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Year 3 > Block 31 Week 6 > Flashcards

Block 31 Week 6 Flashcards

1
Q

occupational and enviromental lung diseases - deaths due to?

A
  • deaths mainly due to PM2.5
  • Deaths are due to IHD/stroke (58%), COPD (18%), lung cancer (6%)
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2
Q

pollutants - particulate matter?

A
  • A mix of solid and liquid droplets arising mainly from fuel combustion and traffic
  • This has the greatest impact on peoples’ health
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3
Q

pollutants - NO2?

A
  • Arising mainly from road traffic and indoor gas cooking
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4
Q

Pollutants - sulphur dioxide?

A
  • Arises mainly from burning fossil fuels
  • Associated with asthma and poor lung function
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5
Q

most toxic PM?

A
  • particulates are a mix of solid and liquid droplets in the air e.g. soot
  • PM 2.5 are the most toxic and are associated with CR disease and lung cancer
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6
Q

pollutants - ozone?

A
  • Caused by the reaction of sunlight with pollutants from vehicle emissions
  • A major factor associated with asthma
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7
Q

indoor air pollution?

A
  • Worldwide smoke fires used for cooking.
  • Biomass fuels produce large amounts of particulate matter
  • contributes to COPD and childhood respiratory infection
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8
Q

occupational asthma?

A
  • commonest cause of occupational lung disease in the UK
  • interactionw smoking and atopy
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9
Q

Work related asthma?

A
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10
Q

occupational asthma causes

A
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11
Q

identifying occupational asthma?

A
  • ask abt occupation - are symptoms worse at work and are they better when they’re away from work - weekends/ holiday?
  • peak flow diary
  • challenge tests
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12
Q

pneumoconiosis?

A
  • lung disease resulting from inhalation of dusts
  • Long latency between exposure and development of disease
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13
Q

types of pneumoconiosis?

A
  • Coal workers pneumoconiosis
  • Silicosis
  • Asbestosis
  • Many other rarer causes (eg. Berylliosos, Bagossis etc).
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14
Q

silicosis?

A
  • rare
  • looks like sarcoidosis
  • predisposes to TB and LC
  • Upper lobe nodules and lymph node calcification
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15
Q

asbestos can cause a range of diseases?

A
  • Benign asbestos related pleural plaques
  • Asbestos related pleural effusions
  • Diffuse pleural thickening
  • Mesothelioma
  • Lung fibrosis (asbestosis)
  • Lung cancer
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16
Q

asbtesosis on CXR

A
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17
Q

Mesothelioma?

A
  • almost always caused by occupational exposure
  • long latency
  • rising prev in UK despite being banned in the 70s
  • incurable
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18
Q

occupational lung cancer?

A
  • Estimated to cause 10% of lung cancers in men
  • Asbestos estimated to cause 60% of these but unclear whether has to cause fibrosis (asbestosis) first or direct effect
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19
Q

other causes of occupational lung cancer?

A
  • Also arsenic,chromium, coal gas, coke production, cadmium, chloromethyl ethers, silica, radon, soot
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20
Q

the health and safety executive?

A
  • independent regulator that aims to prevent work related death, injury and ill-health
  • produce guidance
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21
Q

organisations with responsibility for the environment and health?

A
  • Deparment for environment, food and rural affairs
  • PHE - air pollution
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22
Q

the lung interstitium?

A
  • the lung interstitium is the space between the linings of the alveolus and the blood capillary
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23
Q

pulmonary fibrosis =

A
  • pulm fibrosis: myofibroblasts increase in number, produce a lot of collagen expanding the interstitum
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24
Q

ILD with known cause/ association?

A
  • rheumatic/ CT disease
  • RA
  • scleoderma
  • dermatomyositis
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25
Q

drugs causing pulm fibrosis?

A
  • bleomycin - anti-cancer drug
  • nitrofurantoin
  • amiodarone - high dose
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26
Q

dust inhalation causing ILD?

A
  • asbestosis
  • silicosis
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27
Q

Smoking related ILD?

A
  • Desquamative interstitial pneumonia
  • respiratory bronchiolitis
  • usual interstitial pneumonia (UIP) - severely fibrotic lung (honeycomb change)
  • IPF if no cause
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28
Q

Clinical findings in pulm fibrosis?

