Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 3 Lecture Content > Cardiovascular Therapeutics > Flashcards

Cardiovascular Therapeutics Flashcards

1
Q

Define the following terms

Stage 1 hypertension:

Stage 2 hypertension:

Severe hypertension:

White coat hypertension:

A

Stage 1 hypertension: • Clinic BP 140/90 mmHg or higher and • ABPM (or home) average is 135/85 mmHg or higher.

Stage 2 hypertension: • Clinic BP 160/100 mmHg or higher and • ABPM daytime average is 150/95 mmHg or higher.

Severe hypertension: • Clinic systolic BP 180 mmHg or higher or • Clinic diastolic BP 110 mmHg or higher.

White coat hypertension: • High BP in clinic setting, normal outside this setting.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q
A

Ace inhibitors not given to black people as their renin levels are lower. However, ACE inhibitors with calcium channel blockers prove to still be effective in black people as ACE affects the renin leve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ACE Inhibitors

When do you use them in hypertensive patients?

What are the names of some ACE inhibitors?

What are the adverse effects?

What needs to be monitored?

Any contrandication?

It is also used for?

A

The angiodema usually lip swelling - more common in african caribbean people

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ANGIOTENSIN RECEPTOR BLOCKERS (ARB)

MOA?

Examples?

Adverse effects?

Contraindication?

What needs to be monitored?

It can also be used for apart from hypertension?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

CALCIUM CHANNEL BLOCKERS

MOA

Dihydropyridines

Non-dihydropyridines

A

MOA: Cause vasodilatation by blocking entry of Ca2+ ions through L-type calcium channels.

  • Dihydropyridines – act preferentially on vascular smooth muscle.
  • Non-dihydropyridines – act on the heart and blood vessels.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dihydropyridines:

When are they used?

Adverse effects?

What are they also used for?

A

Non-rate limiting CCBs.

  • Examples: amlodipine, felodipine, nifedipine*
  • 1 st line drugs for African Caribbean patients and those over 55 years of age.
  • Adverse effects: ankle swelling, acid reflux, flushing, can cause gingival hyperplasia.
  • Also used for: Raynaud’s, angina.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Non-dihydropyridines

What are 2 examples of these?

What are the adverse effect?

What is it used in?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the diuretics affecting each part of the nephron?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

THIAZIDE/THIAZIDELIKE DIURETICS

Give names for a thiazide and a thiazide like diuretic?

MOA

A

They aren’t used as much due to type 2 diabetes occuring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

LOOP DIURETICS

Examples?

MOA?

Adverse effect?

Useful for?

A

Examples: furosemide, bumetanide.

  • Mechanism of action:
  • Block the sodium potassium chloride pump in the thick ascending limb of loop of Henle.
  • Greater diuretic effect, short-lived antihypertensive effect.
  • Adverse effects: electrolyte disturbance, polyuria, dehydration.
  • Useful for: pulmonary oedema, CCF(congestive cardiac failure), nephrotic syndrome, ascites.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

POTASSIUM-SPARING DIURETICS

MOA?

Name 2 drugs

What are they useful in?

What are the adverse effect?

There are other potassium sparing diuretics which are weak what are they?

A

Aldosterone antagonists • Aldosterone stimulates sodium and water re-absorption and potassium excretion in the collecting ducts.

  • Spironolactone – competitive aldosterone antagonist. • Eplerenone – mineralocorticoid receptor antagonist (lacks anti-androgen)
  • Low doses in hypertension e.g. 12.5 – 25 mg.
  • Useful in: hyperaldosteronism, Conn’s.
  • Adverse effects: hyperkalaemia, gynaecomastia, erectile dysfunction.
  • Also used in: heart failure, ascites due to portal hypertension.

Amiloride, triamterene.
• Act on the collecting duct, block epithelial Na+ channels and inhibit K+ excretion.

