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Year 3 > Block 31 PPT > Flashcards

Block 31 PPT Flashcards

1
Q

Offer antihypertensive drug Tx to people aged 80 and under with stage 1 hypertension who have one or more of the following:

A
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2
Q

Assessment of HTN:

offer

A
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3
Q

Drug classes for HTN

A
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4
Q

Step approach of anti-hypertensives

A
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5
Q

choice of anti-hypertensive

A
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6
Q

ACEI side effects?

A
  • dry cough
  • constipation
  • angiodema - can occur years afterwards
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7
Q

when would ACEi need to be stopped?

A
  • if they’re unwell and they’re not eating or drinking, patient needs to stop ACEi
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8
Q

statins mechanism?

A
  • inhibition of HMG CoA reductase
  • reducing IC cholesterol levels so the liver expresses more LDL receptors and takes up more LDL
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9
Q

what do statins interact with?

A
  • Statins interact with erythromycin and clarithromycin
  • statins and macrolides interact
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10
Q

fibrates interact with?

A
  • interact w statins
  • risk of rhabdomyalysis
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11
Q

how do fibrates work?

A
  • activation of gene transription factors known as PPARs which regulate genes that control lipoprotein metabolism
  • increase lipoprotein lipase activity
  • increases hepatic free fatty acid uptake and increases plasma HDL
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12
Q

side effects of fibrates?

A
  • GI upset
  • rash/ pruitus
  • dizziness and headache
  • myalgia - uncommon
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13
Q

which anticoagulants act on factor Xa?

A
  • heparin
  • fondaparinux
  • apixaban, rivaroxaban
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14
Q

UFH, LMWH and fondaparinux all bind to…

A
  • UFH, LMWH and fondaparinux all bind to antithrombin and accelerate its inhibition of proteases primarly factor Xa
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15
Q

LMWH is a once a day?

A

injection that doesn’t require monitoring

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16
Q

UFH vs LMWH admin?

A
  • IV admin for UFH and subcutaneous for LMWH
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17
Q

LMWH side effects?

A
  • haemorrhage
  • heparin induced thrombocytopenia
  • skin reactions
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18
Q

prescribing

Warfarin?

A
  • vit K antagonist
  • takes 3-4 days to work, u have to give min of 5 days of LMWH first
  • INR has to be above 2 for 48 hrs before the LMWH can be discontinued
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19
Q

warfarin interactions?

A
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20
Q

monitoring w warfarin?

A
  • INR monitoring required
  • usually needs to be between 2-3
  • patients need to carry an alert card and a yellow book
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21
Q

Vit K dependent coagulation factors are?

A

2 (prothrombin), 7, 9, 10

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22
Q

DOACs e.g. dabigatran, apixaban, rivaroxaban?

A
  • -abans inhibits factor 10
  • dabigatran inhibits thrombin directly
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23
Q

reversal of warfarin?

A
  • vitamin K
  • prothrombin complex concentreate
  • (fresh frozen plasma)
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24
Q

dabigatran reversal?

A
  • idarucizumab - mAb fragment
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25
Q

Factor 10 inhibitors reversal?

A
  • andexanet alfa
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26
Q

IHD - amlodepine?

A
  • amlodipine = peripheral vasodilation which reduces afterload. Symptomatic but doesn’t impact long term survival
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27
Q

IHD - beta blocker?

A
  • bisoprolol: reduces work of heart which reduces the angina
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28
Q

NSTEMI Tx - avoid which 2 things?

A
  • avoid morphine due to risk of resp depression
  • avoid O2 unless patient hypoxic due to free radicals and risk of reflex coronary artery constriction
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29
Q

ACS drug therapy?

A
  • aspirin
  • clopidogrel/ ticagrelor
  • fondaparinux or LMWH
  • BB
  • statin
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30
Q

Antiplatelet drugs - COX inhibitors?

A

aspirin

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31
Q

Antiplatelet drugs - phosphodiesterase inhibitors?

A

dipyridamole

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32
Q

antiplatelet drugs - adenosone disphosphate receptor antagonists?

