pace your MRCP-PACES

*Announcement for Online Session No 89* *28 May 2023* DEAR DOCTORS : MAY I HAVE YOUR ATTENTION PLEASE : *Today we will have an online session on Zoom discussing 2 station 5 ( BCC )* 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. The candidates for today's session have been selected. GOOD LUCK.

*paceUrMRCP-PACES HALL OF FAME* We are thankful to our respected coalleagues who have made us proud by their success in PACES MRCP ( UK ). We believe that this number will keep on increasing 136.Dr Hanadi ( MRCPI ) 135.Dr Azher ( MRCPI ) 134.Dr Noman Hossain 133.Dr Abhinav Meelu 132.Dr Nurul Islam 131.Dr kadhaum ibrahem 130.Dr Inayut 129.Dr Susovan Mitra 128.Dr Bhavesh Kaswala 127.Dr Rashid Ali Khan 126.Dr Bisma 125.Dr Samiah 124.Dr Madiha Mahmood 123.Dr Ratan Kumar 122.Dr Dilfuza Usmanova 121.Dr Mohd Hafiz 120.Dr Colin Cheah 119.Dr Kuan Yau Yeh 118.Dr Satesh Ramasundram 117.Dr Calvin 116.Dr Wan Mohamad 115.Dr Aravinthan Balakrishnan 114.Dr Athirah Azizol 113.Dr Massum 112.Dr Rafa Faaria Alam 111.Dr Benojeer Akter 110.Dr Sonal Karpe 109.Dr Shahla 108.Dr Muhammad Faizal 107.Dr Aisha Sohail 106.Dr Sheetal 105.Dr Anand Kumar 104.Dr Paul 103.Dr Ehsan Ul Haq 102.Dr Amna Gardezi 101.Dr Muhammad Rahib 100.Dr Shilpa 99.Dr Nagaraj Patil 98.Dr Vincent Jose ( MRCPI ) 97.Dr Hana Abdalla Adam Mohamed ( MRCPI ) 96.Dr Thanuja Alahakoon 95.Dr Farehah ( MRCPI ) 94.Dr Sankar Nath Jha ( MRCPI ) 93.Dr Saadia Khan 92.Dr Montasir Elmobark 91.Dr Kiran 90.Dr Ai Yun Loh 89.Dr Eow 88.Dr Lim 87.Dr Lalitha 86.Dr Ashwin Mathew 85.Dr Kasthuri 84.Dr Rohit 83.Dr Sangshaptak Saha 82.Dr Hira Jamil 81.Dr Santa Subhra Chatterjee 80.Dr Shishir 79.Dr Rubeya Ahmad 78.Dr Javaria Imran 77.Dr Rishi Gopalakrishnan 76.Dr Ramandeep Kaur 75.Dr Shakeel 74.Dr Shamla 73.Dr Murtaza 72.Dr Urvashi 71.Dr Urmimala Bhattacharjee 70.Dr Jayalakshmi 69.Dr Steffin Methai Kattor 68.Dr Yew 67.Dr Cyrin 66.Dr Farhat Nazneen 65.Dr Meenal 64.Dr Adil 63.Dr Umar Iftikhar 62.Dr Sohail ( MRCPI ) 61.Dr Amarnath duraikannan 60.Dr Maha 59.Dr Samar 58.Dr Sidra German 57.Dr Mahmood Akhtar 56.Dr Muhammad Hashim 55.Dr Manmohan 54.Dr Pooja 53.Dr Haithem Alghebra ( MRCPI ) 52.Dr Amna 51.Dr Nandhakumar 50.Dr Ew Ju Vern 49.Dr Mohamed Muslim 48.Dr Jerry John 47.Dr Majid Iqbal 46.Dr Phoebe 45.Dr Aimi N Zainudin 44.Dr Tahseen Azim 43.Dr Samina 42.Dr Suzi 41.Dr Samia 40.Dr Tan 39.Dr Kalpesh Kondalkar 38.Dr Sunil Abhishek 37.Dr Faiz Mashood ( MRCPI ) 36.Dr Sharalaa Engatramana 35.Dr Prasad ( MRCPI ) 34.Dr Kalyan Nath ( MRCPI ) 33.Dr Reshma Thalikan 32.Dr Aneesa Shahul 31.Dr Arooj 30.Dr Esraa Soliman 29.Dr Amitave Chatterjee 28.Dr Malik Dilaver 27.Dr Ravi 26.Dr Priya 25.Dr Mujtaba Waris 24.Dr Shaheen Noman 23.Dr Apoorv Tiwari 22.Dr Niaz 21.Dr Janaki 20.Dr Lavanya Devi Palaniswamy 19.Dr Waqas 18.Dr Sadaf Hammad 17.Dr Osama Abdelaziz 16.Dr Rajeev Sharma 15.Dr Nehal Kunjomoidu 14.Dr Steffy 13.Dr Mustafizur Rahman (MRCPI) 12.Dr Vareeja Kasibian 11.Dr Niya Jamaludheen 10.Dr Farook Abdelgioum 9.Dr Kamran Ali 8.Dr Anik Rahman 7.Dr Manoj Dodiyah 6.Dr Madhusha 5.Dr Komal Zahid 4.Dr Hina Shaikh 3.Dr Sameer Abdus Samad 2.Dr Saurabh Gaba 1.Dr Rithik Mohan

