OSCE Flashcards
What are the indications for a CT head following an acute head injury?
Within 1 hour:
- GCS<12 on first assessment
- GCS <15 2hrs following injury
- Suspected open/depressed skull fracture
- Sign of base of skull fracture - panda eyes, CSF leakage, bruising behind ears
- Post-traumatic seizure
- >1 episode vomiting
- Focal neurological deficit
Within 8hrs:
- anyone on anticoagulation or with a coagulopathy
What is the medical management options for type 2 diabetes?
- 1st line → metformin
- Once settled, add SGLT-2 inhibitor if the following are present → existing CVD, heart failure, or QRISK >10%
- 2nd line → sulfonylurea, pioglitazone, DPP-4 inhibitor, SGLT2 inhibitor
- 3rd line → triple therapy, insulin therapy
- 4th line → if triple therapy fails & BMI >35, switch one of the drugs to a GLP-1 mimetic
How does metformin work & what are the common side effects?
- Mechanism → increases insulin sensitivity & decreases glucose production by the liver
- S/E → GI symptoms (pain, nausea, diarrhoea), lactic acidosis secondary to AKI
NB: no weight changes or hypoglycaemia
What are the 2 main examples of SGLT-2 inhibitors, how do they work, and what are the side-effects?
- Examples → dapagliflozin, empagliflozin
- Mechanism → block Na-Glucose transporters in the kidneys causing increased glucose secretion in the urine. Also cardio/reno-protective.
- S/E → glycosuria, polyuria, genital infections, UTI, euglycaemic DKA
NB: causes weight loss, and doesn’t cause hypoglycaemia by itself
What is the main example of a sulfonylurea, how does it work, and what are the side-effects?
- Examples → gliclazide
- Mechanism → stimulate insulin release from the pancreas
- S/E → Weight gain, hypoglycaemia, hyponatraemia
What are the examples of a DPP-4 inhibitor, how do they work, and what are the side-effects?
- Examples → sitagliptin, alogliptin
- Mechanism → allow increased incretin activity (increased insulin secretion, inhibiting glucagon production, slowing GI absorption)
- S/E → headaches, low risk of acute pancreatitis
- Hypoglycaemia → no
- Weight changes → no
What are the differentials for an ejection systolic murmur? How are they differentiated?
Ejection -> aortic stenosis or pulmonary stenosis
AS -> crescendo-decrescendo, loudest over aortic area, radiates to carotids
PS -> loudest over pulmonary area, widely split S2
What are the differentials for a pansystolic murmur? How are they differentiated?
Pansystolic -> mitral/tricuspid regurgitation, VSD
MR -> loudest over mitral area, radiation to axilla
TR -> loudest over tricuspid area, loudest during inspiration
What is the cause of a late systolic murmur?
mitral valve prolapse -> mid-systolic click followed by mid-late systolic murmur
What is the cause of an early diastolic murmur?
aortic regurgitation -> decrescendo, loudest at LSE or aortic area, collapsing pulse
What is the cause of a mid-late diastolic murmur?
mitral stenosis -> low pitched, rumbling, opening click in mid-diastole
What is the secondary prevention given following ACS?
(6As) -> Aspirin, Another antiplatelet, atorvastatin, ACE inhibitors, Atenolol, Aldosterone antagonist (if CCF)
How is hyperkalaemia managed if >6.5 and/or there are ECG changes?
If K+>6.5 and/or there are hyperkalaemia ECG changes, then urgent treatment is required.
Stop further accumulation -> stop IVF with potassium, appropriate medications or supplements
Stabilise cardiac membrane if ECG changes-> 10mls 10% calcium chloride
Shift K+ intracellularly -> insulin-glucose infusion (10 units insulin & 25g glucose over 30 minutes), salbutamol
Remove K+ from body -> K+ binders, correction of underlying cause, haemodialysis if unresponsive
How is hypoglycaemia managed?
Management if conscious:
- 15-20g fast-acting carbohydrates or glucose gel by mouth (glucogel)
- Repeat BMs after 10 minutes, if still low then repeat gel a further 2-3 times
- Then provide a longer-acting carbohydrate, eg toast
Management if unconscious:
- IV glucose -> 150ml 10% dextrose
- If patient regains consciousness, then switch to oral
- If IV access not available, then glucagon 1mg IM or SC
How is SVT managed?
Management if life-threatening features -> synchronised DC cardioversion under sedation/GA. IV amiodarone if initial shocks (x3) are unsuccesssful
Management if NO life-threatening features
Vagal maneuvers -> Valsalva (blow hard into a 10ml syringe for 15s), carotid sinus massage (check for carotid bruit)
Adenosine -> slows cardiac conduction through AVN, give rapid bolus into large proximal cannula, warn patient of impending doom feeling. Doses are 6mg, 12mg, 18mg
If unsuccessful, either the adenosine is being metabolised before it reaches the heart, or this is actually a ventricular tachycardia
Verapamil or beta-blocker
Synchronised DC cardioversion
Wolff-Parkinson White Syndrome
Do not give adenosine, verapamil, or a beta-blocker -> these will block the AVN, promoting conduction through accessory pathway, causing life-threatening ventricular rhythms.
