OSCE Questions Flashcards
Causes of clubbing other than CVS?
Lung Ca CF Bronchiectasis Idiopathic pulmonary fibrosis (IPF/CFA) Sarcoidosis IBD Liver cirrhosis Celiac disease
CVS causes of clubbing?
Cyanotic congenital heart disease
Infective endocarditis
explain the difference between central and peripheral cyanosis?
central: results from a problem getting oxygen into the blood, so blood leaving the heart is deoxygenated, and hence arrives at the peripheries deoxygenated.
peripheral: result of too much oxygen being taken out of the blood at the peripheries.
for cyanosis, concentration of deoxygenated Hb is more than 5g/dL.
define cyanosis
an abnormal bluish discolouration of the skin and mucous membranes that results from a higher than normal level of deoxygenated Hb in the blood (more than 5g/dL).
causes of central cyanosis?
PE R to L shunt e.g. tetralogy of fallot, Eisenmenger syndrome acute severe asthma COPD severe pneumonia pulmonary oedema polycythaemia rubra vera
causes of peripheral cyanosis?
those conditions assoc. with peripheral vasoconstriction and blood stasis in the extremities: congestive heart failure circulatory shock exposure to cold temps PAD-thrombosis, embolism or atheroma Raynauds acrocyanosis erythrocyanosis beta blockers SVC obstruction
all that cause central?
why can central cyanosis be confirmed by looking underneath the tongue?
this is very vascular, and is not a sufficient enough mass to be able to extract enough oxygen out of the blood to cause peripheral cyanosis, and can therefore say for definite that a blue tongue is the result of central cyanosis.
why might a pt with previous valvular heart disease present with jaundice?
if the pt has had a prosthetic heart valve, rbc travelling through this can be subject to damage, and so result in a haemolytic anaemia, where increased rbc breakdown increases the concentration of unconjugated bilirubin in the blood, producing jaundice.
CVS causes of a mild jaundice?
prosthetic heart valve resulting in a haemolytic anaemia and subsequent unconjugated hyperbilirubinaemia
RHF resulting in hepatic venous congestion and hepatocyte damage producing hepatic jaundice with a conjugated and unconjugated hyperbilirubinaemia.
most common cause of loss of cardiac and liver dullness?
COPD- lung hyperinflation
how should metered dose inhalers (MDI) e.g. easibreathe e.g. salbutamol reliever inhaler, be breathed in?
slowly and deeply
how should dry powder inhalers (DPI) e.g. symbicort turbohaler-budesonide and formoterol, be breathed in?
quickly and deeply
important components to explanation of inhaler technique?
check patient’s understanding
explain what inhaler is, how it works, when pt should take it and how much and why
remind pt to rinse mouth out after steroid inhaler use e.g. Qvar-beclometasone, and symbicort-budesonide and formoterol, to reduce risk of oral candidiasis.
ask pt to summarise key points back to check understanding
give demonstration: prepare inhaler, load dose, breathe out gently as far as is comfortable, tightly seal lips around mouth piece, then breathe in slowly and deeply for MDIs, quickly and deeply for DPIs and slowly and deeply for soft mist inhalers. remove inhaler from mouth and hold breath for as long as is comfortable. rpt procedure as directed.
then assess pt technique, critique good and bad points
spacer devices may be used to improve drug deposition in the lungs in those who cannot master aerosol inhaler technique, pt should breathe in and out through spacer mouthpiece several times after dose has been released into device.
important components to assessing a patient’s peak flow?**
explain what peak flow is and why you are measuring it
patient must breathe out as hard and as fast as possible, and maintain good seal around mouth piece
patient must be asked to stand
3 attempts, and best of 3 is taken
ADRs of salbutamol?
Fine tremor, palpitations, tachycardia, nervous tension, peripheral vasodilatation, headache, hypokalaemia, hypersensitivity, paradoxical bronchospasm, hypotension, arrhythmias, oropharyngeal irritation
causes of upper zone opacification on a CXR?