A
  • clopidogrel
  • ticagrelor
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33
Q

antiplatelet drugs - glycoprotein 2b/ 3a receptor antagonist?

A
  • abciximab
  • tirofiban
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34
Q

aspirin - low dose?

A
  • LOW DOSE in heart disease: irreversible inhibition of COX-1
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35
Q

aspirin - high/ intermediate dose?

A
  • high dose/ intermediate dose in pain relief and as an anti-inflammatory inhibits COX-2 as well as COX-1
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36
Q

clopidogrel vs ticagrelor?

A
  • clopidogrel: irreversible PY12 inhibitor
  • ticagrelor: reversible inhibition and more rapid onset of action
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37
Q

dipyridamole mechanism?

A
  • inhibits cellular reuptake of adenosine
  • increased plasma conc of adenosine which inhibits expression of cell surface GPIIb/IIIa receptors
  • inhibits platelet aggregation and causes vasodilation
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38
Q

angina - BBs mechanism?

A
  • slows heart and reduces strength of contractility, reduces cardiac ouput
  • reduces O2 demand and increases diastole time
  • B1 receptors on the heart
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39
Q

what can BBs cause as a side effect?

A
  • can cause AV block as a side effect - AV block is CI
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40
Q

asthma and COPD with beta blockers?

A
  • asthma is CI but COPD is a caution for beta blockers
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41
Q

Whatis made worse by them?

CCB - negative chronotropic effect?

A
  • diltiazem and verapamil
  • non-DPH
  • make HF worse as they reduce the HR
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42
Q

amlodepine?

A
  • DPH CCB
    • DPH cause peripheral arterial dilation and coronary artery dilatation
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43
Q

CCB that reduce cardiac contractility?

A
  • verapamil
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44
Q

nitrates in angina?

A
  • vasodilators causing vascular SM relaxation mimicking the impacts of endogenous NO
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45
Q

What happens if nitrates are used continiously?

A
  • if used continously the effect rapidly diminishes
  • body gets used to having a high NO level
  • asymmetric dosing and nitrate free period to reduce this effect
  • more of an issue with the longer acting nitrates like isosorbine mononitrate or dinitrate
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46
Q

side effects of nitrates?

A
  • headaches - paticularly with the GTN spray
  • syncope - nitrate syncope
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47
Q

which drug when used alongside a nitrate can cause profound hypotension?

A

slidenafil

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48
Q

HF - pulm oedema tx?

A
  • IV furosemide - loop diuretic
  • drops BP
  • In very high doses cause ototoxicity
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49
Q

bolus =

A

drug peaks over short time

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50
Q

bolus-infusion?

A

over e.g. half an hour, less risk of toxicity

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51
Q

infusion =

A

given consistently over a long period e.g. adrenaline in ICU

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52
Q

how does furosemide help in LVF?

A
  • IV furosemide releases vasodilator prostaglandins into the circ which produces venodilation -> helps in LVF
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53
Q

CHF drugs?

A
  • loop diuretics
  • ACEi/ ARBs
  • aldosterone antagonists
  • BBs
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54
Q

drugs used in AF?

A
  • BBs
  • digoxin
  • verapamil
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55
Q

VW classification of drugs?

A
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56
Q

what are the 2 shockable rhythms?

A

VF and pulseless VT

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57
Q

reversible causes of cardiac arrest

A
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58
Q

drugs used in ALS?

A
  • adrenaline
  • amiodarone after 3 shocks to stabilise myocardium
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59
Q

Adenosine?

A
  • adenosine works for SVT
  • especially for AVNRT
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60
Q

what can adenosine cause?

A
  • Adenosine can cause severe bronchospasms - don’t use for asthma
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61
Q

bradycardia Tx?

A
  • atropine
  • or isoprenaline (B1 stimulant drug)
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62
Q

antibiotic stewardship =

A
  • healthcare system wide approach to promotoing and monitoring judicious use of antimicrobials to preserve their future effectiveness
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63
Q

points to remember when using ab in hospital

A
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64
Q

what can cause upper lobe pneumonia?

A

klebsiella and TB

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65
Q

Atypical pneumonia?