A
  • persistent bilateral basal fine inspiratory crackles on auscultation suggests pulm fibrosis
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29
Q

ILD Ix?

A
  • high resolution CT scan
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30
Q

UIP CT

A
  • peripheral and basal reticulation
  • honeycomb cysts
  • traction bronchiectasis - airways wider than they should be
  • little ground glass changes
  • no nodules
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31
Q

UIP pattern?

A
  • IPF - IPF requires other causes of PF to be excluded on history and examination
  • RA and other CTDs
  • asbestosis
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32
Q

pathophys of IPF?

A
  • lung epithelial injury e.g. from viral infection, tobacco smoke, dust inhalation, GORD or autoimmunity
  • in a susceptibile indiv
  • causes production of pro-fibrotic cytokines - TGFbeta, PDGF, CTGF
  • causes activation and proliferation of fibroblasts which normally produce elastin into myofibroblasts which produce collagen
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33
Q

Genetic mutations in IPF?

A
  • MUC5B - most common
  • TERT telomerase reverse transcriptase
  • SFTPC - surfactant protein C
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34
Q

epidemiology of IPF?

A
  • mean age 70
  • M:F 1.5-2: 1
  • Median survival 3 years
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35
Q

CFs of IPF?

A
  • progressive SOB on exertion, typically over 1 year or more in an older person (>50 yrs)
  • sometimes a dry cough
  • bibasal fine inspiratory (velcro) crackles
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36
Q

Spirometry pattern in IPF?

A
  • spirometry shows restriction - reduced FVC and normal FEV1/FVC ratio but may be normal in mild disease
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37
Q

history and examination in IPF?

A
  • history - environmental and occupational exposures
  • physical examination - look for CT disease
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38
Q

clinical course in PF?

A
  • can be stable
  • slow progression
  • rapid progression
  • acute exacerbations
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39
Q

ARDS?

A
  • also shows diffuse ground glass change
  • can occur after traumatic injury
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40
Q

Tx of IPF?

A
  • do not use steroids
  • home oxygen
  • breathlessness management - breathlessness clinic, pulmonary rehabilitation, low dose morphine
  • lung transplantation for those who qualify - under 65
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41
Q

IPF - anti-fibrotics?

A
  • nintedanib or pirfenidone
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42
Q

PF and scleroderma?

A
  • pulmonary fibrosis is the commonest cause of death in scleroderma
  • about 10% of ppl w RA will have clin sig PF
  • Half of patients w scleroderma
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43
Q

NSIP pattern?

A
  • ground glass change
  • traction bronchiectasis
  • biopsy: diffuse interstitial fibrosis
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44
Q

Organising pneumonia pattern?

A
  • patchy consolidation
  • air bronchograms
  • biopsy: buds of granulation and fibroblastic tissue within air spaces
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45
Q

in a patient with a non-UIP pattern of ILD look for a?

A

CTD

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46
Q

NSIP and organsing pneumonia pattern

A
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47
Q

hypersensitivity pneumonitis?

A
  • hypersensitivity pneumonitis
  • inhalation of avian antigens can cause bird breeders lung
  • IgG against bird antigens
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48
Q

common cause of HP

A
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49
Q

sarcoidosis?

A
  • systemic inflammatory disease
  • non caseating granulomas replacing lymph node tissue
  • may self resolve or can progress into pulm fibrosis
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50
Q

acute sarcoidosis triad?

A
  • arthiritis
  • erythema nodosum - painful red patches on the shins
  • bilateral hilar lymphadenopathy
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51
Q

sarcidosis can cause ?

A
  • can cause hypercalcaemia by causing hydroxylation of vitamin D
  • tends to get worse when vitamin D levels
  • sarcoid granulomas can also produce ACE - cannot be used alone to diagnose or exclude sarcoidosis
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52
Q

diagnosing sarcoid?

A
  • non caseating granulomas in one or more organs
  • exclusion of infection - contacts and travel history, stains for mycobacteria and fungi
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53
Q

SOB - CV exam?

A
  • Shortness of breath:may indicate underlying cardiovascular (e.g. congestive heart failure, pericarditis) or respiratory disease (e.g. pneumonia, pulmonary embolism).
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54
Q

Malar flush?

A
  • Malar flush:plum-red discolouration of the cheeks associated with mitral stenosis.
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55
Q

pedal oedema/ ascites?