TB sarcoidosis ankylosing spondylitis extrinsic allergic alveolitis radiation fibrosis
causes of lower zone opacification on a CXR?
pneumonia
idiopathic pulmonary fibrosis
drug induced ILD e.g. MTX, nitrofurantoin, amiodarone
ILD assoc. with CT diseases and AI systemic diseases e.g. RA
how does a patient’s airflow limitation relate to use of corticosteroid treatment in COPD?
if FEV1.0 less than 50% predicted, regular treatment improves symptoms, lung function, QOL and reduces exacerbations.
causes of a cavitating lesion on a CXR?
TB bronchial Ca (espec. squamous CC) pulmonary metastases lung abscess aspergillus infection? cavitating pneumonia wegener's granulomatosis rheumatoid nodule
indications for LTOT in COPD?
PaO2 persistently less than 7.3kPa, OR between 7.3kPa and 8.0kPa with evidence of either pulmonary HTN, peripheral oedema or polycythaemia-haematocrit more than 55% (or evidence of cor pulmonale)
only effective for increasing LT survival if given for at least 16 hours per day
COPD non-pharmacological management?
smoking cessation
exercise, pulmonary rehabilitation programmes
influenza and pneumococcal vaccinations
?RF management in terms of other comorbidities e.g CVD-reduce LDLs, BP, manage DM.
when might the phosphodiesterase 4 inhibitor roflumilast be used in the treatment of COPD?
to reduce exacerbations in those with chronic bronchitis, severe or very severe airflow limitation (FEV1.0 less than 50% of that predicted) and for frequent exacerbations that are not controlled by long acting bronchodilators.
in which pts should Abx be given in an exacerbation of COPD?
those with the 3 cardinal features: increased SOB, increased volume of sputum and increased sputum purulence
increased sputum purulence and 1 other cardinal feature
those requiring mechanical ventilation
comorbidities in COPD?
CVD-IHD, HF, HTN and AF, cardioselective beta blockers e.g. atenolol and bisoprolol are NOT contraindicated in COPD, and important as beta blockers known to improve survival and patients with HF and IHD e.g. post MI
lung Ca-most frequent cause of death in pts with mild COPD
metabolic syndrome and DM
OP, and anxiety/depression-often underdiagnosed
serious infections
what is FEV1.0 influenced by?
age
sex
height
ethnicity
why is spirometry performed for COPD?
to make the clinical diagnosis-FEV1.0/FVC ratio less than 70%
along with presence of symptoms to give idea of severity and guide specific treatment steps e.g. inhaled corticosteroids considered long term if FEV1.0 less than 50% of that predicted
a normal value effectively excludes a diagnosis of clinically relevant COPD
the lower the percentage predicted FEV1.0, the worse the prognosis
can monitor disease progression as FEV1.0 declines over time and usually faster in those with COPD, but must be at least 12 months between measurements to be reliable.
pharamcologic therapy for COPD patients with an FEV1.0 50% or more of that predicted?
if less symptoms, 1st choice is SA anticholinergic e.g. ipratropium bromide, as required OR SA beta 2 agonist e.g. salbutamol, as required
alternatives=LA anticholinergic, or LA beta 2 agonist, or SA beta 2 agonist and SA anticholinergic, could possibly use theophylline
if more symptoms, 1st choice is LA anticholinergic e.g. tiotropium bromide OR LA beta 2 agonist, alternatives=LA anticholinergic and LA beta 2 agonist, could also consider SA beta 2 agonist and/or SA anticholinergic, or theophylline
pharmacologic therapy for COPD patients with an FEV1.0 less than 50% of that predicted?
if less symptoms, 1st choice is an inhaled corticosteroid and a LA beta 2 agonist, or could give a LA anticholinergic
alternatives include LA anticolinergic and LA beta 2 agonist, or LA anticholinergic and PDE-4 inhibtor, or a LA beta 2 agonist and PDE-4 inhibitor, others=SA beta 2 agonsit and/or SA anticholinergic, or theophylline
if more symptoms, 1st choice=inhaled corticosteroid, and LA beta 2 agonist and/or LA anticholinergic
alternatives=ICS and LA beta 2 agonist and LA anticholinergic, or ICS and LA beta 2 agonsit and PDE-4 inhibtor, or LA anticholinergic and LA beta 2 agonsit, or LA anticholinergic and PDE-4 inhibtor.
