Ultimate Finals List - Writtens

1st paper (SBA path +)*
* Picture of ECG: was difficult choices were ectopic (supraventricular or
ventricular), capture or fusion beat
* X-ray pictures:
- ARDS in pancreatitis
- Mantoux test +ve/-ve
- Gram stain: group B strep, campylobacter
- Knee X ray: fractured? compound?
- Lumbar X ray: ank spond
- Hand X ray: rheumatoid hand
* Path pictures (mostly from Utah path site)
- mesothelioma
- pneumonia
- CLL or CML
- adeno/squamous oesophageal ca
- myeloma
- PE
- question on focal segmental glomerulonephritis
* Epidemiology questions: do questions on LAPT lite as these are very
similar and some have been transferred from T/F to SBA format.
* Picture of eyes: bilateral ptosis (hx consistent with myasthenia)
* Diagram of blood levels of antigens/antibodies in HIV (it's in baby Kumar
and Clarke) and ask to label one of the lines (although they ended up
withdrawing this question as wasn't printed well).
* Slide of giardia
* Picture of psoriasis and question surprisingly on pathophysiology of
psoriasis
* Detailed question about high dose/low dose dexamethasone suppression test,
length of test
* Question on gallstones and knowing significance that colour of gallstones
is yellow
* Many questions on interpreting sodium/potassium, ALP, Ca

*2nd paper*
* Do and know all questions from Moodle, 2 came up (question on hyoscine for
dying patient and question on lung function)
* AF management
* Scleritis
* Chronic supparative otitis media
* Pleomorphic adenoma
* CSF changes with viral encephalitis
* Polycythaemia - primary or secondary? Few questions on this.
* Paralytic ileus, causes
* Rx of hyponatremia: water restriction?
* Anal fissure
* Haemorrhoids
* Ulcerative colitis treatment
* Vomiting in adult: pyloric stenosis
* Lateral medullary syndrome
* Headache: cavernous sinus thrombosis
* Acute glomerulonephritis
* Carpal tunnel syndrome: hand pain in man with DM
* 1st thing would do in anaphylactic shock
* Acne treatment
* Woman with sores around mouth
* Breathlessness in GP setting: would give salbutamol?

Ultimate Finals List - Cardiology

Cardiology Stations

• CABG, heard no heart sounds initially, then listened again and again, then thought dextracardia, then got asked what sternotomy scar could indicate
• CABG, aortic valve replacement and systolic murmur, all due to alcoholic liver disease (?) // Gentleman with a very impressive nicotine stained beard! Plus AF, a raised JVP, midline CABG scar, clicking valve replacement and graft scars on his leg. We had to examine, report our findings and then state what drugs we would expect him to be on 
• Cardiology st: Pt looked well. Had midline sternotomy scar and click THUD which I could hear from end of bed. Pt had no other leg or arm scars. I said it was aortic valve replacement and talked about infective endo.Then time was up. I wish there had been time to recite the causes of AF!
• Cardio - prosthetic at S2, midline sternotomy. Asked about how I knew it was aortic. When I would replace the valve. Porcine vs prosthetic
• Cardiovascular- Patient with sternotomy scar. I couldn’t hear a metallic click (in fact he had incredibly quiet heart sounds) and started to panic when I looked for a scar on the upper thigh but couldn’t see one. So I presented and said if it was a CABG I would expect a scar which was not present. At that point the examiner pointed out a scar near the guy’s ankle! It turned out he had had a CABG and valve replacement (biological) and I was asked what valve was most likely to have been replaced and why. I didn’t know and guessed the mitral- wrong! I didn’t mind this station as it all seemed to make sense and the examiner was lovely.
• CVS – Aortic valve replacement, had collapsing pulse, asked for BP, examiner said 160/60 (wide pulse pressure). Auscultation revealed a click at S2, midline sternotomy scar also. Also a diastolic murmur heard with patient sat forwards in expiration. Asked for diagnosis and reasons for my thinking it is aortic regurgitation.
• CVS - Not 100% certain, CABG scar, and ankle scar, loud 2nd sound, but not metallic, I gave CABG and aortic (porcine) valve replacement (examiner said I did really really well). Unable to hear the mitral heart sounds (everyone found this).
• The patient had a large sternotomy scar and metallic sounding S2 and some people also heard a murmur and he had AF. I only mentioned the prosthetic valves and said it was a aortic valve replacement because of the position of the scar and because I heard it loudest in the aortic area. He seemed happy enough with that cos I saw him tick the pass box.

• Mitral valve replacement in a Marfans patient - then asked about JVP waves
• CVS - young afro-Caribbean lady with a midline sternotomy scar - when palpating for her apex beat I could hear the clicking sound of a valve replacement without even my stethoscope! Nice straightforward station - presented my case and gave some differentials as to the type of valve (mitral/aortic etc), examiner asked what else I would consider giving the patient (warfarin with INR between 3-4) and that was about it // Cardio – MVR – mechanical, heard from bedside!! Q’s on likely causes, warfarin

• CV - lady had clubbing and a metallic valve with massive midline sternotomy, which I thought was aortic valve replacement but now I think was pulm secondary to Fallot's. Asked about what I thought she had and why, and complications of valve replacement