A

CHF

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56
Q

Signs associated with endocarditis?

A
  • splinter haemorrhages
  • janeway lesions
  • osler’s nodes
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57
Q

splinter haemorrhages?

A
  • Splinter haemorrhages:a longitudinal, red-brown haemorrhage under a nail that looks like a wood splinter.
  • Causes include local trauma, infective endocarditis, sepsis, vasculitis and psoriatic nail disease.
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58
Q

janeway lesions?

A
  • Janeway lesions:non-tender, haemorrhagic lesions that occur on the thenar and hypothenar eminences of the palms (and soles).
  • Janeway lesions are typically associated with infective endocarditis.
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59
Q

Osler’s nodes?

A
  • Osler’snodes:red-purple, slightly raised, tender lumps, often with a pale centre, typically found on the fingers or toes.
  • They are typically associated with infective endocarditis.
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60
Q

Causes of radio-radial delay include:

A
  • Subclavian artery stenosis (e.g. compression by a cervical rib)
  • Aortic dissection
  • Aortic coarctation
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61
Q

collapsing pulse/ water hammer pulse?

A
  • Normal physiological states (e.g. fever, pregnancy)
  • Cardiac lesions (e.g. aortic regurgitation, patent ductus arteriosus)
  • High output states (e.g. anaemia, arteriovenous fistula, thyrotoxicosis)
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62
Q

slow rising pulse is associated with?

A

aortic stenosis

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63
Q

occupational lung diseases?

A
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64
Q

Patients withidiopathic pulmonary fibrosishave typical findings on examination:

A
  • Bibasal fine end-inspiratory crackles
  • Finger clubbing
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65
Q

Diagnosis of interstitial lung disease involves:

A
  • Clinical features
  • High-resolution CT scan (HRCT) of the thorax (showing a typical “ground glass” appearance)
  • Spirometry
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66
Q

Pirfenidone?

A

reduces fibrosis and inflammation through various mechanisms

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67
Q

Nintedanib?

A

reduces fibrosis and inflammation by inhibitingtyrosine kinase

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68
Q

Several drugs can cause pulmonary fibrosis:

A
  • Amiodarone (also causes grey/blue skin)
  • Cyclophosphamide
  • Methotrexate
  • Nitrofurantoin
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69
Q

Pulmonary fibrosis can occur secondary to other conditions:

A
  • Alpha-1 antitrypsin deficiency
  • Rheumatoid arthritis
  • Systemic lupus erythematosus (SLE)
  • Systemic sclerosis
  • Sarcoidosis
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70
Q

hypersensitivity pneumonitis?

A
  • a.k.a allergic alveolitis - involves type III and type 4 hypersensitivity reaction to an envionmental allergen
  • Inhalation of allergens in patients sensitised to that allergen causes an immune response, leading to inflammation and damage to the lung tissue.
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71
Q

what is suggestive of hypersensitivity pneumonitis?

A
  • raised lymphcoytes in bronchoalveolar lavage
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72
Q

HP - bird fancier’s lung?

A

a reaction to bird droppings

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73
Q

HP - farmer’s lung?

A

reaction to mouldy spores in hay

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74
Q

HP - mushroom workers lung?

A

reaction to specific mushroom antigens

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75
Q

HP - malt workers lung?

A

reaction to mould on barley

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76
Q

cryptogenic organising pneumonia
?

A
  • involves a focal area of inflammation of the lung tissue.
  • It can be idiopathic or triggered by infection, inflammatory disorders, medications, radiation, environmental toxins, or allergens.
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77
Q

COP - presentation?

A
  • Presentation is similar to infectious pneumonia, with shortness of breath, cough, fever and lethargy.
  • Inspiratory crackles may be heard on auscultation.
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78
Q

findings of COP?

A
  • focal consolidation can be found on CXR
  • lung biopsy is the definitive Ix
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79
Q

Bounding pulse = associated with

A

aortic regurg and CO2 retention

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80
Q

thready pulse =

A

associated with intravascular hypovolaemia in conditions such as sepsis

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81
Q

causes of raised JVP?

A
  • RSHF (can be from PE)
  • Tricuspid regurg
  • constrictive pericarditis
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82
Q

Tricuspid regurg?