*paceUrMRCP-Part 2 WRITTEN SUCCESS STORIES* We are thankful to our respected coalleagues who have made us proud by their success in MRCP ( UK ) Part 2 WRITTEN We believe that this number will keep on increasing 56.Dr Ayesha Kamran 55.Dr Sabiha Nusrat 54.Dr Ashif Istiak 53.Dr Kerolos Wagdy 52.Dr Ahmed mohamed 51.Dr Aqsa Khan 50.Dr Nabil 49.Dr Usman 48.Dr Hina Ali 47.Dr Abdul Wahab 46.Dr rabia islam abbasi 45.Dr Farina 44.Dr Ihsanullah 43.Dr Kunza tarar 42.Dr Jeevan Kumar 41.Dr Sowndhariya VA 40. Dr Hina Umar 39.Dr Berkas Khadidja 38.Dr Kiran 37.Dr Warda ( not in the group before ) 36.Dr Shaista Qamar 35.Dr Nasir 34.Dr Ahmed Sayed Hamada 33.Dr Shafiq ul Islam 32.Dr Jawaria Shuja 31.Dr May 30.Dr Aliyah Abdalla 29.Dr Ashraf Jafrani 28.Dr Muhammad Sher Ali 27.Dr Mumtaz ahmad 26.25.Dr Yousaf 24..Dr Salman Afridi 23.Dr Zaheer 22.Dr Mohammad Sohail 21. Dr Raed Khan 20.Dr Maria Syed 19.Dr Divya 18.Dr Cindy Heaster 17.Dr Hira Aftab 16.Dr Sajjad Ali 15.Dr John Wesley 14.Dr Ehdaa Mohammed 13.Dr Khorshed Alam 12.Dr Mohammed Abu Noman 11.Dr Alashima Rabie 10.Dr Karmel Omer 9.Dr Ghena 8.Dr Muhammad Zaheer Ahmed 7.Dr Sumaiya 6.Dr Amer Mazher Sethi 5.Dr Ashiru Sikirat Yetunde 4.Dr Sadaf Fatima 3.Dr Inas Abdullah 2.Dr Mehwish Usman 1.Dr Najwan

*paceUrMRCP-Part 1 SUCCESS STORIES* We are thankful to our respected coalleagues who have made us proud by their success in MRCP ( UK ) Part 1 We believe that this number will keep on increasing 53.Dr Stalin P John Benz 52.Dr MM Mohamed Sufad 51.Dr Aqsa Nizamani 50.Dr Kanta 49.Dr Munmun Nipa 48.Dr Suleman khan 47.Dr Sana Rafique 46.Dr Ali 45.Dr Izza 44.Dr Kerolos Wagdy 43.Dr Bushra 42.Dr Mubaraq Mustapha 41.Dr Bajrang Kumawat 40.Dr Iffat 39.Hotchand 38.Dr Banan Rasool 37.Dr Shilpi Shukla 36.Dr Usman 35.Dr Hasseeb 34.Dr Meena 33.Dr Ahmad 32. Dr Bushra Hossain 31.Dr.Mahwish Mustafa 30.Dr.Mehak Lakhani 29.Dr Nabil 28.Dr Zakia Zulfiqar 27.Dr Laxmikant Chavan ( MRCPI ) 26.Dr Hussain Baloch 25.Dr Jeevan Kumar 24.Dr Muhammad Usman Majeed 23.Dr Muhammad Shoaib Niazi 22.Dr Ahmed Abdelakher 21.Dr Sowndhariya 20.Dr Fatema 19.Dr Asifa 18.Dr Shabbir Ahmed 17.Dr Kiran 16.Dr Cindy Heaster 15.Dr Harshini 14.Dr Shiasta Qamar 13.Dr Jay Dev 12.Dr Nasir 11.Dr Jamila Noor 10.Dr Aparajita Day 9.Dr Haleem Baksh 8.Dr Salman 7.Dr Rabia 6.Dr Manjunath 5.Dr Barkas Khadija 4.Dr Afsana 3.Dr Imran 2.Dr Anam Qadeer 1.Dr Joyce Phua