• Cardiology – Radial scar with sternotomy scar and mechanical aortic valve!! Patient had a CABG replacement with the radial artery, and an AV replacement. REMEMBER if there is a scar on the radial side and NO pulse use the other hand, many people made the pulse up!!// CARDIO- the lead in was this lady has high cholesterol and hypertension, please do an cardiovascular examination. I had done a specialist module in cardiology so I was pretty confident with my murmurs, however, this lady had no murmurs, the only things I could find were quiet heart sounds in the aortic and pulmonary regions, and a very weak left radial, I presented my findings and was asked about the causes of a weak left radial, I started going through a list of things I had learnt and then I said possibly cardiac catheterisation via the right radial artery for angioplasty/stent insertion, I think that’s what he wanted as he didn’t ask me any more

• Cardio - difficult, very loud systolic murmur and obvious artifical valve sound (? ball and cage) loudest at left sternal edge, no radiation. Pt had massive sternotomy scar which looked like it had been re-opened at least once. Also thought she had a waterhammer pulse. Examiner asked me which valve, we had been told by numerous consultants that it would be either a mitral or an aortic pathology so I guessed aortic. Examiner didn't seem too bothered but asked me to look at her abdomen and arms, covered in what looked like multiple biopsy or cigarette burns - had no idea. Turns out pt was a former IVDU and thus it was tricuspid valve replacement - haven't met anybody else who got it yet, most people said mitral though

• Congenital cyanotic heart disease with a right-left shunt. I was asked about causes of central cyanosis.

• Cardio exam - irregular pulse in thin old man with rheumatoid hands, no peripheral oedema. JVP very elevated. Thrill over mitral valve. Systolic murmur, louder on expiration and leaning forward, radiated to carotids not to axilla. I said it was aortic stenosis, examiner guided me to mitral valve prolapse.
• Patient had AF and mitral prolaspe, I thought it was Aortic stenosis but the examiner was very nice and led me round to describing mitral prolapse. He then asked me about the pathogenesis of mitral regurg and how it caused LVF

• Some thought it was aortic stenosis but others thought it was mitral regurgitation. He had subconjunctival haemorrhage which they also wanted you to note and this tied in with his being on Warfarin

• CVS - AF and aortic stenosis. Causes, investigations and managament of aortic stenosis and asked about pulse deficit in AF

• Cardio – gentleman with a beautiful pansystolic murmur also heard at the apex but NOWHERE else. Almost too good to be true. Anyway he also had a pacemaker so had to discuss reasons why – big MI I suggested as likely although he was quite thin and the examiner seemed to enjoy taking a few of us along the HOCM route...
• cardio: excellent station...MR murmur, but apex was undisplaced, examiner asked: give me differentials of just systolic murmurs: MR, VSD, TR, AS, A sclerosis, PS....then he said one investigation: ECHO......y is his JVP raised if he doesn’t have oedema or crackles or other signs of HF....the bell went and I said not sure n he said ur right its difficult to say why!:)
• This was quite straight forward until the questioning. Examiner was again ridiculously nice. The case was mitral regurgitation. The examiner asked me to name the causes (which was fun!). When I said Marfan’s, the examiner asked me what valve is more commonly affected with Marfan’s, I said aortic and he nodded and smiled (see..nice!!!). Then when I said mitral valve prolapse, he also asked me the causes of mitral valve prolapse. He then asked what I would hear with a mitral valve prolapse, I said a mid systolic click and he nodded again. Then he asked me the clinical features of mitral valve prolapse, I think he was getting at signs of left ventricular failure. Then he asked me how many cusps the mitral valve has. I had a moment of madness when I said 2..er no 3....er no 2......about twenty times. He then asked me which cusp more commonly prolapses with mitral valve prolapse, I do believe the answer was anterior (because he told me) but I'm not repeating my answer here because I had a REAL moment of madness!!! Still passed though (despite the examiner laughing in my face).

• My CVS station was AS. Nothing much to say. maybe transoesophageal vs transthroracic echo, and when to have surgery
• Cardiovascular exam: Young Patient with audible clicking and midline sternotomy scar. Ejection systolic murmur radiating to the carotids. Asked about causes of aortic stenosis (marfan’s?)

• Blalock shunts

• Examine pulse, JVP, precordium of Harvey, mitral stenosis & tricuspid regurg // With Harvey, we were told that 'the patient has ankle oedema and bibasal crackles, please examine his precordium' .the murmur was pansystolic, radiating to axilla and was associated with S3 and S4. I said mitral regurg but the examiner kept pressing me saying 'but it can't just be mitral regurg, what is it?' I didn't understand and didn't get the answer, but after my time was up I asked what he meant and the answer he wanted was biventricular failure. causes of mitral regurgitation
• Harvey – cardiac murmur simulator – told to inspect and auscultate the precordium only without talking and then to present our findings. Was mitral regurgitation. Displaced apex beat, Pansystolic murmur @ apex radiating to axilla – s1 obliterated, s3 present giving short diastolic sound. Normal splitting in Pulmonary area, Normal in Aortic area and Tricuspid regurgitation at the tricuspid region - Asked Dx (chronic MR with TR due to R sided dilation). Ask what would do – look for signs RH Failure and do an echo. Asked re causes (I said Rheumatic heart disease, SBE, MV Prolapse and Pap muscle Rupture (although said last would be acute so no displ apex). Told under ECHO that the valve was normal – what is the cause ? No idea I guessed must have been cardiomyopathy. Bell went and as I was leaving I was asked what I would look for on Examination – I said signs of alcohol use?! No idea what he wanted there as I had already mentioned RH failure signs>?
• HARVEY cardiac patient simulator. He had dilated cardiomyopathy but most people said mitral regurgiation.

• CVS - aortic stenosis and mitral regurgitation

• There was a soft ejection systolic murmur which I said was a flow murmur, and he asked the other possible reasons that there could be a flow murmur but I didn't know so he moved on.

