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Cardio/Resp > Acute Coronary Syndromes > Flashcards

Acute Coronary Syndromes Flashcards

1
Q

Some causes of chest pain (10)

A

Broken rib
Collapsed lung
Nerve infection (shingles)
“Pulled” muscle
Infection
Heart burn (hernia)
Pericarditis
Blood clot in the lungs (PE)
Angina
Myocardial infarction

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2
Q

Why is it important to define the type of IHD? (4)

A

need to know if Stable Angina vs Acute Myocardial Infarction

for:
Treatment
Prognosis
Management

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3
Q

Assessment of IHD (6)

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

Chronic and acute coronary heart disease branching graph (6)

A

image
chronic HD vs acute CS

c:
- stable angina
-variant angina
-silent myocardial ischaemia

a:
- unstable angina
-non ST-segment elevation MI
- ST-segment elevation MI

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5
Q

Characterisation of acute coronary syndromes

A

flowchart for diagnosis

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6
Q

Acute coronary syndromes (3)

A

thinking about vessel occlusion

unstable: more flow + potential thrombus

Non-stemi: sig reduced lumen + sig platelet + thrombus activation (areas of necrosis)

stemi: full occlusion - severe disease

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7
Q

Treatment aims (4)

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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8
Q

2 options for ST segment(2)

A

Surgical/Intervention: PCI
 Balloon angioplasty
 Stent
 Coronary bypass

or

Pharmacological treatment - thrombolytic therapy (if no access to primary angioplasty)

image

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9
Q

imaging -Cardiac CT angiography benefits (4)

A

vital for patient management

location of occlusion

location of stent

follow up

images

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10
Q

ST-segment elevation myocardial infarction - initial (5)

A

oxygen (shortness of breath)

anti-emetic (IV morphine)

aspirin + clopidogrel

betablocker

GTN (reduce work of heart)

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11
Q

Thrombolytics/Fibrinolytics (3)

A
  • Streptokinase
  • Urokinase
  • Tissue plasminogen activators
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12
Q

Tissue plasminogen activator-mediated
thrombolysis (5)

A

image

t-PA + urokinase- A: both convert plasminogen > plasmin

plasmin = potent proteolytic enzyme - degrades fibrin net (fibrin degradation products)

  • tPA is a plasminogen
    activator
  • Catalyst
  • Fibrin selectivity

fibrin binding sites on t-PA + plasminogen: fibrinolysis specific to this

t-pa kept in inactive conformation (t-PAi complex) = prevents activating circulating plasminogen

because t-PA has high affinity for fibrin so can dissociate and bind to it = degradation

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13
Q

Tissue plasminogen activator versus
streptokinase (4)

A

SK is bacterial (beta-haemolytic streptococci)
possible immune recognition (allergic)

  • SK will bind circulating plasminogen not associated with fibrin – generalised plasmin generation (bleeding)
  • SK is less fibrin specific, more systemic plasminogen activation and bleeding
  • Antibodies generated that thwart subsequent doses and possible allergic reaction
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14
Q

MoA Streptokinase (2)

A
  • SK binds with free circulating
    plasminogen/plasmin
  • Forms an active complex that can convert additional
    plasminogen to plasmin
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15
Q

Structural differences b/w Alteplase and newer
formulations of tPA (Reteplase and Tenecteplase):
how structural differences affect mode of action (3)

A

Alteplase (Actilyse/Activase) - full length t-PA

  • Reteplase - t-PA deriv (fragment)
  • Tenecteplase - modifed t-PA
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16
Q

t-PA structure (3)

A
  • finger domain (N term):
    GF/ GF-like domain = High affinity for fibrin, Low affinity receptor binding/clearance

-kringles: 2x
1 = Liver clearance, Glycosylation
2=Interaction with PAI-1, Fibrin binding

-protease: Proteolytic activity, Interaction with PAI-1

17
Q

Kringle domains (4)

A

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

  • evolutionary conserved
  • in GF’s
  • in coag factors
  • etc

Apolipoprotein A= 38 copies
Blood coagulation factor XII= 1 copy
Hepatocyte growth factor (HGF) (4 copies)
Hepatocyte growth factor like protein (4
copies)
Plasminogen (5 copies)
Thrombin (2 copies)
Tissue plasminogen activator (tPA) (2
copies)
Urokinase-type plasminogen activator (1
copy)

18
Q

derivatives of t-PA (4)

A

Alteplase=tPA

Reteplase =r-PA or K2P

Lanoteplase =nPA (not as useful)

Tenecteplase =TNK-PA

19
Q

Reteplase =r-PA or K2P (4)

A
  • Deletion of finger region, EGF-like domain and kringle 1, & carbohydrate side chains
  • Hepatic elimination of the
    molecule is reduced
  • Plasma half life is increased to 14–18 minutes (versus 3–4 minutes with alteplase)
  • Diminished fibrin binding
20
Q

Tenecteplase modifications (2)

A

has: EGF-like domain, 2 kringles + protease domain (full length)

Modified glycosylation
residues/sites (in K1 Asn-103 for Thr Gln-117 for Asn) =prolonged half-life (necessary in liver clearance)

4 alanine substitutions at
296-299 in Protease = enhanced fibrin specificity and resistance to PAI-1 inhibition, reduced systemic
plasmin activation

21
Q

Treatment of
ACS summary (6)

A

Time from onset and severity of symptoms is critical

medical:
* General myocardial
oxygenation
* Antiplatelet/Antithrombotic
* Analgesia
* Myocardial energy
consumption
* Coronary vasodilatation
* Anticoagulation
* Thrombolysis
* Plaque stabilization

surgical:
* Reperfusion
* Re-vascularisation

  • Arrival to ECG: within10 min
  • Door-to-needle for thrombolysis: within 20 min
  • Door-to-balloon time for PCI: within 60 min
22
Q

Thrombolysis versus Angioplasty: Pros and Cons (12)

A

Thrombolysis:
* 55-60% recanalisation 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

Angioplasty:
* 95% recanalisation within 60 mins
* No systemic fibrinolysis
* Reduced rates of death,
cerebrovascular events and
re-infarction
* Costly
* Specialist facilities and staff

23
Q

Long term management after a myocardial infarction (8)

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/Resp (34 decks)

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