*Announcement for Online Session No 89* *28 May 2023* DEAR DOCTORS : MAY I HAVE YOUR ATTENTION PLEASE : *Tomorrow we will have an online session on Zoom discussing 2 station 5 ( BCC )* 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.

*👉 IMPORTANT 673 👈* *Some info about heart sounds* The 2nd heart sound ( S2) Represents aortic ( A2 )and pulmonary valve ( P2) closure. The most important abnormality of A2 is softening in aortic stenosis. • A2 is said to be loud in tachycardia, hypertension, and transposition, but this is probably not a useful clinical entity. • P2 is loud in pulmonary hypertension and soft in pulmonary stenosis. • Splitting of S2 in inspiration is normal and is mainly due to the variation of right heart venous return with respiration, delaying the pulmonary component. • Wide splitting occurs in right bundle branch block (BBB), pulmonary stenosis, deep inspiration, mitral regurgitation, and VSD. • Wide fixed splitting occurs in atrial septal defect (ASD). • Reversed splitting (ie A2 following P2, with splitting increasing on expiration) occurs in left bundle branch block, aortic stenosis, PDA (patent ductus arteriosus), and right ventricular pacing. • A single S2 occurs in Fallot’s tetralogy, severe aortic or pulmonary stenosis, pulmonary atresia, Eisenmenger’s syndrome, large VSD, or hypertension. NB: splitting and P2 are heard best in the pulmonary area. Good luck.

*👉 IMPORTANT 672 👈* Please note that Elderly patients with BPH might be taking alpha 1 blockers which may cause postural (orthostatic) hypotension, a common case of dizziness in elderly patients in exams. examples (tamsulosin, prazocin) Good Luck.

*👉 IMPORTANT 671 👈* *Brief management summary for Ankylosing Spondylitis* The following is partly based on the 2010 EULAR guidelines : encourage regular exercise such as swimming NSAIDs are the first-line treatment physiotherapy the disease-modifying drugs which are used to treat rheumatoid arthritis (such as sulphasalazine) are only really useful if there is peripheral joint involvement the 2010 EULAR guidelines suggest: 'Anti-TNF therapy should be given to patients with persistently high disease activity despite conventional treatments' research is ongoing to see whether anti-TNF therapies such as etanercept and adalimumab should be used earlier in the course of the disease Good Luck

*👉 IMPORTANT 670 👈* *Few Investigations for Ankylosing Spondylitis* Inflammatory markers (ESR, CRP) are typically raised although normal levels do not exclude ankylosing spondylitis. HLA-B27 is of little use in making the diagnosis as it is positive in: 90% of patients with ankylosing spondylitis 10% of normal patients Plain x-ray of the sacroiliac joints is the most useful investigation in establishing the diagnosis. Radiographs may be normal early in disease, later changes include: sacroiliitis: subchondral erosions, sclerosis squaring of lumbar vertebrae 'bamboo spine' (late & uncommon) syndesmophytes: due to ossification of outer fibers of annulus fibrosus chest x-ray: apical fibrosis If the x-ray is negative for sacroiliac joint involvement in ankylosing spondylitis but suspicion for AS remains high, the next step in the evaluation should be obtaining an MRI. Signs of early inflammation involving sacroiliac joints (bone marrow oedema) confirm the diagnosis of AS and prompt further treatment. Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints. Good Luck.

