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Chapter 2: Cardiovascular Flashcards

1
Q

Classes of Anti-arrhythmic drugs ?

A

CLASS 1 - membrane stabilising drugs; Na+ blockers

CLASS 2 - Beta-blocker

CLASS 3 - K+ channel blockers

CLASS 4 - Calcium Channel blockers (rate limiting)

OTHER

  • adenoside
  • digoxin (effective in sedentary patients with non-paroxysmal AF and in patients with associative CHF)
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2
Q

What is included in the CLASS 1 antiarrhthmic drugs?

A

MEMBRANE STABILISING DRUGS ; Na+ blockers

  • disopyramide
  • lidocaine
  • flecainide/propafenone (c/i in asthma/ severe COPD. Avoid in structural ischameic heart disease)
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3
Q

What is flecainide/propafenone c/i in?

A

c/i in asthma/ severe COPD. Avoid in structural ischameic heart disease

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4
Q

What is CLASS 2 antiarrhythmic drugs?

A

BETA-BLOCKERS

- propanolol, bisoprolol etc

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5
Q

What is included in CLASS 3 antiarrhythmic drugs?

A

K+ CHANNEL BLOCKERS

  • amiodarone (4 weeks before and 12 months after electrical cardioversion to increase success)
  • sotalol
  • dronedarone (hepatotoxicity and heart failure side effects)
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6
Q

What is included in CLASS 4 antiarrhthmic drugs?

A

CALCIUM CHANNEL BLOCKERS (rate limiting)

  • verapamil
  • diltiazem (unlicensed)
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7
Q

OTHER antiarrhythmic drugs?

A
  • adenosine

- digoxin (effective in sedentary patients with non-paroxysmal AF and in patients with associative CHF)

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8
Q

What is AF?

A
  • abnormal, disorganised electrical signals fired caused the atria to quiver or fibrillate = rapid and irregular heartbeat
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9
Q

Symptoms of AF?

A
  • heart palpitations = pounding/fluttering

- dizziness, SOB, tiredness

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10
Q

Complications of AF?

A

stroke and heart failure

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11
Q

Classifications of AF?

A

LONE
- Single self limiting episode of AF in ‘normal’ patients i.e. those that are defined by a normal clinical history and examination, ECG, chest x ray and echocardiogram

CHRONIC: recurring episodes of AF

  1. Paroxysmal: when symptoms stop spontaneously without treatment within 2-7 days
  2. Persistent: when AF is persistently occurring and does not terminate spontaneously, therefore requiring either electrical or pharmacological cardioversion to stop it (> 7 days)
  3. Permanent: if the cardioversion is not successful or not indicated for that particular patient (present all the time)

POST-OP
- Occurs in a third of patients who have cardiothoracic surgery. This type is associated with greater morbidity, mortality and risks of complications

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12
Q

2 types of control in AF?

A

RATE CONTROL (controls ventricular rate)

RHYTHM CONTROL (restores and maintains sinus rhythm)
- Cardioversion : restores sinus rhythm
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13
Q

Explain cardioversion process

A

CARDIOVERSION; restores sinus rhythm (RHYTHM CONTROL)

  1. electrical = direct current
  2. pharmacological = anti-arrhythmic
  • cannot give if symptoms > 48 hours; increased risk of stroke
  • electrical preffered if > 48 hours, but should wait until fully anticoagulated for 3 weeks before cardioversion and continue 4 weeks after
  • if haemodynamically unstable (perfusion/heart failure) = electrical cardioversion; give parenteral anticoagulant and rule our left atrial thrombus immediately before procedure
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14
Q

For an acute new-onset presentation of AF what would you do?

A
  • life threatening haemodynamic instability: electrical cardiversion
  • without life threatening haemodynamic instability:
    • <48 hours = rate or rhythm control (electrical or amiodarone/flecainide)
    • > 48 hours = rate control (verapamil, beta blocker)
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15
Q

Maintenance drug treatment for AF?

A

First line = rate control
- betablockers (NOT sotalol)*
- rate limiting CCBs (verapamil, dlitiazem)
- Digoxin
monotherapy –> dual therapy –> rhythm control

Second line = rhythm control
- bbs or oral anti-arrhythmic drug
e.g. sotalol, amiodarone, flecainide, propafenone, dronedarone
(also given if rhythm control is stil required post-cardioversion

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16
Q

Treatment for paroxysmal and symptomatic AF?

A
  • rate or rhythm control = standard bb or oral antiarrhtymic drug
  • “pill in pocket” if infrequent episodes - self treatment = flecainide or propafenone restores sinus rhythm if episode occurs
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17
Q

Treatment for atrial flutter?

A

Similar treatment as AF but catheter ablation more suitable

*A catheter ablation involves passing thin, flexible tubes, called catheters, through the blood vessels to the heart. The catheters record the heart’s electrical activity and can pinpoint where the arrhythmia is coming from. The area of heart muscle at the affected site is then destroyed using either heat (radiofrequency ablation) or by freezing (cryoablation). This creates scar tissue, which doesn’t conduct electricity and so knocks out a trouble spot or acts as a fence around the problem area to prevent the electrical signals from reaching the rest of the heart and causing the arrhythmia.

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18
Q

Stroke prevention: when to give anticoagulant ?

A

Give if risk of thromboembolic stroke > risk of bleeding (HAS-BLED)
Risk of stroke CHAD2=DS2-VASc
C = chronic heart failure or left ventricular dysfunction
H = hypertension
A2 = age 75+
D = diabetes mellitus
S2 = stroke/TIA/venous thromboembolism history
V = vascular history
A = age 65-74 yrs
Sc = sex i.e. female

Give anticoagulant is 2 or more
male= 0 and female = 1

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19
Q

What anticoagulant given in new onset AF?

A

parenteral anticoagulant

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20
Q

What anticoagulant given in diagnosed AF?

A

Warfarin OR NOAC

*NOAC in non-valvular AF with 1 or more rusj factors

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21
Q

What is ventricular tachycardia ?

A

Ventricular tachycardia (VT) is a fast, abnormal heart rate. It starts in your heart’s lower chambers, called the ventricles. VT is defined as 3 or more heartbeats in a row, at a rate of more than 100 beats a minute. If VT lasts for more than a few seconds at a time, it can become life-threatening.

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22
Q

How should pulseless VT be treated?

A

immediate defibrillation + CP; IV amiodarone is given refractory to defibrillation

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23
Q

How should patients with unstable sustained VT be treated?

A

direct current cardioversion. If this fails give IV amiodarone and repeat direct current. If this fails, IV amiodraone should be administered and dc cardioversion repeated

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24
Q

How should stable sustained VT be treated?

A

IV antiarrhythmic drug (amiodarone preferred). Flecainide, propafenone and lidocaine (less effective) can be used.

If sinus rhythm is not restored, direct current cardioversion or pacing should be considered. Catheter ablation is an alternative if cessation of arrhythmia is not urgent

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25
Q

How should non-sustained VT be treated?

A

beta blocker

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26
Q

Maintenance treatment for ventricular tachycardia?

A

For patients at high risk of cardiac arrest

  • most patients: cardioverter defibrillator implant (ICD)
  • some patients also require a drug: sotalol, bb alone or bb with amiodarone

*ICD sends electrical pulses to regulate abnormal heart rhythms, especially those that could be dangerous and cause a cardiac arrest.

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27
Q

What is torsade de pointes ?

A

A form of VT associated with a prolonged QT interval

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28
Q

Causes and treatment for torsade de pointes?

A

Causes: sotalol and other drugs that prolong QT, hyPOkalaemia, and bradycardia

Treatment: Magnesium sulphate

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29
Q

What is paroxysmal supraventricular tachycardia (PSVT)?

A

Paroxysmal supraventricular tachycardia (PSVT) is a type of abnormal heart rhythm, or arrhythmia. It occurs when a short circuit rhythm develops in the upper chamber of the heart. This results in a regular but rapid heartbeat that starts and stops abruptly.

This will often terminate spontaneosuly or with reflex vagal stimulation such as a valsalva mmanoeuvre, immersing the face in ice-cold water or carotid sinus massage - performed with ECG monitoring

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30
Q

What can be done is PSVT is still present after reflex vagal stimulation or is causing severe symptoms?

A

IV adenosine (c/i in COPD/asthma)

  if ineffective or c/i

Alternative: IV verapamil (avoid in patients recently treated with beta blockers)

  • if haemodynamicaly ly unstable = direct current cardioversion
  • recurrent episodes = cather ablation OR drugs (rate limiting CCBs, sotalol, flecainide ir propafenone)
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31
Q

What class arrhythmic drug is amiodarone, what is it used to treat and what is the initial loading dose?

A

CLASS 3 - used in arrhythmias e.g. supraventricular and ventricular arrhythmia

INITIAL LOADING DOSE:

  • 200mg TDS for 7 days,
  • 200mg BD for 7 days and then,
  • 200mg OD as maintenance
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32
Q

Amiodarone side effects

A

EYES:
- corneal micro-deposits pt counselling = night time glares when driving
- optic neuropathy/ neuritis (blindness). counselling = STOP if impaired vision
SKIN:
- phototoxicity (burning, erythema)
- slate-grey skin on light exposed areas
counselling = shiled skin from light, wide spec SPF for months after stopping
NERVES:
- peripheral neuropathy, counselling = numbness, tingling hands and feet, tremors
LUNGS:
- pneumonitis, pulmonary fibrosis, Counselling = SOB, dry cough
LIVER:
- hepatoxicity. counselling = report jaundice, N+V, malaise, itching, bruising, abdominal pain. 3X raised liver transaminases)
THYROID DYSFUNCTION (contains iodine)
- hyperthyroidism (weight loss, heat intolerance, tachycardia) –> give carbimazole if nec. stop amiodarone
- hypothyroidism (weight gain, cold intolerance, bradycardia). start levothyroxine without stopping amiodarone if essential

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33
Q

Amiodarone monitoring?

A
  • annual eye test
  • chest xray before treatment
  • LFTs every 6 months
  • monitor TSH, T3, T4 before treatment and every 6 months
  • blood pressure and ECG (causes hypotension and bradycardia)
  • serum K (causes hypokalaemia; enhances arrhythmogenic effect of amiodarone)
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34
Q

Amiodarone interactions?

A

AMIODARONE HAS EXTREMELY LONG HALF LIFE = 50 days (danger of interactions several months after stopping)

  • increased plasma amiodarone concs = grapefruit juice (enzyme inhibitor)
  • amiodarone is an enzyme inhibitor = warfarin, phenytoin, digoxin (half dose)
  • increased risk of myopathy = statins
  • bradycardia, AV block and myocardial depression = bbs, rate limiting CCBs
  • QT prolongation = increased risk of ventricular arrhythmia = quinolones, macrolides, TCAs, SSRIs, lithium, quinine, hydroxychloroquine, anti-malarials (chloroquine and mefloquine), antipsychotics (especially sulpiride, pimozide, amisulpride)
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35
Q

What type of drug is digoxin?

A

Cardiac glycoside: increases force of myocardial contraction (positive ionotrope) reduces conductivity in the AV node (negative chronotrope)

(INCREASE OUTPUT FORCE + DECREASE RATE OF CONTRACTIONS)
high risk drug

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36
Q

Digoxin therapeutic levels?

A

1-2 microgram/L (Cp 6 hours after dose)

Monitoring is not required during maintenance treatment unless toxicity suspected OR in renal impairment (renally cleared

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37
Q

Digoxin doses?

A
  • loading dose required due to long half life
  • maintenance once daily:
    • atrial flutter and non-paroxysmal AF in sedentary patients = 125-250 mcg
    • worsening or severe HF (in sinus rhythm) = 62.5 - 125mcg
  • different dosage forms have different bioavailabiility e.g.
    elixir = 75%
    tablet = 90%
    IV = 100%
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38
Q

Signs of digoxin toxicity

A

“Slow and sick”.
Risk of toxcitiy in hypO K+, hypO Mg2+, hypER Ca2+, hpoxia and renal impairment

  • bradycardia/heart block
  • nausea, vomiting and diarrhoea, abdominal pain
  • blurred or yellow vision
  • confusion, delirium
  • rash
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39
Q

Treatment for digoxin toxcitiy ?

A

WITHDRAW. Correct electrolyte imbalances

Digoxin-specific antibody for life threatning ventricular arrthymias unresponsive to atropine

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40
Q

Digoxin interactions?

A
  • HyPOkalaemia predisposes to digosin toxicity; diuretics (loop/thiazide), b2 agonist, steroids, theophylline (if K+<4.5mmol/L: give K+ supplements OR K+ sparing diuretic preferred)
  • increase plasma digoxin conc = toxicity: amiodarone (half digoxin dose), rate limiting CCBs, macrolides, ciclosporin (enzyme inhibitors)
  • decreased plasma digoxin conc = subtherapeutic dose: st johns wort, rifampicin (enxyme inducers)
  • reduced renal excretion = toxicity (digoxin renally excreted): NSAIDs, ACEis/ARBs
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41
Q

Digoxin interactions acronym ?

A

CRASED

Calcium channel blockers (verapamin/diltiiazem)
Rifampicin
Amiodarone
St Johns wort 
Erythromycin
Diuretics
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42
Q

2 types of venous thromboembolsim (VTE)?

A
  1. Deep vein thrombosis (DVT): a blood clot occurs in a deep vein, usually in calf of one leg
  2. Pulmonary embolism (PE): detachment of blood clot which travels to the lungs and blocks the pulmonary artery
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43
Q

VTE RISK ASSESSMENT (for all patients admitted to hospital) (12)

A
  • immobility
  • obesity BMI >30
  • malignant disease
  • 60+ years
  • personal history of VTE
  • thrombophilic disorders
  • 1st degree of relative with VTE
  • HRT/combined oral contraceptive
  • varicose veins with phlebitis (inflammation of vein)
  • pregnancy
  • crticial care
  • significant co-morbidities
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44
Q

Risk of bleeding:

A
  • thrombocytopenia (low platelet)
  • acute stroke
  • bleeding disorders
    • acquired: liver failure
    • inherited: haemophilia, Von Willebrands disease
  • anticoagulants
  • systolic hypertension
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45
Q

What is mechanical VTE prophylaixis?

A
  • compressin stockings - for patients scheduled for surgery continued until sufficiently mobile
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46
Q

Pharmacological VTE prophylaxis ?

A
  • for high VTE risk patients undergoing general/orthopaedic surgery OR admitted to hospital as general medical patients. (if c/i offer mechanical prophylaxis)

PARENTERAL ANTICOAGULANTS:

  • low molecular weight herapin OR
  • unfractionated heparin in renal failure OR
  • fondaparinux

NOACs:

  • prophylaxis AFTER knee/hip replacement surgery
  • edoxaban: treatment and prevention of recurrent VTE
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47
Q

Durations for VTE prophylaxis?

A
  • general surgery: 5-7 days or until sufficient mobility
  • major cancer surgery in abdomen or pelvis: 28 days
  • knee/hip replacement sugery: extended duration
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48
Q

Treatment of VTE?

A
  • LMWH OR unfractionated heparin in renal failure . For at least 5 days and until INR at 2 or more for at least 24 hours. Monitor APTT if unfractionated heparin given.
  • Start oral anticoagulant at same time; usually warfarin
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49
Q

VTE in pregnancy

A
  • heparins
  • LMWH is the preferred choice
  • lower risk of osteoporosis and heparin-induced thrombocytopenia
  • stop at labour onset. seek specialist advice on continuing after birth
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50
Q

What is APTT?

A
  • Activated partial thromboplastin time
  • Blood test that characterizes coagulation of the blood, with a substance added to make it clot faster
  • A typical aPTT value is 30 to 40 seconds
  • Important to monitor with unfractionated heparin
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51
Q

Heparin types

A

(parenteral anticoagulant)

  • unfractionated heparin activates antithrombin
  • low molecular weight heparin inactivate factor Xa
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52
Q

Unfractionated heparin

A
  • standard heparin
  • shorter duration of action
  • preferred choice if:
    = high risk of bleeding
    = renal impairment
  • essential to measure APTT (activated partial thromboplastin time)
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53
Q

Low molecular weight heparin

A
  • tinzeparin
  • enoxaparin
  • dalteparin
  • longer duration of action
  • generally preferred choice; lower risk of:
    = osteoporosis
    = heparin-induced thrombocytopeonia
  • used in pregnancy
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54
Q

Heparin side effects?

A
  • haemorrhage: withdraw heparin, if rapid reversal required = antidote protamine
  • hyperkalaemia: heparins inhibit aldosterone secretion. Higher risk in diabetes and CKD. Monitor before treatment and if >7 days use
  • osteoporosis
  • heparin-induced thrombocytopoenia: occurs 5-10 days after. Clnical signs: 30% reduction in platelets, skin allergy, thrombosis. Monitoring: before treatment and if >4 days use
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55
Q

What is the reversal antidote for Heparin?

A

Protamine

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56
Q

Other parenteral anticoagulants?

A
  • heparinoid
  • argatroban
  • hirudin
  • flushes
  • epoprostenol
  • fondaparinux
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57
Q

What is warfarin?

A
  • oral anticoagulant (high risk drug)
  • antagonise actions of vitamin K in blood clotting
  • takes 48-72 hours to work
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58
Q

Warfarin doses?

A
  • 5mg initially and monitor every 1-2 days

- maintenance dose: 3-9mg at same time every day

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59
Q

Warfarin monitoring?

A
  • INR every 3 months once stable
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60
Q

Duration of warfarin treatment?

A
  • isolated calf DVT = 6 weeks
  • provoked VTE (COCs, pregnancy, leg plaster cast) = 3 months
  • unprovoked (e.g. AF) = at least 3 months/ long term
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61
Q

What is the target INR?

A
  • 2.5 = VTE, AF, MI, cardioversion, bioprosthetic mitral valve.
  • 3.5 = recurrent VTE in patients recieving antocoagulant and INR > 2
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62
Q

Warfarin patient counselling

A
  • yellow treatment booklet

- anticoagulant alert card

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63
Q

Warfarin interactions?

A

Changes in INRL
- MHRA/CHM advice: direct acting anti-virals to treat chronic hepatitis C: risk of infection with vitamin K antagonsts and changes in INR; affects efficacy of warfarin. Closely monitor INR

Increased INR = increased risk of bleeding
- MHRA/CH< advice: OTC oral miconazole gel (daktarin) c/i in patients taking warfarin, Closely monitor if miconazole prescribed. Miconazole permanent enzyme inhibitor; increases anticoagulant effect of warfarin

counselling: stop and seek immediate medical attention if any sign of bleeding e.g. nose bleeds or blood in urine

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64
Q

Warfarin side effects?

A
  • Bleeding e.g. nose bleeds <10 mins, bleeding gums, bruising. antidote = vitamin K; phytomenadione
  • Calciphylaxis (a serious, uncommon disease in which calcium accumulates in small blood vessels of the fat and skin tissues. Calciphylaxis causes blood clots, painful skin ulcers and may cause serious infections that can lead to death)
  • MHRA/CHM advice: warfarin reports of calciphylaxis. counselling: report painful skin rash. Consider stopping if calc diagnosed. risk factor: end stage renal disease
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65
Q

What to do when bleeding on warfarin?

A
  • MAJOR BLEEDING
  • stop warfarin
  • IV phytomenadione (vit k)
  • dried prothrombin complex or fresh frozen plasma
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66
Q

What to do with INR 5-8 + no bleeding ?

A
  • withhold 1-2 dose
  • reduce maintenance dose
  • measure INR after 2-3 days
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67
Q

What to do with INR 5-8 + minor bleeding?

A
  • omit warfarin
  • IV phytomenadione
  • repeat if INR still high after 24 hours
  • ## restart warfarin when INR < 5
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68
Q

What to do if INR > 8 + no bleeding?

A
  • omit warfarin
  • oral phytomenadione
  • repeat if INR still high after 24 hours
  • restart warfarin when INR < 5
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69
Q

What to do if INR > 8 + minor bleeding?

A
  • omit warfarin
  • IV phytomenadione
  • repeat if INR still high after 24 hours
  • restart warfarin when INR <5
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70
Q

Warfarin and surgery?? (elective/emergncy/high risk VTE and or bleeding)

A

ELECTIVE

  • stop warfarin 5 days before elective surgery
  • give oral phytomenadione one day if INR > 1.5
  • restart warfain on evening or next day

EMERGENCY

  • delay 6-12 hours
  • no delay; give IV phytomenadione and dried prothrombin complex

IF HIGH RISK OF VTE
- VTE in last 3 months, AF with previous stroke/TIA, mechanical valve = bridge with LMWH (treatment dose) and stop 24 hours before surgery

HIGH RISK OF BLEEDING
- start LMWH 48 hours after surgery

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71
Q

What are NOACs?

A

Novel Oral Anticoagulants: inhibits specific clotting factors i.e. thrombin or factor Xa

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72
Q

NOACs examples

A
  • dabigatran - direct thrombin inhibitor, special container - 4 month expiry
  • apixaban*
  • edoxaban*
  • rivaroxaban*
  • direct factor Xa inhibitors

USE: increasingly used as an alternative to warfarin.
Advantages: rarely causes bleeding and no monitoring required

NOACs come with patiet alert card

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73
Q

2 classifications of stroke management ?

A
  1. ISCHAEMIC = BLOOD CLOT OBSTRUCTS BLOOD SUPPLY
    - ischaemic strokes
    - transient iscaemic attack (mini strokes)
  2. HAEMORRHAGIC = WEAK BLOOD VESSEL IN BRAIN BURSTS
    - intracerebral haemorrhage
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74
Q

Long term stroke management?

A

TIA : MR dipyridamole and aspirin

ISCHAEMIC STROKE: clopidogrel, in AF-related stroke - review for anticoagulant

BOTH TIA/ISCHAEMIC STROKES: statin irrespective of serum cholesterol, treat hypertension; not with beta blockers unless indicated for another condition

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75
Q

How is intracerebral haemorrhage managed?

A
  • avoid aspirin, statin and anticoagulants (increases risk of bleeding; only give if essential)
  • treat hypertension and take care to avoid hypoperfusion
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76
Q

Antiplatelet drug action?

A

Decrease platelet aggregation and inhibit thrombus formation in the arterial circulation

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77
Q

antiplatalet drugs?

A
  • aspirin
  • clopidogrel
  • dipyridamole
  • cangrelor
  • prasugrel
  • ticagrelor
  • abciximab (monoclonal antibody)*
  • eptifibatide *
  • tirofiban*
  • glycoprotein IIa/IIb inhibitors
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78
Q

Dose of aspirin used in 2nd prevention of CVD?

A

75mg daily

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79
Q

In what indications is clopidogrel given?

A

following ACS or PCI

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80
Q

When is dipyridamole given?

A

2nd preventionn of strokes. Take tabs 30-60 mins before food. Persantin retard capsules special container - 6 week expiry

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81
Q

How are people under 55 initially treated for hypertension (STEP 1)?

A

ACEi or ARB

*if not c/i or not tolerated: beta blocker

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82
Q

How are people over 55 yrs and/or if patient is of african/carribbean origin initially treated for hypertension ? (step 1)

A

CCB

*if high risk of heart failure or CCB not tolerated: thiazide like diuretic

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83
Q

Step 2 hypertensive treatment for patients under 55 yrs ?

A

ADD CCB

*if high risk heart failure or CCB not tolerated: thiazide like diuretic

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84
Q

Step 2 hypertensive treatment for over 55/ of african/carribbean origin?

A

ADD ACEi or ARB

*ARB preferred in african/carribbean patients

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85
Q

Step 3 in antihypertensive treatment?

A

ACEi/ARB + CCB +TLD

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86
Q

Step 4, resistent hypertenison?

A

low dose sprionolactone
OR high dose TLD if K+ > 4.5
If other diuretics c/i or ineffective, add alpha or beta blocker

87
Q

Stages of hypertension?

A

1: 140/90mmHg = offer lifestyle advice, only treat if under 80 with: target organ damage (LV hypertrophy, CKS, retinopathy), CVD or QRISK >20%, renal disease, diabetes
2. 160/100mmHg = treat all

  1. > 180 systolic >110 diastolic = hypertensive crisis. Hypertensive emergency = acute target organ damage, IV reduce BP slowly; otherwise reduced organ perfusion = blindness, MI, cerebral infarction and severe renal impairment.
    Hypertensive urgency = without target organ damage - oral reduce Bp slowly over 24-48 hrs
88
Q

BP target for under 80yrs ?

A

<140/90

130/80 in atherosclerotic CVD OR diabetes with kidney, eye or cerebrovascular disease

89
Q

BP target for over 80 yrs ?

A

<150/90

90
Q

BP target for renal disease?

A

<140/90

<130/80 if CKD, diabetes, proteinuria >1g in 24 hours . Consider ACEi/ARB if proteinuria present

91
Q

BP target for diabetes?

A

<140/80

<130/80 if compliacations; eye, kidney or cerebrovascular disease

92
Q

BP target for pregnancy? (what classifies hypertenison)?

A

< 150/100 chronic hypertension

<140/90 chronic hypertension and if target organ damage or given birth
LABETALOL (hepatotoxic) is widely used and first choice in gestational hypertension. METHYLDOPA (stop 2 days after birth)/ MR NIFEDIPINE (unlincensed

93
Q

ACE inhibitors MOA?

A

Inhibits the conversion of angiotensin 1 to angiotensin 2

94
Q

ACE inhibitors examples?

A 
Captopril (BD)
Enalapril
Fosinipril
Imidapril
Lisinopril
Moexipril
Perindopril (30-60 mins before food)
Quinapril
Ramipril
Trandolapril

Taken OD except captopril.
Take first dose at bed time

95
Q

Angiotensin 2 receptor blockers (ARBs) examples?

A 
Azilsartan
Candesartan
Eprosartan
Irbesartan
Losartan
Olmesartan
Telmisartan
Valsartan
96
Q

ACE inhib side effects?

A
  • persistent dry cough (give ARB as alternative)
  • hyperkalaemia *higher risk in renal impairment and diabetes mellitus
  • anaphylactoid reactions e.g. angioedema
  • nephrotoxic
  • oral ulcer
  • taste disturbance
  • hypoglycaemia
  • avoid in pregnancy
97
Q

ACE/ARB renal effects?

A
  • renoprotective in renal disease e.g. CKD
  • nephrotoxic = acute kidney injury; avoid DAMN
    Diuretics, ACE/ARB, Metformin, Nsaids
  • reduces egfr via efferent arteriole dilation
  • avoid in renovascular disease (may give in unilateral renal artery stenosis NOT severe bilateral stenosis)
98
Q

ACE/ARB hepatic effects?

A
  • cholestatic jaundice, hepatic failure

- stop if liver transaminases 3x normal or jaundice occurs

99
Q

ACE inhibitors drug interactions?

A
  • hyperkalaemia: aliskeren, ARB, K+ sparing diuretics/aldosterone antagonists
  • nephrotoxicity and reduced eGFR: NSAIDs (afferent arteriole constriction)
  • hypotension: diuretics (volume depletion = low BP)
  • renal impairment, hyperkalaemia and hypotension: renin-angiotensin system drugs ACE/ARB, renin inhibitor. Avoid concomitant ACE + ARB in diabetic nephropathy
100
Q

ARB MOA?

A

blocks angiotensin 2 receptor, does not inhibit the breakdown of bradykinin; alterntaive to ACE if persistent dry cough present

101
Q

Centrally acting anti-hypertensives ?

A
  • methyldopa (side effects = driving; drowsiness)
  • clonidine (side effects = flushing)
  • moxonidine
102
Q

Vasodilator antihypertensives ?

A
  • hydralazine (side effects = fluid retention, tachycardia)

- minoxidil (side effects = tachycardia, fluid retention and increase cardiac output)

103
Q

Alpha blockers?

A
  • prazosin
  • terazosin
  • indoramin
104
Q

beta -adrenoreceptor blocker MOA?

A

Beta-blockers block beta-adrenoreceptors in the heart, peripheral vasculature, bronchi, pancreas and liver

105
Q

4 different types of beta blockers? (anagrams)

A

ice PACO
water CANS
Be A MAN
BACoN

106
Q

ice PACO beta blockers?

A

Pindolol
Acebutol
Celiprolol
Oxprenolol

  • intrinsic sympathomimetic activity
  • less bradycardia
  • less coldness of extremeties
107
Q

water CANS beta blockers (anagram)?

A

Celiprolol
Atenolol
Nadolol
Sotalol

  • water soluble; less likely to cross BBB
  • less nightmares and sleep disturbances
  • reduce dose in renal impairment as renally cleared
108
Q

Be A MAN beta blockers?

A 
Bisoprolol
Atenolol
Metoprolol
Acebutol
Nebivolol
  • cardio-selective = less bronchospasm
  • well-controlled asthma under a specialist if no other choice
109
Q

BACON beta blockers?

A

Bisoprolol
Atenolol
Celiprolol
Nadolol

  • once daily dosing
  • intrinsically long duration of action
110
Q

Beta blocker side effects?

A
  • bradycardia, hypotension

- hyperglycaemia OR hypoglycaemia (masks symptoms of hyPO e.g. tachycardia)

111
Q

Beta blocker contra-indications ?

A
  • asthma: causes bronchospasm (includes b-blocker eye drops e.g. timolol)
  • worsening unstable heart failure
  • second/third degree heart block
  • severe hypotension and bradycardia
112
Q

Beta blocker interactions?

A
  • Asystole and hypotension (verapamil injection)

- hypERglycaemia; avoid in diabetes/high risk (thiazide-like diuretcis)

113
Q

Calcium channel blockers (CCBs) MOA?

A
  • blocks calcium channels to reduce force of contraction, conductivity and vascular tone
114
Q

2 classifications of CCBs?

A
  • dihydropyridine: vasodilation

- rate limiting

115
Q

Dihydropyridine CCBs?

A
  • amlodipine
  • felodipine
  • lacidipine
  • lercanidipine
  • nifedipine (maintain the same MR brand)

side effects: ankle swelling, flushing, headaches (common)

116
Q

Rate limiting CCBs?

A
  • verapamil (causes constipation, only CCB licensed for arrhythmias)
  • diltiazem (maintain on same brand when doses >60mg)

*AVOID IN HEART FAILURE

117
Q

CCB interactions?

A
  • increased CCB concentrations with grapefruit juice(enzyme inhibitor) (avoid)
118
Q

What is Pheochrocytoma and how is it treated ?

A

Pheochromocytoma is a type of neuroendocrine tumor that grows from cells called chromaffin cells. The tumor releases hormones that may cause high blood pressure, headache, sweating and symptoms of a panic attack

Beta-blocker + alpha blocker (phenoxybenzamine)

treats symptoms: headache, excess sweating and a hard, fast heartbeat (palpitations).

119
Q

What class of drugs are used for hypotension and shock and how do they work?

A

Vasoconstrictor sympathomimetics: raise blood pressure transiently by acting on alpha-adrenergic receptors to constrict peripheral blood vessels

120
Q

Vasoconstrictor sympathomimetics examples?

A
  • noradrenaline
  • phenylephrine (longer acting: prolonged rise in BP)

side effects: reduced perfusion to vital organs e.g. kidneys

121
Q

Heart failure symptoms?

A
  • dysponea (sudden severe SOB) during an activity or at rest
  • exercise intolerance/ fatigue
  • oedema:
    * pulmonary oedema = breathlessmess
    * peripheral oedema = swollen ankles/legs
122
Q

What should be measured in diagnosing a patient with suspected heart failure?

A
  • N-terminal pro-B-type natriuretic hormone (NT-proBNP)
  • refer people with suspected HF with NT-proBNP above 2000ng/L (236pmol/L) urgently to specialist for echocardiography within 2 weeks
  • refer between 400 and 2000 for echo within 6 weeks
123
Q

What can reduce levels of serum natriuretic peptides?

A

obesity, African or African–Caribbean family background, or treatment with diuretics, ACE inhibitors, BBs, ARBs or mineralocorticoid receptor antagonists (MRAs) can reduce levels of
serum natriuretic peptides

124
Q

What is another explanation for high NT-proBNP levels?

A

high levels of serum natriuretic peptides can have causes other than heart failure (e.g., age over 70 years, left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia [including pulmonary embolism], renal dysfunction
[eGFR less than 60 ml/minute/1.73], sepsis, chronic obstructive pulmonary disease, diabetes, or cirrhosis of the liver).

REFER TO NICE FOR MORE ON HF

125
Q

What are the first line steps in drug treatment in heart failure ?

A

ACE/ARB + B-BLOCKER

  • perindopril, ramipril, captopril, enalapril, lisinopril, quinapril or fosinopril
  • and beta blocker licensed for HF (bisoprolol, carvedilol in all grades or nebivolol in mild-mod)
  • first line treatment to reduce morbidity and mortality
  • ARB licensed for heart failure (candesartan, losartan, valsartan) considered if ACE not tolerated
126
Q

Alternative first line treatment for HF?

A

hydralazine + isosorbide dinitrate (specialist use)

127
Q

Second line treatmemt in HF if symtpoms persist despite treatment?

A
  • Add spironolactone OR eplerenone after acute MI with LVSD or mild HF (unless c/i due to hyperkalaemia or renal impairment)

ALT:

  • hydralazine +isosorbide dinitrate considered under specialist advoce in patients intolerant of ACE/ARB (in particular african/caribbean origin with mod-sev HF)
  • sacubutril valsartan (LVEF <35% and taking ACE/ARB)
128
Q

Third line treatment for HF if symptoms still persist?

A

Add ivabradine (added to standard therapy if patient in sinus rhytmm and heart rate >75)

OR

Add digoxin (worsening or severe heart failure - does not reduce mortality but may reduce symptoms and hospitalisation)

OR

amiodarone

129
Q

What else should be considered in patients in sinus rhytmn with HF if they have a history of thromboembolism, LV aneurysm or intracardiac thrombus?

A

anticoagulation

130
Q

What monitoring is required when initiating ACE/ARB and aldosterone antagonists in HF?

A
  • serum potassium and sodium, renal function and BP should be checked prior to starting, 1-2 weeks after and at each dose increment . Once taret dose is reached, monitor monthly for 3 months and then at least every 6 months
131
Q

When inititaing BB treatment what monitoring is required in HF*?

A
  • heart rate, BP and symptom control should be assessed at the start of treatment and after each dose change
132
Q

In what condition should lower doses and slower titrations of ACE, ARBs, aldosterone antagonists and digoxin be considered?

A

CKD

133
Q

What drug treatment can be added on in HF for fluid overload?

A
  • loop diuretics

- thiazide diuretucs in mild HF (ineffective in renal failure eGFR <30)

134
Q

What is hyperlipidaemia ?

A

high blood levels of cholesterol, triglycerides or both

135
Q

What complications can hyperlipidaemia cause?

A

CVD

  • hyperlipidaemia causes atherosclerosis and in turn:
  • coronary heart disease (angina, MI)
  • strokes and TIA
  • peripheral arterial disease
136
Q

What patient groups are eligible for primary prevention of CVD?

A
  • type 1 diabetes mellitus
  • type 2 diabetes mellitus only if CVD risk >10%
  • QRISK >10%
  • CKD or albuminuria
  • familial hypercholesterolaemia
  • 85 years + (reduce risk of non-fatal MI)
137
Q

Who is included in secondary prevention of CVD?

A
  • In patients with established CVD (coronary heart disease (angina/MI), cerebrovascular disease (stroke/TIA) and peripheral arterial disease)
138
Q

In which patient groups is QRISK2 not suitable?

A
  • type 1 diabetes mellitus
  • established CVD
  • over 85 yrs
  • CKD (eGFR <60)
  • familial hypercholesterolemia

(score will be underestimated)

139
Q

What cholesterol level classifies hyperlipidaemia?

A

6mmol/L total cholesterol

140
Q

What is the target total cholesterol ?

A

=/< 5mmol/L total for healthy adults

=/< 4mmol/L for high risk adults

141
Q

What is the target for LDL cholesterol?

A

=/<3mmol/L LDL for healthy adults

=/<2mmol/L for high risk adults

142
Q

What is the target for HDL cholesterol?

A

> 1mmol/L HDL (“good cholesterol - higher the better)

143
Q

What is the target for triglycerides?

A

<1.7mmol/L

144
Q

Drugs that cause hyperlipidaemia?

A
  • antipsychotics
  • immunosuppressants
  • corticosteroids
  • antiretrovirals (HIV drugs)
145
Q

Conditions that cause hyperlipidaemia?

A
  • hypothyroidism
  • liver or kidney disease
  • diabetes mellitus
  • family history of high cholesterol
  • lifestyle factors : smoking, excess alcohol, obesity and poor fatty diet
146
Q

Types of lipid regulating drugs?

A
  • statins
  • fibrates (bezafibrate, ciprofibrate, fenofibrate, gemfibrozil)
  • ezetimibe
  • bile acid sequestrants (colesevelam, colestipol. colestyramine)
  • nicotinic acid group (acipimox, nicotinic acid, omega-3 fatty acid)
  • lomitapide
  • alirocumab
147
Q

Statins MOA?

A
  • lowers LDL cholesterol synthesis by the liver via inhibition of HMG-CoA reductase (indirectly reduces triglycerides and increase HDL cholesterol)
148
Q

5 types of statins?

A 
Atorvastatin*
Rosuvastain *
Pravastatin
Simvastatin
Fluvastatin

*dont need to be taken at night

ONCE DAILY (for other statins cholesterol synthesis is greater at night; more effective)

149
Q

Use of statins in CVD prevention?

A

atorvastatin 20mg OD (primary)

atorvastatin 80mg OD (secondary)

150
Q

High intensity statins?

A

Defined as the dose at which a reduction in LDL greater than 40%

  • rosuvastatin 10, 20,40mg
  • atorvastatin 20,40,80mg
  • simvastatin 80mg (MHRA WARNING high risk of myopathy: give only if high risk of CVD complications or severe hypercholesterolaemia and treatment goals not achieved at lower dose)
151
Q

What drug treatment is used for primary and familial hypercholesterolaemia?

A

High intesnsity statin or ezetimibe if statin c/i or not tolerated

152
Q

What drug treatment is used for moderate hypertriglyceridaemia?

A

If statin not tolerated or c/o = fibrate

153
Q

What can be added on to treatment in severe hyperlipidaemia?

A

ezetimibe

154
Q

What can be added onto treatment if triglycerides still high after LDL reduced?

A

Fibrate OR nicotinic acid (also lowers LDL)

155
Q

Before starting statins, what underlying causes of dyslipidaemia could be addressed?

A
  • hypothyroidism
  • uncontrolled diabetes mellitus
  • nephrotoxic synfrome (albuminuria)
  • liver disease e.g. alcohol cirrhosis
156
Q

Before starting statins, what underlying causes of dyslipidaemia could be addressed?

A
  • hypothyroidism
  • uncontrolled diabetes mellitus
  • nephrotoxic synfrome (albuminuria)
  • liver disease e.g. alcohol cirrhosis
157
Q

Statins side effects?

A
  • myopathy, myositis, rhabdomyolysis (report tender, weak and painful muscles)
  • higher risk of muscle toxicity in:
    • -> personal or family history of muscle disorder
    • -> high alcohol intake
    • -> renal impairment
    • -> hypothyroidism; treat before starting statin
  • increased risk of myopathy with:
    • -> concomitant ezetimibe or fibrates, especially gemfibrozil
    • -> concomitant fusidic acid: restart statin 7 days after last dose (increased risk of rhabdomyolysis)
  • interstitial lung disease (report SOB, cough, weight loss)
  • raised HcA1c or BG levels (caution in diabetes)
158
Q

Statin monitoring?

A
  • baseline lipid profile
  • renal function
  • thyroid function
  • HbA1c if high risk of developing diabetes
  • if severe muscle symptoms: DISCONTINUE
  • creatine kinase: discontinue if 5x normal (if level returns to normal and muscle symptoms resolve a statin can be reintroduced at a lower dose and monitor)
  • liver function: discontinue if liver transaminases 3x normal
159
Q

Statin interactions?

A
  • increased statin levels = increased myopathy risk: amiodarone, grapefruit juice, CCBs e.g. diltiazem, amlodipine, imidazole/triazole antifungals e.g. itraconazole, ciclosporin
  • macrolide antibiotic e.g. clarithromycin: stop taking statin until antibiotic course completed
  • fibrates (esp gemfibrozil): Avoid
  • fusidic acid: restart statin 7 days after last fusidic acid (oral) dose
160
Q

Statin dose adjustments due to interactions?

A

Simvastatin:
max 10mg with fibrate
max 20mg with amiodarone, amlodipine, diltiazem, verapamil

Atorvastatin:
max 10mg with ciclosporin

Rosuvastatin
initially 5mg, max 20mg with clopidogrel

161
Q

Statins and pregnancy?

A

TERATOGENIC

  • effective contraception during and 1 month after stopping
  • stop taking 3 months before conceiving and restart after breastfeeding finished
162
Q

Ezetimibe MOA?

A
  • reduces blood cholesterol by inhibiting the absorption of cholesterol by the small intestine
  • alternative to statin in familial and primary hypercholesterolaemia
163
Q

ezetimibe interactions?

A

Can increase risk of myopathy when used together with statins

164
Q

Fibrates MOA?

A

lowers blood triglyceride levels by reducing the livers production of VLDL (the triglyceride-carrying particle that circulates in the blood) and by speeding up the removal of triglycerides from the blood

Interactions: myopathy with statins

165
Q

What treatment is used in severe hypertriglyceridaemia >10mmol/L or in those who cannot tolerate a statin?

A
  • bezafibrate
  • fenofibrate
  • ciprofibrate
  • gemfibrozil: do not use with stain as high risk of myopathy (rhabdomyolysis)
166
Q

Bile acid sequestrants MOA?

A

Binds and sequesters bile acids. The liver then produces more bile acids to replace those that have been lost. The body used cholesterol to make bile acids, this reduces the amount of LDL cholesterol circulating in the blood

(SPECIALIST USE)

167
Q

Bile acid sequestrants examples?

A
  • colesevelam
  • colestipol
  • colestyramine

Interactions: impaired absorption of fat-soluble vitamins ADEK and other drugs. Take other drugs 1 hour before (4hrs for coleveselam) or 4 hours after bile acid sequestrant

168
Q

Short acting nitrates used in acute angina attacks ?

A 
GTN
Isosorbide dinitrate (s/l)
169
Q

Long acting nitrates used in long term prophylaxis of angina?

A
  • MR isosorbide dinitrate
  • isosorbide mononitrates

Also used in prophylaxis

  • BBs
  • CCBs
  • Ivabradine
  • Ranolazine
  • Nicorandil
170
Q

How does GTN work?

A
  • converted to nitric oxide which is a short acting vasodilator; improves blood supply
171
Q

GTN formulations?

A
  • sublingual tablet/spray
  • effects last 20-30 mins
  • if using more than twice a week –> need long term prophylaxis
  • *special container for tablets, expires 8 weeks ater opening, foil-lined container with no cotton wadding
172
Q

How to take GTN?

A
  • when required OR
  • before angina inducing activities e.g. exercise
  • take sitting down as dizziness can occur
  • take 1st dose under tongue and wait 5 mins
  • take 2nd dose and wait 5 mins
  • take 3rd dose and wait 5 mins
  • if pain is still present call 999
173
Q

What is used first line in angina prophylaxis?

A
  • Beta blocker (atenolol, bisoprolol, metoprolol or propranolol)
    OR
  • rate limiting CCB (diltiazem/verapamil) if bb are c/i

*BB + dihydropyridine CCB (amlodipine, nifedipine MR, felodipine) may be effective in patients with prinzmetal’s angina

174
Q

What can be added/used for second line angina prophylaxis if first line c/i ?

A

VASODILATORS:

  • long acting nitrate
  • ivabradine (only in normal sinus rhythm)
  • ranolazine
  • nicorandil in adults only (K-channel activator) MHRA/CHM warning: now given 2nd line risk of ulcer complications: mouth, skin, eye, GI. Do not drive until it is established performance is not impaired
175
Q

Nitrates MOA?

A
  • nitrates are potent coronary vasodilators and reduce venous return and cardiac output
176
Q

Nitrate tolerance?

A
  • with long acting preparations or transdermal patches
  • maintain effectiveness by reducing blood nitrate concentrations to low levels for 4-12 hours a day
    1. leave patches off for 8-12 hrs (overnight) per day
    2. take second dose after 8 hours not 12 hours for MR isosorbide dinitrate BD and isosorbide mononitriate BD
    3. MR isosorbide mononitrate is taken OD therefore does not produce tolerance
177
Q

Nitrates side effects?

A
  • vasodilation, flushing, throbbing headache, dizziness, postural hypotension, tachycardia, dyspepsia, heartburn
  • injection (GTN and isosorbide dinitrate in MI) = severe hypotension, sweating, apprehension, restlessness, muscle twitching, retrosternal discomfort
  • avoid abrupt withdrawal of nitrates (and CCB) –> worsens angina
178
Q

5 steps that need to be taken in the treatment of MI (NSTEMI/STEMI/UA)?

A
  1. O2 if hypoxia
  2. ISCHAEMIC PAIN: - GTN/IV isosorbide dinitrate - IV diamorphine/morphine with metoclopramide
  3. REPERFUSION: - aspirin 300mg + clopidogrel 300mg. - PCI or thrombolytic (altepase within 4.5 hrs; steptokinase within 12hrs - avoid 4 days)
  4. PREVENT RE-OCCLUSION SYSTEMIC AND EMBOLISATION: parenteral anticoagulant
  5. LONG TERM MANAGEMENT = SAAB: Statin, ACE inhibitor, Aspirin indefinitely, Beta blocker. Clopidogrel (4 weeks = STEMI, 12 months = NSTEMI/Unstable angina)
179
Q

PCI?

A

Percutaneous coronary intervention (PCI), can be gievn with glycoprotein IIb/IIa inhibitor

- Dual antiplatelet therapy: 
  Aspirin (forever)
\+ Clopidogrel OR ticagrelor/prasugrel 
elective = one month 
bare metal stent = 12 months 
drug-eluting stent = 12 months
180
Q

Medical emergeny in the community STEMI/NSTEMI/UA

A

UNSTABLE ANGINA AND NSTEMI

  • disp/chew aspirin 300mg STAT + note
  • GTN as required sublingually or spray

STEMI;
- as above but add on IV diamorphine/morphine + metoclopramide

181
Q

Cardiac arrest actions?

A

CARDIOPULMONARY RESUSCITATION

  • 30 compressions: 2 breaths
  • approx 100 compressions/min

IV adrenaline 1 in 1000 every 3-5 mins (sympathetomimetic ionotrope used in cardiogenic shock)

If ventricular fibrillation present: IV amiodarone

182
Q

When should you take diuretics?

A

in the morning to avoid sleep disruption

183
Q

Loop diuretics?

A
  • bumetanide (most potent)
  • furosemide (gout)
  • torasemide (musculoskeletal pain)

Used in pulmonary oedema due to left ventricular failure and in patients with chronic heart failure

184
Q

Thiazide diuretics?

A
  • bendroflumethiazide
  • cyclopenthiazide

Used to relieve oedema due to chronic heart failure and in lower doses, reduce BP

185
Q

Thiazide related diruretics?

A
  • chlortalidone (long half life)
  • indapamide (less aggrevation of diabetes)
  • metolazone (still works in severe renal failure)
  • xipamide
186
Q

Potassium-sparing diuretics?

A
  • amiloride
  • triamterene (blue urine in some lights)

+spironolactone + eplerenone

187
Q

Aldosterone antagonists?

A
  • sprionolactone (ascites liver failure)
  • eplerernone (used in post-acute MI)

*(also known as K-sparing)

188
Q

Osmotic diuretic ?

A

Mannitol (used in cerebral oedema)

189
Q

Carbonic anhydrase inhibitors ?

A
  • acetozolamide (used in glaucoma)
190
Q

Diuretics MOA?

A

Increased urine output by the kidneys e.g. promotes diuresis by inhibiting sodium reabsorption at different parts of the renal tubular system (nephron)

191
Q

Loop diuretics action, onset and side effects?

A
  • inhibit Na+/K+/Cl- co transporter in ascending limb of loop of henle
  • 1 hour onset
  • 6 hour duration
  • side effects:
    • -> ototoxicity (tinnitus, deafness),
    • -> acute urinary retention (too rapid diuresis, *caution in benign prostatic hyperplasia although less likely in low doses)
    • -> hyperglycaemia (diabetes - can exacerbate) although less likely than with thiazides
    • -> hyperuricaemia (gout) - can exacerbate
    • -> HYPO K+, Na+, Cl-, Mg2+ (alcoholic cirrhosis)
    • -> HYPER Ca2+
192
Q

Loop diuretic indications?