A
  • patchy inflammatory changes
  • mycoplasma pneumoniae
  • chlamydophila pneumoniae
  • legionalla pneumophilia
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66
Q

what can be added for atypical pneumonias?

A
  • macrolides like clarithromycin or tetracyclines like doxycycline can be added
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67
Q

what else can cause the clinical picture of atypical pneumonia?

A
  • viral and fungal pathogens can also create the radiological and clinical picture of atypical pneumonia
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68
Q

principles of TB drug therapy?

A
  • intensive phase (2 months) + continuation phase (4 -7 months)
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69
Q

intensive phase of TB treatment?

A
  • isoniazid
  • rifampicin
  • pyrazinamide
  • ethambutol
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70
Q

contination phase of TB treatment?

A
  • isoniazid
  • rifampicin
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71
Q

Pyrazinamide?

A
  • can never be used alone due to risk of resistance
  • crosses BBB and good in TB meningitis
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72
Q

ethambutol side effects - main?

A
  • optic neuritis - produces intial red green colour blindness and then reduced visual acuity - vision needs to be monitored
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73
Q

other ethambutol side effects?

A
  • peripheral neuritits
  • hyperuricaemia, gout
  • nephrotoxicity
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74
Q

pathophys of endocarditis

A
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75
Q

right vs left sided endocarditis?

A
  • right sided: usually IV drug user
  • left side: usually a native or prosthetic heart valve
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76
Q

ab used in endocarditis?

A
  • penicillin G and gentamicin
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77
Q

non-pharmacological Tx of asthma and COPD?

A
  • lifestyle advice
  • weight loss
  • smoking cessation
  • avoiding triggers
  • breathing exercise programs
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78
Q

SABA?

A
  • salbutamol, terbutaline
  • activates B2 receptors which relaxes the SM in the lung, dilating and opening the airways
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79
Q

Side effects of SABA?

A

arryhtmias, headache, palpiptations, fine tremor

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80
Q

ICS?

A
  • beclometasone
  • fluticasone
  • by-passes first pass metabolism
  • potent inhibitors of inflammatory process
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81
Q

Reliever vs preventer therapy in asthma?

A
  • SABA = reliever therapy, only taken to relieve symptoms
  • ICS = preventer, tackles underlying problem
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82
Q

LABAs - formoterol vs salmeterol?

A
  • formoterol: fast onset, but long duration of action
  • salmeterol: delayed onset, long duration of action
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83
Q

never give LABA without ? in asthma

A

ICS - risk of excess cardiovascular events

84
Q

never give ? alone in COPD

85
Q

short acting muscarinic antagonists?

A
  • SAMA: ipatropium binds to muscarnic receptors
86
Q

LAMA?

A
  • tiotropium - long acting anti-muscarinic that is selective for M3
87
Q

MRA are mainly beneficial in?

A

COPD but ipatropium can be added to a B2 agonist in severe asthma exacerbations

88
Q

theophylline?

A
  • inhibits phosphodiesterase and blocks adenosine receptors
  • used for status asthmaticus
89
Q

Monteleukast?

A

leukotriene receptor antagonist

90
Q

steroids?

A
  • oral: prednisolone
  • IV: hydrocortisone
91
Q

oxygen alert card for?

A

hypercapnic respiratory failure

92
Q

COPD pathway

93
Q

HTN flowchart

A
  • offer HTN drug in addition to lifestyle advice to adults of any age with stage 2 hypertension
94
Q

HTN lifestyle interventions?

A
  • encourage exercise and reduction in alcohol intake
  • encourage low dietary sodium intake
  • inform people abt local initiatives e.g. patient organisations that provide support and promote healthy lifestyle change
95
Q

ACEi side effects?

A

dry cough, headaches, dizziness, rash

96
Q

ARBs side effects?

A

dizziness, headaches, cold/ flu like symptoms

97
Q

CCBS side effects?

A

headaches, swollen ankles and constipation. Drinking grapefruit juice can inc risk of side effects

98
Q

diuretics side effects?

A

postural hypotension, increased thirst

99
Q

BBs side effects?

