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Year 3 > Block 31 Week 4 > Flashcards

Block 31 Week 4 Flashcards

1
Q

which ab can cause QT interval prolongation?

A

macrolides

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1
Q

what is the normal QT interval?

A
  • QT interval needs to be less than half of the R-R interval (less than 500ms)
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2
Q

causes of sinus bradycardia?

A
  • acute MI/ ischemia
  • beta blockers, CCB, digoxin, anticholinergics
  • hypothyroidism
  • hyperkalemia
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3
Q

what could bradycardia suggest?

A
  • RCA supplies SAN so bradycardia could suggest inferior ischemia
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4
Q

Tx for bradycardia?

A
  • atropine
  • noradrenaline
  • isoprenaline
  • dopamine
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5
Q

drug for BB overdose?

A

glucagon

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6
Q

if these drugs don’t work for bradycardia then?

A

pacemaker

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7
Q

positive aVR and broad QRS complexes = Treat as

A

VT unless proven otherwise

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8
Q

Tx of VT?

A
  • amiodarone
  • ICDs
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9
Q

why does aVR become positive in VT?

A
  • current firing around the area of fibrosis in the infract in the ventricle
  • aVR becomes positive
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10
Q

which ab to avoid in a LRTI when the patient is on warfarin?

A

macrolides

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11
Q

infectious HD?

A
  • endocarditis
  • myocarditis
  • pericarditis
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12
Q

New murmur and fever think?

A

endocardititis

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13
Q

RF for endocarditis?

A
  • prosthetic valve
  • elderly patient w degenerated valves
  • IV drug users - tricuspid valve
  • catheters, pacemaker electrodes
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14
Q

Relapse vs reinfection - endocarditis?

A
  • relapse - repeat within 6 months and proven identical pathogen
  • reinfection - new MO or same species but > 6 months
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15
Q

CP of endocarditis?

A
  • fever & systemic disease signs like weight loss
  • murmur
  • septic embolization - brain, kidneys, spleen
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16
Q

most common causes of endo?

A
  • streptoccoi, staphy, enterococci most common causes
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17
Q

less common causes of endocarditis?

A
  • less commonly HACEK
  • haemophilus
  • actinobacillus
  • cardiobacterium
  • eikenella
  • kingella
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18
Q

think ? in resistant cases of endocarditis?

A
  • fungi - candida, aspergillus
  • think fungi in resistant endocarditis
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19
Q

echo (transoesophageal) for endo?

A
  • vegetations/ abscess/ new prosthetic valve dehiscence = specific
  • new regurgitation/ obstruction = not specific
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20
Q

clinical signs of endocarditis?

A
  • splinter haemorrhage
  • roth’s spot on the retina
  • osler’s node
  • janeway lesions
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21
Q

Tx of endo?

A
  • amoxicillin
  • gentamicin
  • MRSA: vancomycin
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22
Q

which type of lung cancer tends to cavitate in the middle?

A

SCC

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23
Q

5 yr survival of lung cancer?

A

less than 20%

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24
Q

SCLC is almost always associated w?

A

active smoking

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25
Q

SCC is strongly assoc w

A

smoking

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26
Q

law on radiation exposure?

A

IRMER

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27
Q

Which type of cancer needs referral to coroner?

A
  • Mesothelioma = prescribed disease, needs referral to coroner
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28
Q

SVCO leads to

A

a swollen face

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29
Q

What else can be seen w lung cancer?

A
  • hoarse voice
  • bovine cough
  • can get seizures when lung cancer metastasised
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30
Q

NSCLC has ? on biopsy

A

genetic tests done

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31
Q

Radical vs stereotactic radiotherapy?

A
  • radical radiotherapy isn’t aimed specifically like palliative radiotherapy is so you run the risk of losing healthy lung
  • stereotactic radiotherapy is aimed and has less risk of damaging the rest of the lung e.g. in COPD
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32
Q

ALK mutation?

A

tend to occur in younger non-smoker women

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33
Q

obstructive vs restrictive pattern of airflow obstruction?

A
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34
Q

narrowing of large airways vs small airways?

A
  • narrowing of large airways causes early symptoms
  • major damage can occur to small airways without producing symptoms
  • resistance inversely proportional to radius
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35
Q

obstructive airway diseases?

A
  • asthma
  • COPD
  • bronchiectasis
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36
Q

asthma?

A
  • variable expiratory airflow limitation
  • defined by the history of respiratory symptoms such as wheeze, shortness of breath, chest tightness and cough that vary over time and in intensity,
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37
Q

acute airway changes in asthma?

A
  • SM contraction
  • mucus hypersecretion
  • plasma leakage
  • oedema
  • sensory nerve activation
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38
Q

chronic changes in asthma

A
  • subepithelial fibrosis
  • smooth muscle hypertrophy
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39
Q

asthma diagnosis steps?

A
  • PEFR
  • testing for variability
  • testing for oesinophilic inflammation
  • all patients should have spirometry with a bronchodilator reversibility (BDR) test
  • all patients should have a FeNO test
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40
Q

asthma diagnosis pathway

A
  • spirometry and bronchodilator reversibility
  • FeNO
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41
Q

A - testing for variability methods?