others=carbocysteine (mucolytic), N-acetylcysteine, SA beta 2 agonsit and/or SA anticholinergic, or theophylline.
cause of sail-like appearance in CXR with hemithorax volume loss?
lobe collapse
3 most common causes of a L lower lobe lung collapse?
central hilar or endobronchial mass e.g. lung Ca
endobronchial FB
endobronchial mucus plug-consider in a post op or ITU patient
FB and mucus plug can be dealt with using bronchoscopy
bronchoscopy and CT chest indicated in L lower lobe collapse in adults, espec. smokers, when querying underlying tumour
major exception to taking a CXR in full inspiration?
if looking for a pneumothorax-this shows better with patient in full expiration
causes of mitral regurgitation?
prolapsing mitral valve, can occur in PKD patients and anorexia nervosa patients
rheumatic mitral regurgitation
papillary muscle rupture post MI
cardiomyopathy of any sort
infective endocarditis
CT disorder e.g. Marfan’s syndrome, Ehlers Danlos and osteogenesis imperfecta
findings o/e of pt with mitral regurgitation?
pulse more likely to be in sinus rhythm
malar flush also seen in mitral stenosis
displaced apex beat due to volume overload, palpable thrill
pansystolic murmur heard best over mitral valve, with radiation to the axilla, no gap between murmur and S2
results of CXR and ECG in mitral regurgitation?
CXR-cardiomegaly due to LA and LV enlargement, cardiac to thoracic ratio more than 50%
ECG-P-mitrale-bifid P waves due to LA hypertrophy, LV hypertrophy-tall R waves V5 and V6, Sokolow-Lyon voltage criteria-S wave in V1 plus R wave in V5 or V6 is more than 35mm or 3.5 large ECG squares.
complications of valve replacement?
complications of surgery-5% mortality
valve failure-acute-valave dehiscience, breakage, thrombus, chronic-incompetence, stenosis
thromboembolism
infective endocarditis-early infection-staph epidermidis, late-strep viridans
anaemia-haemolytic anemia-may be noromochromic, due to red cell breakdown across valve, increase reticulocytes, bilirubin and urobilinogen, decrease haptoglobin
differences between mechanical and biological heart valves?
mechanical: longer life span, require oral anticoag-warfarin, INR 2.5-3.5
uses-bileaflet valves most commonly used, use in younger pts as lower revision rate, and those already on warfarin
biological-less durable, but don’t require long term anticoag, do take aspirin
used in older patients, women of child-bearing age and those with bleeding risk e.g. peptic ulcer disease, frequent falls.
how are patients with mitral regurgitation assessed?
ECHO, especially TOE
can look at left ventricular end-systolic diameter and left ventricular ejection fraction
indications for surgery in mitral regurgitation?
surgery can involve valve repair or valve replacement
general indications: severe MR and symptomatic
severe MR in asymptomatic patients with mild-moderate LV dysfunction-EF 30-60% and LVESD 4.5-5.5 cm
medical therapy in mitral regurgitation?
largely use of diuretics ? due to pulmonary HTN complication causing pulmonary oedema
if functional or ischaemic MR resulting from dilated or ischaemic cardiomyopathy, ACEIs may be of benefit
if LV systolic dysfunction present, ACEIs, beta blockers and CRT can all reduce severity of mitral regurge
how are patients with aortic stenosis monitored?
if symptomatic, no matter degree of stenosis, require referral to cardiologist
if asymptomatic and mild stenosis (mean valve gradient less than 25mmHg), annual OP r/v including ECHO
asymp and moderate stenosis, 6mnthly r/v and at least annual ECHO
asymp and severe stenosis, r/f to cardiologist for further assessment
indications for surgery in AS?
