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Vascular > Atherosclerosis and prevention > Flashcards

Atherosclerosis and prevention Flashcards

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1
Q

Causes of left ventricular hypertrophy:

A

Hypertension
Aortic valve stenosis
Hypertrophic cardiomyopathy

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2
Q

What drugs can be used to lower LDL?

A

Simvastatin

Ezetimibe

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3
Q

Pathology of hypertension?

A

Damages endothelium that can no longer release NO
Increased after load causes left ventricular hypertrophy and cardiac ischaemia (as tissue grows faster than vessels)
Brain and kidney are high flow, low resistance systems so they are exposed to high pressures + pulses: RF + stroke

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4
Q

Pathology of smoking?

A

Endothelial dysfunction and inflammation
Increased plaque vulnerability
Increased thrombosis and decreased fibrinolysis
Activation of sympathetic nervous system
Increased risk of insulin resistance and T2DM

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5
Q

Pathology of T2DM?

A

Promotes plaque formation and vulnerability (inflammation)

Associated with other factors of cardiometabolic disease

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6
Q

How is obesity a risk factor for atherosclerosis?

A

Causes same increase in risk whether you are metabolically unhealthy or not but obesity puts you at an increased risk of being metabolically unhealthy
CHD and stroke associated risk

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7
Q

Effect of exercise?

A

Reduce CV risk
OR normalise CV risk in the obese preventing the transition to cardiometabolic disease
Reduces TAGs and oxidative stress, increases HDL and NO release
Reduces inflammation, improves endothelial function

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8
Q

What is relevant family history in a QRISK assessment?

A

CVD in a first degree relative under the age of 60

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9
Q

Management for patient with >10% risk of CVD within 10 years?

A

Lifestyle advice and offer atorvastatin

Most patients >60 y/o

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10
Q

80 y/o with stage 1 hypertension (BP between 130/85 - 150/95) and >1 of organ damage, established CVD, renal disease, diabetes or 20% 10 year risk?

A

Offer antihypertensive drug

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11
Q

Protocol with statins?

A

Higher risk you are, the more statin you should receive as it lowers risk more

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12
Q

What causes wide pulse pressure (systolic hypertension)?

A

Aortic/great vessel stenosis as walls cannot store energy (high systolic) and there is no rebound pressure (low diastolic)

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13
Q

When is BP highest and lowest?

A

BP is highest at the peak of ventricular contraction (systolic pressure)
BP is lowest at the end of ventricular relaxation (diastolic pressure)

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14
Q

What is the dicrotic notch?

A

A small pulse in pressure caused by the aortic valve closing

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15
Q

BP =

A

Blood flow through stem x the peripheral resistance

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16
Q

Blood flow is determined by?

A

Heart rate and stroke volume which are in turn determined by preload and blood volume

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17
Q

Effects of the sympathetic system?

A

Can directly increase CO and the resistance of the system to flow
Stimulates RAAS

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18
Q

How doe you reduce the blood volume?

A

Antihypertensives

Diuretics

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19
Q

How do you reduce CO?

A

Beta-blockers

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20
Q

How do you reduce resistance?

A

CCBs
ACE-inhibitors
Angiotensin-receptor blockers

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21
Q

Effect of aggressively treating high systolic BP in elderly?

A

Diastolic pressure drops even more causing postural hypotension

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22
Q

What is pulse pressure defined by?

A

CO and aortic stiffness

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23
Q

For a given systolic pressure…

A

The CHD hazard ratio goes down with increasing diastolic pressure

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24
Q

Presentation of high BP?

A

Usually asymptomatic so present after complication e.g. MI or stroke
Erectile dysfunction in males