A

causes include infective endocarditis and rheumatic heart disease.

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83
Q

Constrictive pericarditis?

A

often idiopathic, but rheumatoid arthritis and tuberculosis are also possible underlying causes.

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84
Q

asterxis causes?

A
  • asterixis - CO2 retention
  • can also be caused by uraemia and hepatic encephalopathy
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85
Q

fine tremor?

A

beta-2 agonist use e.g. salbutamol

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86
Q

tracheal deviation?

A
  • The trachea deviatesawayfromtensionpneumothoraxandlarge pleural effusions.
  • The trachea deviatestowardslobar collapseandpneumonectomy.
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87
Q

increased TVF?

A

consolidation, tumour, lobar collapse

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88
Q

Decreased TVF ?

A

suggests the presence of fluid or air outside of the lung (e.g. pleural effusion, pneumothorax).

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89
Q

Bronchial breathing?

A
  • harsh-sounding (similar to auscultating over the trachea), inspiration and expiration are equal and there is a pause between.
  • This type of breath sound is associated with consolidation.
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90
Q

coarse crackles?

A
  • Coarse crackles:discontinuous, brief, popping lung sounds typically associated with pneumonia, bronchiectasis and pulmonary oedema.
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91
Q

fine- end inspiratory crackles?

A
  • often described as sounding similar to the noise generated when separating velcro.
  • Fine end-inspiratory crackles are associated with pulmonary fibrosis.
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92
Q

increased vocal resonance?

A
  • Increased volumeover an area suggests increased tissue density (e.g. consolidation, tumour, lobar collapse).
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93
Q

decreased VR?

A
  • Decreased volumeover an area suggests the presence of fluid or air outside of the lung (e.g. pleural effusion, pneumothorax).
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94
Q

Cardiac cycle?

A
  • ventricular diastole
  • lub = first heart sound = mitral and triscupid pulled closed
  • venticular systole
  • dub = second heart sound = aortic + pulmonary pushed closed
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95
Q

murmurs made louder by inspiration vs expiration?

A
  • murmurs made louder by inspiration = right sided
  • by expiration = left sided
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96
Q

systolic murmurs are?

A
  • aortic stenosis
  • mitral regurg
  • MR ASS - mit regurg, aortic stenosis, systolic
97
Q

aortic stenosis?

A
  • turbulent blood flow through narrowed valve
  • murmur may muffle the heart sound - second heart sound can be quieter or louder - associated with pulm hypertension
98
Q

congenital aortic stenosis - causes?

A
  • bicuspid aortic valve
  • presents in infancy
99
Q

aortic stenosis causes in 30-40 year olds?

A

*Bicuspid, typically symptoms develop from 30-40 years+

100
Q

calcification of normal/ tricuspid valve?

A
  • most common
  • 65+ years
  • occurs earlier in renal failure and high cholesterol
101
Q

triad of aortic stenosis?

A
  • effort dyspnoea
  • effort dizziness/ syncope
  • effort angina
102
Q

sudden cardiac death in aortic stenosis?

A
  • sudden cardiac death - rare without classic triad first
103
Q

where is the aortic stenosis murmur heard?

A
  • heard over the aortic area, radiation to the carotids
104
Q

other features of AS?

A
  • slow rising pulse and narrow pulse pressure - below 30
  • absent second heart sound or loud P2
105
Q

apex beat and signs of? in AF

A
  • forceful apex beat - indicated LVH
  • possible signs of heart failure
106
Q

signs of severe aortic stenosis?

A
  • radiation to carotids
  • slow rising pulse and narrow pulse pressure
  • loud p2
  • signs of HF
107
Q

Ix of AS?

A

echo

108
Q

Tx of AS?

A
  • monitoring - symptoms, severity of stenosis, LV function
  • surgery
  • TAVI for high risk
109
Q

Mitral regurg?

A
  • 2nd most common murmur
  • leaky mitral valve which allows blood to backflow into the atria after ventricular systole
  • pansystolic murmur - occurs all throughout systole
110
Q

causes of mitral regurg - intrinsic valve problems?

A
  • Myxomatous degeneration
  • Rheumatic Heart Disease - most common cause of mitral regurg
  • Infective Endocarditis
  • Chordal Rupture/Prolapse - cords not attached to PM and flails backwards causing regurg
  • Papillary Muscle Rupture (IHD)
111
Q

MR causes - secondary/ functional (dilatation of ventricle)?

