Patient Flashcards
An adult patient presents with signs and symptoms giving you suspicion of Asthma. What is the initial plan of management?
6 weeks of low ICS
then review in 3 months
smoking cessation
Adult patient returns after initial step of management complaining of asthma symptoms persisting and not getting better. How do you escalate further?
How would you escalate further still if the Pt. symptoms remain uncontrolled?
*+SABA (salbutamol) and ICS
then if not better => +LABA (salmetarol) or MART
Patient returns to you saying asthma symptoms are not getting better after being prescribed salmetarol in addition to their salbutamol and ICS. What is the next stage of management?
Add-ons:
- INCREASE [ICS]
- LAMA (
- +LTRA
Patient w/ acute asthma attack presents to AE. They have received nebulised SABA already as well as O2 and remain unwell. What would you next prescribe?
Steroid: prednisolone (SOS).
If stays worse, escalate with IV SABA, IPRA, or IV Mg.
Child presents to AE with acute asthma attack. What is the plan of treatment?
O2 via face mask or NC
oral prednisolone
nebulised salbutamol
After initial treatment, child patient’s acute asthma attack persists (already on O2, had oral prednisolone, and nebulised salbutamol)?
+IPRA (neb) (+ nebulised Mg)
2º:
IV SABA
+ Aminophylline
IV Mg. sulphate if poor respiratory funct.
What are risk factors for PE in a patient?
- sedentary
- pregnancy
- combined oral contraceptive
- smoking
Patient presents with query PE in AE. What is first line Tx?
WELLS
anticoagulation: offer apixaban or rivaroxaban.
If neither of these are suitable, alternatives include:
Low molecular weight heparin (LMWH) for at least 5 days followed by dabigatran or edoxaban.
LMWH concurrently with vitamin K antagonists for at least 5 days.
Note relevant bloods:
full blood count, renal and hepatic function, prothrombin time (PT) and activated partial thromboplastin time (APTT).
Patient in AE presents with suspected pneumothorax of less than 2cm on CXR. What are Tx options?
What are Tx options if pneumothorax much larger?
observe but if symptomatic: needle aspiration (2nd intercostal midclavic)
For large pneumothorax: O2;needle aspiration (2nd intercostal midclavic); and talc-pleuredesis if Pt is high-risk/recurrent.
What qualifying findings would you expect in an adult patient presenting with severe acute asthma attack?
- PEF 33–50% best or predicted
- RR 25+
- HR 110+
- inability to complete sentences in one breath
=>
Patient (70 y/o)presenting with Shortness of breath, chest pain, dry cough and fatigue, with working history of construction labourer 44 years ago. Family have noticed Wt. loss. No significant smoking Hx. Suspected pleural effusion. Nil signs of infection.
Pleural effusion secondary to malignant mesothelioma, think ASBESTOS EXPOSURE (occupation).
=> biopsy and imaging ESSENTIAL!
A patient presents with progressive non-productive cough, exertional dyspnea and general exhaustion developed. Nil infection but atelectasis in lower lobes.. LFT show restrictive nature with BAL revealing active inflammation.
PMHx: started immunotherapy 2 months ago for MS
Thoughts?
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7510011/)
- acute restrictive disease (no significant lung infection or chronic lung disease) and significant LFTs
- DAD: exudate stage
- Drug-induced (Type (C)HRONIC if dose-related and can alleviate, Type B if definite drug allergy nature)
In what direction would you expect a foetal O2 dissociation curve to shift to?
Shift to the left giving higher affinity of Hb for O2 at lower PP ensuring good ventilation allowing greater O2 loading since maternal O2 decreases d/t mother’s consumption
(same as organisms living at higher altitudes w/ lower O2)
What adaptations do higher metabolic muscles’ haemoglobin require to be advantageous? What direction will their curves shift at and why?
Fast metabolic cells require LOWER AFFINITY to achieve HIGHER UNLOADING of O2 to surrounding cells/tissue; therefore the O2 dissociation curve would shift to the RIGHT