A
  • reversibility
  • PEF charting
  • challenge tests
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42
Q

methods of testing for oesinophilic inflammation?

A
  • FeNO
  • blood eosinophils
  • skin prick test, Ig-E
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43
Q

steps of brochodilator reversibility testing?

A
  • 1) Prebronchodilator Spirometry
  • If possible, withhold usual inhaled therapy before test (SABA ≥ 4 hours, LABA ≥ 15 hours)
  • 2) Administer short acting beta-2 agonist (400 micrograms salbutamol)
  • 3) Post-bronchodilator Spirometry
  • Perform 15 minutes after salbutamol inhalation
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44
Q

positive bronchodilator test?

A

Test considered positive if:
* FEV-1 increases by 200mls and 12%
* Greater confidence of a positive test if FEV increases by 400mls and 15%

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45
Q

Asthma - peak flow monitoring?

A
  • twice daily for 2 to 4 weeks
  • Calculating variability:
  • ([Days highest – Days lowest] / mean of days highest and lowest PEFR), averaged over 1 week.
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46
Q

peak flow variability that is considered significant?

A
  • > 10% (GINA) to 20% (NICE) variability considered significant
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47
Q

bronchial challenge testing options?

A
  • hyperpnoea, mannitol, saline
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48
Q

mannitol challenge testing?

A
  • highly spec for bronchial hyperresponsiveness consistent w asthma
  • acts on inflammatory cells to trigger release of mediators like PGD, LTE4, histamine that cause bronchoconstriction in those w hyperactivity
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49
Q

FeNO levels supporting an asthma diagnosis?

A
  • NICE say FeNO >40ppb supportive of an asthma diagnosis
  • Elevated FeNO predicts response to inhaled corticosteroids in asthma
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50
Q

peripheral blood oesinophilia?

A
  • more useful in COPD to predict response to inhaled corticosteroids than asthma
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51
Q

sputum eosinophilia?

A
  • gold standard
  • limited to academic centers
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52
Q

evidence of atopy in asthma?

A
  • Blood tests - total IgE and specific IgE to aeroallergens (RAST)
  • Skin prick testing
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53
Q

allergic/ atopic asthma?

A
  • Often childhood onset and may be associated with other atopic disease
  • Associated with eosinophilic airway inflammation.
  • Identifiable triggers (clinically and objectively)
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54
Q

asthma with persistent airflow limitation?

A
  • Some asthma patients develop airflow obstruction that is fixed or incompletely
    reverses with treatment.
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55
Q

asthma and obesity?

A
  • Prominent respiratory symptoms
  • Little evidence of eosinophilic inflammation
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56
Q

COPD?

A
  • persistent resp symptoms and airflow limitation due to airway and/or alveolar abn usually caused by sig exposure to noxious particles or gases
  • The most common respiratory symptoms include breathlessness, cough and/or sputum production.
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57
Q

RF for COPD?

A
  • smoking
  • genetic factors
  • abn lung development
  • accelerated lung aging
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58
Q

Causes of COPD?

A
  • Tobacco
  • Recreational drug use
  • E-cigarettes
  • Passive smoking
  • Chronic asthma
  • Biofuels
  • Occupation
  • Familial
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59
Q

emphysema on a CT

A

looks like holes

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60
Q

pathology of chronic bronchitis?

A
  • Mucus gland hypertrophy
  • Smooth muscle hypertrophy
  • Goblet cell hyperplasia
  • Inflammatory cell infiltrate
  • Excess mucus
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61
Q

emphysema =

A
  • Abnormal enlargement of airspace distal to the terminal bronchiole accompanied by destruction of their walls and without obvious fibrosis
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62
Q

why does emphysema cause airflow obstruction?

A
  • Alveolar pressure reflects sum of pleural pressure + elastic recoil
  • Combination of reduced radial traction and reduced intraluminal pressure leads to airway narrowing/collapse
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63
Q

COPD and cycle of inactivity

A
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64
Q

asthma vs COPD age of onset?

A
  • asthma usually childhood but can be any age, COPD usually >40yrs
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65
Q

asthma vs COPD symptoms?

A
  • asthma: symptoms vary over time, often triggers
  • COPD: chronic and continous symptoms with good and bad days
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66
Q

Asthma vs COPD - bronchodilator response?

A
  • asthma: Variable airflow limitation. Bronchodilator reversibility
  • COPD: Post bronchodilator FEV1/FVC <0.7
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67
Q

A vs COPD - history?

A
  • asthma: Often have personal or family history of asthma
  • COPD: Relevant exposure (cigarette smoke)
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68
Q

A vs C - reversible?

A
  • asthma: reversible and can resolve
  • COPD: progressive
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69
Q

Asthma vs COPD X ray changes?

A
  • asthma: X ray usually normal
  • COPD:Hyperinflation and other chronic changes
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70
Q

asthma vs COPD type of inflammation?

A
  • asthma: inflammation is usually eosinophilic
  • COPD: typically neutrophilic
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71
Q

Asthma and COPD overlap syndrome?

A
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72
Q

why airflow obstruction causes hypoxia?