• HARVEY (mitral regurg and 3rd heart sound)

• 2 murmurs to trick me! mitral regurg and aortic stenosis both radiating loudly... everywhere, in a really talkative patient making it rather difficult to auscultate the pracordium!

• CVS: VSD

• Tetrallogy of fallot!!

• cardio - was asked to explain my understanding of pulmonary hypertension and right sided heart failure and how this might fit with the murmur

• cardio- great my cardio patient must of been ill so I got a normal medical student! no murmurs after all those hours of learning! however his intro led u to believe it may be hocm, however examination was normal. I was then asked why else he may have collapsed while playing football on a hot summers day. duh dehydration- I forgot to do cap refill!

Ultimate Finals List - History Stations

History Stations

• Take a history of abdo pain...he had renal colic and told me when the bell went his urine was pink! You had to specifically ask if there was blood in the urine/changed colour- otherwise he said it was all normal. 
• ... next station was a follow on...u had to ring up the hospital and on the phone refer ur patient n the doc on the line asks u why u referring and what management plan do u propose...pt had a family history of gout so I said to screen for that, analgesia and further investigations cos he was male // Telephone referral of the case - not sure what they wanted. Finished way early. Looked like an idiot again as asked to speak to the med registrar, so the examiner hiding behind the screen said he was the surgical reg.. oh I said.. no, I want you!! :S // Talk to a Dr on a fake phone, I didn't check who I was talking to - so I gave all of the info to the man who picked up the phone, which could have been anyone- so check! // He then asked you for a differential and what tests you wanted to do. They provided you with urine analysis results and examination results, which confirmed renal stones - no signs of inf, but haematuria, plus tenderness in the loins 

• Cough hx, due to ACEi, so never omit the drug history. Was even asked about why ACEI give you cough and ATR blockers don’t. I discussed a chemical building up in body, normally broken down, some people mentioned bradykinin specifically. I’m not sure how much technical info a patient would want to hear // but u must say at the end that well change ur antihypertensive medication and see if cough improves n if it doesn’t well call u back in for more tests. cos they waned u to discuss a management plan with the pt in the quest // Smoking history with 40 pack year history, hence differentials are ACEi cough and maybe some underlying cancer of the lung. 

• History - diabetes history from knowledgeable patient, asked about complications. Had no differential diagnosis to make. 
• Hx Diabetes Mellitus in 19 yo girl with abdo pain and weight loss

• Splenectomy + pancreatectomy, HCV + HIV etc. 

• Hx - Rheumatoid Arthritis. You get 5 minutes before you start but no info. So just wrote down headings and surreptitiously studied the patient for clues! History taking was fine, but I missed the clue about TB in the family - he didn’t want to go on biologicals because of the risk of TB reactivation. Also re chronic conditions make sure you ask about previous medications patient have been on rather than just the current ones. Presented a differential diagnosis at the end. I also forgot smoking and alcohol till I heard my neighbour ask about it swiftly followed by the next door cubicle too! Questions on how to monitor RA (Esr/ Crp I think) How to diagnose, Dmards, how to protect vs possible Tb reactivation. Cjd from biologicals possibility? Should people with RA have joint replacements? Was straightforward I think. // rheum arthritis, also going through MJ THREADS was important as patients had TB in the past and lots of people didn’t pick that up. Asked to present the hx then asked about differentials, what the drugs were Anti TNF therapy what it was, Ix I would do...I mentioned anti ccp and the examiner seemed very impressed. // History for 20 mins from pt then 10 mins of qus from examiner. Lovely patient with rheum arthritis and kidney failure. Then she went out and I was asked about her meds etc and differentials for her kidney failure. I then asked examiner what the cause of it actually was- he didn't know! So I think as long as you gave a differential, it was fine. // Others histories that came up: stroke, scleroderma examiner asked me about RA so known ur stuff about chronic conditions in particular!! she waned to know all the drugs she was on and their side effects especially steroids and she was also on etanercept so u must say u give it when 2 DMARDS including methotrexate have failed hence don’t forget to ask patient if they’ve been on methotrexate ever like I did!!

• Hx Adhesions 

• History - guy with MS. Needed to elicit that his main problem was urinary dysfunction 

• Peripheral vascular disease in a man who smokes and drinks a lot!!!! Take a good social history because most of his problem list was to do with this and I spent most of my time discussing his drinking and smoking with the examiner as opposed to his PVD. General questions I got asked about PVD was investigations and management (conservative, medical and surgical). In terms of his drinking, she asked me how I would know that he has problem drinking - eye openers, interference with work and social/family life, putting alcohol above all other priorities and if he's ever been admitted into hospital with an alcohol related illness. It turns out he's on iron tablets. You are asked how this relates to his drinking - GI bleeds? 
• hx - 25year history or arterial and venous disease. Discussion of all surgical options and complications of such disease

• SAH history (Know Cushing’s response) 

• Ankle swelling history - patient was on amlodipine 

• Focused history - Chest pain - given a short case scenario of a woman who presented with epigastric pain radiating round both sides 'like a strap' worse when hungry, not on any medication. ECG and cardiac enzymes show no features of MI. - take a history and then answer examiners questions - patient had no CVS symptoms other than the chest pain, but had features suggestive of peptic ulcer disease/GORD. - examiner asked: whats ur differential diagnosis (GORD/PUD/DUD); what further investigations could you do; and what the management would be if patient had PUD (examiner stressed MEDICAL management, didnt want any conservative management! hurried me along!) Overall comment: you don't have very long to do the history so it's important to focus in on the really important things eg. does patient smoke/drink lots of alcohol/use of NSAIDS important if suspecting PUD etc.. Triple therapy for treating H Pylori
• answer questions about PUD and its aetiology/risk factors/diagnosis/management - had to ask if taking any medication over counter cos only then she said NSAIDS and paracetomol.... . // As I was leaving I was asked what it was important to rule out – said cancer and that I should have asked the patient about weight loss. The examiner asked how I would investigate this possibility and I said endoscopy. 

