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Cardiology > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What does Athero mean?

A

Soft/porridge like

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2
Q

what does sclerosis mean?

A

Hardening

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3
Q

Define Atherosclerosis

A

Atherosclerosis is the combination of atheromas (fatty deposits in the artery wall) and sclerosis (hardening or stiffening of the blood vessel wall)

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4
Q

what arteries does AS affect?

A

Medium and large

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5
Q

What is AS caused by?

A

Chronic inflammation and activation of immune system by artery walls.

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6
Q

This causes deposition of _____ and development of _______ _________ ______

A

Lipids
Fibrous atheromatous plaques

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7
Q

What do the Plaques result in?

A

Stiffening, stenosis and plaque rupture

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8
Q

Stiffening of the artery walls leads to?

A

hypertension and strain as the blood is working to pump blood against the increased resistance

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9
Q

Stenosis?

A

Stenosis is narrowing of the artery walls and leads to reduced blood flow e.g Angina

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10
Q

Plaque ruptures lead to?

A

Thrombus forming and can block a distal vessel causing ischaemia. e.g acute coronary syndrome where the coronary artery becomes blocked.

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11
Q

What three things happen to an artery during AS?

A
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12
Q

What are the non-modifiable risk factors?

A

Older ages
Male
Family history

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13
Q

What are the 8 modifiable risk factors?

A

Raised cholesterol
Smoking
Alcohol consumption
Stress
Obesity
Poor diet
Poor sleep
Lack of sleep

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14
Q

What are the 5 medical Co-morbidities?

A

Diabetes
Inflammatory conditions e.g rheumatoid arthritis
Hypertension
Chronic Kidney Disease (CKD)
Atypical Antipsychotic Medication

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15
Q

What are the 6 End results of AS?

A

Stroke
Transient Ischaemic Attack
Myocardial Infarction
Angina
Chronic Mesenteric Ischaemia
Peripheral Artery Disease

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16
Q

Primary prevention…

A

Only possible when there’s no other cardiovascular condition diagnosed

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17
Q

Secondary prevention…

A

After a diagnosis of MI, Angina, Stroke etc…

18
Q

How to optimise modifiable risk factors?

A

Fix patient diet, incorporate more exercise, stress management, stop smoking, reduce alcohol consumption, manage medical treatment for co-morbidites

19
Q

7 NICE guidelines for diet?

A

Total fat consumed <30% of total calories (primarily monounsaturated and polyunsaturated fats)
Saturated fat <7% of total calories consumed
Reduced sugar intake
Wholegrains
5 fruits and veg daily
2 fish a week (one oily)
4 times a week legumes seeds and nuts

20
Q

NICE guidelines for activity?

A

Anaerobic exercise 150 minutes per week if moderate intensity and 75 minutes for vigorous
Strength training activities 2 times a week

21
Q

Primary prevention of AS?

A

QRISK3 score >10% = initially offered atorvastatin 20mg at night

22
Q

what is the QRISK score?

A

The QRISK score is the percentage risk of a patient having a stroke of MI in the next 10 years.

23
Q

When else is 20mg Atorvastatin offered?

A

Chronic Kidney Disease (eGFR less than 60ml/min/1.73m2)
Type 1 Diabetes for more than 10 years or if patient over 40

24
Q

How do Statins work?

A

Statins Reduce cholesterol production in the liver by inhibiting HMG CoA reductase

25
Q

NICE recommendations for Statins regarding Lipids?

A

NICE recommend checking lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol. Check adherence (are they taking the medications?) before increasing the dose.

26
Q

NICE recommendations for Statins regarding LFTS?

A

NICE also recommend checking LFTs within 3 months of starting a statin and again at 12 months. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use. They usually do not need to be stopped if the rise is less than 3 times the upper limit of normal.

27
Q

Side effects of Statins?

A

Myopathy (muscle weakness and pain)
Rhabdomylosis ( muscle damage and check creatine kinase if patients report muscle weakness)
Hemorrhagic Stroke (rarely)
Type 2 Diabetes

28
Q

Other Cholesterol lowering Drugs?

A

Ezetimibe and PCSkG Inhibitors

29
Q

How does Ezetimibe work?

A

It lowers the absorption of cholesterol in the intestine, it can be used when statins are not tolerated or alongside statins when they are inadequate

30
Q

How do PCSkG Inhibitors work?

A

They are monoclonal antibodies that lower cholesterol. They are highly specialised and are given as subcutaneous injections every 2-4 weeks.

31
Q

Secondary Prevention of AS?

A

A- Atorvastatin 80mg
A- Ace inhibitors ( commonly ramipril) titrated to its maximum tolerated dose
A- Atenolol (or other beta blockers e.g bisoprolol) titrated to its maximum tolerated dose
A- Antiplatelet medication ( Aspirin, clopidogrel, ticagroler)

32
Q

What dual antiplatelet treatment is offered to MI patients?

A

Aspirin 75mg (continued indefinitely)
Clopidogrel or ticagroler ( max. 12months usually)

33
Q

What can be used for patients with Peripheral artery disease or after an ischaemic attack?

A

Clopidogrel

34
Q

What is family Hypercholestreolaemia?

A

It is an autosomal dominated condition that causes high levels of cholesterol. Several genes can cause the condition.

35
Q

Heterozygous =

A

Only one copy of the gene is abnormal. 1 in 250 people

36
Q

Homozygous =

A

both copies of abnormal gene, this is rare. Extremely high levels of cholesterol (> 13 mmol/L). Early CV disease almost guaranteed.

37
Q

Two criteria’s for clinical diagnosis of Familial Hypercholestreolaemia?

A

Simone Broome Criteria
Dutch Lipid Network Criteria

38
Q

Features of the two Criteria’s?

A

Family history ( anyone under 60 that has CV disease)
High levels of Cholesterol (>7.5 mmol/L)
Tendon Xanthomata (Hard nodules in the tendons that contain cholesterol, usually found in the hands or Achilles)

39
Q

Clinical management of Familial Hypercholestreolaemia?

A

Specialist referral for gene testing and family testing
Statins

40
Q

Clinical management of Familial Hypercholestreolaemia?

A

Cardiology (2 decks)

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