  • Weak diuretic activity.
  • Often used in combination with furosemide (e.g. co-amilofruse 5/40mg).
  • Adverse effects: hyperkalaemia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

42 year old Caucasian female

  • 24h ABPM 150/95 mmHg
  • Which antihypertensive drug would you prescribe? • Amlodipine 5mg • Amlodipine 10mg • Indapamide 2.5mg • Ramipril 10mg • Ramipril 2.5mg
  • What would you need to check before you started it?
A

Ramipril - 2.5mg

What you need to check? -> pregnancy and baseline kidney function - U+E

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

ALPHA-ADRENOCEPTOR ANTAGONISTS

What’s the MOA

What’s the common side effect?

What is it useful in?

A

e.g. doxazosin, terazosin, prazosin.

  • Vasodilation by blocking α-mediated vasoconstriction.
  • Postural hypotension common.
  • Useful in men with BPH (tamsulosin).
  • Generally used as add-on therapy.(4th or 5th line as it does not have a protective effect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

BETA-ADRENOCEPTOR ANTAGONISTS

MOA

Examples which are:

Cardioselective

Non selective

With weak alpha blockade

Acting on B1 receptor vs B2 receptor?

Adverse effects?

Multiple Clinical Uses

Contraindication? (absolute one and relative one)

A

β-blockers • Reduce heart rate and force of contraction. • Reduce renin release.

  • Examples:
  • Cardioselective (β1): bisoprolol, metoprolol, atenolol, nebivolol.
  • Non-selective: propranolol.
  • With weak α-blockade: carvedilol, labetalol.
  • β1 receptors: increased cardiac rate and force.

• β2 receptors: vasodilatation, bronchodilatation, visceral smooth muscle relaxation, hepatic glycogenolysis, muscle tremor.

Adverse effects: • Tiredness, bradycardia, bronchoconstriction, cold extremities, erectile dysfunction, depression, hypoglycaemia*

  • Multiple clinical uses: • Heart failure, IHD, arrhythmias, anxiety, migraine prophylaxis, oesophageal varices, glaucoma, thyrotoxicosis, essential tremor.
  • Contra-indications: • Absolute – asthma.
  • Relative – peripheral arterial disease, acute HF.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

CENTRALLY ACTING DRUGS

Examples

A

Moxonidine (imidazoline I1 receptor agonist)

  • Methyldopa (pre-synaptic α2 -agonist) - Used in pregnancy • Can cause depression • Monitor FBC, LFTs, DCT
  • Clonidine – acts on both receptors above - Anxiolytic
  • Avoid abrupt discontinuation – rebound hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

DIRECT RENIN INHIBITORS

Where is renin released from?

Give an example?

A

Aliskiren is a direct renin inhibitor.

  • Limited clinical use.
  • Adverse effects: diarrhoea, AKI.

Not very effective so not used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Direct vasodilators

What are the problems of using hydralazine and minoxidil

A
  • Hydralazine • Can cause lupus-like syndrome (monitor ANA at higher doses)
  • Reflex tachycardia and tachyphylaxis
  • Minoxidil • Hypertrichosis(hair growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

POSTURAL (ORTHOSTATIC) HYPOTENSION

Define?

Causes?

Management: Non pharmacological and pharmcological

A

Definition: • ≥20mmHg drop in SBP ± ≥10mmHg drop in DBP on standing*

• Adrenal insufficiency, autonomic failure (diabetes, alcoholism, Parkinson’s disease, MSA), drugs(e.g doxazosin).

Management

  • Non-pharmacological: Discontinuing offending medications, standing slowly, drinking water, small meals, compression hosiery, counter-manoeuvres.
  • Pharmacological:
  • Fludrocortisone (mineralocorticoid agonist - salt and water retention)
  • Midodrine (now licensed)- alpha agonist
  • Droxydopa (FDA approved)
  • Can cause supine hypertension.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Why does oedema occur in heart failure?

What are the 2 main categories of heart failure?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

HEART FAILURE WITH REDUCED EF

RCT trials have shown improvement in mortality with what drugs?

