pace your MRCP-PACES

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr Hanadi* For passing CLINICAL MRCP Ireland from Musqat. We wish her the best for her future.

*Announcement for Online Session No 88* *21 May 2023* DEAR DOCTORS : MAY I HAVE YOUR ATTENTION PLEASE : *Tomorrow we will have an online session on Zoom discussing 1 station 4 ( Communication Skills )* regarding our preparation for MRCP PACES ( UK ) TIMINGS : Saudia Arabia: 4 00 pm Pakistan : 6 00 pm Bangladesh : 7 00 pm India : 6 30 pm Singapore : 9 00 pm Hong Kong : 9 00 pm Malaysia : 9 00 pm Egypt : 4 00 pm Libya : 3 00 pm Bahrain : 4 00 pm Burma ( Myanmar ) :7 30 pm Sudan : 3 00 pm UAE : 5 00 pm UK : 2 00 pm Ireland ( Dublin ) : 2 00 pm Afghanistan : 5 30 pm Kenya : 4 00 pm Germany ( Berlin ) : 3 00 pm Nigeria : 2 00 pm Japan ( Tokyo ) : 10 00 pm Denmark : 3 00 pm Qatar : 4 00 pm Oman : 5 00 pm Italy : 3 00 pm Indonesia : 8 00 pm Mauritius : 5 00 pm Iraq : 4 00 pm Texas Usa : 8 00 am Kuwait : 4 00 pm ( please Google for your local time zones to avoid any inconvenience ) Zoom meeting link will be shared 5 minutes before start time. Interested candidate may send a personal message to take the case GOOD LUCK.

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr Stalin P John Benz* For passing MRCP UK part 1. We wish him the best for his future.

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr Pei Shing* For passing MRCP UK part 1. We wish her the best for her future.

*👉 IMPORTANT 655 👈* *Important points in the management of Psoriasis* Regular emollients may help to reduce scale loss and reduce pruritus First-line: NICE recommend a potent corticosteroid applied once daily plus vitamin D analogue applied once daily for up to 4 weeks as initial treatment These should be applied separately, one in the morning and the other in the evening Second-line: if no improvement after 8 weeks then offer a vitamin D analogue twice daily Third-line: if no improvement after 8-12 weeks then offer either: A potent corticosteroid applied twice daily for up to 4 weeks or A coal tar preparation applied once or twice daily Short-acting dithranol can also be used Good Luck

*👉 IMPORTANT 654 👈* *Few words about Chronic plaque psoriasis* Clinical features Erythematous plaques covered with a silvery-white scale Typically on the extensor surfaces such as the elbows and knees. Also common on the scalp, trunk, buttocks and periumbilical area Clear delineation between normal and affected skin Plaques typically range from 1 to 10 cm in size If the scale is removed, a red membrane with pinpoint bleeding points may be seen (Auspitz's sign) Good Luck

*👉 IMPORTANT 653 👈* *Few words about prognosis of SAH* If SAH is untreated the prognosis is often poor: around 50% within 1 month of the haemorrhage, and of those who survive the first month, 50% will remain dependent for help with activities of daily living. However, survival improves to 85% in patients with confirmed SAH admitted to a specialist neurosurgical unit. Good Luck

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr Azher* For passing CLINICAL MRCP Ireland from Musqat. We wish him the best for his future.

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr Aqsa nizamani* For passing MRCP UK part 1. We wish her the best for her future.

*✌✌ HEARTIEST CONGRATULATIONS ✌✌* To *Dr MM Mohamed Sufad* For passing MRCP UK part 1. We wish him the best for his future.

