Cardiac Difficult Drugs Flashcards
Bendoflumethiazide
THIAZIDE LIKE DIURETICS. Works by blocking the Na+/Cl- co transporter on the DCT of the kidney stopping Na from being re-absorbed and hence also stopping water from being re-absorbed (osmosis). Reduces blood volume and hence pressure. In the long term they also appear to have vasodilatory effects.
IND: alternative first line treatment when CCBs are not tolerated (e.g. due to oedema, headaches or gastro upset) - anti-hypertensive in >55s
AE: can cause HYPONATRAEMIA and HYPOKALAEMIA (can lead to arrhythmias) avoid when there are other drugs that might cause low electrolytes such as loop diuretics
DOSE: usually 2.5mg OD
Indapamide
THIAZIDE LIKE DIURETICS. Works by blocking the Na+/Cl- co transporter on the DCT of the kidney stopping Na from being re-absorbed and hence also stopping water from being re-absorbed (osmosis). Reduces blood volume and hence pressure. In the long term they also appear to have vasodilatory effects.
IND: alternative first line treatment when CCBs are not tolerated (e.g. due to oedema, headaches or gastro upset) - anti-hypertensive in >55s
AE: can cause HYPONATRAEMIA and HYPOKALAEMIA (can lead to arrhythmias) avoid when there are other drugs that might cause low electrolytes such as loop diuretics
DOSE: usually 2.5mg OD
Chlortalidone
THIAZIDE LIKE DIURETICS. Works by blocking the Na+/Cl- co transporter on the DCT of the kidney stopping Na from being re-absorbed and hence also stopping water from being re-absorbed (osmosis). Reduces blood volume and hence pressure. In the long term they also appear to have vasodilatory effects.
IND: alternative first line treatment when CCBs are not tolerated (e.g. due to oedema, headaches or gastro upset) - anti-hypertensive in >55s
AE: can cause HYPONATRAEMIA and HYPOKALAEMIA (can lead to arrhythmias) avoid when there are other drugs that might cause low electrolytes such as loop diuretics
DOSE: usually 2.5mg OD
Amlodipine, Nifedipine and lercandapine
CALCIUM CHANNEL BLOCKERS - Dihydropyridine.
CCBs work by blocking the passage of Ca into cells and hence preventing muscle contraction.
The dihydropyridines have effects focussed around vasculature: they prevent SMC contraction in arteries and hence vasodilator bringing BP down
IND: first line anti-hypertensive in >55y
- Added on as second line in <55y
- Used in stable angina treatment (alt. beta-blocker)
AE: Oedema, palpitations, headache and flushing
Verapamil, Diltiazem
CALCIUM CHANNEL BLOCKERS - Non-dihydropyridine.
CCBs work by blocking the passage of Ca into cells and hence preventing muscle contraction.
Non-dihydropyridines have more of a cardiac specific effect - they lower force of contraction (negative inotrope) and also have negative chronotropic and dromotropic effects
IND: Used to control heart rate in people with supra ventricular arrhythmias (alt. beta-blockers)
AE: Verapamil can cause constipation and worsen heart failure
Losartan, Irbesartan, Candesartan
ANGIOTENSIN-RECEPTOR BLOCKERS. Prevents Angiotensin II from attaching to its receptor on SMCs and hence blocks vasoconstriction. Specifically it blocks to AT1 receptor. Leads to vasodilation. Also dilates efferent arteriole of kidney and decreases production of aldosterone meaning Na+ and water are excreted and BP drops further
Useful for HTN in <55ys as well as diabetic nephropathy and CKD and protection against IHD and heart failure
AEs: hypotension and hyperkalaemia
DOSE: 50mg OD PO
Ramipril, Lisonopril and perindopril
ACEis - prevent the production of angiotensin 2 by blocking the angiotensin converting enzyme. Hence causes global vasodilation (inc of the efferent nephron arteriole) decreases production of aldosterone and hence decreases blood volume.
IND: first line treatment for HTN in <55ys also good for IHD protection and CKD (diabetic neuropathy)
AE: key one is BRADYKININ DRY COUGH, hypotension and hyperkalaemia also common (less than ARBs)
DOSE: 2.5mg OD PO and titrate up
Furosemide, Bumentanide
LOOP DIURETICS: these are diuretics acting not he Na+/K+/Cl- channels on the LOOP OF HENLE (mostly the ascending loop) - blocking these channels prevents reabsorption of electrolytes and hence of water dropping blood volume and hence pressure. Also have a dilatory effect on capacitance veins (the big veins) this helps to decrease preload into the heart helping a failing, baggy heart to keep up its force of contractility and cardiac output.
IND: HEART FAILURE is main indication as well as HTN to reduce OEDEMATOUS STATES (can also be used in liver failure and renal failure as well)
AE: can cause hypotension and dehydration. Also can cause LOW ELECTROLYTE STATES: this is particularly noticeable in the endolymph of the ear where loop diuretics can cause tinnitus and hearing loss.