A

ACEI or ARBs • Reduce preload and afterload. • Decrease symptoms, slow disease progression and prolong life.

  • β-blockers • Bisoprolol, carvedilol, nebivolol. • Reduce sympathetic overactivity. • Long-term administration improves survival. • Can worsen heart failure in the acute setting.
  • Aldosterone antagonists • Spironolactone, eplerenone. • Reduce mortality.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

HEART FAILURE WITH REDUCED EF

What drugs can be used to have symptomatic relief of oedema?

What is used for heart failures caused by atrial fibrillation?

What drug is given when beta blockers are not tolerated?

A

Diuretics • Symptomatic treatment of oedema. • Reduces preload by reducing circulating volume. • Do not improve mortality. • Thiazides e.g. bendroflumethiazide, metolazone(very strong). • Loop diuretics e.g. furosemide, bumetanide. • IV furosemide infusion.

  • Digoxin • Increases force of contraction. • Useful when heart failure caused by AF.
  • Ivabradine (when β-blockers not tolerated).
  • Hydralazine(vasolidator) with a nitrate.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Licensed for symptomatic chronic heart failure with reduced EF.

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

HEART FAILURE WITH PRESERVED EF

What do you do

A

Optimise blood pressure control
• Symptomatic treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give examples of drugs from class 1a,b,c, 2, 3 and 4

A

Class I: drugs that block voltage-gated sodium channels. • Class Ia (intermediate dissociation): disopyramide, quinidine

  • Class Ib (fast dissociation): lidocaine, mexiletine, phenytoin
  • Class Ic (slow dissociation): flecainide, propafenone
  • Class II: β-blockers (block sympathetic-dependent AVN conduction).
  • Class III: drugs that substantially prolong the cardiac action potential. • Amiodarone
  • Class IV: calcium channel blockers: verapamil, diltiazem • Not classified: digoxin, adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does this person have?

What is the treatment you would give?

How will the management change from having no other disease to: Hypertension of HFpEF,

A

ATRIAL FIBRILLATION • Paroxysmal • Persistent • Permanent

Treatment • Anticoagulation

AND

  • Rate control or rhythm control
  • Pharmacological
  • Non-pharmacological -> • DC cardioversion • Ablation • Left atrial appendage closure

Rate control • β-blockers, diltiazem, verapamil, digoxin Rhythm control • Amiodarone • Flecainide Anticoagulation • Warfarin • DOACs – rivaroxaban, apixaban, edoxaban, dabigatran.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does this person have?

A

Atrial flutter - saw tooth pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does the person have?

What is the treatment for it?

What is given for prophylaxis?

A

They have superventricular tachychardia

• Treatment • Place defibrillator pads • Vagal manoeuvres • Carotid sinus massage • Large bore cannula, proximal vein(to get to the heart quickly) • Adenosine 6mg IV, 12mg IV etc* • Short-acting (seconds) • If ineffective: verapamil 5-10mg IV slow injection • DC cardioversion if haemodynamically compromised

• Prophylaxis • Disopyramide, digoxin, verapamil, β-blockers, sotalol

30
Q

ADENOSINE

MOA

What problems can occur?

A

A1 adenosine receptor agonist. • (Theophylline, caffeine are antagonists).

  • Hyperpolarisation.
  • Transient AV block. • Unpleasant chest tightness, flushing, feeling of ‘impending doom’.
  • Effects are short-lived (seconds).
31
Q

DIGOXIN

MOA?

When is it usually used?

What is the loading dose?

What individuals is the half prolonged in?

What are the adverse reactions?

What do you give in overdose?