• Patient had rectal bleeding and history of aortic dissection, bladder cancer and angina. Asked about bladder cancer. 
• Hx - Bleeding episodes PR twice yesterday on background of weight loss and increased diarrhoea with mucous in a 59 year old lady with an aunt who has just been diagnosed with colorectal carcinoma.
• ... Writing a referral letter to hospital re: PR bleed - write referral letter to Med Reg on call regarding an urgent referral for this woman – quite tight for time. 

• Hx lady with Marfans - presented with 12 year hx of back pain. Asked diff dx, then why you get lens dislocation and mx of patients with marfans. Examiner was impressed when I said genetic counselling. 

• history - a man with hypothyroid, this was annoying - presenting complaint was just increasing tiredness. eventually got to the fact that he had carpel tunnel as well. // TATT -  History of tiredness...pt is only tired absolutely no other symptom...okay this comes up yearly n we figured that last year she had a change in her diet so you had to ask in particular have you changed ur diet...but this yr when I asked that she said no...so I asked r u a veg and she goes yes for 20 yrs she’s been a veg!!! only other problem was weight gain in past 5 months...so hypothyroid??? but examiner didn’t ask any questions so still not sure what her prob was exactly.
• History station – tiredness. She was a vegetarian, taking vitamin tablets, recent weight gain, slightly depressed. Take a full focused history, and then give differentials (main were anemia, depression and hypothyroidism), then mention to patient you will take some blood tests looking for anemia and thyroid problems and will review her later at GP // Hx - tiredness (vegetarian and swollen glands and sore throat: ?infectious mononucleosis) - told her I would ix her for anaemia, TFTs, EBV, depression hx- tiredness. // Young girl with tiredness for 2 months, some bowel problems, a viral infection a few months ago, vegetarian (but had been all her life). No heat/cold intolerance or menstrual changes. No idea. He asked what bloods I would do at the end and I said Fbc but it wasn’t until I was on the tube home that I thought of TFTs! and to keep a food diary for review

• Some weird skin condition where the patient had what looked like multiple skin tags for a history taking station (not neurofibromatosis - it was really random, but the friend of mine who had this didn't know what either of these things was and still got a distinction, so I don't think they really care that much about you getting the correct diagnosis).

• Had to take a history from a guy who had been vomiting small amounts of blood for the past two days and who had a family history of gastric cancer which he was worried about but no other symptoms. He was taking shed loads of ibuprofen for a sprained ankle. Learning point: make time for the drug history!!!
• ... 10) Referral letter for above patient. This was a strange station, we had to refer the patient we had taken a history from for further investigation, the main issue here was time and getting all the patient details down.
• History station on Gastrointestinal stromal tumour. Viva mainly on upper GI bleeds, differentials, emergency treatment etc.

• Hx – Chronic Pancreatitis – asked differential, problem list, summary etc. + causes, Ix, differences between chronic and acute
• Hx - BPH
• ... Referral for patient above via telephone - examiner kept asking what else??

• Hx - Acute shortness of breath. O/E legs for swelling - signs of tension pneumothorax and P.E management.

• Hx station - Stevens Johnsons syndrome (doesn't really matter what the Dx is - just have to take a thorough Hx and then summarise, give DDx, problem list, management plan)

• History - IHD

• Hx - crohn's disease - Dx, Rx, prognosis, aetiology etc

• Hx - perianal abscess in lady with nonspecific colitis - causes, crohns, diabetes, COPD, Qs on diabetic Cx and Ix of colitis

• My history was really hard as the patient was jaundiced, but had left abdo pain, urinary frequency and a hx of diverticulitis. I couldn't put it together but stuck to my format for the history and it must have gone OK because my score was good in the end

• History of feeling odd with frothy urine and a rash - SLE // History of gentleman with recently diagnosed hypertension (i.e. that day) and urine dip showing nephritic syndrome. Nice history of two months increasing tiredness and joint aches and spotty red rash over legs and gluteals ... Can you guess what it is yet... Two questions – most likely diagnosis and which investigations // History from a person with hypertension, with protein and blood in urine. Does not have any cardiovascular risk factors...was kinda stuck because secondary causes such as phaechromocytoma and coarctation of aorta could not be ruled out. Turned out infact patient had a rash and diffuse joint ache. Other students said the patient had SLE?? Asked what 2 investigations would you do? Answer depended on what you got out of the history, I went for renal ultrasound and ECG. // Urinalysis with nephrotic syndrome picture - history taking of hypertension, haematuria and proteinuria. - You are a GP and a patient who has just moved house had just registered- has a urine dipstick and u get given the result - ++++proteinuria and ++blood He had swollen ankles and face and a rash on shine 2/52 agon ? Nephritic sx? Asked 3 Ix would do. . 
• Think most people like me fumbled around with renal failure as most likely diagnosis and said we'd like to do U&E, FBC, glucose, creatinine clearence... and prayed for the bell to go... I said SLE, although other people think it might have been IgA - who knows? // history of (i think) glomerolonephritis secondary to SLE. He didn't question my diagnosis anyway like he did with other people who said things like pyelonephritis, nephrotic syndrome. Asked to name three tests you would do eg urine culture, microscopy, U and Es, autoantibodies for SLE

• History station - obstructive jaundice

• Hx station: very long and complicated UC history from a real patient but they just wanted to see hoe you cope with taking a complicated history.