A
  • those w LV dysfunction develop a dilated ventricle which doesn’t work very well, mitral annulus stretches apart and leaflets can’t compensate for that and the valve becomes incompetent
  • Tx aims to improve dilatation of the ventricle
112
Q

MR from dilatation of ventricle - patients often present with?

A
  • patients often asymptomatic for years so presentation and signs often that of heart failure
113
Q

CFs of MR?

A
  • Displaced (down and round), diffuse apex beat resulting from volume overload (dilated LV)
  • Loud pan systolic murmur at apex - same intensity throughout
  • Radiation of murmur to (usually left) axilla/back
114
Q

markers of severity in mitral regurg?

A
  • displaced apex
  • loud pan systolic murmur - loudness reflects seveity in regurgitation murmurs
  • radiation to axilla/ back
115
Q

medical Tx of MR?

A

HF Tx

  • diuretics
  • ACEi to maintain systolic function of LV
116
Q

surgical Tx of MR?

A
  • indicated if LV is enlarging progressively or if intrusive symptoms
  • mitral valve repair or mitral valve replacement
117
Q

causes of systolic murmurs?

A
  • AS
  • MR
  • pulmonary stenosus
  • tricuspid regurg
118
Q

pulm stenosis?

A
  • radiation to axilla/ back
  • present in younger population
  • one of the most common types of congenital HD
119
Q

pulm stenosis is louder in?

A

inspiration

120
Q

tricuspid regurg?

A
  • radiation to the liver (blood goes down to IJV)
  • accenuated in end inspiration
121
Q

tricuspid regurg - hypertrophic cardiomyopathy?

A

Outflow tract mumur

122
Q

tricuspid regurg - coarction of aorta?

A

radio-radio delays and BP change

123
Q

tricuspid regurg - VSD?

A

very loud, no accenuation

124
Q

what are the diastolic murmurs?

A
  • aortic regurg
  • mitral stenosis
  • De ARMS
125
Q

aortic regurg?

A
  • backflow of blood into LV
  • pressure equalizes much quicker so flow stops
  • described as decreshendo diastolic murmur
126
Q

aortic regurg signs?

A
  • collapsing pulse
  • Wide PP
  • early diastolic murmur
127
Q

aortic regurg - murmur?

A

murmur heard at left sternal edge (patient leaning forward, end-expiration)

128
Q

Signs of AR - Corrigan’s sign?

A

visible carotid pulsations

129
Q

Signs of AR - De Musset sign?

A

head bobbing

130
Q

Signs of AR - Quinke’s sign?

A

nail bed pulsations - red flashes within the nail bed. marker of serverity

131
Q

Signs of AR - pistol shot femorals?

A

due to large forward stroke volume

132
Q

Signs of AR -Duroziez’s murmur?

A

to-and fro- murmur in femoral (large forward and backward flow in aorta)

133
Q

causes of AR - diseases affecting the aortic valve?

A
  • Rheumatic Heart Disease
  • Infective Endocarditis
  • Lupus
134
Q

causes of AR - diseases resulting in dilatation of the aortic root?

A
  • Aortic Aneurysm (hypertension)
  • Marfan’s syndrome
  • (Ankylosing spondylitis)
  • Syphilis (late sign)
135
Q

aortic dissection =

A

acute AR

136
Q

Aortic regurg Tx?

A
  • Diuretics-symptom control
  • ACEi - maintains systolic function of left ventricle
137
Q

mitral stenosis murmur?

A
  • low pitched mid diastolic murmur - use bell
  • stops at first heart sound
138
Q

mitral stenosis is almost exclusively ? in origin?

A

rheumatic in origin so may also have aortic valve problems

139
Q

MS signs?

A
  • Low-pitched rumbling mid-diastolic murmur (apex in left lateral position)
  • Opening snap (rigid valve opening) precedes murmur
  • Malar Flush / ‘Mitral Facies’
140
Q

Other signs of MS - cardiac?

A
  • Signs of Heart Failure
  • Usually in AF
  • Right ventricular Heave if secondary pulmonary hypertension
141
Q

MS - tapping?

A

apex beat (palpable S1)

142
Q

markers of severity of MS?

