Acute coronary syndromes Flashcards
What can be the causes of chest pain
broken rib
collapsed lungs
infection
pulled muscle
ANGINA
MYOCARDIAL INFARCTION
What are the classification of coronary artery disease
- Chronic ischemic heart disease
-stable angina - Acute coronary syndromes
- Unstable angina
-N-STEMI
-STEMI
What are the differences between unstable and stable angina, N-STEMI and STEMI
- Stable angina: the atherosclerotic plaque has a strong fibrous cap which prevents it from rupturing. It occludes 70% of the artery. Upon exertion - stable angina is triggered causing ischemia of the endocardial tissue
acute coronary syndromes:
-Unstable angina
The atherosclerotic plaque ruptures, platelets will form on the surface of the plaque. This will cause 90% occlusion of the artery and lead to the ischemia of the endocardial tissue. The unstable angina is triggered upon exertion
-N-STEMI: (Non-ST segment elevation MI)
The atherosclerotic plaque ruptures, platelets will form on the surface of the plaque. This will cause 90% occlusion of the artery and lead to the ischemia of the endocardial tissue for MORE THAN 30 MINUTES- this leads to INFARCTION
(triggered at rest)
-STEMI: (ST segment elevation MI)
The atherosclerotic plaque ruptures, platelets will form on the surface of the plaque. This will cause 100% occlusion of the artery and lead to the ischemia of the endocardial tissue for MORE THAN 30 MINUTES- this leads to INFARCTION
(triggered at rest)
How is ischemic heart disease measured
- Medical history
- Signs/symptoms
-ECG
-Biomarkers
-Imaging and scans- CT angiography
What are the treatments for Acute STEMI (Acute ST segment elevation myocardial infarction)
- Pharmacological treatment
-thrombolytics and fibrolytics: streptokinase, urokinase, tissue plasminogen activators - Surgical Intervention
-Balloon Angioplasty: using a balloon to stretch open an artery
-Stent
- coronary bypass
How does t-PA cause thrombolysis
t-PA results in plasminogen activation
Plasminogen converts into plasmin
Plasmin degrades fibrin into fibrin degredation products.
- t-PA is more like a catalyst
normally in the body: t-PA is bound to PA-I
How is streptokinase different to t-PA
- Streptokinase is bacterial- possible immune recognition
- Streptokinase binds to circulating plasminogen not plasminogen associated with fibrin
- SK is less specific to fibrin
- SK generates antibodies which may lead to a possible allergic reaction
- Streptokinase forms a complex that converts additional plasminogen to plasmin
What is the structure of Alteplase
structural differences in t-PA affect the mode of action
- Kringle domain 1: glycosylation, liver clearance
- Kringle domain 2: interacts with t-PA, interaction with Fibrin
- Growth factor and finger domain: high affinity for fibrin and low affinity for receptor binding and clearance
4.Protease domain: proteolytic activity
What are Kringle domains
triple looped domains linked by disulphide bonds
What is the structure of Reteplase and how does this enhance the function of t-PA
- Removed kringle 1: reduced liver clearance
- removed glycosylation: an increased half life
- Removed growth factor and finger domain: dec binding to fibrin
What is the structure of tenectaplase?
- Modified glycosylation: inc plasma half life
- 4- Alanine substitutions: inc. affinity for fibrin, increased resistance to PA-1 and reduced systemic plasmin activation
Steps for treating N-STEMI
- ECG
-Myocardial oxygenation
-Thrombolysis - Baloon angioplasty
What are the PROs& CONs of Angioplasty
PROS:
- in 60 mins, there is a 95% rate of recanalisation
- No systemic fibrinolysis
- Reduced rate of death and reinfarction
Cons:
-costly
-requires specialist staff
What are the PROs& CONs of thrombolysis
PROS: -In 90 mins, recanalisation rate is 55-60%
CONS:
-Re-occlusion rate is 5-15%
- Risk of Intracranial haemorrhage with mortality rate
- Some patients are contraindicated for fibrinolytics
What is the long term management after a myocardial infarction
reduce BMI
Improve diet
blood pressure management
Lipid management
smoking cessation
management of LV dysfunction