• I had a stable patient with diabetes brought on by steroids she was on for Crohn's. Quite straightforward Others had diabetes, SLE, and there was one with gauler's disease which noone had heard of!!

• Liver transplant history

• Hx - pt with lymphoedema and median nerve compression post-radiotherapy for breast cancer
• History of a 79 year old woman with a history of breast cancer. “Please talk to this woman regarding any problems she had with this diagnosis”. More psychological rather than medical but still talked briefly (in the history and with the examiner afterwards) about triple assessment, oestrogen receptor inhibitors, staging and grading and non-medical treatments for breast cancer.

• I got SLE (I almost cried). the patient had recently been discharged from hospital with heart failure, but I asked her every question under the sun (systems review in the best!) and she was feeling very well and had no rashes or anything. She mentioned that she sometimes gets "cold fingers" and the penny dropped after that. The examiner was really nice and asked me to present my findings as a problem list. I was then asked about the features of SLE and why this patient had heart failure. I said cardiomyopathy (which I think might have been wrong) and then pericarditis/pericardial effusion (which I think made more sense). I was asked about investigations for the patient and how often I would review this patient in clinic. I said monthly for the first six months then perhaps six months. I actually was making it up.

• History: (20 mins observed + 10 mins questions) This was ridiculous. My young patient was referred to clinic with recurrent shoulder dislocations and stretchy skin. She had long complicated history involving hyperextendible joints and operations for shoulder and broken tibia, fundoplication for GORD, arthroscopies. She had osteoporosis and secondary amenorrhea because of a pituitary adenoma. On many meds - remember to ask about doses and any side effects. Diagnosis was Ehler Danlos. Differentials include osteogenesis imperfecta, Marfans, pseudoxantha elasticum. Examiner then asked questions about ED - what type of collagen affected? how would you treat? referrals? At the end the examiner said he would never have expected to see an Ehler Danlos patient in finals and that he did not feel it was fair. I did ok though!

• History – 30 minutes station, 17 minutes history, rest of time questioning by examiner. I had history of elderly man with chronic fatigue and episodes of melaena. Main differential was colon cancer. Take a FULL history, you have 5 minutes before station starts to read the scenario and write whatever questions you may want to ask so use this time efficiently to write down differentials etc before you have even taken the history. Examiner then asks you to present the history briefly and then asks for differentials, investigations and a management plan.

• Other people had a scleroderma history (shortness of breath and skin changes so know that inside out).

• Remember they like chronic diseases for histories, like HIV (nasty one as you need to know about anti retrovirals and their side effects etc), rheumatoid, SLE, IBD (UC and Crohn’s is world famous history to come up). // Hx - HIV clinic please take Hx of lady with known HIV. Turns out she has a cough, so disuses differential/management afterwards with

• hx of woman who had lung ca 4 yrs ago, had to find out how this affected her life. I was only asked questions about things I brought up. for example, when asked what investigations I would do I said fbc to start looking for high calcium - I was asked how having cancer may raise your calcium. and how on a scan they may differentiate cancer from fibrosis due to previous radiotherapy

• long hx- Mine was on thyroid cancer- initially hypothyroid, then developed thyroid cancer & Mx. A nice history in comparison to what other people got. The questioning was relatively difficult, but the doctor was very nice and there's not much you can do to prepare for it anyway

• History – took history from patient with history of several valve replacements and infective endocarditis more recently. Then asked questions by examiner on infective endocarditis and valves etc.

• Long History station - was a little baffled by this at first, the instructions were just to take a full med history from this lady, who when I asked for her presenting complaint, said 'I don't know dear, I've come in today because I always come in for exams and the doctors asked me to'. But just moved onto her PMH etc and she had a lot to go through, to which I really had to rush by the end to get a complete history! But then the 10 min discussion I just presented my case (who had diabetes, AF, OA, cancer of the breast and skin, a stroke and a few other chronic problems) and then was asked how I would manage these different parts as a GP. Again

• Hx - Patient is new to GP practice. Please take her medical history. My patient just would not stop talking and kept going off on tangents. At 17mins, I was still on HPC. Had to rush through social hx. Moral: feel free to interrupt patients!!

• History of acute cord compression and a linked station with the next one being a telephone referral (which was actually really fun!)

MI & Liver Enzymes

Remember - does the investigation rule out/in? Dx

MI Enzymes

CK
- rises 3-6hrs after event
- only 50% pts show rise > ULofN @ 4hrs
- CK rises by over 50% over 12 hrs

CK-MB
- rises earlier than CK
- 3% CK-MB in skeletal muscle
- rhabdomyolysis = raised absolute levels
- better test = CK-MB/CK

+
Sys + ECG
CK-MB to confirm CK

Troponin

Myofibrillar protein fr damaged cells
- subtypes inc trop-T/trop-I
Measured at 12hrs post onset
Elevation persistent up to 10 days
Can indicate low-grade myocardial damage before infarction, requiring acute treatment
Good specificity

Liver Enzymes

ALT - cytosolic enzyme

ALP - biliary brush border enzyme
GGT - ribosomal test, x liver specificity

Enzymes

Raised Levels
*most significant finding
- increased synthesis/cell proliferation
- cell membrane damage
- cell death
- defective/slow blood clearance
Level increased can = extent of injury
Isoenzyme = greater tiss specificity

Enzyme profiles

1) tissue of origin
2) isoenz pattern in tiss
3) timing in relation to disease
4) lab availability