A
  • Ventilation / perfusion mismatch. Many alveoli will be poorly ventilated because of bronchial narrowing
  • Emphysema also reduces the surface area of the gas exchanging part of the lung impairing diffusion of gasses.
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73
Q

consequences of pulm hypertension - cor pulmonale?

A
  • Right sided heart failure as a result of chronic lung disease.
  • Right heart failure leads to raised venous pressure and oedema
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74
Q

bronchiectasis can be divided into?

A
  • CF
  • non-CF
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75
Q

what is bronchiectasis?

A
  • Abnormal dilatation of the airways
  • Chronic purulent sputum production
  • Recurrent infection
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76
Q

causes of bronchiectasis

A
  • Many causes – most commonly idiopathic
  • Cystic fibrosis is the most common fata genetic disease
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77
Q

how is the diagnosis of bronchiectasis confirmed?

A
  • Diagnosis of bronchiectasis is confirmed using high resolution CT (HRCT)
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78
Q

airflow obstruction in bronchiectasis?

A
  • Paradox of airway narrowing in a disease defined by dilatation of one or more bronchi
  • Secretions and fibrosis affecting predominantly small airways causes airflow obstruction
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79
Q

Asthma vs COPD spirometry results?

A
  • Reversibility can be established using before and after measurements after an inhaled beta-agonist( after 30 minutes) or taking oral prednisolone (after 2 weeks).
  • A positive response is increase in FEV1by 15% and >200ml = ASTHMA, less than this is COPD
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80
Q

COPD FEV1/ FVC ratio?

A

has to be less than 70%

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81
Q

COPD grading?

A
  • FEV1 - 60-80% predicted:mild
  • FEV1 - 40-60% predicted:moderate
  • FEV1 -<40% predicted :severe
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82
Q

regular cough and sputum in a smoker usually indicates?

A

chronic hypersecretory bronchitis

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83
Q

features of COPD?

A
  • Dyspnoea varying from mild (exertional) to severe at rest
  • Cough and sputum if CHB
  • Recurrent exacerbations
  • Respiratory failure if severe
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84
Q

Chronic features of COPD?

A
  • Respiratory failure if severe
  • Odema, secondary polycythaemia - as a result of chronic hypoxia
  • Pulmonary hypertension (and cor pulmonale)
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85
Q

other features of COPD?

A
  • weight loss
  • depression and social isolation
  • premature retirement
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86
Q

Smoking cessation?

A
  • only intervention that can halt decline in FEV1
  • nicotine replacement therapy, bupropion and vareninicline can be used in a smoking cessation package
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87
Q

inhaled bronchodilators in COPD?

A
  • Usually combine inhaled beta-agonist (sabutamol) and anticholinergic agent (ipatropum and tiotropium)
  • often in a nebuliser
  • Large measurable response usually suggests an asthmatic component.
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88
Q

Steroids in COPD?

A
  • useful if reversibility testing suggests asthmatic component to airflow obstruction
  • short course of oral steroids can also be used in exacerbations
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89
Q

Carbocysteine in COPD?

A

mucolytic, reduce cough and sputum production

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90
Q

pulm rehab for COPD?

A
  • Pulmonary rehabilitation is the most effective treatment for reducing dyspnoea and disability
  • It is best delivered as a multidisciplinary and exercise based programme (combined with emotional and nutritional support)
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91
Q

recognition of COPD exacerbations?

A
  • Increased dyspnoea,sputum volume or purulence
  • More wheezy
  • Peripheral odema
  • Fever or symptoms of upper respiratory tract infection
  • Confusion or drowsiness (implies respiratory failure)
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92
Q

Causes of Copd exacerbations?

A
  • infections
  • other - reflux
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93
Q

Tx of COPD exacerbations?

A
  • ab to cover H influenza/ S pneumoniae/M catarrhalis
  • increase bronchodilator dose (nebulized) if worsening airflow obstruction
  • steroids
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94
Q

when is admission for COPD required?

A
  • Admission required if severely breathless, suspicion of respiratory failure,need to exclude other conditions,social factors
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95
Q

type 1 resp failure?

A

hypoxia (under 8kPa) and normal to low CO2

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96
Q

type 2 resp failure?

A

hypoxia and hypercapnia - CO2 over 6kPa

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97
Q

which type of resp failure are ppl usually in during exacerbations?

A
  • most people have type 1 failure during exacerbations and then when stable and then type 2 in exacerbations and then permanently
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98
Q

mechanisms of hypoxia - low inspired oxygen

A

e.g. altitude

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99
Q

mechanisms of hypoxia - hypoventilation?

A

opiate overdose

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100
Q

mechanisms of hypoxia - diffusion defect?

A

lung fibrosis (alveoli abn, initially hypoxic only on exercise but as it progresses gas exchange becomes worse causing severe hypoxia which needs a lot of oxygen to correct)

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101
Q

mechanisms of hypoxia - V/Q mismatch?

A

COPD or asthma

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102
Q

mechanisms of hypoxia - right to left shunt?

A
  • pulmonary AVM: deox blood enters the LA bypassing alveoli so it doesn’t get oxygenated, blood leaving via arteries is still deoxygenated
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103
Q

Mechanisms of hypercapnia?

A
  • Same as those that lower paO2 apart from altitude
  • The CO2 dissociation curve is steeper and more linear than for oxygen so carbon dioxide elimination is more ventilation dependent
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104
Q

how can oxygen worsen hypoxia in COPD?