A

• Inhibits Na+ /K+ ATPase in cardiac myocytes -> Increase in intracellular sodium -> Inhibits Na+ /Ca2+ exchange ->Increased intracellular Ca2+

Positive inotropic effect. • Enhance vagal inhibition of SAN automaticity and AVN conduction. • Decreased ventricular rate in AF (diminished on exercise due to withdrawal of underlying vagal tone). • Useful in sedentary elderly patients with heart failure and AF

• Loading dose required in urgent situations. • 500 mcg + 500 mcg after 6 hours. • Maintenance dose 62.5 – 250 mcg daily thereafter. • Narrow therapeutic index - monitor plasma concentration. • Elimination t1/2 approximately 36 hours. • Half-life prolonged in renal impairment.

Hypo/hyperkalaemia concerns. • Adverse effects: • cardiac arrhythmias, N+V, diarrhoea, fatigue, confusion, xanthopsia(yellow tinge)

• In overdose: • Atropine • Digoxin-specific antibody (Fab) fragments.

32
Q

Amiodarone

MOA

ECG changes

Non cardiac effects

A
  • Prolongs action potential duration and effective refractory period in all cardiac tissues.
  • Has class I, III and IV activity.
  • Prolongs QT interval.
  • Minimal negative inotropic effect.
  • Loading dose required. • Highly lipophilic - considerable accumulation in fat and muscle.
  • Extremely long elimination half-life (more than 30 days).

Non-cardiac side effects:

  • Lungs – fibrosis
  • Liver – hepatitis
  • Thyroid dysfunction - goitre
  • Neurological – tremors, ataxia
  • Skin – photosensitivity
  • Eyes – corneal microdeposits, optic neuritis
  • Testes – orchitis
33
Q

FLECAINIDE

What are the main uses

Who should you avoid giving it to?
What can it excarcerbate?

A

Specialist use only.

  • Main uses: • ‘Pill in the pocket’ for PAF • Chemical cardioversion in recent onset AF • Tachycardias involving accessory pathways e.g. WPW
  • Avoid in patients with previous MI or LV dysfunction or structural heart disease. - they would have an echo and coronary angiogram
  • May exacerbate pre-existing conduction disorders (great care in SA or AV node diseases, or BBB).
34
Q

AF AND ANTICOAGULATION

What is the difference between HAS-BLED score and CHA2DS2-VASc score?

What are the highest scoring points for both?

A
35
Q

What are examples of ORAL ANTICOAGULANTS

A

Vitamin K antagonists

• Warfarin, acenocoumarol, phenindione

Direct oral anticoagulants (DOACs)

  • Direct thrombin (IIa) inhibitors - Dabigatran
  • Factor Xa inhibitors - Rivaroxaban, apixaban, edoxaban
36
Q

WARFARIN

MOA

Target INR

Adverse effect?

What are the antidotes available?

A

Inhibits synthesis of vitamin K-dependent clotting factors: II, VII, IX and X. • Anticoagulant effect takes several days to develop.

  • Inter-individual variability – monitor INR (International normalised ratio).
  • Target INR: AF 2-3, metallic valve replacement 3-4.
  • TTR(time in therapeutic range) is key.

Adverse effects: bleeding (intracranial, GIT, epistaxis etc.)

Antidotes: • Vitamin K (~6 hours to reverse) e.g. phytomenadione.

  • FFP
  • Prothrombin complex concentrate e.g. Beriplex®
37
Q

What increases and decreases INR when interacting with warfarin?

A

Increases INR - Cranberry juice • Ciprofloxacin • Clarithromycin • Metronidazole

Decreases INR - Dietary vitamin K • Rifampicin • Carbamazepine • St John’s wort

38
Q

DOACS

What are the 2 mechanism of action?

Example of DOAC

Do you need to monitor INR

A

No need for INR monitoring.

  • Well tolerated.
  • Licensed for non-valvular AF, VTE treatment and prophylaxis.
  • Not suitable for metallic heart valves or antiphospholipid syndrome.
  • Once or twice daily.
  • Rivaroxaban needs to be taken with food. (less bioavailability without it)
  • Dose reductions in renal impairment.
  • Reversal - Idarucizumab for dabigatran
39
Q

What is angina pectoris?