Normal variations of enzyme levels

1) Age/sex variation in reference range (ALP higher in adolescents)
2) Race (CK higher in afro-Caribbean)
3) Analytical interference (transaminases & LDH - haemolysis from red cells)
4) Renal failure (Amylase increased, as excreted renal-ly)
5) 'Macro enzymes' - binding of enzyme to immunoglobulin - lowers rate of degradation
- primary protein (immunoglobulin) disease eg myeloma
- temp
- *CK & AMY
- = req alt of Ix w/ documentation

Dx

MI
CK & CK-MB
troponin (non-enzyme)

x transamimases/LDH

Liver
ALT
ALP
GGT

Pancreatitis
Amy

Skeletal

CK for muscles
ALP for bone

Osteoporosis

Reduction in bone mass via loss of matrix
Excessive bone loss
Normal mineral:matrix ratio

Causes
Old age (post-menopause)
Endocrine
 - premature ovarian failure (early menopause)
- Cushings
- thyrotoxicosis
Drugs
Steroids
Heparin

Ix
pl Bone profile = normal
DEXA
- Identify fast bone losers
- Monitor therapy (HRT, bisphosphonates)

Osteomalacia

...aka rickets in children

Defective mineralisation of bone (calcium deficiency) + Increased osteoid

Causes
Dietary/Malab - Ca/vit D def
x Exp to sunlight
Disordered vit D metabolism
- renal Dis (decreased 1-hydroxylation)
- vit D-dep rickets (1alpha-hydroxylase def)
- a-convulsive therapy (induces metabolism)
Low phosphate (Renal Tubular Leak)

Ix
low sCa & PO4
high ALP (osteoblastic response) - interpret with age-related ref range
low circulating 25-OH cholecalciferol (?diet def)
elev sPTH (2ry HPThm)

Hypocalcaemia

Hypocalcaemia

Sy & Si
MSK - numbness, parasthesia, muscle cramps, convulsions
+ve Chvostek's & Trousseau's signs

Bone - myopathy & bone pain (low vit D)

Eyes - cataracts (chronic)
Brain - behav disturbances

Ix

ECG = Prolonged QT

Causes (NB hypoalbuminaemia)
Low vit D
Disordered vit D metabolismm (eg Renal Failure)
hPTH (congenital, AI, post Thyroid Sx, infiltrations)
PseudohPTH (PTH resistance)
Mg depletion (impaired PTH synthesis/release)
Acute pancreatitis
Neonatal
Massive blood transfusion (citrated blood)
Artefactual ( Blood sample collected into EDTA/citrate)

hCa + low/undetectable PTH = hPTm

hCA+elevated PTH = non-PT causes (except pseudo hPT)

Hypercalcaemia

"Bones, Stones, Abdo Groans & Moans"

Si&Sy
GI - Anorexia, N&V, Abdo pain & Constipation, Peptic ulceration & Acute pancreatitis
Renal - Polyuria & polydipsia, calculi & nephrocalcinosis, renal failure
CVS - HTN, heart arrhythmias
MSK - weakness, lassitude
Eyes - corneal calcification
Mental changes
Underlying Disease

Causes
*
1ry HPTH (1/1000)
Malignancy (*myeloma)
- Bony mets
- Tumour - PTH related peptide
- Tumour - HCa agonists
Other
Sarcoidosis (increased calcitriol synth)
Vit D intox
3ry HPTH (eg CRF - post Tx)
Immobilisation (Paget's, Adolescents)
Thyrotoxicosis (severe)
Tz diuretics
Familial hypocalciuric HCa (v rare)

HCa + supp PTH = non-PTH Cause
HCa + raised/detectable PTH = PTH-mediated cause

Calcium Haemostasis

Haemostasis
Skeleton = 1kg/25000mmol/99% body Ca
Dietary Intake of Ca = 25mmol/day
Exchange between ECF and bone = 10mmol/day
*renal (imp in regulation)
GIT... also involved

Pathology
... occus with...
- Gut, renal, skeletal problems
- Parathyroid disorders
- Abnormal Vitamin D metabolism

Ix
*Total plasma calcium
plCa = alb-bound 40%, complexed 10%, free ionised fractions 50%
Ionised Ca = active fraction - roles in bone, teeth, neuromuscular activity, coagulation (enzyme co-factor)

Corrected Ca = Ca + 0.02(40-Albumin)


Parathyroid Hormone
Increase in PTH - stim by
 - low Ca
 - raised PO4 (Chronic effect only)
Only intact PTH is active
...act on...
Kidneys
 - incrs Ca reabsorption
 - decrs PO4 reabsorption
 - decrs HCO3 reabsorption
 - incrs 1-alpha-hydroxylation of vit D (activated)
Bone
 - incrs osteolclastic resorption


Vit D
Dermal synthesis & Diet
Liver = 25-OH cholecalciferol - 'inactive'
Renal = 1,25 dihydroxycholecalciferol (calcitriol - 'active')
Calcitriol stim by...
- low ionised Ca (via PTH)
- low PO4
- low vit D
Calcitriol acts on...
- gut = incrs Ca & PO4 absorption
- renal = incrs Ca & PO4 reabsorption
- bone - incrs resorption/mineralisation, remodelling


Calcitonin (Thyroid 'C' Cells)
hCa actions
- stim by increased Ca ions

Septicaemia

Bacteraemia = "presence of bacteria in blood"

