Acute coronary syndromes Flashcards
(15 cards)
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
