IHD Flashcards
2 Main causes of IHD - what does this centre around?
Disease of the coronary arteries (fatty plaque build up / atherosclerosis)
Non-acute coronary syndrome: stable angina
Angina
Atherosclerosis
What is meant by ischaemia?
Resitriction of blood flow to tissues
Atherosclerosis features
Atherosclerosis –> restricts blood flow to tissues (ISCHAEMIA), blocks arteries, progressive with age, has modifiable risk factors
Angina features
Blood, o2, nutrients, cannot reach the myocardium
Results in chest pain and cell death of the myocardium
Pain in chest seems to occur with less and less exertion
Stable angina - why is it different?
NOT an acute coronary syndrome
Occurs due to emotional or physical stress
Acute coronary syndromes- what are they ?
Unstable angina
NSTEMI (non st elevation myocardial infarction)
STEMI (st elevated myocardial infarction)
What can normally be found in a completely blocked artery
Both a thrombus and a fatty plaque
What is seen to distinguish a STEMI from other ACS
No relief from GTN (nitrate treatment) Troponin present (released as a result of damaged cardiac muscle) Abnormal ECG (elevated ST)
What is seen to distinguish a N-STEMI from other ACS
No relief from GTN
Troponin present
Abnormal ECG (but no elevation of ST)
What is seen to distinguish stable angina from other ACS
Relief from GTN
No troponin present
Normal ECG
What is seen to distinguish unstable angina from other ACS
Relief from GTN
No troponin
Normal ECG
Angina treatment - stable and unstable?
Characterised by crushing pain in the chest
Relieved by rest (no exercise)
- Stable = asparin, ca2+ channel blocker
- Unstable = TREAT AS MI - anti platelet meds, asparin
Treatment of ischaemia - what do we aim to do?
Restore blood flow (prevents HF and death of myocardium)
Stenting (opens blocked arteries)
Reduce coagulation (prevents blockage of arteries - warfarin and asparin)
Reduce myocardial o2 demand (reducing work/contractility of the heart)
Control risk factors (stop smoking/good diet!)
Features of stent - how soon does it need to be applied? Drugs coating device? Overall process?
PCI (percutaneous coronary intervention)
Ideally needs to happen <120 minutes (door -> balloon time)
Catheter used to dilate vessel and push plaques away
Stent coated with RAPAMYCIN which inhibits proliferation of cells
Stenting - overall process, what does it aim to do, how can it be personalised
- Restores blood flow in coronary arteries
- Balloon placed inside the stent, balloon inflated, balloon removed
- Can get balloons of different sizes for personalised aspect
What must be done after PCI? Additional benefits?
- After treatment DAPT (dual anti platelet therapy)
Plavix/asparin - Up to a year after stenting
- Adverse effects = excessive bleeding
- Additional benefits = anti inflammatory as has positive pleiotropic effects on neutrophils
Pharmacological treatments for IHD - prognostic (in anticipation of future event)
- Statins
- Ace –|s
- Asparin/DAPT
Pharmacological treatments for IHD - symptomatic (reduces associated symtoms)
- Nitrates
- Asparin/antiplatelet
- Ca2+/K+ channel blockers
Nitrates – what is their mechanism of action?
Metabolises release of NO (causes production of GNP from GTP –> activates PKG)
Relaxes vascular smooth muscle and veins
Where do nitrates mainly target/
Large muscular arteries
They decrease cardiac work and redirect ischaemic flow
Adverse effects of nitrates
- Tolerance
- Headaches
- Hypotension
- Dilation in the collateral vessels of the heart
How is IHD treatment personalised?
- Length of stents
- Mapping of coronary arteries
- Can measure activity of platelets in patients to work out the best drugs for their dynamics
Ca2+ channel blockers - name an example? Features and mechanism?
VERAPAMIL Target L type channels Cardioselective Few side effects Disrupt movement of Ca2+ through channels to prevent release from sarcoplasmic reticulum
ASPARIN - adverse effects?
Gastric bleeding
Resistance
Self poisoning risk
Deafness/tinnitus
Asparin - mechanism of action?
Bind to active site of COX1 enzyme - acetylates serine residue
Prevents Arachodonic acid from doing so
This prevents the production of Prostoglandin H2 which means it cannot be converted into Thromboxane A2 which activates platelets via TP receptors
Platelets don’t have nucleus so until more COX1 is produced platelets cannot coagulate (IRREVERSIBLE)
HEPARINS - mechanism of action, adverse effects
Activation of anti clotting factors including ANTITHROMBIN |||a - this inactivates Thrombin and Factor Xa which prevents clot formation
Can result in EXCESSIVE BLEEDING
Analgesia - main example - why is it used and where does it exert its’ action?
Very powerful painkiller which is well tolerated when correctly administered
Binds to Opoid receptors Go and Gi in the brain
Coupled to ion channels
Analgesia - adverse effects
Induces release of histamines Dependance Vomiting and nausea Decreased gut tone and mobility Respiratory depression
Treatment summary - unstable angina -
1) DAPT
2) Heparin
3) Analgesics
Then move onto secondary prevention drugs such as ACE–|s, B blockers and Statins
Treatment summary - NSTEMI
1) DAPT
2) Heparin
3) Platelet inhibitor
Then if ECG changes, stent within 72 hours and analgesics must be applied
Treatment summary - STEMI
1) PCI
2) IV clot buster (catheterisation)
3) Antiplatelet drugs (DAPT - asparin + clopidogrel)
If this doesn’t work you’re fucked (lifelong meds ACE-|s, asparin, statins, b blockers)