- Can have an effect on drugs that are really excreted so important to keep an eye on these: LITHIUM and DIGOXIN.
DOSE: PO or IV 40mg (tell the patient it’s going to be making them go the toilet a lot more - commonly given in the morning so the patient isn’t up all night)
Spironolactone and Amiloride
K+ SPARING DIURETICS - these are useful to clear fluid from people who have hypokalaemia or low electrolytes states - they work by inhibiting the ALDOSTERONE RECEPTOR on the kidney tubules hence stopping the reabsorption of Na and thus water. Amiloride works slightly differently: block Na channels directly on the DCT.
IND: fluid overload in low electrolyte states. Particularly useful at treating HTN in HYPERALDOSTERONAEMIA (AKA CONN’S SYNDROME)
- Also useful to treat acne and excessive hair growth in females and early puberty in boys
AE: Spironolactone: Hyperkalaemia, Decreased libido, gynecomastia, dizziness, headache etc
Amiloride: GI upset and urinary symptoms
ROUTE: Spironolactone 25-50mg PO
Co-amilofruse
COMBINATION OF FUROSEMIDE AND AMILORIDE
2.5mg Amiloride and 20mg furosemide
Warfarin
ANTI-COAGULANT. Works by blocking the enzyme Vitamin K epoxide reductase which is responsible for reducing vitamin K. Reduced vitamin K is needed for the production of clotting factors II, VII, IX and X in the liver.
IND: people in AF or with new heart valves or any other reason why they might be at increased risk of developing clots (slowly going out of fashion in favour of NOACs). Also prevent DVT and PE.
NO USE against ARTERIAL THROMBUS FORMATION because this is driven by platelet aggregation (venous is not - more emphasis on clotting factors and fibrinogen)
AE: TI is very narrow and dose is very variable from person to person and so can be hard to control - people need very regular reviews.
METABOLISED BY CYP450 so be aware if prescribed in conjunction with any inhibitors or inducers
Always stop 4 days prior to surgery (replaced by heparin)
DOSE: Very variable but should be aiming for an INR between 2.0 and 3.0 (3.5 in valve patients). INR = PatientPT/Normal population PT
Aspirin and Clopidogrel
ANTI-PLATELETS
Aspirin is a COX inhibitor (for both COX-2 and COX-1 but weakly more selective for COX-1) hence stops the production of thromboxane and prostaglandins from arachidonic acid. Thromboxane cause vasoconstriction and platelet aggregation and prostaglandins cause vasodilation and increased vascular permeability (aspiring can also be useful as an anti-inflammatory as well)
Clopidogrel works by blocking the ADP receptors on platelet surfaces hence stopping platelets from aggregating.
IND: ACS and stroke treatment and prevention. People with AF to stop cardiac thrombus. Aspiring can also be used for mild to moderate pain
AE: ASP: GI upset, ulceration and haemorrhage, tinnitus and hearing problems, hyperventilation due to bronchoconstriction (consider in asthma)
DOSE: PO ACS: 300mg loading dose then 75mg thereafter
Stroke 300mg loading dose for 3/52 then 75mg thereafter
Streptokinase, Altepase
TISSUE PLASMINOGEN ACTIVATORS (THROMBLYTICS). These are enzyme agents which help to promote the break down of blood clots. They work by directly binding to active sites of plasminogen helping to turn it into plasmin which breaks down fibrin meshes and helps to degrade clots.
IND: they are useful in Cerebral infarcts due to thrombus and are also commonly used in MIs and PEs
AE: they have very short half lives and can cause over-bleeding and haemorrhage. When used in stroke patients they can cause haemorrhagic transformation from an ischaemic clot.
People can have hyper-sensitivity reactions to them as well as they are antigenic and sourced from bacteria
DOSE: IV 100mg over 3 hours
Apixaban, Rivaroxaban
NOACs: these are new oral anti-coagulants they are slowly replacing warfarin. They work in a similar way to heparins by directly inhibiting factor Xa hence stopping the formation of clots
IND: AF, treatment for DVT and PE, prophylaxis for VTE, prophylaxis for stroke (not licensed for use in valve patients)
AE: Bruising and bleeding, hypotension, nausea and anaemia. Avoid in patients ho have had recent surgeries and patients who have malignant neoplasms or any kind of active bleeding
DOSE: PO 2.5mg BD - dose can be increased if being given as treatment and not prophylactic.
Fondaparinux, Tinzaparin, Enoxaparin, Dalteparin
ANTI-COAGULANTS: HEPARIN. Two types of heparin, most commonly used in LMWH which works by inhibiting thrombin and factor Xa directly (common pathway of clotting cascade). Other form is unfractioned heparin (just called heparin) that has a slightly less predictable effect and works by activating anti-thrombin and hence inactivation thrombin and Xa indirectly.
IND: Commonly used for VTE prophylaxis in hospital as well as stroke and ACS prophylaxis. Can be used to treat ACD
AE: bleeding risk and use with caution in renal impairment
DOSE: 40mg SC for prophylaxis can use higher dose if being used as treatment