A

cold hands and feet, dizziness and headaches

100
Q

primary prevention =

A
  • Primary prevention refers to the steps taken by an individual to prevent the onset of the disease.
    This is achieved by maintaining a healthy lifestyle choice such as diet and exercise.
101
Q

secondary prevention =

A
  • Secondary prevention focuses on reducing the impact of the disease by early diagnosis prior to any critical and permanent damage.
  • This facilitates avoiding life threatening situations and long term impairments from a disease
102
Q

secondary prevention of CVD involves…

A
  • The secondary prevention of CVD includes diagnosis and prevention.
  • Most critical step of secondary prevention is early diagnosis
  • requires identifying risk factors, criticality of risk factors, and how the variation of these factors relates to CVD.
103
Q

Tx of hypercholesteroleamia/ hypertriglyceridaemia?

A
  • first line: statins
  • if not well controlled with a statin, use ezetimibe
  • fenofibrate can be added to statin therapy if triglycerides remain high even after LDL-choleserol levels have been reduced
104
Q

HTN lifestyle advice?

A
  • dietary advice - reduced saturated fats, intake of sugar and refined sugar
  • physical activity: at least 150 minutes of moderate-intensity aerobic activity per week or 75 mins of vigorous intensity activity
  • weight management
  • alcohol reduction
  • smoking cessation
105
Q

stroke prevention in AF patients?

A
  • Apixaban
  • dabigatran
  • edoxaban
  • ribaroxaban
  • CHADS-VASC score of >2
106
Q

anticoagulation in AF - if DOACs don’t work use?

A
  • if DOACs not tolerated/ suitabled use a vitamin K antagonist
107
Q

rate control in AF?

A
  • beta blocker (not sotalol) or a rate limiting CCB like diltiazem or verapamil
  • digoxin monotherapy if other drugs ruled out due to comorbities/ patient preferences
108
Q

AF - if monotherapy doesn’t control symptoms and if symptoms thought to be due to poor ventricular rate control, consider combination therapy with 2 of;

A
  • beta blocker
  • diltiazem
  • digoxin
109
Q

rhythm control in AF?

A
  • if symptoms continue after HR controlled or if rate control strategy not been successful
  • first line: BB
  • dronedarone as a second line after successful cardioversion
110
Q

and the drug used w

AF - cardioversion?

A
  • electrical cardioversion if AF >48 hrs
  • amiodarone therapy 4 weeks before and up to 12 months after
111
Q

AF - left atrial ablation?

A
  • drug Tx unsuccessful, unsuitable or not tolerated
  • radiofrequency point by point ablation
  • cryoballoon ablation
  • laser balloon ablation
112
Q

which patients need a CHADS-VASC score calculating?

A
  • symptomatic or asymptomatic paroxysmal, persistent or permanent atrial fibrillation
  • atrial flutter
  • a continuing risk of arrhythmia recurrence after cardioversion back to sinus rhythm or catheter ablation
113
Q

anticoagulation is initiated in patients with a CHADS-VASC score of?

A
  • all patients >2
  • men with a score of 1
114
Q

DVT - anticoagulation?

A
  • apixaban or rivaroxaban
  • LMWH followed by at least five days dabigatran or edoxaban
  • or LMWH with Vit K antagonist
  • for a minimum period of 3 months
115
Q

identify patients who should be considered for prophylaxis of deepvein thrombosis

116
Q

factors temporarily increasing risk of DVT

117
Q

prevention of DVTs?

A
  • Graduated compression stockings
  • DOACs
118
Q

PE management - before confirmation?

119
Q

PE management?

A
  • Fondaparinux.
  • Low molecular weight heparin (LMWH).
  • LMWH followed by an oral anticoagulant (dabigatran oredoxaban).
  • Oral anticoagulant treatment (warfarin, apixaban, or rivaroxaban).
  • Unfractionated heparin.
120
Q

mechanical interventions of PE?

A
  • IVC filters - these are designed to trap fragmented thromboemboli from the deep leg veins en route to the pulmonary circulation (whilst preserving blood flow in the IVC filter)
  • thrombolysis
121
Q

Warfarin reversal?