Aet
- N flora - access to bloodstream
eg dental & soft tissue abscesses/cholecystitis/appendicitis/diverticulitis/upper renal tract infection
- **prosthetic surgery (orthop, CVS, neuro) - prosth can be 'seeded' by organism & infect irrev
- Pneumonia - S pneum
- Skin - S pyogenes/S aureus

Sy&Si

Asy (pray that it's not)
or
Severely ill
Fever (absent with child/eld)
Shock (later presentation)
Depressed consciousness (confused/drowsy)
?GN-ve vs G+ve - cannot clinically differentiate

h/e signs poss...
- N meningitidis - purpura
- S Aureus - embolic lesions
- N Gonorrhoeae - arthritis

Dx
x2 peripheral blood cultures b4 Tx
Septic screen
- blood cultures

- urine cult

- sputum cult

- CSF

- skin swabs

- CXR/AXR
- abdo US

Tx
1) empirical DO NOT WAIT!!! - BSp

Empirical Therapies

Skin - strep & staph
-Flucloxacillin
Abdo sepsis - enterobacteriaceae & obligate anerobes
-Ceftazidime & metronidazole/meropenem
Prosthetic devices - staphylococci
-Fluclox/vanc
Urinary Tract - enterobacteriaceae & enterococci
-Piperacillin/tazobactam (init if Hosp acq & sev)
Meninges - N Meningitidis, S pneumoniae, H influenzae
-Benzyl penicillin/Cefotaxime

Line-related septicaemia
- increased risk with time
- S aureus, S epidermidis, Klebsiella
- look for inflammation - remove if susp infection

- Ix - blood cultures from peripherally through cannula
- Tx - ABs, Glycopeptide (MRSA)

- Prevention - ANTT, device w/o dead space/side ports, good dressing, staff hygiene, regular inspection, periph resited every 48hrs, central & tunnelled lines - inspection changed with evidence of infection

- Cx - septicaemia, endocarditis, metastatic infection (eg OMyelitis)

Puerperal Fever
Sev
*bacteraemic infection
Entry of pathogens throo placental bed/cervix following delivery
*w/i 7d of deliv

Sy
Fever
Back pain
Offensive lochia
Shock

Ix

Fever - if in early puerperium = Ix! - bl/ur cult/endocervical swabs

Tx
Empirical
3rd gen cephalosporin & metronidazole
Remove any retained products of contraception
Intensive care if necess

Cx
DIC

Systemic Causes of Haematological Changes #3

Liver Disease

Bleeding
 - deficiency of vitamin K factors (II, VII, IX, X), Factor V, fibrinogen
 - functional abnormalities of fibrinogen
 - increased fibrinolytic activity
 - decreased plts (Hsplen, direct alcohol effect)
 - portal HT - varices

Anaemia
 - bleeding & iron deficiency
 - alcohol - direct toxic effect
 - folate def (megaloblastic An)

 - Hsplen
 - Hlysis - alcohol, Copper (Wilson's), AI (a/w hepatitis)

Red cell changes (macrocytosis, target cells, spur cells)


Chronic Renal Failure

Bleeding

 - abn plt function
 - thrombocytopenia (AI, HUS)

Anaemia
 - decrsd erythropoetin production
 - Fe def (dialysis, venesection, poor plt function)
 - aluminium toxicity
 - folate def (chr dialysis)
 - Hlysis (HUS)
 - anaemia of chronic disease

Red cell changes (Burr cells, fragmented cells in HUS)

Anaemia
 - chronic disease
 - Fe deficiency (Chronic bleeding, *GI tract tumours)
 - immune haemolytic anaemia *NHL
 - pure RC aplasia a/w/ thymoma
 - BM infiltration (extensive)
 - folate deficiency (anorexia, drugs)


Polycythaemia
 - erythropoietin-producing tumours eg kidney, cerebellum, liver

Platelets & coagulation
 - thrombocytosis - eg GI bleeding, reactive
 - DIC - eg mucin-secreting carcinoma
 - coagulation factor aB - eg to factor VIII


Hsplenism
Incrsd pooling, sequestration, destruction

Causes An, Leucop, Tbcytop

Hyposplenism

- splenectomy
- sickle cell dis

- essential thrombocythaemia
- adult coeliac dis

Splenic function impaired by
- corticosteroids
- radiation

Haematological changes
RCCs:
- Target cells

- Howell-Jolly bodies (DNA remnants)

- siderotic granules (iron-containing)

- nucleated RBCs

WCCs:
- early after splenectomy = Nphilia
- ltr = lymphocytosis, monocytosis

Plts:

- early post-splen = marked tbcytosis
- ltr = plts slightly elevated

Cxs:
Increased risk of fulminant infection (*encapsulated bact, malaria)
- S Pneumoniae
- N meningitidis
- H influenzae

Tx

Life-long prophylactic penicillin/erythromycin (prior to splenectomy if poss)
Immunisation - pneumococcus, HiB, meningococcus

Systemic Causes of Haematological Changes #2

Acute Phase Reactants
- general indication of inflammatory resp
eg
Fibrinogen
Complement
CRP
Haptoglobin
Ferritin
Serum amyloid protein

Ix
Presence & extent of inflamation + resp to Tx


ESR
Red cell sedimentation through plasma in 1hr
 - cheap
 - dependant on plasma concentration of large proteins - immglob/fibrinogen
 - raised - chronic infection/myeloma/dissem malig/AI
 - aff by red cell concentration - low in polycythaemia & high in An

Normal range
Men < 5mm/hr
Females < 15mm/hr
Increases with age


Plasma Viscosity
n(1.5-1.7 mPa/s)
15min test
Slight increase with age
Unaffected by red cell changes


