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Cardio and Resp diseases > Acute coronary syndromes > Flashcards

Acute coronary syndromes Flashcards

1
Q

What are some causes of chest pain?

A
  • Blood clot in the lungs (PE)
  • Angina
  • Myocardial infarction – most severe
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2
Q

Why is it important to define the type of IHD (ischaemic heart disease)?

A

Need to know if it’s stable Angina or Acute Myocardial Infarction (needs rapid intervention)
• Treatment
• Prognosis
• Management

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3
Q

What is considered in the assessment of IHD?

A
  • Medical history
  • Risk factors
  • Presenting signs and symptoms
  • ECG
  • Biomarkers
  • Imaging/scans
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4
Q

What 2 major diseases is coronary heart disease divided into it?

A
  • Acute coronary syndromes

- Chronic ischaemic heart diseases

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5
Q

Examples of chronic ischaemic heart diseases?

A
  • Stable angina: pain gets worst with exertion
  • Variant angina: due to vascular spasm of the vessels
  • Silent myocardial ischaemia: fewer symptoms, low oxygen levels, not feeling chest pain
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6
Q

Examples of acute coronary syndrome?

A
  • Unstable angina: pain even without exertion, ECG and cardiac marker elevation differentiates it
  • Non ST-segment elevation MI
  • ST-segment elevation MI: more serious than NON ST-segment elevation MI
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7
Q

How is acute cardiac ischemia caused?

A
  • Plaque disruption or erosion
  • Thrombus formation with or without embolization
  • acute cardiac ischemia happens
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8
Q

What is the difference between ST segment elevation and non-ST segment elevation?

A
  • No necrosis (troponin markers are normal) – it’s unstable angina
  • If there is necrosis – it’s a non ST segment elevation
  • If there’s markers of necrosis and the ST segment elevation on ECG, it’s ST segment elevation
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9
Q

What is seen in unstable angina patients?

A

More flow in unstable angina patients – flow is reduced but not enough to increases markers

• The lumen is wider than non-ST segment elevation MI/ST segment elevation MI

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10
Q

What is seen in non-ST segment elevation?

A

In non-ST segment elevation there’s a significant reduction in lumen – thrombus and platelet activation aggregation is more significant

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11
Q

What is seen in ST segment elevation?

A

In ST segment elevation – full occlusion of vessel

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12
Q

What are the treatment aims for acute coronary syndromes?

A
  • Relieve symptoms
  • Improve survival
  • Minimise cardiac risk

Major aim of treatment should be to facilitate a return to normal activities

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13
Q

What are the methods of recanalisation for acute myocardial infarction?

A

With ST segment 2 options:

– PCI (percutaneous coronary intervention), balloon angioplasty with stent
– thrombolytic therapy, usually if there’s no access to PCI/primary angioplasty

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14
Q

What happens if there is no recanalization after thrombolytic treatment?

A

If there’s no recanalization after thrombolytic treatment, delayed/rescue angioplasty is used

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15
Q

What is used to monitor and manage the patients?

A

Cardiac CT angiography

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16
Q

What are the treatments of acute coronary syndromes?

A

• Surgical/Intervention
o Balloon angioplasty
o Stent
o Coronary bypass

• Pharmacological treatment

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17
Q

What is the initial pharmacological approach for ST-segment elevation myocardial infarction?

A
  • Given O2 (2-4 L/min) if patient has short of breath
  • IV diamorphine with IV anti-emetic (metaclopramide or cyclizine) – pain relief
  • Aspirin and Clopidogrel – anti-platelet
  • IV beta adrenergic antagonists - beta blocker
18
Q

What are some thrombolytics/fibrinolytics used for treatment?

A
  • Streptokinase - cheap
  • Urokinase
  • Tissue plasminogen activators – mainly used
19
Q

What are 2 plasminogen activators?

A
  • Tissue plasminogen activator (tPA)

- urokinase plasminogen activator (uPA)

20
Q

What does thrombin do?

A

converts fibrinogen into fibrin which cross links with other fibrin – forms net

21
Q

Describe tissue plasminogen activator-mediated thrombolysis?

A
  • Tissue plasminogen activator (tPA) and urokinase plasminogen activator (uPA) are plasminogen activators – convert plasminogen to plasmin (potent proteolytic enzyme that degrades cross linked fibrin net into small pieces)
  • Binding sites on tPA and plasminogen for fibrin – makes fibrinolysis very specific to fibrin formation/where the clot is
22
Q

What is the normal conformation for tPA and why is it kept in that conformation normally?

A

tPA normally kept in inactivate conformation by plasminogen activator inhibitor type 1 (tPAI1)

  • tPA-PAI1 complex tethered to EC – prevents tPA from activating circulating plasminogen
  • when there’s fibrin tPA has greater affinity for it, can disassociate from its complex and bind to fibrin and plasminogen and form the degradation products
23
Q

What is a plasmin inhibitor?