What conditions come under acute coronary syndrome?

A

Angina pectoris

• Stable and unstable • Coronary artery vasospasm

• Acute coronary syndrome (ACS)

• STEMI • NSTEMI • Unstable angina

40
Q

What are primary prevention modifiable risks?

What is the cardiovascular risk predictor score called?

A

Addressing modifiable risk factors:

• Smoking • Obesity • Blood pressure • Dyslipidaemia • Thrombophilia • Diabetes • Alcohol • Diet

Cardiovascular risk predictors

• QRISK3 (NICE recommended)

41
Q

SMOKING CESSATION

What drugs are available and what support is available?

A

With behavioural support.

Nicotine replacement therapy (NRT)

  • Patches, gums, lozenges, nasal sprays, inhalators.
  • Vaporised nicotine.

Varenicline

  • Nicotine receptor partial agonist.
  • Suicidal ideation.

Buproprion

  • Noradrenaline (and dopamine) re-uptake inhibitor.
  • Lowers seizure threshold.
42
Q

Obesity

What pharmaological interventions are available?
What are there MOA?

A

Non-pharmacological measures are fundamental.

• Surgery

• Pharmacological:

  • Orlistat:
  • Lipase inhibitor. • Prevents breakdown of dietary fats therefore decreases absorption. • Abdominal cramps, faecal urgency/incontinence, steatorrhoea.
  • In diabetic patients(shown to lose weight):
  • GLP1 agonists e.g. liraglutide.
  • SGLT2 inhibitors e.g. empagliflozin. (excrete more glucose)

• Not recommended:

• Sibutramine – increased risk of stroke.

43
Q

DYSLIPIDAEMIA

Familial disorders should be suspected if cholesterol is higher than?

What drugs are given for thos with dyslipidemias

A

Hypercholesterolaemia & hypertriglyceridaemia.

• Familial disorders
• FH; especially if total cholesterol >9 mmol/L.

  • RCT evidence for lipid-lowering drugs (statins). • 30-40% relative risk reduction in CAD events. • Primary (10% or greater 10-year risk of CVD). • Secondary prevention.
  • Lipid-lowering drugs: • HMG CoA reductase inhibitors (statins) • Ezetimibe • Fibrates • PCSK9 inhibitors
44
Q

STATINS

MOA?

A

HMG CoA reductase inhibitors. • Rate-limiting enzyme in hepatic synthesis of cholesterol.

  • Upregulation of LDL cholesterol receptors.
  • Reduce LDL cholesterol by 20-55%.
  • Examples: atorvastatin, simvastatin, pravastatin, rosuvastatin.
  • Adverse effects:
  • Myalgia, myositis, raised LFTs • 12% increased risk of new onset diabetes. • Rhabdomyolysis (rare).
45
Q

EZETIMIBE

What is the MOA?

A

Blocks NPC1L1 transport protein in the brush border of enterocytes in the duodenum. • Inhibits intestinal absorption of cholesterol.

  • Augments effects of statins.
  • May be useful if statin contra-indicated or not tolerated.
  • Modest improvement in cardiovascular outcomes when used with statin.
  • Adverse effects: mainly GI symptoms.
46
Q

PCSK9 INHIBITORS

MOA

A

PCSK9 (proprotein convertase subtilisin/kexin type 9) is an enzyme which binds to the receptor for LDL cholesterol.

• Monoclonal Abs - alirocumab and evolocumab.

  • Subcutaneous injections every 2 weeks.
  • Highly effective at lowering LDL cholesterol (up to 62%).
  • Expensive.
  • Recommended by NICE for certain high risk patients with persistent high cholesterol.
47
Q

Fibrates

A

Complex mechanism of action.

• Markedly reduce circulating VLDL and hence triglyceride, modest effect on LDL and HDL.

• Examples: bezafibrate, fenofibrate, gemfibrozil.