*👉 IMPORTANT 669 👈* *Referral criteria for ankylosong spondylitis* NICE advise: all patients with suspected ankylosing spondylitis should be referred to a specialist 'Do not rule out the possibility that a person has spondyloarthritis solely on the presence or absence of any individual sign, symptom or test result.' Good Luck

*👉 IMPORTANT 668 👈* *Few clinical features of Ankylosing spondylitis* *Introduction* Ankylosing spondylitis is a HLA-B27 associated spondyloarthropathy. It typically presents in males (sex ratio 3:1) aged 20-30 years old. *Clinical features* *Features* typically a young man who presents with lower back pain and stiffness of insidious onset stiffness is usually worse in the morning and improves with exercise the patient may experience pain at night which improves on getting up *Clinical examination* reduced lateral flexion reduced forward flexion - Schober's test - a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible reduced chest expansion Other features - the 'A's Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis and cauda equina syndrome peripheral arthritis (25%, more common if female Good Luck

*👉 IMPORTANT 667 👈* *Few complications of ITP* Complications of treatment are related to side effects of specific drugs used for treatment of ITP. A referral to local haematology department is desirable to weigh up the risks and benefits of choosing a particular modality of treatment against the risks of bleeding. I.e. if platelet counts are stable and above a certain acceptable threshold (depending on hospital guidelines, i.e. >50 and asymptomatic), it may be reasonable to continue monitoring. Patients who received splenectomy require long term prophylactic penicillin V and pneumococcal/meningococcal vaccines. Most patients with ITP do not have severe bleeding. In a review of adult ITP cases in Oklahoma over a 10 year period, 83% patients were managed on an outpatient bases. Indications for inpatient management of ITP include: Large bleeding; Haemodynamic compromise; Intracranial haemorrhage; Platelet count of less than < 30. Inadequate response to conventional therapy agents. Good Luck

*👉 IMPORTANT 666 👈* *Some treatment options for ITP* ITP at first presentation should be referred to and managed by haematologists. The requirement for treatment varies between patient to patient; as such, clinical status is a key determinant for these considerations - i.e. asymptomatic, bleeding or planned surgical/dental procedures. Treatment is only given to those patients that absolutely require it, hence decreasing the risks of adverse effects such as infection as a result of immunosuppression. Below are the recommendations as according to British society of haematology. First line treatment for ITP is oral prednisone at 1mg/kg daily with proton pump inhibitors . This is given over a period of 2 - 4 weeks and weaned off a few weeks after. Most patients respond to this treatment within a week of commencing steroids. Pooled normal human immunoglobulin (IVIG) is also listed as first line treatment. Intravenous immunoglobulin is administered at 1g/kg. The mechanism of action is unknown but it was thought that one way is by blocking the Fc receptor of macrophages. Splenectomy had been used for many years, long before steroids were used. It is now second line for ITP in steroid refractory cases. It works by avoiding platelet destruction by removing the spleen. Other immunomodulatory drugs such as rituximab, cyclophosphamide and dapsone have also been used to treat ITP. Romiplostim works by activating the thrombopoietin receptor and stimulating JAK2, thus it stimulates platelet production. It has been approved by NICE as an option for ITP. Indications for usage include: ITP is refractory to standard active treatments and rescue therapies or Patients have severe disease and a high risk of bleeding that needs frequent courses of rescue therapies. Additionally it is important to avoid drugs which make bleeding worse. It is important to avoid antiplatelet drugs such as aspirin and clopidogrel. In cases of severe bleeding, it is important to treat promptly with transfusion of platelets, IVIG, tranexamic acids and initiate major haemorrhage protocol. Although transfusion of platelets may not improve platelet count, it has been shown to be effective at relieving the symptoms in acutely severe bleeding. Good Luck

👉 IMPORTANT 665 👈 *Some investigations for ITP* There are a number of investigations to be considered in patients presenting with bleeding and in those with incidental findings of thrombocytopenia. There is no single blood marker for ITP. Rather it is a diagnosis of exclusion. Minimum investigations to be done if thrombocytopenia is found include: Firstly, full blood count and blood film need to be requested. This would demonstrate isolated decrease in platelet counts, with normal counts in all other cell lineages. Additionally, there should be no evidence of fragments on the film. Secondly, a virology screen including HIV, EBV, hepatitis screen. Further investigations to be considered, as guided by history and examination findings: Clotting screen including PT and APTT, especially in those with severe bleeding. Thyroid function tests Malarial screen Myeloma screen. Immunological tests including ANA is considered especially if coexisting rheumatological features are present. Imaging including CT may be useful if there is a high index of suspicion for cancer. Bone marrow biopsy is no longer a standard investigation for ITP. If there are blood count abnormalities such as anaemia, leucopenia or other unexplained haematological findings, a bone marrow biopsy is warranted. In cases where ITP is not responsive to treatment and there is a high clinical suspicion for MDS, bone marrow biopsy should be carried out. Good Luck