A 
HEART FAILURE 
(BD take last dose at 4pm)
20-40mg OM - furosemide doses

RESISTANT HYPERTENSION
Bumetanide (most potent)
Torasemide (musculoskeletal pain)
Furosemide

193
Q

Thiazide and related action, onset and side effects?

A
  • Inhibits Na+/Cl- transporter in distal convoluted tubule
  • 1-2 hour onset
  • 12-24hr duration
  • side effects:
    • -> GI disturbances
    • -> impotence
    • -> high LDL/triglycerides
    • -> hyperglycaemia (diabetes)
    • -> hyperuricaemia (gout)
    • -> HYPO K+, Na+, Cl-, Mg2+ (alcohol cirrhosis)
    • -> HYPER Ca2+
  • ineffective if eGFR <30ml/min except metolazone
194
Q

Thiazide and related action, onset and side effects?

A
  • Inhibits Na+/Cl- transporter in distal convoluted tubule
  • 1-2 hour onset
  • 12-24hr duration
  • side effects:
    • -> GI disturbances
    • -> impotence
    • -> high LDL/triglycerides
    • -> hyperglycaemia (diabetes)
    • -> hyperuricaemia (gout)
    • -> HYPO K+, Na+, Cl-, Mg2+ (alcohol cirrhosis)
    • -> HYPER Ca2+
  • ineffective if eGFR <30ml/min except metolazone
195
Q

Thiazides and related indications?

A

HEART FAILURE OM 5mg
HYPERTENSION OM 2.5mg
- bendroflumethiazide doses

  • indapamide (less diabetes exacerbation)
  • metolazone (use in severe RF)
  • chlortalidone (long half life given on alternate days if acute retention is a problem or dislikes frequent urination)
196
Q

Potassium sparing diuretics MOA?

A

Promotes urination (diuresis) without the loss of potassium by inhibiting sodium channels in the distal convoluted tubule. They are weak diuretics used as an adjunct to loop and thiazide diuretics

197
Q

Potassium sparing diuretics use, side effects and interactions?

A
  • triamterene (urine can look blue)
  • amiloride

USE:
- preferred over K+ supplements in counteracting HYPOkalaemia
SIDE EFFECTS:
- hyperkalaemia
INTERACTIONS:
- hyperkalaemia: avoid concomitant ACE/ARB, K+ supplements, aldosterone antagonist

198
Q

Aldosterone antagonist MOA

A

Inhibits aldosterone which causes sodium reabsorption via the Na+/K+/H+ co transporter. Less potassium and hydrogen ions are exchanged for sodium and therefore less lost to the urine

199
Q

Aldosterone antagonsit side effects and interactions?

A
  • spironolactone (use in ascites in liver failure)
  • eplerenone

SIDE EFFECTS:

  • gynaecomastia, benign breast tumours, menstrual disturbances
  • hypertrichosis
  • change in libido
  • HYPERkalaemia, hyperuraemia, HYPOnatraemia

INTERACTIONS:
- severe hyPERkalaemia: K+sparing diuretics, K+ supplements, ACE/ARBs
MHRA: aldosterone antagonists and ACEi/ARB in heart failure: risk of potentially fatal/severe hyperkalaemia. Monitoring of blood electrolytes is essential

200
Q

Osmotic diuretics MOA?

A

Inhibits sodium and water reabsorption by increasing the osmolarity (solute concentration) of blood and renal filtrate. Osmotic diuretics act on the parts of nephron that are water permeable; proximal convoluted tubule and descending limb of the loop of henle

201
Q

Osmotic diuretic uses?

A

MANNITOL (pharmacologically inert sugar)

USES:

  • cerebral oedema
  • high intracranial pressure
202
Q

What is used for simple gravitational oedema in the elderly ?

A
  • low dose diuretic

- not for long term use, try alternatives first e.g. stockings, raising legs and movement

203
Q

What is peripheral vascular disease?

A
  • either occlusive (intermittent claudication) in which occlusion of the peripheral arteries is caused by atherosclerosis (peripheral arterial disease)

OR

  • vasospastic (e.g raynauds syndrome)
204
Q

Treatment for peripheral arterial disease?

A
  • aspirin 75mg daily and statin as secondary prevention of CVD
205
Q

Treatment for raynauds?

A
  • stop smoking and avoid exposure to cold

- nifedipine used to reduce the frequency and severity of vasospastic attacks

206
Q

What does tranexamic acid do?

A
  • anti-fibrinolytic drug
  • inhibits fibrinolysis, can be used to prevent bleeding or to treat bleeding associated with excessive fibrinolysis (e.g. in surgery, dental extraction, obstetric disorders, and traumatic hyphaema) and in the management of menorrhagia
207
Q

What is desmopressin used for?

A
  • used in the management of mild-moderate haemophilia and von willebrands dosease. also used for fibrinolytic response testing
208
Q

What are thrombolytic drugs?

A
  • streptokinase (given within 12 hours)
  • altepase (given within 6-12 hours)

Been shown to reduce mortality in MI. Reteplase (within 12 hours) and tenecteplase (early as poss) also licensed in MI. Thrombolytic drugs are indicated for patients with acute MI for whom benefit outweigh risk

  • Altepase, streptokinase and urokinase can be used for other thromboembolic disorders such as DVT and pulmonary embolism
209
Q

Thrombolytic drugs MOA?

A

Dissolve blood clots by activating plasminogen, which forms a cleaved product called plasmin. Plasmin is a proteolytic enzyme that is capable of breaking cross-links between fibrin molecules, which provide the structural integrity of blood clots

210
Q

Which beta blockers have intrinsic sympathomimetic activity?

A
  • oxprenolol
  • pindolol
  • acebutolol
  • celiprolol
  • cause less bradycardia
  • causes less coldness of the extremeties
211
Q

Which beta blockers are water soluble?

A
  • atenolol
  • celiprolol
  • nadolol
  • sotalol
  • less likely to cross the blood - brain barrier
  • less likely to cause nightmares and disrput sleep
  • excreted renally
212
Q

Which beta blockers have a long duration of action?

A
  • atenolol
  • bisoprolol
  • celiprolol
  • nadolol
  • once daily dosing
213
Q

Which beta blockers have arteriolar vasodilating action?

A
  • labetolol
  • celiprolol
  • carvedilol
  • nebivolol
  • lower peripheral resistance (*the resistance of the arteries to blood flow. As the arteries constrict, the resistance increases and as they dilate, resistance decreases. Peripheral resistance is determined by three factors: Autonomic activity: sympathetic activity constricts peripheral arteries.)
  • no evidence that these have any important advantages over others
214
Q

Which beta blockers are cardioselective?

A
  • atenolol
  • bisoprolol
  • metoprolol
  • nebivolol
  • acebutolol (to a lesser extent(
  • good for patients with well-controlled asthma/copd where there’s no alternative available
  • good for patients who have suffered heart failure or MI
  • lesser effect om airway resistance
  • less effect on beta-2 receptors
  • preferred in diabetic patients

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