👉 *IMPORTANT 652* 👈 *Few complications of aneurysmal SAH* Re-bleeding (in around 30%) Vasospasm (also termed delayed cerebral ischaemia), typically 7-14 days after onset Hyponatraemia (most typically due to syndrome inappropriate anti-diuretic hormone (SIADH)) Seizures Good Luck

👉 *IMPORTANT 651* 👈 *Few lines about treatment of Subarchanoid Haemorrhage* The treatment in spontaneous SAH is in accordance with the causative pathology Intracranial aneurysms are at risk of rebleeding and therefore require prompt intervention, preferably within 24 hours Most intracranial aneurysms are now treated with a coil by interventional neuroradiologists, but a minority require a craniotomy and clipping by a neurosurgeon Until the aneurysm is treated, the patient should be kept on strict bed rest, well controlled blood pressure and should avoid straining in order to prevent a re-bleed of the aneurysm Vasospasm is prevented using a 21-day course of nimodipine (a calcium channel inhibitor targeting the brain vasculature) and treated with hypervolaemia, induced-hypertension and haemodilution Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or, if required, a long-term ventriculo-peritoneal shunt Good Luck

👉 *IMPORTANT 650* 👈 *Few investigations for the diagnosis of Subarchanoid Haemorrhage* *Confirmation of SAH:* Computed tomography (CT) head Acute blood (hyperdense/bright on CT) is typically distributed in the basal cisterns, sulci and in severe cases the ventricular system. CT is negative for SAH (no blood seen) in 7% of cases. Lumbar puncture (LP) Used to confirm SAH if CT is negative. LP is performed at least 12 hours following the onset of symptoms to allow the development of xanthochromia (the result of red blood cell breakdown). Xanthochromia helps to distinguish true SAH from a ‘traumatic tap’ (blood introduced by the LP procedure) Referral to neurosurgery to be made as soon as SAH is confirmed After spontaneous SAH is confirmed, the aim of investigation is to *identify a causative pathology* that needs urgent treatment: CT intracranial angiogram (to identify a vascular lesion e.g. aneurysm or AVM) +/- digital subtraction angiogram (catheter angiogram) Good Luck

👉 *IMPORTANT 649* 👈 *Few Clinical features of Subarchanoid Haemorrhage* Classical presenting features include: Headache: typically sudden-onset (‘thunderclap’ or ‘baseball bat’), severe (‘worst of my life’) and occipital Nausea and vomiting Meningism (photophobia, neck stiffness) Coma Seizures Sudden death ECG changes including ST elevation may be seen Good Luck

👉 *IMPORTANT 648* 👈 *Few causes of Subarchnoid Haemorrhage* The most common cause of SAH is head injury and this is called traumatic SAH . In the absence of trauma, SAH is termed spontaneous SAH . The rest of this note focuses on spontaneous SAH. Intracranial aneurysm* (saccular ‘berry’ aneurysms): this accounts for around 85% of cases. Conditions associated with berry aneurysms include adult polycystic kidney disease, Ehlers-Danlos syndrome and coarctation of the aorta Arteriovenous malformation Pituitary apoplexy Arterial dissection Mycotic (infective) aneurysms Perimesencephalic (an idiopathic venous bleed) Good Luck

👉 *IMPORTANT 647* 👈 *Few causes of weight gain* Depression Hypothyroidism Corticosteroids: side-effects Chronic heart failure Polycystic ovarian syndrome Chronic kidney disease Sulfonylureas: side-effects Cushing's disease Focal segmental glomerulosclerosis Membranous glomerulonephritis Minimal change disease Good Luck

👉 *IMPORTANT 646* 👈 *Brief management of Wilson,s disease* penicillamine (chelates copper) has been the traditional first-line treatment trientine hydrochloride is an alternative chelating agent which may become first-line treatment in the future Zinc has also been used. tetrathiomolybdate is a newer agent that is currently under investigation Good Luck

👉 *IMPORTANT 645* 👈 *Few investigations for Wilson’s disease* Reduced serum caeruloplasmin Reduced serum copper (counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin) increased 24hr urinary copper excretion Good Luc

👉 *IMPORTANT 644* 👈 *Some clinical features of Wilson’s disease* The onset of symptoms is usually between 10 - 25 years. Children usually present with liver disease whereas the first sign of disease in young adults is often neurological disease Features result from excessive copper deposition in the tissues, especially the brain, liver and cornea: liver: hepatitis, cirrhosis neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, parkinsonism, dementia Kayser-Fleischer rings renal tubular acidosis (esp. Fanconi syndrome) haemolysis blue nails Good Luck

👉 *IMPORTANT 643* 👈 *Some info about Wilson’s disease* Wilson's disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues. *Pathophysiology* Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson's disease is caused by a defect in the ATP7B gene located on chromosome 13. Good Luck