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.