A

Vitamin K1(phytomenadione)

122
Q

apixaban reversal?

A

Andexanet alfa reverses bleeding in those treated with apixaban or rivaroxaban (direct factor 10 inhibitor)

123
Q

dabigatran reversal?

A

Idarucizumab reverses bleeding caused by dabigatran

124
Q

heparin reversal?

A
  • protamine sulfate is a specific antidote (but only partially reverses the effects of low molecular weight heparins).
125
Q

ALI initial management?

A
  • analgesia and heparin
126
Q

ALI - endovascular interventions?

A
  • Percutaneous catheter-directed thrombolytic therapy.
  • Percutaneous mechanical thrombus extraction.
127
Q

ALI - surgical interventions?

A
  • Surgical thromboembolectomy.
  • Endarterectomy.
  • Bypass surgery.
  • Amputation if the limb is unsalvageable.
128
Q

chronic limb ischemia management?

A
  • Urgent referral to vascular MDT
  • pain management: paracetamol and opioids
  • refer to pain management service if pain isn’t managed well or persists after revascularisation or amputation
129
Q

CLI - advice on?

A
  • foot care - for example daily foot inspection,keeping ischaemic feet clean to avoid infection, being careful to avoid injury when cutting the toenails, avoiding walking barefoot, and wearing well-fitting shoes.
130
Q

conservative management of CLI?

A
  • secondary prevention to improve long term outcomes
  • addressing modifiable RFs - smoking cessation
  • supervised exercise program - Excercise typically involves walking until the onset of symptoms, and where possible until the maximal pain is reached.
131
Q

which therapies should be offered to CLI patients?

A
  • Lipid therapy: statins should typically be offered to patients with peripheral vascular disease.
  • Anti-platelet therapy: all patients with peripheral arterial disease should be offered Aspirin or Clopidogrel as secondary prevention.
132
Q

Naftidrofuryl oxalate?

A

this is a peripheral vasodilator that may be considered in patients with CLI in whom conservative measures have failed and decline surgical options.

133
Q

Revascularisation in CLI?

A
  • angioplasty +/- stent
  • remote endarterctomy
134
Q

Surgical management of CLI?

A
  • bypass - vessel used to bypass diseased segment of artery
135
Q

When should oxygen be given?

A

<94% O2 sats

136
Q

oxygen delivery in a patient w COPD?

A
  • Use a 24% Venturi mask at 2-3 L/min (or a 28% Venturi mask at 4 L/min, or nasal cannulae at 1-2 L/min if a 24% mask is not available) for people with suspected chronic obstructive pulmonary disease (COPD),morbid obesity, a chest wall deformity, or a neuromuscular disorder
  • if sats remain <88% afteruse of a 28% venturi mask, change to either a nasal cannulae at 2-6 L/min or a simple face mask at 5 L/min
137
Q

Oxygen delivery in hypoxaemic patients?

A
  • use a nasal cannulae at 2-6 L/min, or a simple face mask at 5-10 L/min.
138
Q

acute asthma exacerbation management?

A
  • oxygen
  • SABA: nebulized salbutamol for life-threatening/ severe asthma or ipatropium bromide with poor initial response
  • oral predinosolone or IV hydrocortisone
139
Q

moderate severity asthma exacerbation management?

A

pressurized metered-dose inhaler with a large volume spacer

140
Q

stepwise management of asthma?

A
  • ICS: Fluticasone and Beclomethasone.
  • LABA: salmeterol
  • LTRA: monteleukast
141
Q

Four

COPD exacerbations?

A
  • Increase SABA use - nebuliser - salbutamol or ipatropium
  • oral corticosteroids - prednisolone
  • antibiotics - amoxicillin, doxycycline, or clarithomycin
  • oxygen
142
Q

NIV may be needed in a COPD exacerbaton if?

A

high levels of oxygen needed but there’s a risk of T2RF

143
Q

chronic COPD management?

A
  • 1) SABA or SAMA for use on PRN basis
  • 2) LABA plus LAMA or LABA plus ICS if features of steroid responsiveness/ asthmatic features
  • 3) triple therapy: LABA + LAMA + ICS
144
Q

oral therapies in COPD?