A
  • In acute exacerbations of COPD uncontrolled oxygen can worsen hypercapnoea by reducing hypoxic drive,causing a degree of hypoventilation and worsening V/Q mismatch by reversing hypoxic vasoconstriction in poorly perfused lung units
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105
Q

management of resp failure - oxygen?

A
  • pulse oximetry and blood gas
  • Controlled oxygen –aim for paO2>6.5-8kPa
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106
Q

management of resp failre - pharm?

A
  • Improve ventilation with high dose combination bronchodilators (salbutamol + ipatropium) and mobilising secretions(physiotherapy)
107
Q

resp failure - ventilation

A
  • consider non-invasive positive pressure ventilation or intubation with mechanical ventilation in ICU (level 3 care) if the patient doesn’t improve and has T2F with acidosis
108
Q

symptoms of resp failure?

A
  • confusion,
  • agitation,
  • headache,
  • drowsy,
  • coma.
109
Q

signs of resp failure?

A
  • cyanosis
  • bounding pulse - high volume radial pulse very suggestive of CO2 retention
  • flapping tremor.
110
Q

O2 therapy for COPD?

A
  • acute for Tx of exacerbations
  • short burst to relieve dyspnoea
  • ppts can have portable cylinders to relieve breathlessness e.g. to improve exercise tolerance
111
Q

LTOT for COPD?

A
  • LTOT is the only treatment shown to prolong survival in COPD patients with chronic respiratory failure.
  • Patients should use oxygen for >15 hrs/day and oxygen is provided from a concentrator.
112
Q

What is type 1 resp failure?

A
  • Type 1 respiratory failureinvolveshypoxaemia(PaO2<8 kPa / 60mmHg) withnormocapnia(PaCO2<6.0 kPa / 45mmHg)
113
Q

what is type 2 resp failure?

A
  • Type 2 respiratory failureinvolveshypoxaemia(PaO2<8 kPa / 60mmHg) withhypercapnia(PaCO2>6.0 kPa / 45mmHg)
114
Q

why does type 1 resp failure occur?

A
  • usually occurs due to V/Q mismatch - volume of air flowing in and out of the lungs isn’t matched w flow of blood to lung tissue
  • as a result of the mismatch, PaO2 falls and PaCO2 rises
  • The rise in PaCO2rapidly triggers an increase in a patient’s overall alveolar ventilation, whichcorrects the PaCO2but not the PaO2
115
Q

examples of type 1 resp failure?

A
  • Reduced ventilation and normal perfusion (e.g. pneumonia, pulmonary oedema, bronchoconstriction)
  • reduced perfusion and normal ventilation e.g. PE
116
Q

type 2 resp failure is caused by?

A
  • It occurs as a result ofalveolar hypoventilation, which prevents patients from being able to adequatelyoxygenateandeliminate CO2from their blood.
  • This leads toPaO2falling(due to lack of oxygenation) andPaCO2rising(due to lack of ventilation and elimination of CO2).
117
Q

why can hypoventilation occur?

A
  • Increased resistance as a result of airway obstruction (e.g.COPD)
  • Reduced compliance of the lung tissue/chest wall (e.g. pneumonia, rib fractures,obesity)
  • Reduced strength of the respiratory muscles (e.g. Guillain-Barré, motor neurone disease)
  • Reduced respiratory drive (e.g.opioidsand other sedatives)
118
Q

normal PaO2 on high glow oxygen

A

this is abnormal as you would expect the patient to have a PaO2well above the normal range with this level of oxygen therapy.

119
Q

A ‘very low’ PaO2in a patient who looks completely well, is not short of breath and has normal O2saturations:

A

this is likely a venous sample.

120
Q

PaO2 on room air in a healthy ppt?

A
  • PaO2 should be >10kPa when oxygenating on room air in a healthy patient
121
Q

PaO2 of a patient on oxygen therapy should be?

A

approximately10kPa less thanthe% inspired concentration FiO2

122
Q

nasal cannulae?

A
  • nasopharynx used as a resevoir for oxygen
  • oxygen flow rate of 2-6 L/min
123
Q

simple face masks?

A
  • O2 flow rate of 5-10L/min
  • These masks should not be used with flow rates less than 5L/min - risk of CO2 retention due to rebreathing
124
Q

non rebreather masks?

A
  • Reservoir masks deliver oxygen at concentrations between 60% and 90% when used at a flow rate of 10–15 l/min.
  • The concentration is not accurate and will depend on the flow of oxygen as well as the patient’s breathing pattern.
125
Q

when should NBM be used?

A

most suitable for trauma and emergency use where carbon dioxide retention is unlikely.

126
Q

NRB - flow rate of under ? leads to risk of CO2 retention due to rebreathing?

A

12L/min

127
Q

fixed performance devices?

A

venturi mask

128
Q

Venturi mask?

A
  • gives accurate conc of oxygen to the patient
  • They are suitable for all patients needing a known concentration of oxygen,
129
Q

COPD venturi mask?

A
  • 24% and 28% Venturi masks are particularly suited to those at risk of carbon dioxide retention (e.g. patients with chronic obstructive pulmonary disease)
130
Q

venturi mask valve colours?