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25
ABCD of BP treatment?
A: ACE inhibitors (ramipril), angiotensin R blockers B: Beta-blockers (bisoprolol) C: Ca channel blockers (amlodipine) D: Diuretics (bendroflumethazide)
26
Diuresis with BP?
Use gentle diuretics like bendroflumethazide | Harsher ones like spironolactone and furesimide are used for severe HF on the ward
27
Examples of ACE inhibitors:
Elanapril Lisinopril Ramipril Trandolapril
28
Mechanismm of ACE inhibitors?
Prevent formation of angiotensin II which constricts blood vessels
29
Advantages of ACE inhibitors?
Beneficial to cardiac function | Tolerated well in diabetes and young people
30
Disadvantages of ACE inhibitors?
Dry cough (bradykinin - can cause angioedema) Can cause renal impairment (if bilateral renovascular disease) Should not be used in pregnancy
31
Examples of angiotensin receptor blockers:
Lorsartan Irbesartan Candesartan
32
Mechanism of angiotensin receptor blockers?
Prevent the action of angiotensin II
33
Advantages and disadvantages of angiotensin receptor blockers?
Same as ACE inhibitors minus the dry cough
34
Examples of beta blockers:
Atenolol Bisoprolol Metoprolol Nebivolol
35
Mechanism of beta blockers?
Reduces contractility and rate of heart therefor reducing CO and BP however it is used less for BP
36
Advantages of beta blockers?
Good for co-existent conditions: anxiety, HF, angina/previous MI
37
Disadvantages of beta blockers?
Effectiveness in preventing CV complications is questionable Cold hands, lethargy and tiredness Should not be used in asthma/chronic emphysema Should not be used if problems with the arterial circulation Can cause sleep disturbances and nightmares
38
Contraindications of beta blockers?
Asthma/COPD Worsening unstable HF Second or third degree heart block
39
Examples of calcium channel blockers:
Nifedipine Amlodipine Verapamil
40
Mechanism of CCBs?
Cause direct dilatation of the arteries
41
Advantages of CCBs?
Powerful Good in elderly Good with co-existent problem e.g. angina, Raynaud/s or other circulatory problems
42
Disadvantages of CCBs?
Ankle oedema Occasionally headache and flushing Constipation (especially verapamil)
43
Examples of diuretics used for hypertension:
``` Chlortalidone Indapamide Bendroflumethiazide Amiloride Hydrochlorthadone (furosemide and spironolactone are more aggressive and are used for HF) ```
44
Advantages of diuretics?
Cheap | Good in elderly
45
Disadvantages of diuretics?
Frequent urination/incontinence Impotence (especially in younger patients) Rarely can precipitate gout and other metabolic problems
46
Thiazides:
Prevent reabsorption of Na in the distal convoluted tubule | Can cause hyperglycaemia
47
Loop diuretics:
Prevent sodium reabsorption in the ascending loop of Henle Furosemide and bumetanide Used for pulmonary oedema in the case of left ventricular failure Can exacerbate diabetes and gout Can be used for resistant hypertension but not 1st line
48
Potassium sparing diuretics and aldosterone agonists:
Amiloride hydrochloride and triamterene are weak K-sparing diuretics Spironolactone is a K-sparing aldosterone agonist, works well with furosemide as an adjunct, used to treat oedema and ascites caused by liver cirrhosis, severe heart failure and resistant hypertension, also Conn's syndrome (primary hypoaldosteronism) Epleronone can be used for left heart failure
49
What must not be given with aldosterone agonists?
K supplements
50
Secondary causes of uncontrolled hypertension?
``` Obstructive sleep apnoea Renal artery stenosis Primary hypoaldosteronism Phaeochromocytoma Cushing's Vasculitides Aortic coarctation Thyroid dysfunction ```
51
Lp(a)
Familial risk of hyperlipidaemia
52
ApoE
Risk of mixed hyperlipidaemia
53
Presentation of familial hyperlipidaemia? (monogenic, autosomal dominant)
``` TC >7.5mmol/L LDL-C >4.7mmol/L Tendon xanthomata (cuboidal achilles tedon, deposits move with tendon unlike H nodes) Arcus Develop CHD at around 50 ```
54
Presentation of homozygous FH of hyperlipidaemia?
``` No functioning LDL receptor TC >16mmol/L Tendon xanth, arcus, CHD at 20, die at 34 Poor response to statins Give ezetimibe, PCSK-9 inhibitors Apheresis or liver transplant ```
55
How do statins work?
Reduces hepatic cholesterol synthesis Upregulates PCSK-9 LDL receptors (SREBP feedback) Switches off LDL receptors in macrophages May cause muscle aches in some people
56
Which drugs block cholesterol reabsorption?
Benicol Solostanol (ezetimibe) Siteserol
57
How does ezetimibe work?
NPC1L1 transporter blocker that blocks cholesterol reabsorption
58
What is PCSK-9?
A receptor that when activated, down-regulates LDL receptors Activated PCSK-9 causes early cardiac disease Alirocumab and evolocumab are human Abs to it Inclisiron is an siRNA that leads to a 50% reduction in LDL Used for high risk population such as ACS population
59
Signs of lipoprotein lipase deficiency?
TAG >20mmol/L Lipaemia retinalis Eruptive xanthomata Pancreatitis
60
Presentation of lipoprotein lipase deficiency?
Homozygous age of onset is 2-12 with severe recurrent pancreatitis Heterozygous age of onset is 30-50 with moderate-severe occasional pancreatitis Refer to hospital if TAG >20 + acute abd pain - worse in pregnancy
61
Which lipid measurements should you take?
Non-fasting | Non-HDL-C
62
Secondary prevention of hyperlipidaemia?
Atorvastatin 80mg - as much as you can tolerate
63
Primary prevention of hyperlipidaemia and in DM?
Moderate dose atorvastatin 20mg
64
Risk of ACS (possibly post stroke or other event)?
Atorvastatin 80mg + Ezetimibe 10mg + PCSK9 inhibitor if LDL-C is high

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