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Flashcards in Vascular Medicine Deck (29)
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1
Q

Describe the formation of the fatty streak

A

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.

2
Q

Describe how the fatty streak then goes on to become a plaque

A

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

3
Q

What are the 6Ps of critical limb ischaemia?

A
Pain
Pallor
Pulselessness
Parathesia
Paralysis
Perishingly Cold
4
Q

Describe how peripheral arterial disease is diagnosed

A

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

5
Q

List the modifiable and non-modifiable cardiovascular risk factors

A

NON-MODIFIABLE
Age, Male Gender, Family Hx, Ethnicity, Previous CVD
MOIFIABLE
Hypertension, Hyperlipidaemia, Smoking, Diabetes

6
Q

When should blood samples for cardiac markers be collected?

A

On admission and 6-9 hours after the onset of symptoms

7
Q

What is levels of troponin are required to make a diagnosis of acute MI?

A

> 99th centile (TnT >14) AND a RISE OR FALL of >20% on the second sample

8
Q

What is the definition of an acute MI?

A

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

9
Q

What does the GRACE score calculate?

A

6 month mortality from cardiovascular disease

10
Q

What is junctional bradycardia?

A

When the rate of the heart is an escape rhythm from the AV node
Rate = 40-60 bpm

11
Q

What medications should patients be on after discharge from ACS?

A

Dual antiplatelet therapy
Beta-Blocker
Ace Inhibitor
Statin

12
Q

Describe the significance of random blood glucose measurements

A

> 11.1 = consistent with a diagnosis of diabetes

7.9-11.1 - reflects impaired glucose handling

13
Q

When should the possibility of familial hypercholesterolaemia be considered?

A

Patient has a total cholesterol >7.5 AND a family history of premature cardiovascular disease
Should be investigated for

14
Q

List some of the effects of NSAIDs on the cardiovascular system that were picked up in the case

A

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

15
Q

What are the 5 different types of MI

A
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
16
Q

Describe the different types of ACS

A

NO ST ELEVATION
Can be unstable angina or an NSTEMI
ST ELEVATION
Non Q wave MI (smaller and less extesnive), Q wave MI

17
Q

Describe the atypical presentation of MI that you may see in the elder or diabetic population

A
Chest pain less of a feature
Breathlessness
Tachycardia
N & V
Sweating and clamminess
18
Q

What does the TIMI score measure?

A

Estimates mortality for patients with unstable angina and non-ST elevation MI.

19
Q

Describe the different ECG changes that can indicate an MI

A
ST elevation
Q waves
ST depression
T wave inversion (low risk ECG)
LBBB
20
Q

Other than acute MI, in what other situations can troponin be increased?

A
PE
Spesis
Post-Operatively
AF
LVF
21
Q

How is the risk of cardiovascular disease related to rise in BP?

A

For every 20/10 mmHg rise in BP the risk of cardiovascular disease doubles
ALSO Elevated systolic is a greater risk than diastolic

22
Q

Describe the pathophysiology of Hypertension

A

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

23
Q

In Hypertension when should phaeochromocytoma be suspected?

A

If there is labile or postural hypotension, headache, palpitations, pallor and profuse sweating

24
Q

Describe the different causes of Hypertension

A

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

25
Q

In people under 80 with Stage 1 Hypertension, when should blood pressure treatment be offered

A
If there is target organ damage
There is established cardiovascular disease
Renal Disease
Diabetes
10 yr cardiovascular risk >10%
26
Q

What should the blood pressure target be in anyone with diabetes, regardless of age?

A
27
Q

What is the pathophysiology of Cushings Syndrome causing hypertension?

A

Excess cortisol binds to aldosterone receptors causing activation of the renin-angiotensin system

28
Q

Describe Liddle Syndrome and how it is treated?

A

Hyperactivity of ENaC - increase Na absorbed, and water follows = hypertension. Also a cause of hypokalaemia
Treat with AMILORIDE -K+ sparing diuretic that block ENac

29
Q

What cancer syndromes is Phaeochromocytoma associated with?

A

MEN 2

Von-Hippel Lindau