A
  • corticosteroids - especially in acute exacerbations
  • theophylline
  • mucolytics e.g. carbocysteine
  • ab - in exacerbations - or prophylactically (azithromycin)
145
Q

non-pharm management of COPD?

A
  • healthy diet and physical activity
  • smoking cessation
  • pulmonary rehabilitation
  • pneumococcal and influenza vaccinations
146
Q

First lines for stable angina?

A
  • first line: BB or a CCB
  • If the person cannot tolerate the beta-blocker or calcium-channel blocker, consider switching
147
Q

stable angina - if BB and CCB are CI/ not toleraed consider:

A
  • A long-actingnitrate(such as isosorbide mononitrate).
  • Nicorandil.
  • Ivabradine.
  • Ranolazine.
148
Q

symptomatic relief of angina?

A
  • sublinguial GTN for reliief of pain
149
Q

anginal chest pain - advise the patient to?

A
  • Stop what they are doing and rest.
  • Use their glyceryl trinitrate spray or tablets
  • Take a second dose after 5minutes if the pain has not eased.
  • Call 999 for an ambulance if the pain has not eased 5minutes after the second dose, or earlier if the pain is intensifying or the person is unwell.
150
Q

secondary prevention for angina?

A
  • antiplatelet treatment - aspirin
  • clopidogrel should be continued if the person is alr on it for stroke or PAD
  • ACEi for ppl w stable angina and diabetes
  • statin
  • antihypertensive treatment
151
Q

initial management of ACS?

A
  • GTN
  • IV morphine - paticularly if acute MI suspected
  • loading dose of aspirin
  • oxygen shouldn’t routinely be given
  • monitoring for hyperglycaemia - insulin should be given
152
Q

STEMI - intervention?

A
  • coronary reperfusion therapy - either primary PCI or fibrinolysis ASAP
  • Primary PCI (if within 12 hours of symptom onset and within 120 minutes of the time when fibrinolysis could have been given) is the preferred strategy for most patients.
153
Q

drug therapy in STEMI?

A
  • aspirin + second antiplatelet: prasugrel,ticagrelor, orclopidogrel
  • Aspirinalone may be appropriate for some patients with a high bleeding risk not undergoing a PCI.
154
Q

unstable angina and NSTEMI tX?

A
  • ASPIRIN plus prasugrel, ticagrelor or clopidogrel
  • antithrombin therapy with fondaparinux sodium should also be offered
155
Q

UA/ NSTEMI with renal impairment offer?

156
Q

Following ACS patients should be offered?

A
  • following ACS, should be offered cardiac rehabilitation programme - including advice for lifestyle changes, stress management and health education.
157
Q

drugs offered after an ACS?

A

-ACEi
- BB
- dual antiplatelet therapy
- statin

158
Q

acute HF management?

A
  • IV diuretic therapy
  • If a person has cardiogenic pulmonary oedema with severe dyspnoea and acidaemia consider starting non‑invasive ventilation without delay
159
Q

Chronic HF - patients should be told to ? everyday

A
  • weighing themselves at a set time of day and to report any weight gain of more than 1.5–2.0kg in 2 days
160
Q

which drugs should be avoided in ppts w reduced ejection fraction HF?

A
  • Rate-limiting calcium-channel blockers (verapamil anddiltiazem)
  • short-acting dihydropyridines e.g.nifedipine, ornicardipine
  • reduce cardiac contractility
161
Q

which calcium channel blocker can be used in those with HF and angina?

A

amlodepine

162
Q

CHF w reduced ejection fraction Tx?

A

1) ACE and BB such as (bisoprolol, carvediolol or nebivolol
2) ARB instead of ACEI
3) MRA

163
Q

ARBs used in HF?

A
  • Candesartan
  • losartan
  • valsartan
164
Q

HF - MRAs such as

A

spironolactone or eplerenone should be added

165
Q

which drugs can be used if the HF persists despite the BB, ACEi/ ARB and MRA?