A
  • malar flush
  • signs of HF
  • AF
  • RV Heave
  • tapping apex
143
Q

medical Tx of Mitral stenosis?

A
  • Diuretics- symptom control
  • Rate control / Anticoag - if in AF
144
Q

surgery in the Tx of mitral stenosis?

A
  • Mitral Valvotomy - balloon used to open the valve
  • Mitral Valve Replacement
145
Q

other causes of diastolic murmurs?

A
  • pulm regurg
  • tricuspid stenosis
  • patent DA
146
Q

common cause

Pulm regurg?

A
  • pulm regurg - loud
  • common consequence of surgery for teratology of fallot
147
Q

tricuspid stenosis?

A
  • tricuspid stenosis - accetuated in end inspiration
148
Q

patent ductus arteriosus?

A
  • patent ductus arteriosus - continous machinery murmur - due to patent duct still being open so there will be a diastolic component
  • not accenuated by respiration
149
Q

valvular lesions Ix?

A
  • echo
  • ECG
  • Stress testing is sometimes done in those who are asymptomatic or have minor symptoms
150
Q

systole =

A

occurs between S1 and S2 heart sounds

151
Q

diastole =

A

between S2 and S1

152
Q

stenosis -> ? murmur?

A
  • Stenosis of the aortic or pulmonic valves will result in a systolic murmur, as blood is ejected through the narrowed orifice.
153
Q

echocardiograms?

A
  • echocardiograms use sound waves to produce images of the heart as it moves
  • shows blood flow through the heart and heart valves
  • can tell us about pumping function of the heart, the valve function, size of the heart chambers
154
Q

Infective endocarditis ?

A
  • can be a life threatening condition associated w severe complications
  • Infection of the endocardium may involveone or more heart valvesor anintracardiac device(e.g. prosthetic valve).
155
Q

types of infective endocarditis?

A
  • native valve endocarditis
  • prosthetic valve endocarditis
  • IVDA
156
Q

Native valve endocarditis?

A

normal valves without previous intervention. May be acute or subacute.

157
Q

PVE?

A

may occur early (< 1 year) or late (> 1 year) following surgical intervention. Account for 10-20% of cases.

158
Q

Intravenous drug abuse (IVDA) endocarditis?

A
  • classically affects the tricuspid valve (50%).
  • Staphylococcus aureusmost common microorganism.
159
Q

IE RF?

A
  • age
  • male
  • IV drug use
  • poor dental hygeine
  • immunosuppression or haemodialysis
160
Q

Cardiac RF for IE?

A
  • Structural or valvular HD
  • Congenital HD
  • prosthetic heart valves
  • previous IE
161
Q

most common cause of IE?

A
  • The most common cause of IE overall isStaphylococcal aureus, which is the usual pathogen in IE associated with intravenous drug use (IVDU) and prosthetic heart valves.
  • Other commonly isolated bacteria areStreptococcalandEnterococcalspecies
162
Q

non infective endocarditis?

A
  • endocarditis may occur in the absence of infection
  • it is due to sterile platelet thrombi on heart valves
  • causes: advanced malignancy, lupus, RA
163
Q

Fungal caues of endocarditis?

A
  • associated w poor prognosis - ~50% mortality
  • Candida species(e.g.C. albicans,C. stellatoidea)
  • Aspergillus species
164
Q

pathophys of IE?

A
  • IE occurs when bacteria enter the bloodstream and deposit onto the endocardial surface of the heart.
  • Classically, adental procedureis associated with a brief bacteraemia that our immune system is able to control.
  • However, in patients with underlying cardiac disease (e.g. rheumatic heart disease) it can lead to deposition and adherence of bacteria.
  • Once deposited on the endocardial surface, the organisms adhere and eventually lead toinvasion and destruction of the valve leaflets.
  • The key pathological process in IE is formation of infectedvegetations.
165
Q

IE is characterised by?

A

formation of vegitations on cardiac valves

166
Q
  • IE vegitations lead to?
A
  • forms vegitations which leads to regurgitant murmurs and eventually congestive cardiac failure
  • If this process occurs acutely (e.g. acute IE secondary toStaphylococcal aureus) it can lead to acute heart failure and cardiogenic shock. T
167
Q

Order of valves affected in endocarditis?

