Ischaemic Heart disease Flashcards

1
Q

What is Ischaemic heart disease?

A
  • Angina (angina pectoris) or Myocardial infarction
  • Impaired blood flow or thromboembolic occlusion in coronary artery
  • Coronary blood flow does not match demand, leading to ischaemia
  • (plaque rupturing can cause platelet buildup and lead to a clot)
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2
Q

What are risk factors for IHD?

A
  • Male gender
  • Family history
  • Smoking–
  • Diabetes mellitus–
  • Hypercholesterolaemia–
  • Hypertension–
  • Sedentary lifestyle–
  • Obesity–
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3
Q

How to manage Angina pectoris?

A

Lifestyle:
* Stop smoking
* Excercise
* Diet
* Weight

  • Dif types e.g. stable, unstable angina
  • Coronary artery bypass grafting
  • Percutaneous transluminal coronary angioplasty & stenting
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4
Q

How to pharmacologically manage angina pectoris? (list)

A
  • Nitric Ocide
  • Nitrates
  • B-adrenoceptor antagonists
  • Ca channel blockers
  • ACEIs
  • Potassium channel activators
  • Ivabradine
  • Antiplatelet drugs
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5
Q

How does Nitric oxide manage Angina pectoris?

A
  • Synthesised in endothelial cells
  • eNOS (endothelial), iNOS (inducible, inv in inflammation), nNOS (neuronal, inv in synth or neuronal NO as neurotransmitter)
  • Nitric oxide=vasodilater-acts on guanylate cyclase to make cGMP which causes dilation
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6
Q

How does Nitrate manage Angina pectoris?

A
  • e.g. glyceryl trinitrate (GTN)
  • Via release of NO-Nitrates converted to NO by aldehyde dehydrogenase
  • Venodilatation(Relaxation of blood vessels) leads to a decrease in preload and a reduction in cardiac work
  • Reduce the heart’s requirement for blood
  • Also, coronary vasodilatation-more blood flows through the coronary circulation
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7
Q

Explain Nitrate tolerence.

A
  • Prolonged exposure can reduce effectiveness
  • Partly due to reduced conversion by aldehyde dehydrogenase
  • Inactivation by reactive oxygen species (ROS) e.g. superoxide (O2-)

Side effects:
* Vasodilation also causes headaches-cerebral vasodilatation
* Also-postural hypotension-impaired distribution of blood

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8
Q

How do B-adrenoreceptor Antagonists manage Angina pectoris?

A
  • First choice drugs for prevention
  • ↓ HR & ↓Force–> ↓Cardiac work and preventing symptoms
  • Slowing HR inc diastolic period, as will the time for coronary blood flow.
  • B-adrenoceptors inc K+ channel closing-red the time betw contractions and therefore inc HR
  • B-blockers-therefore block this and red HR
  • Coronary blood flow occurs during diastole
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9
Q

How do calcium channel blockers manage Angina pectoris?

A
  • Dihydropyridines: Block vasoconstriction so improve coronary blood flow
  • Verapamil & diltiazem-effects on HR so reducing Cardiac work
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10
Q

How do ACEIs manage Angina pectoris?

A
  • Vasodilation-reduced workload on the heart
  • Reduction in MI and stroke
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11
Q

How do potassium channel activators manage Angina pectoris?

A
  • Nicorandil: combined NO donor and activator of ATP-sensitive K-channels
  • The target is the ATP-sensitive K+-channel
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12
Q

How does Ivabradine manage Angina pectoris?

A
  • Inhibits If channels (pacemaker Na/K currents in the SAN)
  • HCN channel
  • Red HR-by slowing rate of depolarisation
  • Ivabradine enters the channel from inside when in open state
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13
Q

How do Antiplatelet drugs manage Angina pectoris?

A
  • Inhibition of platelet aggregation prevents clot formation
  • Ensures blood flow through coronary artery
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14
Q

What is a Myocardial infarction?

A
  • Thromoembolism or rupture of plaque
  • Thrombus forms in a blood vessel (blocks blood flow), leading to infarction (tissue death due to inadequate blood supply)
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15
Q

What are the symptoms of MI?

A
  • Prolonged cardiac pain-chest, throat, arms, epigastrum or back
  • Breathlessness
  • Collapse
  • Anxiety
  • Nausea/vomiting
  • May be ‘silent’ MI
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16
Q

What are the signs of MI?

A
  • Pallor/sweating/tachycardia (due to symp activation), and signs of impaired cardiac functions
17
Q

How to diagnose MI?

A

Cardiac Enzymes:
(Creatine Kinase(CK)), Aspartate aminotransferase(AST)), Lactate dehydrogenase(LDH))
* MI tissue damage leads to inc in plasma conc of enzymes in cardiac cells

Troponin T
* Released within hours
* Peaks at 36 hours
* Small amounts released in unstable angina

18
Q

What are the goals of treatment?

A
  • Restore coronary flow/limit infarct size
  • Prevent/reduce arrhythmias
  • Prevent reinfarction
19
Q

What is the immediate treatment for MI?

A

Thrombolysis:
* Dissolves the clot, with reperfusion, salvages cardiac muscle
* Fibrinolytics convert plasminogen to plasmin-degrades fibrin
* If indicated, the earlier the better-damage is irreversible 6h post MI. Only really effective in 1st 12h
* E.g. streptokinase

20
Q

What is the immediate treatment for MI?

A

Thrombolysis:
* Dissolves the clot, with reperfusion, salvages cardiac muscle
* Fibrinolytics convert plasminogen to plasmin-degrades fibrin
* If indicated, the earlier the better-damage is irreversible 6h post MI. Only really effective in 1st 12h
* E.g. streptokinase

21
Q

What to give once discharged from hospital?

A
  • Antiplatelet drugs
  • B-adrenoreceptors antagonist (Ca channel blocker)
  • ACEi
  • Statin
  • All lower risk-additive