Cardiovascular Flashcards

1
Q

loop diuretics:

  • examples? 2
  • mechanisms of action? 2
A
  • furosemide
  • bumetanide
  • INHIBITS Na+/K+/2Cl-CO-TRANSPORTER in loop of henle -> less osmosis back into cells -> potent diuretic effect
  • causes direct DILATION OF VEINS, thus reducing pre-load of heart
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2
Q

loop diuretics:

  • examples? 2
  • indications? 3
  • contraindications? 4
A
  • furosemide
  • bumetanide
  • acute pulmonary oedema (used w nitrates + O2)
  • to treat fluid overload in CCF
  • treat fluid overload in other oedematous states (eg dt renal or liver disease)

contraindications:

  • dehydration/severe hypovolemia (worsens!)
  • severe hypokalaemia +/or hyponatraemia
  • patients at risk of hepatic encephalopathy (hypokalaemia worsens this!)
  • worsens gout (if used chronically)
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3
Q

loop diuretics:

  • examples? 2
  • side-effects? 3
  • interactions? 3
A
  • furosemide
  • bumetanide
  • dehydration + hypotension
  • low electrolyte states
  • hearing loss/tinnitus (loss of electrolytes affect cochlea)
  • lithium
  • digoxin
    (levels of these are increased as diuretic reduces excretion of them)
  • aminoglycosides (eg gentamicin)
    (dt diuretic-induced hypokalaemia, increases risk of ototoxicity and nephrotoxicity of these drugs)
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4
Q

info for patients taking loop diuretics:

  • how they work?
  • desired effect?
  • when should NOT take dose?
A
  • there is too much water in your body so giving you a drug to help you pee off excess water
  • should improved breathlessness, oedema etc
  • it will mean that you need to go to the toilet more often
  • don’t take dose at night as this will mean you have to wake up to pee
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5
Q

thiazide-like diuretics:

  • examples? 3
  • mechanisms of action? 2
A
  • bendroflumethiazide
  • indapamide
  • chlortalidone
  • INHIBIT Na+/Cl- CO-TRANSPORTER in the DISTAL CONVOLUTED TUBULE -> prevents reabsorption of sodium (+ thus water) -> diuretic effect
  • VASODILATOR effect of unknown mechanism
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6
Q

thiazide-like diuretics:

  • examples? 3
  • indications? 2
  • contraindications? 2
A
  • bendroflumethiazide
  • indapamide
  • chlortalidone
  • alternative 1st line treatment for HTN (when Ca+ channel blocker can’t be used, eg in heart failure)
  • ADD-ON treatment for HTN not controlled using other cardiac drugs
  • patients with hypokalaemia +/or hyponatraemia
  • patients with gout
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7
Q

thiazide-like diuretics:

  • examples? 3
  • side effects? 2
  • interactions? 2
A
  • bendroflumethiazide
  • indapamide
  • chlortalidone
  • hyponatraemia + hypokalaemia (can -> arrhythmias)
  • impotence in men
  • NSAIDs may reduce efficacy of these diuretics
  • cution using with other drugs that lower potassium (ie loop diuretics)
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8
Q

info for patients taking thiazide-like diuretics:

  • effect it should have?
  • what OTC drugs should they refrain from using?
  • which side effect must you ask about?
A

should lower BP as well as reducing any oedema

will increase amount you go to the toilet (make sure no mobility issues)

  • taking NSAIDs will reduce effectiveness
  • ask men directly about impotence as unlikely to volunteer it
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9
Q

potassium-sparing diuretics:

  • examples? 2
  • mechanism of action
A
  • spironolactone
  • amiloride (as co-amilofruse, co-amilozide)

Amiloride:

  • works at the distal convoluted tubule by inhibiting reabsorption of Na+ by epithelial Na+ channels (ENaC) -> excretion of sodium + water BUT retention of potassium
  • nb rarely used alone as diuretic effect is weak, used with other diuretics

Spironolactone:

  • is an aldosterone antagonist, competitively binding to the aldosterone receptor (aldosterone norm stimulates ENaCs) -> same effect as above
  • nb effect is greatest in primary hyperaldosteronism or when circulating aldosterone is increased (eg liver cirrhosis)
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10
Q

Potassium-sparing diuretics:

  • examples? 2
  • indications? 2
  • contraindications? 5
A

spironolactone

  • ascites + oedema dt liver cirrhosis
  • primary hyperaldosterone

Amiloride
- combination therapy w other diuretics for treatment of HYPOKALAEMIA

contra for BOTH types:

  • hyperkalaemia
  • severe renal impairment
  • hypovoloemia

contra for spironolactone (aldosterone antagonist)

  • addison’s disease
  • pregnant or lactating women
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11
Q

potassium-sparing diuretics:

  • side effects of spironolactone? 3
  • side effects of amiloride? 3
  • interactions for both? 3
A
spironolactone
- hyperkalaemia
- gynaecomastia + impotence in men
- liver impairment/jaundice
(- nb can cause steven-johnson syndrome)

amiloride

  • GI upset
  • hypotension/dizziness
  • electrolyte imbalances
  • other potassium elevating drugs (eg ACEi, angiotensin receptor blockers)
  • potassium supplements
  • digoxin + lithium reduce clearance (requiring dose adjustment)
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12
Q

patient info for potassium-sparing diuretics/aldosterone antagonists:

  • what time to take meds?
  • what monitoring should they undergo?
  • extra info for men taking spironolactone?
A
  • take diuretics (aka water tablets) in morning to recude likelihood of nocturia
  • should attend regular blood tests to ensure good electrolyte balance

possibility of growth + tenderness of tissue under the nipples + impotence
- this is harmless + reversible but know it can be uncomfortable/embarassing

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13
Q

Beta blockers:

  • examples? 4 (incl type)
  • suffix?
  • mechanism of action
A

Cardiac (B1) selective

  • atenolol
  • bisoprolol
  • metoprolol

Non-selective
- propranolol

-olol suffix

B1 recptors - mainly in heart
B2 receptors - mainly in blood vessels

In heart:

  • reduce force of contraction + speed of conduction (increasing myocardial perfusion)
  • prolong
  • lower blood pressure (via reducing renin secretion - mediated by B1 receptors)
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14
Q

Beta blockers:

  • examples? 4 (incl types)
  • indications? 6
  • contraindications? 4
A

Cardiac selective (B1)

  • bisoprolol
  • atenolol
  • metoprolol

Non-selective
- propranolol

Indications:

  • ischaemic heart disease (first line)
  • chronic heart failure (first line - but start slowly)
  • AF (first line)
  • superventricular tachycardia (first line)
  • hypertension (2nd line, if others are insufficient/inappropriate)

Contraindications:

  • asthma (nb cardio-selective can be used in COPD)
  • heart block
  • hypotension (should be avoided)
  • severe hepatic failure (dose should be reduced!)
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15
Q

Beta blockers:

  • examples? 4 (incl types)
  • adverse effects? 6
  • interactions? 1
A

Cardiac-selective

  • bisoprolol
  • atenolol
  • metoprolol

Non-selective
- propranolol

  • fatigue
  • cold extremities
  • headache
  • GI disturbances (eg nausea)
  • sleep disturbances/nightmares
  • impotence (in men)
  • non-dihydropyrine Ca channel blockers (eg verapamil, diltazem)
  • – can cause heart failure, brady cardia + even asystole used together
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16
Q

Info for patients taking beta blockers:

  • specific warning for treatment of heart failure?
  • specific warning for patients w COPD?
  • other possible effects to mention?
A

Warn patients w heart failure that symptoms may get worse initially (+ to tell docs this)

Warn patients w COPD to stop drug + see dr if breathing difficulties occur

Discuss common side effects, incl impotence

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17
Q

Calcium channel blockers (aka antagonists)

  • examples? 4 (incl 2 types)
  • mechanism of action?
A

Dihydropyridines (vascular selective)

  • amlodipine
  • nifedipine

Non-dihydropyridines (heart selective)

  • diltiazem
  • verapamil

Nb different suffixes, just learn these 4 well!!

Reduce intracellular Ca conc

  • vasodilation in arterial smooth muscle
  • reduce myocardial contractility (reducing myocardial oxygen demand)
  • suppress cardiac conduction
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18
Q

Calcium channel blockers:

  • examples? (2 of each)
  • indications for dihydropyridines? 1
  • indications for non-dihydropyridines? 1
  • indication for both? 1
A

Dihydropyridines (amlodipine, nifedipine):
– hypertension (1st/2nd line)

Non-dihydropyridines (diltiazem, verapamil):
– supraventricular arrhythmias (incl AF)

both:
– stable angina (1st/2nd line)

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19
Q

Calcium channel blockers:

  • examples? (2 of each)
  • contraindications for dihydropyridines? 2
  • contraindications for non-dihydropyridines? 2
A

dihydropyridines (nifedipine, amlodipine):

  • unstable angina (may trigger reflex constriction)
  • severe aortic stenosis (can provoke collapse)

non-dihydropyridines (diltiazem, verapamil):

  • poor LV function (may worsen HF)
  • AV nodal conduction delay (may provoke complete heart block)
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20
Q

calcium channel blockers:

  • examples (2 of each type)?
  • common adverse effects of dihydropyridines? 4
  • common adverse effect of non-dihydropyridines? 1
  • rare adverse effects of non-dihydropyridines? 3
A

dihydropyridines (amlodipine, nifedipine)
- ankle oedema
- flushing
- head ache
- palpitations
(nb all dt vasodilation + compensatory tachycardia)

non-dihydropyridines (diltiazem, verapamil)

  • constipation (common)
  • bradycardia
  • heart block
  • heart failure
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21
Q

calcium channel blockers:

  • interaction of non-dihydcropyridines? 1
  • interaction of both?1
A

non-dihydropyridines (diltiazem + verapamil):
- beta blockers

both
- should not be used together (as additive effect)

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22
Q

info for patients taking calcium channel blockers:

- 3 things to discuss?

A
  • why drug being given
  • other self-help measures to reduce CV risk
  • discuss common side effects (esp ankle oedema, if relevant)
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23
Q

ACE inhibitors:

  • examples? 3
  • suffix?
  • mechanism of action?
A
  • ramipril
  • lisinopril
  • perindopril

-pril

decreases action of RAAAS pathway by blocking AT1 -> AT2

  • reduces peripheral resistance
  • by reducing aldosterone secretion, promotes Na + water secretion
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24
Q

ACE inhibitors:

  • examples? 3
  • indications? 4
  • contraindications? 3
A
  • ramipril
  • lisinopril
  • perindopril
  • hypertension (1st/2nd line)
  • chronic heart failure (1st line)
  • ischaemic heart disease (2ndary prevention)
  • diabetic nephropathy + CKD w proteinuria
  • AKI (but restart afterwards)
  • renal artery stenosis
  • pregnancy/breastfeeding
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25
Q

ACE inhibitors:

  • examples? 3
  • adverse effects? 4
  • interactions? 2
A
  • ramipril
  • lisinopril
  • perindopril
  • hypotension (esp after first dose)
  • persistent dry cough
  • hyperkalaemia (as aldosterone norm -> K excretion)
  • anaphylactoid reactions (rare)
  • potassium elevating drugs (increases risk of hyperkalaemia)
  • NSAIDs (increases risk of renal failure)
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26
Q

info for patients taking ACE inhibitors:

  • what does drug do?
  • side effects to mention?
  • what monitoring do they need?
  • what shouldn’t they take?
A
  • improve blood pressure + reduce strain on heart
  • dry cough
  • dizziness (w first dose esp)
  • severe allergic reaction (call 999)
  • blood tests to monitor kidney function + K levels
  • don’t take OTC NSAIDs as could make kidney worse
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27
Q

angiotensin receptor blockers (ARBs)

  • examples? 3
  • suffix?
  • mechanism of action?
A
  • Losartan
  • Candesartan
  • irbesartan

-sartan
“to avoid the cough that SATAN gives when taking ACE inhibitors”

block RAAS pathway
- block action of angiotensin 2 on the AT1 receptor

  • reducing peripheral vascular resistance
  • particularly dilates efferent glomerular arteriole, reducing long term strain on kidneys
  • reducing aldosterone secretion -> more water + salt excretion
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28
Q

angiotensin receptor blockers (ARBs)

  • examples? 3
  • indications? 4
  • contraindications? 3
A
  • Losartan
  • candesartan
  • irbesartan

indications are same as for ACE inhibitors but ARBs are used when dry cough cannot be tolerated

  • hypertension
  • chronic heart failure
  • ischaemic heart disease
  • diabetic nephropathy + CKD w proteinuria
  • AKI (but restart after)
  • renal artery stenosis
  • pregnancy/breastfeeding
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29
Q

angiotensin receptor blockers (ARBs):

  • examples? 3
  • adverse effects? 2
  • interactions? 2
A
  • Losartan
  • candesartan
  • irbesartan
  • hypotension (esp first dose)
  • hyperkalaemia

nb doesn’t cause dry cough or risk of angioedema as bradykinnen breakdown is further upstream in RAAAS pathway

  • potassium elevating drugs
  • NSAIDs
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30
Q

info for patients taking angiotensin receptor blockers (ARBs):

  • why are you giving it to them?
  • side effects?
  • what monitoring do they need?
  • what shouldn’t they take?
A
  • same effect as ACEi but won’t give you the cough
  • dizziness (esp first dose)
  • blood test monitoring for kidney function + K levels
  • don’t take OTC NSAIDs
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31
Q

Nitrates:

  • examples? 2
  • which is long acting, which short acting?
  • mechanism of action?
A
  • isosorbide mononitrate (long acting)
  • glyceryl trinitrate (short acting - GTN spray)

converted to nitric oxide (NO) which causes muscles to relax -> vasodilation

-> reduced cardiac preload -> lower cardiac work + myocardial oxygen demand

(nb they also act on arteries to reduce afterload but most of their effect is to reduce preload)

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32
Q

Nitrates:

  • examples? 2
  • indications for short acting?
  • indications for long acting? 2
  • contraindications? 2
A

isosorbide mononitrate

  • prophylaxis of angina (when B blocker of Ca channel blocker not tolerated)
  • used IV for pulm oedema (alongside furosemide + O2)

glyceryl trinirate

  • acute angina
  • acute coronary syndrome

contraindications:

  • severe aortic stenosis (risk of coronary collapse)
  • hypotension/haemodynamically unstable
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33
Q

Nitrates:

  • examples? 2
  • adverse effects? 5
  • interactions?
A
  • isosorbide mononitrate (long acting)
  • glyceryl trinitrate (short acting)
  • flushing
  • headaches
  • light-headedness
  • hypotension
  • tolerance
  • phosphodiesterase inhibitors (eg sildenafil)
    (enhance + prolong hypotensive effects of nitrates)

nb should be used in caution w people on anti-hypertensive medication as may cause hypotension

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34
Q

info for patients taking nitrates:

  • what the effect should be?
  • when most effective?
  • main 2 side effects?
  • advice for long-acting nitrates?
A

relieve chest pain +/or breathlessness

more effecting at preventing that terminating angina
- take BEFORE you exert yourself

  • headaches (will normally pass)
  • postural hypotension, advice to sit down

can develop tolerance so have periods of no nitrates - norm over night

35
Q

cardiac glycosides:

  • example? 1
  • effects on the heart? 2
A

digoxin (only one)

negatively chronotropic

  • reduces heart rate
  • “CHRONOlogy is time”

positively inotropic

  • increase force of contraction
  • “you need IONs for muscles to contract”
36
Q

cardiac glycosides:

  • example? 1
  • indications? 2
  • absolute contraindications?
  • relative contraindications?
A

digoxin

  • AF (+ atrial flutter) - after B blockers + Ca blockers
  • severe heart failure (third line after B blocker + ACEi)

absolute:

  • heart block (will worsen)
  • people at risk of ventricular arrythmias

relative:

  • renal failure (reduce dose, narrow therapeutic index)
  • electrolyte abnormalities, esp hypokalaemia (increases risk of arrythmias)
37
Q

cardiac glycosides:

  • example? 1
  • mild side effects? 5
  • serious adverse effect?
  • interactions? 5
A

digoxin

  • bradycardia
  • dizziness
  • visual disturbances (blurred or yellow vision)
  • GI disturbance
  • rash
  • cardiac arrythmias (very narrow therapeutic margin)
  • loop + thiazide diuretics increase digoxin dose (as they reduce conc of K+)
  • amiodarone
  • Ca channel blockers
  • spironolactone
  • quinine
    (all the above increase plasma conc of digoxin)
38
Q

info for patients taking digoxin (cardiac glycoside):

  • effect on ECG?
  • what to watch out for?
  • what needs monitoring?
A

therapeutic doses of digoxin can give ST-depression (reverse tick sign)
- this is expected and does not indicate toxicity!

  • side effects getting worse, could be a sign of toxicity
  • electrolytes and kidney function
39
Q

Antidysrhythmics:

  • example? 1
  • mechanism of action?
A

Amiodarone (only one)

Many effects on myocardial cells but basically acts to reduce spontaneous depolarisation, increase the likelihood of sinus rhythm and reduces the ventricular rate

40
Q

Anti-dysrhythmics

  • example?
  • indications? 5
  • contraindications? 3
A

Amiodarone (only one)

Wide range of TACHYarrhythmias
- AF
- atrial flutter
- superventricular tachycardia (SVT)
- ventricular tachycardia (VT)
- refractory ventricular fibrillation (VF)
Nb generally only used when other options (drugs or electrical cardioversion) are ineffective/innapropriate

  • severe hypotension
  • heart block
  • active thyroid disease
41
Q

Antidysrrhythmics

  • example? 1
  • acute side effect? 1
  • chronic adverse effect on lungs? 1
  • chronic adverse effects on heart? 2
  • chronic adverse effect on liver? 1
  • chronic adverse effects on skin? 2
  • chronic adverse effect on thyroid? 1
A

Amiodarone (only one)

Acute:
- hypotension (during IV infusion)

Chronic lungs:
- pneumonitia

Chronic heart:

  • bradycardia
  • AV block

Chronic liver:
- hepatitis

Chronic skin:

  • photosensitivity
  • grey discolouration

Chronic thyroid
- hypo/hyperthyroidism
(Dt iodine content and structural similarity to thyroid hormone)

Nb amiodarone has a very long half life, after discontinuation it may take months to be completely eliminated!

42
Q

Antidysryhthmics

  • example? 1
  • notable interactions? 3
A

Amiodarone (only one)

Amiodarone interacts eith many drugs (always check before prescribing!)

Increases plasma conc of:

  • digoxin
  • diltiazem
  • verapamil

Increasing risk of bradycardia, AV block and heart failure

43
Q

Info for patients taking amiodarone:

  • explanation of action/risks?
  • side effects to look out for and report? 7
  • what should they not have/avoid? 2
A

Aims to correct their fast +/or irregular heart rhythm
- has lots of side effects but being used because your condition is serious and doesn’t respond to anything else

  • breathlessness
  • persistent cough
  • jaundice
  • restlessness
  • weight loss
  • tiredness
  • weight gain

Avoid

  • grapefruit juice (increase risk of side effects)
  • sunlight (photosensitive skin)
44
Q

Aspirin:

- mechanism of action?

A

irreversibly binds COX enzyme

-> reduction in platelet aggregation

nb platelets cannot make new COX so half-life of aspirin is long as COX stores only increase when new platelets are made

45
Q

Aspirin:

- main indications? 4

A

1) treatment of ACS and acute ischaemic stroke
2) secondary prevention of MI/stroke/peripheral arterial disease
3) control mild-moderate pain + fever (though other NSAIDs are often preferred)
4) reduce risk of cardiac thrombus in AF (where warfarin + NOACs are contraindicated)

46
Q

Aspirin:

  • absolute contraindications? 3
  • relative contraindications? 2
A
  • children under 16 (risk of Reye’s syndrome*)
  • aspirin hypersensitivity
  • third trimester of pregnancy (may lead to premature closure of ductus arteriosus)
  • peptic ulcer disease (use PPIs alongside)
  • gout (may trigger acute attack)
47
Q

Aspirin:

  • mild side effect? 2
  • severe GI side effects? 2
  • other severe side effect? 1
  • effect of overdose?
A
  • GI irritation
  • tinnitus (if on long-term)
  • peptic ulcer
  • GI bleed
  • hypersensitivity reaction (incl bronchospasm)

overdose:
tachypnoea, hearing changes, metabolic acidosis, confusion, convulsions, CV collapse and rest rest

48
Q

Aspirin:

- interactions? 2

A

acts synergistically with other anti-platelet agents which is good but does increase risk of bleeding

use with caution with:

  • other anti-platelets
  • anti-coagulants
49
Q

Aspirin prescribing:

  • high dose amount?
  • low dose amount?
  • dose for pain?
  • drug often prescribed alongside?
A

high dose: 300mg
low lose: 75mg

pain dose: max daily dose of 4g (taken in divided doses)

lansoprazole (or other PPI)

  • 20mg daily
  • in >65 or any other gastric risk factors
50
Q

Patient info for aspirin:

  • when to take tablet?
  • what to look out for?
A
  • take AFTER food
  • signs of bleeding
  • gastric upset
51
Q

clopidogrel:

- mechanism of action?

A

bind irreversibly to ADP on the surface of platelets

-> prevention of platelet aggregation

nb this pathway is different to aspirin so its effects are synergistic

52
Q

clopidogrel:

- indications? 4

A

nb norm prescribed with aspirin (though may be used alone when aspirin contraindicated or not tolerated)

1) treatment of ACS and acute ischaemic stroke
2) secondary prevention of MI/stroke/peripheral arterial disease
3) prevent occlusion of coronary artery stents
4) reduce risk of cardiac thrombus in AF (where warfarin + NOACs are contraindicated)

53
Q

Clopidogrel:

  • absolute contraindication?
  • relative contraindications? 2
A

absolute:
- active bleeding

relative:

  • stop 7 days before elective surgery (normally)
  • renal and hepatic impairment
54
Q

clopidogrel:

  • commonest adverse effect?
  • other adverse effects? 2
A

commonest = bleeding

  • GI upset (dyspepsia, abdo pain, diarrhoea)
  • thrombocytopenia (i.e. can reduce numbers as well as function)

nb UNLIKE aspirin, clopidogrel does NOT need to be taken after food!

55
Q

clopidogrel:

  • interactions related to increased bleeding risk? 2
  • interactions which reduce efficacy? 5
A
  • aspirin (+ other NSAIDs)
  • anti-coagulants

any cytochrome P450 inhibitor

  • omeprazole (use lansoprazole or pantoprazle instead)
  • ciprofloxacin
  • erythromycin
  • some anti fungals
  • some SSRIs
56
Q

thrombolytics:

  • example? (incl drug class)
  • mechanism of action?
A

alteplase
- recombinant TPA

TPA catalyses plasminogen -> plasmin which breaks down clots

nb streptokinase is NOT a rTPA but has similar effects but is used less commonly!

57
Q

thrombolytics:

  • main example?
  • indications? 3
A

alteplase (an rTPA)

1) acute ischaemic stroke (give within 4.5 hrs)
2) acute STEMI (must give within 12 hrs, nb PCI is now often used instead)
3) massive PE with haemodynamic instability (evidence base not great)

nb only given in wards where patients are fully monitored and on sign off of senior clinician

58
Q

thrombolytics:

  • main example?
  • main contraindications? 5
  • contraindication for streptokinase?
A

alteplase (an rTPA)

ANY bleeding

  • use CT to rule out haemorrhage on stroke presentation
  • recent haemorrhage
  • recent trauma/surgery
  • bleeding disorders
  • peptic ulcers

previous streptokinase treatment

  • due to anti-streptokinase anti-bodies being produced
  • nb can still use alteplase
59
Q

thrombolytics:

  • main example?
  • common mild side effects? 3
  • serious adverse effects? 4
  • effects of repercussion on (a) brain and (b) heart muscle?
A

alteplase

  • nausea/vomiting
  • bruising (around injection site)
  • hypotension
  • serious bleeding
  • allergic reaction
  • cariogenic shock
  • cardiac arrest
  • cerebral oedema
  • arrhythmias
60
Q

thrombolytics:
- main example?
- interactions which increase bleeding risk? 2
- interaction which increases risk of anaphylaxis?

A

alteplase

  • anti-platelets
  • anti-coagulants
  • ACE inhibitors (unknown mechanism)
61
Q

heparin:

  • examples of LMWH?
  • LMWH mechanism of action?
  • unfractioned heparin mechanism of action?
A
  • tinzeparin
  • enoxaparin
  • dalteparin

both bind to anti-thrombin

LMWH
- helps to inhibit factor Xa ONLY

unfractioned
- helps to inhibit factor Xa AND thrombin

(nb fondaparinux is also an anticoagulant and works similarly to LMWHs)

62
Q

LMW heparin:

  • examples of LMWH? 3
  • indications?
A
  • tinzeparin
  • enoxaparin
  • dalteparin

1) VTE (first line for both DVT + PE)
2) VTE prophylaxis
3) ACS (incl fondaparinux)

63
Q

heparin:

  • examples of LMWH? 3
  • relative contraindications (related to bleeding)?
  • other relative contraindication?
A
  • tinzeparin
  • enoxaparin
  • dalteparin
  • clotting disorders
  • severe uncontrolled HTN
  • recent surgery/trauma
  • invasive procedures (e.g. lumbar puncture + spinal anaesthesia)
  • renal impairment (can use lower dose or unfractioned heparin instead)
64
Q

heparin:

  • examples of LMWH? 3
  • commonish adverse effects? 2
  • rare adverse effect?
  • interactions?
A
  • dalteparin
  • enoxaparin
  • tinzaparin
  • bleeding
  • injection site reactions (sub cut)
  • heparin-induced thrombocytopenia

increased risk of bleeding with any anti platelet or other anticoagulant
- nb used w warfarin for VTE treatment at start and used w anti-platelets for ACS

65
Q

heparin:

  • test used to monitor UH
  • test used to monitor for side effect?
A

activated partial thromboplastin ratio (APTR)
- nb this is not commonly measured in LMWH or fondaparinux

  • monitor platelet levels if long term therapy (>4 days)
66
Q

NOACs:

  • examples? 4
  • mechanism of action?
  • indications? 4
A
  • rivaroXABAN
  • dabigatran
  • edoXABAN
  • apiXABAN

directly inhibits factor Xa (in the common pathway)

  • non-valvular AF
  • VTE prophylaxis
  • VTE treatment
  • following ACS
67
Q

NOACs:

  • examples? 4
  • contraindications? 6
A
  • rivaroXABAN
  • dabigatran
  • apiXABAN
  • edoXABAN
  • pregnancy
  • breastfeeding
  • liver failure (w coagulopathy)
  • severe renal failure
  • active bleeding
  • bleeding disorders
68
Q

NOACs:

  • examples? 4
  • side effects?
A
  • dabigatran
  • rivaroxaban
  • enoxaban
  • apixaban
  • bleeding (incl bruising + brain haemorrhages)
  • dyspepsia
  • headaches/dizziness
  • diarrhoea/constipation

make it clear to patients the signs of bleeding (incl bruising and epistaxis) and tell them to visit GP if notice

nb side effects are not as well known as new drugs

nb unlike warfarin + heparin there is currently NO reversal agent for NOACs

69
Q

NOACs:

  • examples? 4
  • interactions?
A
  • dabigatran
  • rivaroxaban
  • apixaban
  • enoxaban

***look up! - likely to increase likelihood of bleeding

70
Q

Warfarin:

- mechanism of action?

A

Warfarin inhibits hepatic production of vitamin K-dependent coagulation factors and cofactors. Vitamin must be in its reduced form for synthesis of coagulation factors. It is then oxidised during the synthetic process. Vitamin K epoxide reductase reactivates vitamin K. Warfarin INHIBITS vitamin K epoxide reductase, preventing reactivation of vitamin K and coagulation factor synthesis

nb essentially makes you vit K deficient

71
Q

Warfarin:

- indications? 3

A
  • DVT + PE prophylaxis
  • AF (prevent embolic complications)
  • post-heart valve replacement (prevent embolic complications)
72
Q

Warfarin:

  • absolute contraindications? 2
  • relative contraindication? 1
A
  • immediate risk of pregnancy
  • during pregnancy
  • liver disease
73
Q

Warfarin:

  • main side effect?
  • three groups of drugs that cause interactions?
A
  • bleeding (prolongs clotting time and, in high doses, causes spontaneous bleeds)

warfarin has a low therapeutic index

  • cytochrome P450 inhibitors decrease warfarin metabolism and INCREASE BLEEDING risk
  • cytochrome P450 inducers increase warfarin metabolism and INCREASE CLOT risk
  • many Abx can increase anticoagulation inpatients on Warfarin by killing gut flora, which synthesise vit K
74
Q

Drugs which are metabolised by the cytochrome P450 pathway (and are thus are affected by cytochrome P450 inducers/inhibitors)

  • effect of c P450 INHIBITORS on these drugs?
  • effect of c P450 INDUCERS on these drugs?
  • affect of alcohol on c P450 pathway?
A
  • Warfarin
  • COCP
  • Theophylline* (asthma + COPD)
  • Corticosteroids
  • Tricyclic antidepressants (also used for neuralgia)
  • Pethidine (synthetic opiod)
  • Statins

INHIBITORS
- inhibit the breakdown of the active drug so the effect of the drug is stronger

INDUCERS
- induce the breakdown of the active drug so the effect of the drug is weaker

alcohol:

  • acute intake: inhibits (“you are disINHIBITED when drunk”)
  • chronic intake: induces (“alcoholism tends to INDUCE many other problems”)
75
Q

Cytochrome P450 INHIBITORS:

  • mneumonic?
  • list? 13
  • summary (4 main groups)
A

P450 Inhibitors

Don’t join this group it will make your spirit go down…

SICKFACES.COM Group

Sodium valproate (epilepsy, bipolar, migraines)
Isoniazid (Abx for TB)
Cimetidine (H2 receptor antagonist)
Ketoconazole (topical antifungal)

Fluconazole 
Alcohol (acute)
Chloramphenicol (Abx)
Erythromycin 
Sulfonamides* (Abx)

Ciprofloxacin (Abx)
Omeprazole (PPI)
Metronidazole (Abx)

Grapefruit juice

SUMMARY

  • Sodium Valproate
  • Some Abx
  • Some Abx
  • A PPI and a H2 antagonist
76
Q

Cytochrome P450 INDUCERS:

  • mneumonic?
  • list? 7
  • summary (3 main groups)
A

P450 Inducers

CRAP GPS induce me to madness!

Carbemazepines (anti-epileptic)
Rifampicin (Abx for TB)
Alcohol (chronic)
Phenytoin (anti-epileptic)

Griseofulvin (anti-fungal)
Phenobarbitone (barbituate, for epilepsy/insomnia)
Sulphonylureas (diabetes med)

SUMMARY:

  • Anti-epileptic (bar sodium valproate)
  • diabetes med
  • weird anti-fungal and Abx
77
Q

Warfarin:

  • what must it be started alongside?
  • method of administration?
  • target INR for AF and VTE?
  • how often measured?
  • what must patients avoid?
  • what should patients look out for?
A
  • LMWH (as warfarin is prothrombotic - dt protein C - for first few days)
  • oral tablets (once a day, at same time)
  • 2-3 INR (normal is 1)
  • everyday for inpatients, every few days for outpatients
  • grapefruit juice (and keep an eye out for other drugs)
  • any signs of bleeding/bruising etc
78
Q

Statins:

  • examples? 4
  • mechanism of action? (incl specific enzyme name)
A
  • simvastatin
  • atorvastatin
  • rosuvastatin
  • pravastatin

Inhibit the enzyme: HMG CoA reductase

  • means less cholesterol produced by liver
  • means increased clearance of LDL from blood

(- may indirectly reduce triglycerides and increase HDL levels)

overall: slow atherosclerotic process (+ may even reverse it)

79
Q

statins:

  • examples? 4
  • indications? 3 (be clear on cut off values)
A
  • rosuvastatin
  • atorvastatin
  • simvastatin
  • pravastatin

1) primary prevention of CVD (over 40 yo with >10% risk over 10 years)
2) secondary prevention of CVD (1st line, alongside lifestyle changes, to prevent CVD events in people known to have CVD)
3) primary hyperlipidaemia (1st line for conditions such as familial hypercholesteraemia)

80
Q

statins:

  • examples? 4
  • absolute contraindication? 1
  • relative contraindications? 3
A
  • rosuvastatin
  • pravastatin
  • atorvastatin
  • simvastatin

absolute
- pregnant women (baby needs cholesterol)

relative

  • breastfeeding women (see above)
  • renal impairment
  • hepatic impairment
81
Q

statins:

  • examples? 4
  • common side effects? 3
  • serious side effects? 3
A
  • atorvastatin
  • rosuvastatin
  • simvastatin
  • pravastatin
  • headache
  • GI disturbances
  • muscle aches (myalgia)
  • myopathy
  • rhabdomyolysis
  • rise in liver enzymes (e.g. ALT) which can -> drug-induced hepatitis
82
Q

statins:

  • examples? 4
  • interactions? 2
A
  • pravastatin
  • atorvastatin
  • simvastatin
  • rosuvastatin

statins are metabolised by CP450 pathway so:

  • inhibitors increase conc of statin (increased side effects)
  • inducers decrease conc of statin (decreased therapeutic benefit)
  • amiodarone has similar effect (mechanism unclear) of a CP450 INHIBITOR (so increases statin side effect risk)
83
Q

statins:

  • time of day taken?
  • side effect to looks out for?
  • what should patients avoid? 2
  • monitoring needed?
A
  • evening
  • muscle symptoms (pain or weakness)
  • grapefruit juice (only relevant for simvastatin or atorvastatin)
  • limit alcohol intake

check LFTs (esp ALT) at:

  • baseline
  • 3 months
  • 12 months