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Cardiovascular > Acute MI > Flashcards

Acute MI Flashcards

1
Q

Types of acute coronary syndrome

A

Unstable angina
Acute NSTEMI
Acute STEMI

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2
Q

Chronic Stable angina

A

Fixed stenosis
Asymptomatic at rest- demand led ischaemia
Predictable and safe
Not ACS

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3
Q

Unstable angina

A

Dynamic stenosis
Symptomatic at rest- supply led ischaemia
Dangerous and unpredictable

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4
Q

Formation of thrombis

A

Normal-> fatty streak-> atherosclerotic plaque-> fibrous plaque-> plaque ruptures spontaneously, causing thrombosis

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5
Q

Factors affecting Plaque Ruptures

A
  • plaque lipid content
  • thickness of fibrous cap
  • shape
  • mechanical injury
  • sudden pressure changes
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6
Q

Typical presentation of patient with STEMI

A

Central crushing chest pain, which can radiate to arms and jaw
More severe and prolonged than angina attack and not relieved by GTN spray
Occurs at rest
N+V, sweating

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7
Q

What happens in initiation stage of platelet cascade?

A

Vascular damage, exposing endothelial tissue

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8
Q

What happens in adhesion stage of platelet cascade?

A

Monolayer of platelets (which are normally blocked by NO and prostacyclin, both of which are low/ absent during injury) stick on site of injury. They stick as VWF is released from endothelial cells onto site of injury to which it binds to as well as platelets. VWF activates platelets

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9
Q

What happens in activation and degranulation stage of platelet cascade?

A

Platelets and G2b/3a change shape when activated, releasing granules into blood allowing for degranulation.
TxA2 is secreted

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10
Q

What are the granules found in platelets and G2b/3a? What do each of them contain?

A

Alpha granule, which contains fibrinogen and VWF

Dense granule, which contains serotonin, ADP and calcium (SAC)

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11
Q

Role of serotonin and its alternative name

A

5-HT

Smooth muscle constrictor

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12
Q

Role of ADP in platelet cascade

A

Platelet activation and promotion of aggregation

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13
Q

TxA2 production and role

A

Made by prostacyclin (a vasodilator)

It is a vasoconstor, activates platelets and promotes aggregation

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14
Q

What happens in aggregation stage of platelet cascade?

A

Activated platelets bind to G2b/3a, causing a conformational change and allowing it to bind to fibrinogen.
Here is clots and creates a plug

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15
Q

Cardiac enzyme and protein markers in MI

A

Troponin I and T, above 99%th percentile, detected within 6hrs, Serum levels- peak at 24-48hrs

Creating Kinase- reach peak at 24hrs

Myoglobin- released rapidly from infarction tissue (detected in 2hrs after acute MI) but has poor sensitivity

BNP

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16
Q

Early treatment for STEMI

A 
Morphine (+ae)
Oxygen (94-98)
Nitrates (GTN spray, monitor BP)
Aspirin (300mg, chewed)
\+
Ticagrelor (180mg or 600mg coplidogrel)
17
Q

Mechanism of clopidorgel

A

P2Y12 antagonist (blocks ADP receptor), preventing conformational change of platelet

18
Q

Mechanism of aspirin

A

Switches of COX (cyclooxygenase) enzyme system, preventing TxA2 production and therefore platelet activation/ aggregation/ vasoconstriction

19
Q

Thrombolysis role, timeframe and risks

A

Clot busting IV drug
>20mins;<12hrs- only if cant get patient in cath lab within 120mins for PCI
Risk of haemorrhage, inability to reperfuse and hypersensitivity

20
Q

Inhibiting the coagulation cascade

A

Heparin/LMWH-> prevents factor X from producing Xa

G2b/3a inhibitors prevent platelet aggregation

21
Q

Medication given post MI

A 
Antiplatelets
- aspirin and ticagrelor
Beta blockers
- bisoprolol
ACEI
- ramipril
Statin
- atorvastatin
22
Q

Type 1 MI

A

Spontaneous, related to ischaemia due to primary coronary event eg plaque erosion

23
Q

Type 2 MI

A

Secondary to ischaemia due to Oxygen imbalance eg in HT

24
Q

Type 3 MI

A

Sudden unexpected cardiac death w symptoms suggestive of MI

25
Q

Type 4a and b MI

A

4a- MI associated with PCI

4b- MI associated with documented in stent thrombosis

26
Q

Type 5 MI

A

MI associated with CABG

Cardiovascular (14 decks)

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