CV Pharmacology Flashcards
How do Beta-Blockers work in:
a) HTN
b) CCF
c) Angina
a) Negative inotropy leading to reduced Cardiac output.
MAP = CO x SVR
b) Reduced heart rate, so more time to fill, hence increased preload and better CO (frank-starling)
c) Reduced heart rate, hence increased diastolic time and time for heart to fill
Drugs in CCF.
a) 3 Drug classes with prognostic impact in heart failure
b) why no prognostic benefit of diuretics?
c) When to consider digoxin. How does digoxin work?
a) ACEI, cardioselective BBs, aldosterone antagonists
b) Possibly due to nephrotoxic effects
c) In AF, or where BB/ACEI has not effectively stabilised patient
Works by inhibiting Na/K/ATPase channel. This slows the heart rate but increases stroke volume. Isolated from the foxglove plant
Antiplatelets and anticoagulants.
a) Why APs useful in thrombosis and ACs in embolism?
b) MoA of aspirin
c) MoA of clopidogrel/ticagrelor
d) MoA of warfarin (affects which coag factors?)
e) MoA of DOACs?
f) MoA of heparin
g) UFH vs LMWH
a) - Platelets more active in high pressure/shearing systems (arterial) whereas coagulation factors more active where there is stasis (venous/heart chambers).
- Anticoagulants prevent thrombin formation (which is needed to activate platelets), hence they also have an anti platelet effect
b) COX inhibition - prevent formation of prostanoids (eg prostaglandins, thromboxane A2)
c) Inhibition of P2Y12 receptor (found on ADP): Prevent platelet aggregation (but no effect on platelet number)
d) Vitamin K antagonist: inhibits production of factors II, VII, IX and X
e) - Dabigatran: Direct thrombin inhibitor
- ApiXaban/ rivaroXaban: indirect thrombin inhibitors (via inhibiting conversion of factor X to factor Xa)
f) Activates antithrombin (which inactivates thrombin); hence it is an indirect thrombin inhibitor
g) - UFH has a shorter half life (quicker onset/offset) so is preferred for patients at high risk of bleeding
- LMWH (dalteparin, enoxaparin, tinzaparin) has a longer duration of action and so is preferred for VTE
NSAIDs.
a) Inhibit what enzyme
b) Which leads to reduced production of…?
c) Explain the GI side effects, with respect to the correct pathway
d) Explain the Cardiac side effects, with respect to the correct pathway
e) What drugs are more COX-1 or COX-2 selective? Explain dosing effects also
f) Explain the effect on GFR
a) Cyclooxygenase (COX)
b) Prostaglandins and thromboxane
c) PGE2 from the COX-1 pathway protect the stomach lining. Hence COX-1 inhibitors increase risk of ulceration and UGIB
d) PGs from the COX-2 pathway lead to increase thrombosis risk, and should be avoided in CCF/heart disease
e) COX-1: Naproxen, aspirin
COX-2: celecoxib, meloxicam, diclofenac
Ibuprofen non selective
In higher doses, COX-1 effects become greater, even in COX-2 selective drugs
f) PGs lead to afférent artériole vasodilation (hence keep GFR high). NSAIDs block this, leading to afférent artériole vasoconstriction and reduced GFR.
(Note: ACEI lead to efferent artériole vasodilation, reducing glomerular pressure and reducing GFR; to remember - ACE has an ‘e’ for ‘efferent’ whereas NSAID does not have an ‘e’)
Management of:
a) NSTEMI
b) STEMI
c) HFREF
d) HFPEF
e) Stable angina
f) Secondary prevention of MI
a) - DAPT, GTN, anticoagulation (+/- opioids and oxygen)
- Angio + PCI may be indicated in patients deemed at moderate-high risk of future cardiac event
b) As above, plus:
- Primary PCI (presentation within 12h of onset and can be carried out within 2h), or
- Thrombolysis
c) 1st line: ACEI + BB + loop diuretic 2nd line: add spiro 3rd line agents: (under specialist supervision): - Long acting nitrates - Digoxin - Ivabradine - Sacubitril valsartan Adjuvants: anticoagulation (AF, hx of VTE/LV aneurysm)
d) Symptom control and manage risk factors
e) - 1st line: Aspirin + BB or CCB + GTN spray
- If indicated: ACEI, statin
- 2nd line: long-acting nitrates, ivabradine, nicorandil, ranolazine
f) - DAPT (aspirin + ticagrelor)
- ACE inhibitor
- Beta-blocker
- Statin
Statins.
a) MoA
b) When to take simvastatin
c) Indications
d) Side effects
e) Monitoring
a) Inhibit HMG CoA reductase, which synthesises cholestérol in the liver
b) At night
c) Hypercholesterolaemia (if conservative measures failed)
- QRISK > 10% / diabetes
d) Constipation, diarrhoea, myalgia/Myopathy
e) HDL/LDL cholesterol, renal function, thyroid disease, liver function
Antiplatelet indications and choice.
a) Primary prevention in CVD
b) Angina
c) PAD or post-stroke/TIA
d) Post-ACS
e) AF
a) Not routinely indicated; only those at high risk of MI/stroke
b) Aspirin 75 mg indefinitely (if CI - clopidogrel 75 mg)
c) Clopidogrel 75 mg (if CI - aspirin in PAD, aspirin + dipyridamole in stroke/TIA)
d) DAPT — aspirin 75 mg daily plus ticagrelor 90 mg twice a day for 12 months
e) If anticoagulation contraindicated - DAPT (aspirin and clopidogrel)
Drug management of intermittent claudication.
a) Secondary prevention
b) Symptomatic medication - consider in who? - MoA?
a) Clopidogrel 75 mg and atorvastatin 80 mg (note: 20 mg is standard dose in primary prevention)
b) Naftidrofuryl oxalate:
- Peripheral vasodilator - increases walking distance
- Only consider in patients with no improvement with exercise programme and who decline revascularisation or are not suitable for surgery
How do these drugs reduce BP.
a) ACEI/ARBs
b) CCBs (dihydropyridines)
c) Diuretics
d) BBs
e) Alpha-blockers
a) - Reduce levels of angiotensin II, which leads to reduced vasoconstriction
- Reduce levels of aldosterone, which leads to reduced sodium and water reabsorption
b) Vasodilation
c)
d)
e)
ACE inhibitors.
a) Indications
b) Contraindications/cautions
c) Initiation and monitoring
a) - HTN: 1st line if < 55 (non-black), diabetic or CKD
- HFREF
- Secondary prevention of MI
- Proteinuria in CKD
- Renal complications in diabetes
- Glomerulonephritis
b) - Pregnancy
- Renal artery stenosis
- Baseline hyperkalaemia (> 5.5)
- Hereditary angio-oedema
c) - Check U+Es, eGFR and BP
- Start low and titrate up every 2 weeks
- Re-check U+Es, eGFR and BP