A

mitral -> aortic -> tricuspid -> pulmonary valves

168
Q

CFs of IE - most common?

A

fever and cardiac murmur

169
Q

symptoms of IE?

A
  • Fever(90%)
  • Malaise, lethargy
  • Anorexia
  • Weight loss
  • Abdominal pain: splenic abscess
170
Q

urinary changes in IE?

A
  • Haematuria: renal embolic phenomenon
171
Q

Cardiac symptoms of IE?

A

shortness of breath, chest pain, palpitations

172
Q

Murmur in endocarditis?

A

pansystolic murmur of mitral regurgitation or early diastolic murmur of aortic regurgitation classical

173
Q

other clinical signs of IE?

A
  • features of HF
  • petechia
  • splinter haemorrhages, janeway lesions, oslers nodes
  • roth spots
174
Q

roth spots?

A

exudative, oedematous hemorrhagic lesions of the retina with pale centre (immune complex deposition). Subacute > acute.

175
Q

Ix for IE?

A
  • TT echo followed by a transoesophageal echo (TOE) to look for local complications
  • blood cultures
  • CT, MRI, CT-PET
176
Q

other tests for IE?

A
  • urine dip (haematuria/proteinuria)
  • ecg - prolonged PR interval is suggestive of para-aortic abscess
  • CT/ US of thorax and abdomen - pulmonary or splenic abscesses
  • CT/ MRI for neuro complications
177
Q

Findings on TTE/TOE suggestive of IE include:

A
  • Vegetation
  • Abscess formation
  • Pseudoaneurysm
  • Valve perforation
  • New dehiscence of a prosthetic valve
178
Q

Staph A endocarditis Tx?

A

flucloxacillin

179
Q

MRSA IE Tx?

A
  • MRSA or penicillin allergy: vancomycin
180
Q

strep IE tx?

A
  • penicillin, or amoxicillin or ceftriaxone or gentamicin or vancomysin
181
Q

surgery for IE?

A
  • Heart failure(e.g.new acute heart failure with haemodynamic compromise)
  • Uncontrolled infection(e.g. abscess formation or persistently positive blood cultures)
  • Prevention of embolisation(e.g. large vegetations)
182
Q

Ab prophylaxis of IE?

A
  • cardiac procedures
  • dental procedures
  • resp tract procedures - e.g. bronchoscopy
  • GI procedures - e.g. TOE, colonoscopy
  • urological procedures - cytoscopy
  • obstetric procedures - vaginal/ caesarian delivery
183
Q

Cardiac complications of IE?

A
  • HF most freq and most severe
  • cardiac: heart failure, perivalvular abscess, pericarditis, cardiac tamponade
184
Q

Neurological complications of IE?

A

stroke, abscess, meningitis, encephalitis, haemorrhage, seizures

185
Q

Metastatic infection from IE?

A

mycotic aneurysm, embolisation, abscess formation

186
Q

Embolisation sequaelae from IE?

A

stroke, blindness, ischaemic limb, splenic/renal infarct, pulmonary embolism, myocardial infarction

187
Q

how can pathogens get to the heart?

A
  • bacteria/ fungi can get to the heart by entering the bloodstream from infectionns elsewhere in the body - e.g. urinary or GI tract ot skin or after surgical or dental procedures
188
Q

what else can you get with IE?

A
  • chills
  • night sweats
189
Q

Later symptoms of IE?

A
  • swelling of feet and legs
  • SOB
  • irregular heartbeat
190
Q

enterococcal IE?

A

*Men > Women
- Median age 59-65 years

191
Q

Jobs at risk of sillicosis?

A
  • mining
  • slate works
  • foundries
  • potteries
192
Q

Features of sillicosis?

A
  • upper zone fibrosing lung disease
  • ‘egg-shell’ calcification of the hilar lymph nodes
193
Q
A
194
Q

Tx of enterococcal IE?

A

*Amoxicillin + gentamicin or ceftriaxone standard treatment

195
Q

ejection systolic murmurs?

A
  • AS
  • hypertrophic obstructive cardiomyopathy
  • PS
  • ASD
  • teratology of fallot
196
Q

Ejection systolic murmurs louder on expiration?

A
  • AS
  • hypertrophic obstructive cardiomyopathy
197
Q

Ejection systolic murmurs louder on insp?

