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Systems: Cardiovascualar AB > SIHD and Angina- Therapy > Flashcards

SIHD and Angina- Therapy Flashcards

1
Q

What is included under the umbrella ischaemic heart disease?

A
  • ACS

- Chronic or stable ischaemia

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2
Q

What is included in chronic or stable ischaemia?

A
  • Angina pectoris

- Silent ischaemia

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3
Q

What are the risk factors for ischaemic heart disease?

A
  • Hypertension
  • Smoking
  • Hyperlipidaemia
  • Hyperglycaemia
  • Male
  • Post-menopausal females
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4
Q

What is the purpose of drug treatment for ischaemic heart disease?

A
  • Relieve symptoms
  • Halt the disease process
  • Regression of the disease process
  • Prevent MI
  • Prevent death
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5
Q

What marks the start of hyperlipidaemia?

A

Atherosclerosis

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6
Q

What is hyperlipidaemia?

A
  • Disease of the muscular arteries

- Progressive deposition of cholesterol esters

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7
Q

What vessels are affected by hyperlipidaemia?

A
  • Coronary arteries

- Cerebral arteries

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8
Q

How do atherosclerotic lesions start?

A
  • As fatty streaks

- Subendothelial accumulation of large foam cells (derived from macrophages plus SM cells) filled with lipid

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9
Q

What are fibrous plaques?

A
  • More advanced than fatty streaks and the cause of disease
  • Develop from fatty streaks
  • Projects into arterial lumen
  • Reduce blood flow
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10
Q

Where do most atherosclerotic changes occur?

A
  • In the intimal layer

- Accumulation of monocytes. lymphocytes, foam cells and connective tissue

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11
Q

What is the origin of most foam cells?

A

Smooth muscle

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12
Q

What is the main structure of an atheroma?

A
  • Necrotic core

- Fibrous cap

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13
Q

What does stable IHD arise as a result of?

A

Mismatch between myocardial blood/oxygen supply and demand

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14
Q

What may precipitate an angina attack?

A
  • Any stress which increases cardiac work and myocardial oxygen demand
  • Anything which increases heart rate, stroke volume or blood pressure
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15
Q

What is demand ischemia?

A

Ischaemia during stress (physical/emotional)

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16
Q

What are the determinants of demand ischaemia?

A
  • Heart rate
  • Systolic blood pressure
  • Myocardial wall stress
  • Myocardial contractility
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17
Q

What is supply ischaemia?

A

Ischaemia at rest

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18
Q

What are the determinants of supply ischaemia?

A
  • Coronary artery diameter and tone
  • Collateral blood flow
  • Perfusion pressure
  • Heart rate (duration of diastole)
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19
Q

What is the common pathology of ischaemic heart disease?

A

-Atherosclerosis

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20
Q

Type III atherosclerotic lesion

A

Preatheroma

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21
Q

Type IV atherosclerotic lesion

A

Atheroma

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22
Q

Type V atherosclerotic lesion

A

Fibroatheroma

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23
Q

Type VI atherosclerotic lesion

A

Complicated lesion

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24
Q

How can drugs help in IHD?