  • Adverse effects: GI symptoms, rash, pruritis, rhabdomyolysis (particularly in combination with statins).
  • Not for routine use.
48
Q

What is angina pectoris?

What are the main strategies for phamacotherapy?

Symptomatic relief?

A

Insufficient blood (oxygen) supply to the heart to meet it’s metabolic needs.

• Main strategies for pharmacotherapy:

  • Slow the heart rate and reduce metabolic demand
  • Improve the blood supply (coronary vasodilatation)
  • Reduce the preload (venodilatation)
  • Reduce the afterload (by lowering systemic blood pressure)

• Symptomatic – acute angina attack

• GTN

49
Q

Stable Angina

What drugs can you give?

A
  • Rate-limiting drugs
  • β-blockers, verapamil, diltiazem, ivabradine • Nitrates e.g. isosorbide mononitrate • Dihydropyridine CCBs e.g. amlodipine • Nicorandil • Ranolazine
50
Q

Ivabradine

What does it’s MOA?

It can be given as an alternative to what drug?

If HR>60 what additionally can be given?

What is it also used in apart from angina pectoris?

What does it increase risk of?

A

Slows the heart rate.

  • Inhibiting the pacemaker If current, which causes spontaneous depolarisation in the SAN.
  • Alternative to β-blockers if not tolerated or contra-indicated.
  • Or, in addition to β-blockers if HR >60bpm.
  • Also used in: chronic systolic heart failure.
  • Increased risk of AF.
51
Q

NITRATES

A

Nitric oxide (N.O.) donation.

  • Immediate release or MR versions e.g. Monomax XL®.
  • Spray, sublingual/buccal tablet, patch.
  • Tolerance develops (need nitrate-free period).
  • Headache, postural hypotension common.
  • Avoid concomitant use of PDE5 inhibitors (sildenafil)
52
Q

NICORANDIL

MOA?

Is it first line or an add on?

Adverce effects?

A
  • Potassium KATP channel activator and N.O. donor.
  • Add-on therapy with other anti-anginal drugs.
  • Adverse effects:
  • Headache, flushing and dizziness.
  • Ulceration – skin, mucosa, eye
53
Q

RANOLAZINE

MOA?

A

Inhibits late sodium current → reduces intracellular calcium → reduces force of contraction.

  • Adjunct to other anti-anginal drugs.
  • Does not affect heart rate.
  • Main use: elderly patients with angina not suitable for invasive intervention (PCI).
54
Q

ACUTE CORONARY SYNDROME

What is the standard treatment?

A

Standard treatment of ACS:

  • Aspirin 300mg loading dose
  • Clopidogrel or ticagrelor loading dose
  • LMWH e.g. enoxaparin 1 mg/kg BD or fondaparinux 2.5 mg OD
  • Glyceryl trinitrate (GTN) sublingual spray or buccal tablet or IV infusion if continuing pain • Analgesia e.g. IV morphine 5-10mg • Anti-emetic e.g. IV metoclopramide 10mg • Oxygen only to maintain SpO2 94-98%
55
Q

ST Elevation MI

What is the treatment option?

A

Primary percutaneous coronary intervention (PCI).

  • Thrombolysis
  • Only if timely primary PCI not available.
  • Sooner the better (up to 12 hours).
  • IV infusion.
56
Q

THROMBOLYSIS

Whaat are the different types of thrombolysis and what is it used for?

What is it’s MOA

What are the adverse effects?

A

Recombinant tissue plasminogen activator (tPA): • Alteplase, tenecteplase, reteplase. • Also used for stroke and massive PE.

  • Streptokinase – no longer used. • Derived from streptococcus – antibodies develop after first use; allergic reactions.
  • Adverse effects: bleeding; haemorrhagic stroke 0.5-1%.
  • Contra-indications: recent surgery/trauma/CPR/stroke, previous haemorrhagic stroke, bleeding disorders, uncontrolled hypertension, pregnancy.
57
Q

HEPARINS

MOA?