A
  • For patients in sinus rhythm,digoxinis recommended as add-on therapy in worsening or severe heart failure despite optimal treatment
  • Ivavradine, SGLT-2 inhibitors like dapagflozin, hydralazine and nitrate if symptoms persist
166
Q

All people w CHF need monitoring:

A
  • clinical assessment of functional capacity, fluid status, cardiac rhythm (minimum of examining the pulse), cognitive status and nutritional status
  • a review of medication, including need for changes and possible side effects
  • an assessment of renal function.
  • at least 6-monthly for people with stable heart failure
167
Q

atrial flutter - ventricular rate control?

A
  • BB, diltiazem, verpamil
  • digoxin can be added if rate not well controlled, paticularly useful in HF
168
Q

other methods of rate control in flutter?

A
  • electric cardioversion by cardiac pacing or direct current), pharmacological cardioversion, or catheter ablation.
169
Q

supraventicular tachycardias?

A
  • Adenosineis usually the treatment of choice for terminating paroxysmal supraventricular tachycardia
  • verapamil (INTERACTS with BB) can be used if this doesn’t work
170
Q

other options in SVT?

A
  • IV Amiodarone hydrocholride
  • flecainide acetete or a BB like esmolol hydrochloride)
171
Q

unsustained VT Tx?

A
  • ppts with unstable unsustained VT should receive direct current cardioversion to restore sinus rhythm
  • if it fails, IV amiodarnone
172
Q

sustained VT who are haemodynamically stable:

A
  • IV amiodarone preferred
  • flecainide, propafenone, lidocaine
  • non sustained VT can be treated with a BB
173
Q

Torsades de pointes?

A
  • polymorphic VT
  • (usually drug-induced, but other factors including hypokalaemia, severe bradycardia, and genetic predisposition are also implicated)
174
Q

Torsades Tx?

A
  • iV infusion of magnesium sulfate
  • beta-blocker (but notsotalol hydrochloride) and atrial (or ventricular) pacing can be considered
175
Q

bradycardia Tx?

A
  • atropine
  • adrenaline
176
Q

pharmacological management of AV block?

A
  • atropine: antimuscarinic: blocks action of the vagus nerve at the SAN/ AVN increasing SAN activity and conduction through AVN
  • isoprenaline (non-selective BA)
177
Q

when is pacing needed for AV block?

A
  • acute bradyarrhythmia
  • following MI
  • long term option in patients w bradyarrythmias
178
Q

ALS pathway for VT/ VF?

A
  • Defibrillation
  • CPR with 30:2 ratio of compressions to rescue breaths
  • continue CPR for 2 minutes and then check to see of VT/ VF persists
  • CPR for 2 minutes then check
  • resume CPR then give adrenaline and amiodraone IV
179
Q

ALS pathway - if VT/ VF persists then give?

A
  • Give further adrenaline 1 mg IV after alternate shocks(approximately every 3–5minutes).
  • Give amiodarone after 5 defibrillations, lidocaine can be used instead
180
Q

ALS pathway for non-shockable dysrhythmias (asystole, PEA)?

A
  • CPR - with a 30:2 ratio of compressions to rescue breathsfor people with pulseless electrical activity (PEA) orasystole.
  • Give adrenaline1mg intravenously (IV) as soon as venous access is achieved.
  • continue CPR until airways secured
  • once the airway is secured, ventilate the lungs at a rate of about 10breaths per minute and continue chest compressions without pausing during ventilation.
181
Q

ALS - non shockable: recheck after 2 minutes then?

A
  • continue CPR if no pulse/ signs of life
  • give adrenaline after every alternate sequence of CPR/rhythm check (approximately every 3–5 minutes).
182
Q

CAP - low severity?

A
  • CURB-65 score 0
  • amoxicillin
  • alternatives: doxycycline or clarithrymoycin if atypical pathogens suspected or amoxicillin unsuitable
183
Q

moderate severity CAP?

A
  • Score of 1 or 2
  • amoxicillin and (if atypical pathogens suspected) clarithromycin/ erythryomycin
  • alternatively doxycyline or clarithromycin
184
Q

High severity CAP?