A
  • blue delivers the least Oxygen and green the most
131
Q

when should flow rate on a venturi be increased?

A
  • BTS guidelines recommend that if the patient has a RR>30 that the flow rate on the Venturi mask is increased above the flow rate given on the adapter, to compensate for the patient’s increased respiratory flow.
  • This will not increase the FiO2 being delivered to the patient.
132
Q

advanced O2 delivery systems?

A
  • capable of delivering upto 100% humidified and heated oxygen at a flow rate of uto 60L/min
  • The high flow rate also creates a small amount of PEEP (positive end-expiratory pressure), which helps to keep the alveoli open at the end of expiration
133
Q

pH values?

A
  • Acidotic: pH <7.35
  • Normal: pH 7.35 – 7.45
  • Alkalotic: pH >7.45
134
Q

changes in ? = respiratory

A
  • changes in CO2 - respiratory
  • changes in HCO3 - metabolic
135
Q

respiratory acidosis vs respiratory alkalosis?

A

Respiratory acidosis: low pH and high CO2
Respiratory alkalosis: high pH and low CO2

136
Q

respiratory acidosis w metabolic compensation?

A

pH low, high CO2, high bicarb

137
Q

resp alkalosis with metabolic compensation?

A

high pH, low CO2, low bicarb

138
Q

metabolic acidosis?

A

pH and HCO3- low, CO2 normal

139
Q

metabolic alkalosis?

A

high pH and bicarb, normal CO2

140
Q

metabolic acidosis with resp compensation:

A

low ph, low bicarb, low CO2

141
Q

metabolic alkalosis with resp compensation:

A

high pH, high bicarb and high CO2

142
Q

Mixed alkalosis and acidosis?

A
  • e.g. respiratory and metabolic acidosis
  • CO2andHCO3–will be moving inoppositedirections (e.g. ↑ CO2↓ HCO3– in mixed respiratory and metabolic acidosis).
143
Q

causes of resp acidosis?

A
  • inadequate alveolar ventilation leading to CO2 retention
  • Respiratory depression (e.g. opiates)
  • Guillain-Barre: paralysis leads to an inability to adequately ventilate
  • Asthma and COPD
  • Iatrogenic (incorrect mechanical ventilation settings)
144
Q

why does resp alkalosis occur?

A
  • caused byexcessivealveolarventilation (hyperventilation) resulting in more CO2than normal being exhaled.
  • As a result, PaCO2is reduced and pH increases causingalkalosis.
145
Q

causes of resp alkalosis?

A
  • Anxiety (i.e. panic attack)
  • Pain: causing an increased respiratory rate.
  • Hypoxia: resulting in increased alveolar ventilation in an attempt to compensate.
  • Pulmonary embolism
  • Pneumothorax
  • Iatrogenic (e.g. excessive mechanical ventilation)
146
Q

2 methods that metabolic acidosis can occur through?

A
  • Increasedacidproductionoracidingestion.
  • Decreasedacidexcretionorincreased rate of gastrointestinalandrenal HCO3– loss.
147
Q

examples of metabolic acidosis?

A
  • diabetic ketoacidosis
  • lactic acidosis
  • aspirin overdose
  • renal failure
  • diarrhoea
  • renal tubular disease or Addinsons disease
148
Q

metabolic alk occurs as a result of?

A
  • occurs as aresult ofdecreased hydrogen ion concentration, leading toincreased bicarbonate, or alternatively a direct result of increased bicarbonate concentrations.
149
Q

Met alk - GI loss of H+ ions e.g.

A

(e.g. vomiting, diarrhoea)

150
Q

met alk - renal loss of hydrogen ions?

A

e.g. loop and thiazide diuretics, heart failure, nephrotic syndrome, cirrhosis, Conn’s syndrome

151
Q

met alk - iatrogenic?

A

e.g. addition of excess alkali such as milk-alkali syndrome

152
Q

Causes of mixed respiratory and metabolic acidosis?

A
  • cardiac arrest
  • multi organ failure
153
Q

target O2 sats?

A
  • target sats 94%-98%
  • unless risk of CO2 retention 88-92%
154
Q

variable performance devices?

A
  • Variable performance devices deliver variable FiO2 depending upon several variables, including the oxygen flow rate and the patient’s ventilation pattern.
  • These devices do not provide all the gas required for minute ventilation; each breath will include a proportion of inspired air and the oxygen supplied.
  • nasal cannulae, simple facemasks, non rebreather masks
155
Q

examples of critical illnesses requiring high levels of oxygen?

A
  • cardiac arrest/ resus
  • shock
  • sepsis
  • major pulmonary haemorrhage
  • status epileptica
  • major head injury
156
Q

? poisoning requires as much oxygen as possible

A

CO

157
Q

Critical illnesses requiring high levels of oxygen - which delivery device to use?

A
  • 15L/min via NRB
  • Patients at risk of hypercapnic respiratory failure (e.g., COPD) who develop a critical illness should have target saturations of 94-98% until proven, on an ABG, that they need controlled oxygen therapy with target saturations of 88-92%
158
Q

BTS table for critical illnesses requring a lot of oxygen

A
159
Q

illnesses requiring moderate levels of supplemental oxygen if patient is hypoxaemic:

A
  • acute hypoxaemia
  • asthma
  • pneumonia
  • lung cancer
  • pneumothorax
  • PE
  • pleural effusions
  • acute HF
  • post op dyspnoea
160
Q

O2 therapy for the illnesses requiring moderate levels of oxygen?

A

Initial oxygen therapy will be:
- 2-6L/min via nasal cannula
- or 5-10L/min via simple face mask, if sats not maintained oxygen delivery to 15L/min via NRM
* For patients not at risk of hypercapnic respiratory

161
Q

sats below 85%?

A

treat as a critical illness and use 15L/min via NRB mask targeting 94-98

162
Q

BTS table for moderate levels of oxygen

A
163
Q

conditions where monitoring is required but oxygen not needed unless ppt is hypoxaemic:

A
  • MI/ ACS
  • Stoke
  • hyperventilation
  • poisoning and drug overdoses (unless CO poisoning)
164
Q

O2 delivery device for when o2 not required unless ppt is hypoaemic?

A
  • If Hypoxaemic aim saturations 94-98%, give 2-6L/min via nasal cannula or 5-10L/min via simple face mask unless saturations are below 85% (use 15L/min via NRB)
165
Q

BTS table for when oxygen is only required when ppt is hypoxaemic

A
166
Q

COPD oxygen?

A
  • Prior to an ABG use a 24% venturi mask at 2-3L/min or 28% venturi at 4L/min or 1-2L/min via nasal cannula aiming target saturations of 88-92%
167
Q

sudden cesation of oxygen therapy?

A

can cause life-threatening rebound hypoxaemia with a rapid fall in oxygen saturations below the starting oxygen saturation prior to the start of supplementary oxygen therapy.

168
Q

phases of a cough?

A
  • inspiratory phase - negative flow phase
  • closed glottis
  • expiratory phase - positive flow phase
169
Q

acute vs chronic cough?

A
  • acute: <3 weeks
  • subacute: 3-8 weeks
  • chronic: 8+ weeks
170
Q

receptors for the cough reflex?

A
  • larynx, tracheo-bronchial tree and the carina have the most sensitive receptors
  • polymodal receptors - respond to mechanical, pharm, chemical stimulation
171
Q

common causes of acute cough?

A
  • pneumonia
  • acute on chronic bronchitis
  • pertussis
172
Q

parenchymal diseases that can cause a cough?

A
  • chronic intersitital lung fibrosis
  • emphysema
  • sarcoidosis
173
Q

tumours that can cause a cough?

A
  • bronchogenic carcinoma
  • mediastinal tumours
  • aveolar cell carcinoma
174
Q

other causes of a cough?

A
  • foreign bodies
  • middle ear pathology in children and elderly
175
Q

CVD causes of a cough?

A
  • LVF
  • pulmonary infarction
  • aortic aneurysm
176
Q

GI causes of a cough?

A
  • reflux oesophagitis
  • recurrent aspiration
177
Q

Ix for a cough?

A
  • spirometry
  • CXR
  • FeNO/ eosinophils
178
Q

cough hypersentitivity syndrome?

A
  • airways
  • upper airways cough syndrome
  • reflux
179
Q

which ab can be used in bronchiectasis prophylactically?

A
  • azithromycin can be used as a prophylactic ab in for its anti-inflammatory and immunomodulatory effects bronchiectasis
180
Q

what can be seen on a TB CXR?

A
  • reticular nodular shadowing in TB on CXR
181
Q

What can be seen on a CXR for bronchiectasis?

A

‘dirty’ lung fields

182
Q

CT findings of bronchiectasis - ? sign?

A
  • signet ring - airways more dilated than vessels
183
Q

resp consequences from excessive cough?

A
  • pneumothorax
  • pneumomediastinum
  • pneumoperitoneum
  • laryngeal damage
184
Q

CV conseuquences of excessive cough?

A
  • cardiac dysarrythmias
  • subconjunctival haemorrhage
  • loss of conciousness
185
Q

CNS consequences of chronic cough?

A
  • syncope
  • headaches
  • central air embolism
186
Q

Tx of cough?

A
  • codeine, morphine, dimorphine are good antitussive agents
  • dextrromethophan (synthetic morphine)
187
Q

obstructive vs restrictive lung diseaseS?

A
  • obstructive: FEV1/ FVC ratio of <70%
  • restrictive: FEV1/FVC >70%
188
Q

examples of restrictive lung diseases?

A
  • pulm fibrosis
  • obesity
  • chest wall deformities
  • NM disorders
189
Q

spirometry findings on an obstructive disease

A
190
Q

COPD epidemology?

A
  • costs the NHS £1.2bn/ annum
  • 2% of the whole population have COPD
  • 25,000 deaths/ year in the UK
191
Q

COPD RF?

A
  • Cigarette smoke
  • occupational dust and chemicals
  • indoor and outdoor air pollution
  • genes
192
Q

mechanisms underlying airflow limitation in COPD - small airways disease?

A
  • airway inflammation and fibrosis, luminal plugs
  • increased airway resistance
193
Q

mechanisms underlying airflow limitation in COPD - parenchymal destruction?

A
  • loss of alveolar attachments
  • decrease of elastic recoil
194
Q

air trapping in COPD?

A
  • Inflammation and thickened airway (SM hypertrophy and constriction)
  • loss of alveolar attachments
  • loss of elasticity (emphysema)
  • airway closure
195
Q

mucosal changes of COPD?

A
  • mucosal oedema
  • mucus hypersecretion
  • loss of alveolar SA and attachments
196
Q

other changes seen in COPD (3)?

A
  • hyperinflation and gas trapping
  • increased work of breathing
  • V/Q mismatch
197
Q

systemic effects of COPD

A
  • IHD
  • cardiac failure
  • osteoporosis
  • diabetic metabolic syndrome
  • normocytic anemia
  • depression
198
Q

how is COPD diagnosed?

A
  • spirometry required to make the diagnosis: the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation.
199
Q

vaccinations that should be offered to COPD patients?

A
  • pneumonia
  • influenza
200
Q

palliative care for COPD?

A
  • opiates, NMES
  • nutritional supplementation can improve resp strength and overall health in malnourished patients
  • fatigue can be improved by self managament, pulm rehab, nutritional support
201
Q

LTOT COPD?

A
  • for patients w an SaO2 level below 88%
  • or if O2 is higher but there’s evidence of pulmonary hypertension, peripheral edema suggesting congestive cardiac failure, or polycythemia
202
Q

COPD bronchodilators?

A
  • increase radius of the small airways and so reduce the resistamce of the airflow during breathing
  • Airflow is inversely proportional to the radius of the small airway to the power of four
203
Q

anti-inflammatory therapies in COPD - steroids?

A
  • ICS - but increased risk of pneumonia
  • oral glucocorticoids
204
Q

anti-inflammatory therapies in COPD - PDE4 inhibitors?

A
  • PDE4 inhibitors - in patients w chronic bronchitis. severe COPD and a history of exacerbations
205
Q

anti-inflammatory therapies in COPD - mucolytics?

A
  • carbocysteine
206
Q

COPD - airflow obstruction -> inhaler?

A
  • airflow obstruction -> LAMA/ LABA combination inhaler
  • eosinophilic airway inflammation -> ICS
207
Q

bronchiectasis =

A

Persistent or recurrent bronchial sepsis, related to irreversibly damaged and dilated bronchi

208
Q

presentation of bronchiectasis?

A
  • cough
  • sputum - excessive volume
  • haemoptysis
  • dyspnoea
  • chest pain
  • recurrent chest infections
209
Q

CXR of bronchiectasis

A
210
Q

CT features of bronchiectasis?

A
  • HRCT is the gold standard for bronchectasis
211
Q

Cystic vs non tapering bronchiectasis on CT

A
212
Q

signs associated with bronchiectasis?

A
  • bronchial wall thickening
  • mucus impaction
  • mosaic perfusion/ air trapping on expiratory CT
213
Q

Allergic bronchopulmonary aspergillosis (ABPA)?

A
  • causes 4% of bronchiectasis in the UK
  • Can get proximal bronchiectasis and high attenuation mucus plugging
214
Q

who should bronchiectasis be suspected in?

A
215
Q

diagnosing ABPA?

A
  • associated clinical deterioration - inc cough, wheeze, increased sputum production, worsening lung function
  • high total IgE >500
  • Either positive Aspergillus-specific IgE or immediate reaction on skin prick testing
  • mucus plugging/ proximal bronchiectasis on imaging
216
Q

immune dysfunction as a cause of bronchiectasis?

A
  • investigate for primary B cell immunodeficiency - IgG replacement therapy
  • check serum ab & electrophoresis
  • measurement of baseline spec ab levels against capsular polysaccharides of strep pneumoniae
217
Q

bronchiectasis - CVID?

A
  • Cardinal feature: recurrent pulm infections with encapsulated organsisms
  • GI infection with Giardia and enteric pathogens is a common complication of CVID
218
Q

CVID ix?

A
  • reduced IgG and IgA/IgM
  • impaired resp to test immunisation
219
Q

Kartagener’s syndrome:

A
  • chronic sinusitis
  • dextrocardia
  • bronchiectasis
220
Q

Causes of bronchiectasis?

A
  • primary ciliary dyskinesia
  • CF
  • youngs syndrome
221
Q

Primary ciliary dyskinesia - are likely to have?

A
  • history going back to childhood
  • upper and lower RT infections
  • chronic rhinosinusitis
  • recurrent otitis media
  • situs inversus
222
Q

which condition has a strong association with bronchiectasis?

A

RA

223
Q

in which adults shoukd CF be investigated in?

A
224
Q

cf?

A
  • newborn screening
  • AR
  • Caucasian population
  • CFTR dysfunction
225
Q

Youngs syndrome?

A
  • Azoospermia(obstructive)
  • Chronic rhinosinusitis
  • Bronchiectasis
  • No ciliary beat frequency or ultrastructural abnormalitiss
226
Q

Bronchiectasis management - airway clearance teachiques?

A
  • chest clearance techniques to keep airways free of secretion
  • resp physio effective in stable patients
227
Q

Bronchiectasis Mx - breathing and devices?