A
58
Q

Unfractionated heparin?

How is it given?

How quickly does it act?

How long is it’s half life?

How is dose monitored?

Advantage

Reversal agent?

Problems it can cause?

A

Given by IV bolus and infusion.

  • Acts immediately.
  • Short elimination half-life.
  • Dose is monitored by measuring APTT.
  • Advantages/disadvantages – needs continuous infusion.
  • Reversal: protamine sulfate – binds to heparin. • Clinical use now limited. • Can cause heparin-induced thrombocytopenia (HIT)
59
Q

LOW MOLECULAR WEIGHT HEPARINS (LMWH)

How is it given?

What are the different names?

What is the half life compared to unfractionated?

Does it affect APTT?

What impairement do we have to reduce the dose in?

What can it be used in?

A

Given by subcutaneous injection.

  • Enoxaparin, tinzaparin, dalteparin.
  • Longer elimination half-life than UFH.
  • Do not prolong the APTT; monitoring not routinely required.
  • Reduced dose in renal impairment.
  • More convenient; can be self-administered.
  • Also used for: PE, DVT, treatment and prophylaxis.
60
Q

ANTIPLATELET AGENTS

Name 4

A

Aspirin • Clopidogrel and prasugrel • Ticagrelor • Dipyridamole

61
Q

ASPIRIN

MOA

What is it used for?

Main side effect?

A

Acetylsalicylic acid (ASA).

  • Irreversibly inhibits cyclo-oxygenase (COX-1).
  • Reduces TXA2 synthesis • Reduces platelet activation and aggregation via expression of the gpIIb/IIIa complex.
  • Used for ACS, secondary prevention of IHD and stroke.
  • Main adverse effects: upper GI bleeding (inhibition of protective prostaglandins in stomach lining).
62
Q

CLOPIDOGREL

MOA?

risk of therapeutic failure in patient with variable alles of what gene

Potential interaction with what drug?

When is it used?

It is also used for prevention of?

A

Adenosine P2Y12 inhibitor. • Irreversibly inhibits ADP-induced platelet aggregation.

  • Prodrug - requires conversion to active metabolite by cytochrome P450 enzymes.
  • Risk of therapeutic failure in patients with variant alleles of CYP2C19 (poor metabolisers).
  • Potential interaction with omeprazole (metabolised by CYP2C19).
  • Used for 1 year post-coronary stent insertion; aspirin lifelong.
  • Secondary prevention of stroke.
63
Q

TICAGRELOR

MOA?

Indicated in?

Advantage over clopidigrel?

Interactions with what inhibitors?

Main adverse effects?

A

Allosteric inhibitor of P2Y12 receptor. • Inhibits ADP-induced platelet aggregation.

  • Indicated for patients with ACS in conjunction with aspirin.
  • Does not require hepatic activation.
  • Interactions with inhibitors of CYP3A4.
  • Main adverse effects: bleeding, shortness of breath.
64
Q

DIPYRIDAMOLE

MOA

It is no longer used for stroke and IHD

What are the adverse effects?

A
  • Inhibits platelet activation including by inhibition of phosphodiesterase.
  • No longer recommended in stroke guidelines.
  • Not used for IHD.
  • Reduced risk of stroke and death in patients with TIA by 15%.
  • Additive effects with aspirin.
  • Adverse effects: dizziness, headache, GI disturbance.
  • Does not increase risk of bleeding.
65
Q

What are secondary prevention after being diagnosed with IHD?

A
  • Duel antiplatelet therapy (DAPT)
  • Aspirin + clopidogrel or prasugrel or ticagrelor
  • More effective but higher risk of UGIB.
  • Optimal duration not known.
  • β-blocker
  • ACE inhibitor
  • Statin
  • Smoking cessation
66
Q
A
67
Q
A
68
Q
A
69
Q
A
70
Q
A

Year 3 Lecture Content (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions