Vascular Medicine Flashcards
Describe the formation of the fatty streak
Deposition of cholesterol underneath the endothelium
Uptake of lipid by macrophages - break down and remove lipid
If macrophages become overloaded with lipid - turn into foam cells - basis of fatty streak
BUT reversible lesion.
Describe how the fatty streak then goes on to become a plaque
Fatty streak = Inflammation
Recruit immune cells to site
If these cells become overwhelmed - leads to lipid peroxidation
This causes the breakdown of macropahes and release of free lipid into the cell wall.
Get lipid core with surrounding inflammation
if the overlying cap of this is thick and fibrous = STABLE plaque
If cap becomes thin, may rupture. Exposes underlying lipid core which prompts thrombosis. If this completely blocks artery can get MI/Stroke/Critical Limb
What are the 6Ps of critical limb ischaemia?
Pain Pallor Pulselessness Parathesia Paralysis Perishingly Cold
Describe how peripheral arterial disease is diagnosed
Using the ABPI - ankle brachial pressure index
Ratio of systolic BP at the ankle to the systolic BP in the brachial artery
0.9 - 1 = Normal
0.7 - 0.9 = Mild
0.4-0.7 = Moderate
List the modifiable and non-modifiable cardiovascular risk factors
NON-MODIFIABLE
Age, Male Gender, Family Hx, Ethnicity, Previous CVD
MOIFIABLE
Hypertension, Hyperlipidaemia, Smoking, Diabetes
When should blood samples for cardiac markers be collected?
On admission and 6-9 hours after the onset of symptoms
What is levels of troponin are required to make a diagnosis of acute MI?
> 99th centile (TnT >14) AND a RISE OR FALL of >20% on the second sample
What is the definition of an acute MI?
Rise in tropinin + at least one of the following
Symptoms of ischaemia
ECG changes indicative of new ischemia
Development of pathological Q waves on ECG
Imaging evidence of loss of viable myocardium
What does the GRACE score calculate?
6 month mortality from cardiovascular disease
What is junctional bradycardia?
When the rate of the heart is an escape rhythm from the AV node
Rate = 40-60 bpm
What medications should patients be on after discharge from ACS?
Dual antiplatelet therapy
Beta-Blocker
Ace Inhibitor
Statin
Describe the significance of random blood glucose measurements
> 11.1 = consistent with a diagnosis of diabetes
7.9-11.1 - reflects impaired glucose handling
When should the possibility of familial hypercholesterolaemia be considered?
Patient has a total cholesterol >7.5 AND a family history of premature cardiovascular disease
Should be investigated for
List some of the effects of NSAIDs on the cardiovascular system that were picked up in the case
In patients who have had a previous MI, NSAIDs increase the risk of death and/or recurrent MI
NSAIDs (especially in combination with aspirin and clopidogrel, increase the risk of developing gastric ulcers
Regular doses of NSAIDs may increase the antiplatelet effect of low dose aspirin
What are the 5 different types of MI
TYPE 1 - usual MI TYPE 2 - imbalance between mycardial O2 supply and demand - ischaemia without definite CAD TYPE 3 - Sudden Death TYPE 4 - PCI associated MI TYPE 5 - CABG associated MI
Describe the different types of ACS
NO ST ELEVATION
Can be unstable angina or an NSTEMI
ST ELEVATION
Non Q wave MI (smaller and less extesnive), Q wave MI
Describe the atypical presentation of MI that you may see in the elder or diabetic population
Chest pain less of a feature Breathlessness Tachycardia N & V Sweating and clamminess
What does the TIMI score measure?
Estimates mortality for patients with unstable angina and non-ST elevation MI.
Describe the different ECG changes that can indicate an MI
ST elevation Q waves ST depression T wave inversion (low risk ECG) LBBB
Other than acute MI, in what other situations can troponin be increased?
PE Spesis Post-Operatively AF LVF
How is the risk of cardiovascular disease related to rise in BP?
For every 20/10 mmHg rise in BP the risk of cardiovascular disease doubles
ALSO Elevated systolic is a greater risk than diastolic
Describe the pathophysiology of Hypertension
Reduced elasticity and compliance of large arteries = part of normal ageing
in hypertension get accelerated accumulation of arterial calcium and collagen, and degradation of elastin
Stiffened vessels increase rate of return of reflect pressure waves - rising peak systolic pressure
Hypertension can also be as a result of excess sodium and therefore fluid rentention
In Hypertension when should phaeochromocytoma be suspected?
If there is labile or postural hypotension, headache, palpitations, pallor and profuse sweating
Describe the different causes of Hypertension
Essential Hypertension (80%) - primary cause unknown
Secondary Hypertension ( has several different causes)
These include
Renal Disease (75% intrinsic renal disease, 25% renovascular disease)
Endocrine Disease e.g Cushing’s syndrome, Conn’s syndrome, Phaeochromocytoma, Acromegaly, Hyperparathyroidism
Co-arctation
Pre-eclampsia/gestational Hypertension
Drugs and Toxins
In people under 80 with Stage 1 Hypertension, when should blood pressure treatment be offered
If there is target organ damage There is established cardiovascular disease Renal Disease Diabetes 10 yr cardiovascular risk >10%
What should the blood pressure target be in anyone with diabetes, regardless of age?
What is the pathophysiology of Cushings Syndrome causing hypertension?
Excess cortisol binds to aldosterone receptors causing activation of the renin-angiotensin system
Describe Liddle Syndrome and how it is treated?
Hyperactivity of ENaC - increase Na absorbed, and water follows = hypertension. Also a cause of hypokalaemia
Treat with AMILORIDE -K+ sparing diuretic that block ENac
What cancer syndromes is Phaeochromocytoma associated with?
MEN 2
Von-Hippel Lindau