A
  • active cycle of breathing, autogenic drainage, use of positive expiratory pressure devices
228
Q

bronchiectasis - rehab?

A
  • pulm rehab
  • improved excercise tolerance and health related QOL
229
Q

Prior to starting long term macrolides:

A
  • avoid in patients w prolonged QT interval
  • azithromycin 3x a week for bronchiectasis
  • caution when patient has hearing loss
230
Q

atopic triad?

A

asthma, eczema, and hay fever

231
Q

ashma affects ? adults

A

1 in 12

232
Q

pathiphys of asthma?

A
  • mural inflammation - eosinophils, mast cells, lymphocytes
  • wall thickening by oedema, hyperaemia, fibrosis
  • SM thickening and spasm
  • mucous plugs
233
Q

which variation is exacerbated in asthma?

A

diurnal variation

234
Q

Ix of asthma?

A
  • PEF
  • to assess severity at that time
  • or to show patterns of disease
  • peak flow diary
  • spirometry
  • FEV1/ FVC ratio of under 0.7
235
Q

beta agonists in asthma?

A
  • salbutamol and terbutaline - stimulation of SNS -> bronchodilation
  • inhaled route normally except in severe and life threatening exacerbartions when the use of nebulisers is recommended
236
Q

occupations at risk of asthma?

A
237
Q

NIV?

A
  • used in NM disease (resp muscle weakness), morbid obesity, kyphoscoliosis
  • resp support to a spontaneously breathing patient using a tight fitting face mask and is an effective alternative to intubation with an endotracheal tube and mechanical ventilation in ICU
238
Q

CPAP?

A
  • not the same as NIV
  • used to treat obstructive sleep apnoea by preventing collapse of upper airway during sleep, but this does not blow air into the lungs
239
Q

NIV is indicated for COPD when?

A
  • indicated for acidotic T2RF in a COPD exacerbation in a patient who isn’t responding to drug Tx
240
Q

how does NIV work?

A
  • increases alveolar ventilation and CO2 elimination through resting fatigued respiratory muscles and decreasing the work of breathing
  • opens airways
241
Q

+ of NIV?

A
  • lower risk of nosocomial pneumonia
  • no sedation required
  • patient can talk ,eat, cough
  • ICU bed not usually needed, reduced costs
242
Q

NIV involves a ?

A

small portable ventilaor

243
Q

overlap syndrome?

A
  • The combination of morbid obesity and COPD (often with an element of sleep apnoea) is called overlap syndrome and is a common cause of type 2 respiratory failure
244
Q

Intubation (invasive ventilation) is used when?

A
  • safer if patient unconscious, vomiting, severe acidosis, unable to protect upper airway, cardiovascular instability
  • better access to airway (particularly important in patients with copious secretions)
  • patient cooperation not required so greater scope to alter ventilator
245
Q

AS features

A

An ejection systolic murmur and splitting of the second heart sound are both signs

246
Q

Heart sound in heart failure?

A

third

247
Q

pulsus paradoxus?

A

In cardiac tamponade, there will be an abnormally large drop in BP during inspiration, known as pulsus paradoxus

248
Q

LV free wall rupture

A

A patient develops acute heart failure 10 days following a myocardial infarction. On examination he has a raised JVP, pulsus paradoxus and diminished heart sounds - left ventricular free wall rupture

249
Q

AHF management

A

IV furosemide

250
Q

CHF management?

A

1: ACEi AND BB
2: aldost antagonist such as spironolactone and elpernone
3: ivabradine, valsartan, hydralazine, nitrate, digoxin, cardiac resync therapy

251
Q

SGLT2 inhib?

A
  • in management of HF w rEF
252
Q

digoxin?

A

does not improve mortality in HF

253
Q

ralazine in combination with nitrate

A

this may be particularly indicated in Afro-Caribbean patients

254
Q

CRT

A

indications include a widened QRS (e.g. left bundle branch block) complex on ECG

255
Q

Other Tx of HF?

A

offer annual influenza vaccine
offer one-off pneumococcal vaccine

256
Q

Initial Mx of ACS?

A
  • Aspirin
  • O2 if sats under 94%
  • morphine in severe pain
  • nitrates - but not if hypotensive
257
Q

STEMI Tx?

A
  • PCI if present within 24 hours and can be done within 2 hrs
  • if not fibrinolysis within 12 hours of onset of symptoms
258
Q

PCI AP THERAPY?

A
  • aspirin
  • plus prasugrel if not alr taking an AC
  • clopidogrel if already taking an AC
259
Q

Drug therau during PCI?

A
  • UFH with gylcoprotein inhibitior as a bailout
260
Q

Fibrinolysis?

A
  • ## give antithombin
261
Q

NSTEMI mX?

A
  • aspirin and fondaparinux if no immediate PCI planned
  • calc GRACE score
262
Q

NSTEMI - low GRACE RISK

A
  • <3%
  • give ticagrelor - conservative management
263
Q

PCI for NSTEMI?

A
  • > 3% GRACE risk
  • give prasuregl or ticareglor
  • give UFH
264
Q

NSTEMI - if ppt alr on AC awap?

A

praugrel/ ticareglor for clopidrogel

265
Q
A

Year 3 (45 decks)

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