👉 IMPORTANT 664 👈 Few differential diagnosis for ITP ITP is a diagnosis of exclusion. Thrombocytopenia can be caused by increased destruction of platelets, and/or reduced production of platelets. Important differential diagnoses to consider include: Non-immunological causes of increased destruction of platelets include disseminated intravascular coagulation (DIC) i.e. in the setting of sepsis or malignancy. Pregnancy and its complications such as HELLP syndrome can also cause thrombocytopenia. Chronic liver disease and hypersplenism is associated with thrombocytopenia. Thrombotic thrombocytopenic purpura (TTP) is life-threatening disease which presents with thrombocytopenia but can result in multi-organ failure, cardiac complications, strokes and other thrombotic events. The hallmark for DIC and TTP is the presence of fragments on the blood film. Additionally, drugs such as heparin may result in thrombocytopenia, known as heparin-induced thrombocytopenia or HIT. Immunomodulatory drugs such as gold, alemtuzumab and more recently immunotherapy agents such as nivolumab and pembrolizumab have been associated with ITP. Thrombocytopenia may be the first sign in well patients with underlying viral infections such as HIV or hepatitis. Many haematological malignancies can result in thrombocytopenia such as leukaemia, lymphoma, myelofibrosis, myelodysplasia and myeloma. Therefore it is important to take a careful history, as patients with these diseases often present with constitutional symptoms. Finally, rheumatological diseases such as SLE and rheumatoid arthritis can present with thrombocytopenia. Good Luck

👉 *IMPORTANT 663* 👈 *Some info about clinical presentation of idiopathic thrombocytopenic purpara ( ITP )* Approximately 1/3 of patients are asymptomatic and have incidental discovery on blood test. Approximately 2/3 of patients have bleeding. Commonly patients with ITP present to their doctors with petechiae , small red dots on the skin. Purpura , formed by petechiae joined together, can also occur. Mild epistaxis is common. Continuous epistaxis requiring nasal packing or cauterisation may pose greater risks of bleeding. In women, patients with ITP may have prolonged and heavy menstrual cycles. Very rarely, nonetheless the most importantly, ITP can present with intracranial bleeding; this occurs in 1.4% of the cases. Severe non-intracranial bleeds such as large gastrointestinal bleed occur in 9.6% of the cases. Patients with ITP can present as generally unwell, i.e. feeling lethargic. Occasionally, patients with ITP may present with strokes and TIA, often referred to as paradoxical thrombotic events in ITP. Good Luck

👉 *IMPORTANT 662* 👈 *Some info about pathophysiology of idiopathic thrombocytopenic purpara ( ITP )* ITP is an autoimmune disorder. In ITP abnormal immune system leads to destruction of own platelets . Although the precise mechanism for ITP is not completely understood, there have been several widely accepted theories: In ITP, autoantibodies are produced by the patient's B cells, principally of IgG. These target against platelet membrane glycoproteins GPIIb/IIIa. These platelets with autoantibodies are then engulfed by macrophages and degraded in the spleen. The bone marrow compensates by producing megakaryocytes (precursor to platelets). Purpura occurs as a result of increased permeability in capillary due to low platelets. In some cases, it is thought that viral infections can precede development of ITP. Antibodies against viral antigens cross react with normal antigens on platelet surfaces thus producing molecular mimicry. Good Luck

👉 *IMPORTANT 661* 👈 *Some info about aetiology of idiopathic thrombocytopenic purpara ( ITP )* It is thought that ITP is an autoimmune disorder resulting in antibodies produced to target against individual’s own platelets, leading to thrombocytopenia. This in turn results in petechiae and in rarer cases more severe bleeding. Furthermore, ITP can be primary or secondary. Primary ITP occurs when there is isolated thrombocytopenia is found with no co-existing conditions. Secondary ITP is associated with co-existing conditions. These include: Rheumatological diseases CLL Lymphoma Viral infections Various pharmacological agents Good Luck

👉 *IMPORTANT 660* 👈 *Important points in the management of sarcoidosis* *Indications for steroids* patients with chest x-ray stage 2 or 3 disease who have moderate to severe or progressive symptoms. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment hypercalcaemia eye, heart or neuro involvement Prognosis *Factors associated with poor prognosis* insidious onset, symptoms > 6 months absence of erythema nodosum extrapulmonary manifestations: e.g. lupus pernio, splenomegaly CXR: stage III-IV features black people Good Luck