A
  • pulm stenosis
  • ASD
  • ToF
198
Q

Pansystolic/ holosytolic murmurs?

A
  • mitral/ tricuspid regurg
  • VSD
199
Q

mitral/ tricuspid regurg character?

A

high-pitched and ‘blowing’ in character

200
Q

Tricuspid regurg vs mitral regrurg?

A

tricuspid regurgitation becomes louder during inspiration, unlike mitral reguritation

201
Q

VSD?

A
  • harsh murmur
  • holosytolic
202
Q

what are the late systolic murmurs?

A
  • mitral valve prolapse
  • coarctation of aorta
203
Q

early diastolic murmurs?

A
  • aortic regurg
  • pulm regurg
204
Q

aortic regurg and pulm regurg?

A

high pitched, blowing murmur

205
Q

Mid-late diastolic murmurs?

A
  • MS
  • austin flint murmur
206
Q

mitral stenosis character?

A

‘rumbling’ in characterA

207
Q

Austin flint murmur?

A

severe aortic regurgitation, again is ‘rumbling’ in character

208
Q

cont machine-like murmur?

A

patent ductus arteriosus

209
Q

RILE?

A

Right-sided murmur → heard best on Inspiration
Left-sided murmur → heard best on Expiration

210
Q

RCA supplies?

A
  • II, III, aVF - inferior leads
211
Q

AS symptoms?

A

syncope, angina, dyspnea (SAD)

212
Q

Murmur in AS?

A

ejection systolic, described as crescendo-decrescendo. Radiates to the carotids.

213
Q

where is AS best heard?

A

expiration in the aortic area

214
Q

Additional signs of AS?

A
  • Sustained apex
  • Slow rising pulse
  • Narrow pulse pressure
  • Heart sounds:
  • Soft S2 (sign of severe disease)
  • S4
  • Reversed splitting of S2
215
Q

cogenital associations of PS?

A
  • ToF
  • congenital rubella syndrome
216
Q

Symptoms of PS?

A

syncope, fatigue

217
Q

acquired causes of PS?

A
  • Carcinoid syndrome
  • rheumatic fever
218
Q

Murmur in PS?

A

ejection systolic, described as crescendo-decrescendo. Often associated with a thrill.

219
Q
A
220
Q

post-mI AV block affects?

A
  • RCA
  • II, III, aVF
221
Q

Anteroseptal MI?

A
  • v1 - v4
  • LAD
222
Q

inferior MI?

A
  • 2, 3, aVF
  • RCA
223
Q

antereolateral MI?

A
  • v1 -v6
  • avL
  • proximal LAD
224
Q

lateral MI?

A
  • I
  • aVL
  • +/- V5-V6
  • Left circumflex
225
Q

Posterior MI?

A
  • changes to V1-V3
  • usually left circumflex also RCA
226
Q

posterior MI - reciprocal changes seen:

A
  • horizontal ST depression
  • tall, broad R waves
  • upright T waves
  • dominant R wave in V2
227
Q

How is posterior MI confirmed?

A

Posterior infarction is confirmed by ST elevation and Q waves in posterior leads (V7-9)

228
Q

moderate asthma exacerbation?

A
  • PEFR 50-75%
  • RR less than 25
  • Pulse less than 110bpm
229
Q

Severe asthma exacerbation features?

A
  • PEFR 33-50%
  • can’t complete sentences
  • RR > 25
  • pulse over 110
230
Q

Can’t complete sentences =

A

severe asthma

231
Q

Life threatening asthma features?

A
  • < 33%
  • O2 below 92 and normal CO2
232
Q

Other features of life threatning asthma?

A
  • silent chest
  • cyanosis
  • bradycardia/ hypotension
  • confusion, coma, exhaustion
233
Q

silent chest =

A

life threatening

234
Q

Near fatal asthma?

A

raised pCO2 and or requiring mechanical ventilation

235
Q

Mx of acute asthma exacerbation?

A
  • O2 if hypoxic
  • bronchodilation - SABA
  • prednisolone for 5 days
236
Q

ipatropium bromide?

A
  • life threatning/ severe asthma
  • pps who haven’t resp to beta agonists, steroids
237
Q

IV magnesium sulfate?

A

mmonly given for severe/life-threatening asthma

238
Q
A

Year 3 (45 decks)

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