symptomatic, and any degree of stenosis
asymptomatic severe with LVSD
asymptomatic severe with abnormal exercise test-symptoms-angina, dyspnoea, syncope, ST changes, drop in BP
asymptomatic severe at time of other cardiac surgery e.g. CABG
investigations to be undertaken before aortic valve replacement in aortic stenosis?
coronary angiography and ascending aortography in older patients
CT scanning of aorta can help determine operative strategy
carotid scan in older patients as radiated murmur may mask underlying carotid disease
contraindications to a transfemoral approach in TAVI-trans catheter aortic valve insertion, in aortic stensosis?
valve annulus less than 18mm or more than 29mm
peripheral arteries less than 6-9mm in diameter
severe peripheral artery calcification or tortuosity
classic triad in aortic stenosis?
chest pain
heart failure
syncope
features of typical angina?
constricting discomfort in front of chest, or in neck, jaw, shoulders or arms
precipitated by physical exertion
relieved by rest or GTN within about 5 mins
all 3=typical angina
2=atypical angina
1 or none=non-anginal chest pain
what are the normal findings to be examined for when assessing the JVP?
JVP-assessed using R IJV
should normally be 4cm or less between sternal angle and upper limit of venous pulsation
2 waves per cardiac cycle: a wave=R atrial contraction, occurs just before S1, absent in AF
v wave- caused by atrial filling during ventricular systole when tricuspid valve closed
rarely c wave seen due to tricuspid valve closure
JVP falls with inspiration due to decreased intrathoracic pressure
JVP waveform obliterated by occluding vein at base of neck
abdomino-jugular test- JVP made to rise if abdomen if firmly pressed as increases venous return temporarily to R side of heart
ADRs of amlodipine-a dihydropyridine Ca2+ blocker?
oedema dizziness flushing headache nausea abdo pain palpitations fatigue
findings on examination of patient with atrial fibrillation?
irregularly irregular pulse-may notice that some heartbeats are not transmitted to the pulse-pulse defect if AF with fast ventricular response-inadequate cardiac output?-narrow complex irregular tachycardia, if all are ?sinus arrhythmia-HR increase on inspiration and decrease on expiration, ?not all transmitted if ventricular ectopics
BP-HTN could be cause of AF
overactive thyroid-tremor, tachycardia, goitre, exophthalmos, weight loss, pre-tibial myxoedema
displaced apex beat-HF
mid-diastolic rumbling murmur over mitral area, accentuated by asking pt to roll over onto their side, of mitral stenosis
evidence of HF-result of AF, raised JVP, ankle oedema, bibasal inspiratory medium crackles, gallop rhythm
patients with aortic regurgitation can remain asymptomatic for many years, when become symptomatic what is their common presentation?
exertional dyspnoea or reduced exercise tolerance
eventually chronic LV overload causes progressive LV dilatation and systolic HF.
how can the rate of LV dilatation in patients with AR be slowed?
give and ACEI to reduce afterload on the LV
surgery for aortic regurgitation?
open surgery for valve replacement
surgey for mitral stenosis?
percutaneous mitral balloon valvuloplasty
surgical mitral valve repair or replacement
must do TOE to determine most appropriate procedure
causes of mitral valve prolapse?
this refers to the flopping back of the mitral valve leaflets into the left atrium during systole, producing a mid systolic click on auscultation
due to excessively large valve leaflets, enlarged mitral valve annulus, abnormally long chordae or disorder papillary muscle contraction.
causes: IHD
rheumatic heart disease
thyrotoxicosis
marfan’s syndrome
polycystic kidney disease
valves most commonly affected by infective endocarditis?
mitral valve then aortic mitral and aortic tricuspid pulmonary (rarely)
features of digoxin toxicity?
cardiac arrhythmias-atrial tacharrhythmia and AVN conduction block-palpitations, syncope
dizziness
confusion
xanthopsia-yellow vision
what name is given to the plan that should be in place for all asthma patient?
personal asthma action plan