A
  • 3-5
  • co-amoxiclav plus clarithromycin
185
Q

Atypical CAP pathogens?

A
  • The addition of a macrolide to amoxicillin if an atypical pathogen is suspected gives a broaderspectrum of activitywith which to target atypical pathogen
  • doxycycline and clarithromycin have good activity aginst strep pneumoniae and atypical infections
186
Q

HAP - first choice ab if non-severe symptoms?

A

co-amoxiclav

187
Q

HAP - Alternative oral antibiotics if non‑severe symptoms or signs, and not at higher risk of resistance, for penicillin allergy or if co‑amoxiclav unsuitable:

A
  • doxycycline
  • cefalexin
  • co-trimoxazole
  • levofloxacin
188
Q

HAP - First-choice intravenous antibiotics if severe symptoms or signs (for example, symptoms or signs of sepsis) or at higher risk of resistance:

A
  • Piperacillin with tazobactam
  • Ceftazidime
  • Ceftriaxone
  • Cefuroxime
  • Levofloxacin
  • Meropenem
189
Q

HAP - Antibiotics to be added if suspected or confirmed meticillin-resistantStaphylococcus aureusinfection(dual therapy with a first-choice intravenous antibiotic)

A
  • Vancomycin
  • Teicoplanin
  • Linezolid
190
Q

latent TB Tx?

A
  • 6 months of isoniazid with pyridoxine (6H)or
  • 3 months of isoniazid (with pyridoxine)and rifampicin(3HR)
191
Q

active TB w/o CNS involvement?

A
  • isoniazid (with pyridoxine), rifampicin, pyrazinamide and ethambutol for 2 months
  • followed by rifampicin and isoniazid for 4 months.
192
Q

TB w CNS involvement?

A
  • RIPE plus pyroxidine for first 2 months
  • then stop pyrazinamide and ethambutol for the last 8 months
  • Patients with CNS involvement are offered dexamethasone or prednisolone at the start of treatment which is then weaned over 4-8 weeks
193
Q

MSSA bacterial endocarditis Tx?

A

flucloxacillin

194
Q

MRSA or penicillin allergy bac endo?

A

vancomycin

195
Q

prosthetic valve bacterial endocardiits?

A

in the presence of a prosthetic valve, rifampicin and gentamicin should be added to both regimens and the duration should be ≥6 weeks

196
Q

streptococcal endocarditis Tx?

A
  • Standard four-week regimen: penicillin G, OR amoxicillin, OR ceftriaxone
197
Q

penicillin allergic strep endo?

A

vancomycin for four weeks

198
Q

Native valve endocarditis or late prothetic valve endocarditis:

A

Ampicillin, flucloxacillin and gentamicin, OR vancomycin and gentamicin.

199
Q

Early prosthetic valve endocarditis:

A

vancomycin, gentamicin and rifampicin.

200
Q

Rational prescribing - aims to (4)

A
  • maximise clinical effectiveness
  • minimise harms
  • avoid wasting scarce healthcare resources
  • respect patient choice.
201
Q

what is rational prescribing?

A
  • Rational use of medicines requires that “patients receive medications appropriate to their clinical needs, in doses that meet their own individual requirements, for an adequate period of time, and at the lowest cost to them and their community.
202
Q

WHO interventions to promote rational use?

A
  • use of clinical guidelines
  • Continuing in-service medical education as a licensure requirement
  • Public education about medicines
  • Use of appropriate and enforced regulation
  • Establishment of a multidisciplinary national body to coordinate policies on medicine use
203
Q

concept of antibiotic resistance?

A
  • if ab are not used in the correct dose or are overused, will cause antibiotic resistance
  • bacteria that survive an treatment will survive and be able to multiply and pass on characteristics to the next generation
  • leading to an increasing number of antibiotic resistant strains of bacteria
  • Consequences are more severe disease, frequent recurrence, long recovery time, high treatment methods and costs.
204
Q

reducing risk of antibiotic resistance?

A
  • only using antibiotics for bacterial diseases
  • finishing the course of antibiotics
  • selecting the correct ab and dosage

Year 3 (45 decks)

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