A

a2 antiplasmin

24
Q

Difference between tissue plasminogen activator and streptokinase (which is also a plasminogen activator)?

A
  • SK is bacterial (beta-haemolytic streptococci) possible immune recognition
  • SK will bind circulating plasminogen not associated with fibrin – generalised plasmin generation aka systemic plasminogen activation
  • SK is less fibrin specific, more systemic plasminogen activation and can cause bleeding
  • Antibodies (because it’s bacterial) generated that thwart subsequent doses and possible allergic reaction
25
Q

What is mechanism of action of Streptokinase?

A
  • SK binds with free circulating plasminogen/plasmin

* Forms an active complex (with plasminogen and plasmin) that can convert additional plasminogen to plasmin

26
Q

What are structural differences between Alteplase and newer formulations of tPA (Reteplase and Tenecteplase)?

A
  • Alteplase (Actilyse/Activase) – full length tPA
  • Reteplase – derivative of tPA
  • Tenecteplase – modification of tPA
27
Q

What are kringle domains?

A

Kringles are triple-looped, disulphide cross-linked domains found in a varying number of copies, in some serine proteases and plasma proteins:

  • Tissue plasminogen activator (tPA) (2 copies)
  • Urokinase-type plasminogen activator (1 copy)
28
Q

What are the different functional domains of tPA/alteplase (rtPA)?

A
  • Finger domain at the n-terminus
  • Growth factor domain/epidermal growth factor domain
  • 2 Kringle domains – each is a triple looped structure held by further bonding
  • Proteolytic domain
29
Q

What is the function of the finger and growth factor domains?

A
  • these structural units have high affinity for fibrin – give the specificity for fibrin
  • have low affinity for receptor binding sites on EC – they bind loosely to EC cells
30
Q

What is the function of the kringle domains?

A
  • Kringle 1: involved in clearance – through the liver the molecule gets cleared by kringle 1 unit cause it had some specific binding sites
  • Glycosylation of kringle 1 domain cause of side chains
  • Kringle 2: interacts with PAI-1
  • There’s also some fibrin binding
  • Kringle 2 leads onto proteolytic domain
31
Q

What is the function of the proteolytic domain?

A
  • Where the catalytic activity of the protein is located
  • Where plasminogen is activated into plasmin
  • Interactions with PAI-1
32
Q

What is the structure of reteplase (r-PA)?

A
  • Only has Kringle 2 domain and protease domain
  • Deletion of finger region, EGF-like domain and kringle 1, & carbohydrate side chains
  • Hepatic elimination of the molecule is reduced – cause kringle 1 domain is removed
  • Plasma half-life is increased to 14–18 minutes (versus 3–4 minutes with alteplase)
  • Diminished fibrin binding
33
Q

What is the structure of Lanoteplase (nPA)?

A
  • Only has 2 kringle domains and protease domains

* Not used clinically

34
Q

What is the structure of Tenecteplase?

A
  • Has all of the domains but has modifications
  • Modified glycosylation residues/glycosylation side chains binding sides in K1
  • Asn-103 for Thr
  • Gln-117 for Asn = prolonged half-life and glycosylation prevented
  • 4 alanine substitutions at 296-299 in Protease domain = enhanced fibrin specificity and resistance to PAI-1 inhibition, reduced systemic plasmin activation
35
Q

What is really critical in acute coronary syndrome treatment?

A

Time from onset and severity of symptoms is critical

  • Arrival to ECG: has to be 10 min of chest pain
  • Door-to-needle for thrombolysis: 20 min
  • Door-to-balloon time for PCI: 60 min
36
Q

What are the pharmacological treatments for acute coronary syndrome?

A

go down in this order, starting from top

  • General myocardial oxygenation
  • Antiplatelet/Antithrombotic
  • Analgesia
  • Myocardial energy consumption
  • Coronary vasodilatation
  • Anticoagulation
  • Thrombolysis
  • Plaque stabilization
37
Q

Surgical interventions for ACS?

A
  • Reperfusion

* Re-vascularisation

38
Q

Pros and cons of thrombolysis?

A
  • 55-60% recanalisation of vessel within 90 mins
  • 5-15% risk of reocclusion
  • Worsening ventricular function
  • 1-2% risk of intracranial haemorrhage with 40% mortality
  • 15-20% of patients have a contraindication to thrombolysis
39
Q

Pros and cons of angioplasty

A
  • 95% recanalisation of vessel within 60 mins
  • No systemic fibrinolysis
  • Reduced rates of death, cerebrovascular events and re-infarction
  • Costly
  • Specialist facilities and staff
40
Q

Long term management after a myocardial infarction?

A
  • Smoking cessation
  • Physical activity
  • Diabetes management
  • Diet and weight reduction
  • Blood pressure control
  • Lipid management
  • Management of heart failure or LV dysfunction
  • Prevention of sudden death

Cardio and Resp diseases (29 decks)

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