A
  • Decreasing myocardial oxygen demand by reducing cardiac workload
  • Increasing the supply of oxygen to ischaemic myocardium
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25
How can cardiac workload be reduced?
- Reduce heart rate - Reduce myocardial contractility - Reduce afterload
26
What is the drug therapy for IHD?
- B-blockers - Ivabridine - Calcium channel blockers - Nitrates - Potassium channel openers - Aspirin/clopidogrel/ticagrelor - Cholesterol lowering agents
27
What drugs are rate limiting?
- B-blockers - Ivabridine - Calcium channel blockers
28
What drugs are vasodilators?
- Calcium channel blockers | - Nitrates
29
What drugs are cholesterol lowering agents?
- HMG CoA reductase inhibitors | - Fibrates
30
Give 2 examples of B blockers.
- Bisoprolol | - Atenolol
31
What are B blockers?
- Reversible antagonists of the B1 and B2 receptors - Newer drugs are cardioselective acting primarily on the B1 receptors - These agents block the physiological responses to adrenaline and noradrenaline
32
What are the 3 major determinant of myocardial oxygen demand that B blockers decrease?
- Heart rate - Contractility - Systolic wall tension
33
What do B blockers allow?
Improved perfusion of the subendocardium by increasing diastolic perfusion time
34
What affect for B blockers have on the heart?
- Decrease heart rate - Decrease the force of myocardial contraction - Decrease cardiac output - Decrease the velocity of contraction - Decrease blood pressure - Protect cardiomyocytes from oxygen free radicals formed during ischaemic episodes
35
What do B blockers do by reducing HR, force of contraction and BP?
Increase the exercise threshold at which angina occurs and so move the balance point at which the demand for oxygen outstrips the supply of oxygenated blood
36
What is rebound phenomena?
Sudden cessation of B blocker therapy may precipitate MI
37
Who is at risk of rebound phenomena?
Patients with angina and men over 50 receiving B blockers for other reasons
38
What are the contraindications for B blockers?
- Asthma - Peripheral vascular disease - Raynauds syndrome - Heart failure - Bradycardia/ heart block
39
What adverse drug reactions can occur with B blockers?
- Tiredness/fatigue - Lethargy - Impotence - Bradycardia - Bronchospasm - Rebound
40
What drug-drug interactions can occur with B blockers?
- Primary pharmacodynamics - Hypotension: hypotensive agents - Bradycardia: verapamil, diltiazem - Cardiac failure: negatively inotropic agents - Exaggerate and mask hypoglycaemic actions of insulin
41
Give 3 examples of calcium channel blockers.
- Diltiazem - Verapamil - Amlodipine
42
What do calcium channel blockers do?
Prevent calcium influx into myocytes and smooth muscle lining arteries and arterioles by blocking the L-type calcium channels
43
What CCBs are rate limiting?
Diltiazem and verapamil reduce heart rate and force of contraction
44
What CCBs are vasodilating?
Nifedipine or amlodipine may produce a reflex tachycardia
45
How do CCBs reduce myocardial work load?
Reduce vascular tone and so produce vasodilation and reduce afterload
46
How do CCBs reduce myocardial oxygen requirements?
Rate limiting CCBs reduce the heart rate and force of myocardial contraction
47
What affect can CCBs have on coronary vessels?
May produce coronary vasodilation
48
What should you never use CCB wise?
NEVER USE NIFEDIPINE IMMEDIATE RELEASE
49
What are the contraindications for CCBs?
- Post MI | - Unstable angina
50
What may rapidly acting vasodilating CCBs do?
Precipitate acute MI or stroke
51
Why should CCBs not be given post MI?
May increase the morbidity and mortality in patients with impaired LV function
52
Why should CCBs not be given to those with unstable angina?
Evidence that dihydropyridines may increase infarction rate and death in the unstable patient
53
What adverse drug reactions can occur with CCBs?
- Ankle oedema - Headache - Flushing - Palpitation
54
Give 3 examples of nitrovasodilators.
- Glyceryl trinitrate - Isosorbide mononitrate - Isosorbide dinitrate
55
How can glyceryl trinitrate (GTN) be administered?
- Sublingual - Buccal - Transdermal
56
How can Isosorbide mononitrate be administered?
- Sustained release formulation | - Tablets
57
How can isosorbide dinitrate be released?
- Sustained release formulation | - Tablets
58
What is the pharmacology behind nitrovasodilators?
-They relax almost all smooth muscle by releasing NO which then stimulated the release of cGMP which produces smooth muscle relaxation
59
How do nitrovasodilators reduce myocardial oxygen consumption?
Reduce preload and afterload
60
How do nitrates relieve angina?
- Arteriolar dilatation and so reduced cardiac afterload and thus myocardial work and oxygen demand - Peripheral venodilation and so reduces venous return, cardiac preload and thus myocardial work load - Relieves coronary vasospasm - Redistributes myocardial blood flow to ischaemic areas of the myocardium
61
Why is GTN used?
- Rapid treatment of angina pain - To avoid first pass metabolism - May be used frequently and prophylactically
62
Why are oral nitrates used?
- Can be give as a once a day sustained release formulation | - Prophylaxis
63
Why are IV nitrates used?
Main stay treatment of unstable angina where they are used combination with heparin
64
How is tolerance to the effects of nitrate therapy overcome?
- Giving asymmetric doses of nitrate 8am and 2pm | - Using a sustained release preparation which incorporates a nitrate free period
65
What are the adverse drug reactions with nitrates?
- Headaches (increase dose slowly) | - Hypotension producing GTN syncope
66
Give an example of a potassium channel opener
Nicorandil
67
What do potassium channel openers do?
- Active silent potassium channels | - The entry of potassium into cardiac myocytes inhibits the calcium influx and so has a negative inotropic action
68
Why are potassium channel openers now third line treatment?
Can result in Crohns like bowel ulcerations
69
What is ivbradine?
A selective sinud node I channel inhibitor
70
What does ivabridine do?
- Slows the diastolic depolarisation slope of the SA node - Results in a reduction in heart rate - Reduces heart rate and myocardial oxygen demand
71
Give an example of an anti-platelet agent.
Low dose aspirin (75-150mg)
72
What is aspirin
A potent inhibitor of platelet thromboxane production
73
What does thromboxane stimulate?
Platelet aggregation and vasoconstriction
74
What is the most common cause of admission with GI bleed?
Low dose aspirin
75
What does clopidogrel do?
Inhibits ADP receptor activated platelet aggregation
76
When is clopidogrel used?
- Prevention of atherosclerotic events in PVD | - ACS
77
How does clopidogrel differ in its incidenc of bleeding to aspirin?
Same incidence of bleeding but possibly lower GI bleeding
78
Give 3 examples of cholesterol lowering agents.
- Simvastatin - Pravastatin - Atorvastatin
79
What are simvastatin, pravastatin and atorvastatin examples of?
HMG CoA reductase inhibitors
80
What is the treatment regime for IHD?
- B blocker - Rate limiting CCB - Dihydropirinde CCB - Ivabridine/ranolazine - Nicorandil - Aspirin - Statin - Long acting nitrate - Refer to cardiology for work up and possible stenting
81
What are the indications for ivabridine?
- In adults unable to tolerate or with contr-indications to B blockers - In combination with B blockers in patients inadequately controlled with an optimal B blocker dose
82
What is ivabradine used for?
Symptomatic treatment of chronic stable angina in adults with normal sinus rhythm and heart rate >70bpm
83
Ivabridine is only effective in reducing the incidence of coronary artery disease in who?
Patients with heart rate of 70 bpm or over

Systems: Cardiovascualar AB (42 decks)

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