wk 1- CVD Flashcards
what age do people need to be screened for CVD risk and recommended times going forward
45+ every 5 years
35years for ASTI people
people regarded as high risk already are
-CVD patients
-DM if >60yrs
-CKD
modifiable and non modifiable risk factors of CVD
MOD:
hypertension
dyslipideamia
smoking
obesity
sedentary
alcohol
DM
NON MOD:
-family history
gender (male)
age
management on how to modify risk factors and dislipidaemia
lifestyle changes of
diet-
1. consume a whole foods diet (mederteranian style),
2. limit foods containing saturated and trans fats
3. limit salts
4 limit alcohol consumption (2standard per day or less)
5. add plant sterol rich foods (milk, cheese, margarine)
physical activity-
minimum 30mins of moderate activity per day
weight-
limit energy intake and increase energy output, goal is BMI less than 25
smoking-
smoking cessation or nicotine replacement therapy
AND
medications-
lipid lowering medication for
1. previous ASCVD, high risk CVD
2. moderate risk CVD after 3-6months of lifestyle changes not helping with also a family history of premature CVD
medication choices and MOA for dislipidaemia
- statin -1st line
MOA: HMG CoA reductase inhibitors, which reduce cholesterol synthesis in liver - ezetimbe
MOA: decreases choelsterol absoprtion in small intestine - fibrates
MAO: complex - fibrates and omega 3
-used for hypertrigylceridaemia
define dyslipidaemia, what serious pathology is it linked to, what are primary/secondary differences
derangement of plasma lipid levels (cholesterol and or triglycerides)
associated with atherosclerosis, PAD, CAD, STROKE- serious pathology that involves blockage of an artery
primary: gene mutations which result in
1. excessive production
2. decreased clearance of LDL/trigylcerides
3. decreased production, increased clearance of HDL
secondary: low levels of activity, excessive dietary intake of sat fats, cholesterol and trans fats
different types of dislipidaemia and ranges
hypercholesterolaemia
1. total Cholestero is 5.5mmol/L or more
2. and or LDL is 3.5mmol/l or more
hypertriglyceriaemia
1. triglycerises is 2mmol/L or more
mixed dyslipidaemia
1. both tri and cholesterol elevated (2mmol/L or more and 5.5mmol/l or more)
LOW HDL
1. HDL is less than 1mmol/L for men and 1.3 for women
patho of ASCVD/ lipid metabolism
- lipids (cholesterol and triglycerides) are insoluble in blood therefore theyre transported within lipoproteins
- Lipids (now monoglycerides, fatty acids and cholesterol) leave micelles and reassemble into chylomicrons which transport lipids around the body
3.liver synthesis lipoproteins to transport cholesterol and cholesterol
-LDL is either cleared by liver or taken up into vascular endotheliium
-HDL are initially cholesterol free and transport cholesterol from tissues to other cells or liver for clearance
dyslipidaemia/ ASCVD symptoms
dislipideamia is usually asymptomatic and manifests as
heart attack
stroke
or picked up on health screening
hypertrigylceride symptoms
acute pancreaitis with severe upper abdominal pain which may radiate to back
nausea
vomiting
pallor
diaphoresis
high levels of LDL symptoms
corneal arcus (deposits of lipids around corneal margin of eye
tendinous xanthomata
management of dyslipidaemia
- lifestyle changes
activity 30mins - decreases TG and increases HDL
diet- mediteranian and low in sat and trans fats - medications when
- patient has ASCVD or
- high CVD risk or
- 3-6months with lifestyle changes at mod risk and fam history of premature CVD
medication is typically lifelong so other causes need to be ruled out
for high LDL cholesterol
1. statin
2. ezetimbe
3. fibrate
for hypertrigylceridaemia
1. fibrate and omega 3 fatty acids
define hypertension and range classification, primary and secondary causes
sustained elvation of BP
systolic BP >140mmHG
diastolic BP >90mmhg
or both
primary: most common due to
1. activation of sympathetic nervous system,
2. RAAS overactivity,
3. vasodilator deficiency in endothelium
secondary: due to
1. primary aldosteronism or
2. chronic kidney disease or
3. other diseases/conditions
hypertension symptoms
asymptomatic usually until complications
diagnosisng hypertension and grades, and medical emergency
calibrated sphygmomanometer
grade 1: 140/90, ambulatory or home monitoring should be used to determine BP, might be white coat
grade 2- 160/100
grade 3: 180/110
> 220/140 is medical emergency
hypertension management
- lifestyle modifications
cease smoking
regular exercise
reduce alcohol and salt
better diet
lose weight
manage obstructive sleep aponea - medications
starts when
- BP 160/100
-mod-high CVD risk and 140/90 BP
antihypertensives
1. ACE/ARB/CCB/BB/thiazide diuretic- first line
2. after 3 months, not controlled, add a second
3.” 3rd, if not signs of secondary hypertension causes
define coronary artery disease
Impairment of blood flow through the coronary arteries, which supply
blood to the heart muscle (myocardium)
can be
angina OR
myocardial infarction
patho of ACS
- Athersclerosis caused by uptake of lipids in vasuclar endothelium of the coronary arteries leads to progressive narrowing
and reduction in blood flow - stabiliy of the plaque influences the presentation
- stable angina
-rupture and thrombosis results in ACS
signs of stable angina and ACS
stable: chest pain that may radiate to left arm, felt under sternum triggered by exertion and settles with rest
ACS: same chest pain present at rest and increased in frequency/severity/duration
testing for CAD (diagnosing)
ECG
cardiac markers
management of CAD- stable
- life style modifications
-activity
-diet
-weight loss
-smoking cessation
-alcohol cessation - medications
-antiplatelets
-statins
-ACE/BB/CCB
-nitrates for angina - surgery
for patients with persistent symptoms and maximum medical intervention
- coronary artery bypass grafting
-PCI
management of ACS
- hospital
-oxygen
-aspirin
-nitrates
-morphine
-BB
-anticoagulants - STEMI OR NSTEMI
-STEMI: urgent coronary angiography and artery bypass or thrombolysis
-NSTEMI: prompt bypass
patients with stent need dual antiplatelet for 12 months following then aspirin alone lifelong
complications of myocardial infarction
- Electrical (arrhythmia, conduction disturbances)
- Mechanical (heart failure, myocardial rupture)
- Thrombotic (recurrent coronary ischaemia, mural thrombosis)
- Inflammatory (pericarditis, effusion, joint pain)
