infiltration
- monocytes to macrophages modification
- internalised to form foam cells
high density lipoprotein functions
- reverse cholesterol transport
- plaque regression?
- monocyte adhesion decrease
- maintain endothelial function
blood lipid levels
- elevated blood lipid profile = over 5.2 (6/7 increases risk)
- LDL = over 3.4 (keep below 3.4)
- HDL = over 1 (should be above 1)
- HDL ratio = over 3.5 (total divided by HDL and should be above 3.5)
- triglycerides (over 1.7)
how does smoking increase CV risk
- increased carboxyhaemoglobin
- decreased myocardial o2 delivery
- increased sympathetic NS + HR + BP (increased myocardial O2 demand)
- increased endothelial damage (platelet aggregation/clotting and increase VC and permeability)
type 1 diabetes
beta cells destroyed (production issues)
- blood glucose does ont produce as much insulin
- cannot get insulin to target organs
type 2 diabetes
- pancreas has normal beta cells
- tissues have insulin resistance (too high BGL and high insulin)
normal fasting BGL
over 5.5 mmol/L
IFG (pre-diabetes)
5.5 - 7mmol/L
Type 2 Diabetes
over 7 mmol/L
HbA1c
glycated haemoglobin
- haemoglobin molecule with glucose bound to it
- excess glucose absorbed to HB to create HbA1c
how exercise is a good intervention for Diabetes
- GLUT4 transporter (GLUT1 is insulin dependent)
- insulin binds to GLUT1 and sucks glucose into cell from blood stream
exercise -> contraction -> movement of GLUT4 –> glucose enters cell
How does CVD risk increase?
direct injury or impairment to endothelium
- increased afterload –> increased myocardial O2 demand –> increased wall stress
- increased likelihood of plaque rupture
- can cause aneurysm or haemorrhage
afterload impact after hypertension
- greater AL -> shorter ejection period -> larger ESV -> lower SV -> increased peripheral resistance -> increased afterload
OR
VC / resistance vessels = increased aortic pressure