CRP
Rapid increase to tiss inj (4-6hrs)
Highly sens
Unaff by RC Changes

?poss - paraproteinaemias

Systemic Causes of Haematological Changes #1

White Cell Changes

Neutrophilia
> 7.5
- Bacterial infection - localised (eg abscess), disseminated (eg septicaemia)
- Inflammation/necrosis - eg MI, vasculitis
- Malignant disease
- Myeloprofilerative disease - eg CML
- Metabolic disease eg uraemia, gout
- Corticosteroid Tx

Leukaemoid reaction
WBC > 50 nt fr leukaemia
Lymphocytes/Neutrophils +/- immature forms
- Severe infections - bacterial eg pneumonia
- Viral - eg infectious mononucleosis
- Severe haemorrhage/haemolysis
- Malignant disease
- Intoxications - eg burns, eclampsia

Ix
BM aspirate/trephine Bp
BM cytogenetics
BM film - Np Granulocytes/Myelocytes
(NB identical to CML, therefore test for Philadelphia chromosone)

Leukoerythroblastic change
Blood shows - nucleated RBCs & primitive WBCs
- Marrow invasion - eg metastatic tumour, Hm malignancy (eg myeloma/lymphoma), fibrosis
- Severe illness - eg trauma, septicaemia, massive haemolysis

Ix
BM trephine biopsy

Neutropenia
< 2
Isolated/pancytopenia

Isolated
- Drugs eg phenylbutazone, co-trimoxazole, carbimazole, anti-psychotics
- Racial
- Congenital eg Kostmann's syndrome, cyclic
- Infections eg hepatitis, typhoid, TB, malaria
- AI eg Felty's, SLE, idiopath

Pancytopenia
- MF - any cause (aplastic anaemia, megaloblastic anaemia, irradiation, malignant infiltration)
- Hypersplenism

Eosinophilia
> 0.5
- Allergies eg asthma, drugs, hayfever
- Parasites eg ankylostoma, ascaris, filaria
- Skin eg eczema, psoriasis, dermatitis herpetiformis
- Malignancy eg Hodgkin's disease
- Inflammatory disease eg sarcoidosis, PAN
- Hypereosinophilic syndrome
- Eosinophilic leukaemia

Hx - for travel, Dx, allerg
Ex - skin, lungs, joints
Ix - as above, stool examination (parasites), RhF, CXR

Lymphocytosis
> 3.5
- Acute infection - *viral eg rubella, mumps, infectious mononucleosis
- Chronic infection - TB, brucellosis, hepatitis
- Thyrotoxicosis
- CLL
- Other Leuks & Lymphomas

Hx - viral illness/night sweats/WL
Ex - throat, LNs, liver, spleen

Viral serology - EBV

Marrow Failure - Myelodysplasia

MDS (myelodysplastic sydromes/myelodysplasia)

Acquired clonal d/o fr haemopoetic stem cells

Epid
Pts *> 70 yrs

Ix & Path
Cytopenias - *An

Morphological evid of dysplasia in blood & BM cells
BM - cellular/Hcellular (NB difference to AA)

Aet
*idiopath
Prev cytotoxic CTx/RTx

Dx
Typical dysplastic changes of Blood & BM
+ Clonal cytogenetic abnormalities on chromosomal examination of BM cells

Prognosis
3 variables
 - % immat blast cells in BM (low blast = best)
 - cytogen abnorms
 - no of cytopenias

Tx

- Supportive - red cell transfusion, iron chelation Tx after multiple transfusions, recombinant erythropoetin therapy
- Cytotoxic CTx - for AML, h/e poor response rate
- Differentiation therapy eg 5-azacytidine (accelerates differentiation of MDS clone, so normal stem cells can regain dominance)
- StC transplantion - definitive cure; only poss 4 small fraction of younger pts

Cx

MDS - *AML

Marrow Failure - Aplastic Anaemia

Features:
- Pancytopenia
- Hypoplastic marrow
- Low reticulocyte count

Si&Sy
Infection/bleeding/anaemia

Causes:
Congenital
Fanconi's (not*)
Acquired
Idiopathic - *AI reaction to BM Stem Cells - eg T suppressor lymphocytes
Radiation - RTx/Occ
Chem - Benzene TNT, DDT
Drugs - Cytotoxic Dx (requires frequent FBCs), other
Viruses

Viral Causes

 - Hepatitis

 - EBV

 - ParvoV

Non-cytotoxic Drug Reactions

 - Chloamphenicol

 - Zidovudine

 - Gold

 - Phenylbutazone

Tx

Remove cause

Supportive - red cell transfusion, ABs, plt transfusion

Stim BM Stem Cells - anabolic steroids

Severe AA
- Np < 0.5
- Plts < 20
- Transfusion-dependant Hb

Tx
BM transplant
- <45yrs
- with HLA matched donor avail
ATG/ALG (anti-thymocyte globulin)
 - removes inhibitory T-cells
 - H/e SE: temp thrombocytopenia & serum sickness
Immsupp
- cyclosporin
- HD steroids

Marrow Failure - Thrombocytopenia

Thrombocytopenia

Decrease in plts prolongs bleeding

(>50 is still okay)
Important to know in case of invasive procedures eg LP

Sy
Purpura/mucosal bleeding

Tx
Plts < 10 = daily transfusion of plt concentrate obtained w/i last 72 hours

Relatives/HLA-matched donors - plt-pheresed on cell separator
Short life-span, so in 24h = x sustained increase in no.

Plt count unreliable mesr of effectiveness

Effective transfusion?
1) Cessation of bleeding
2) Incrs in plt count >20 over baseline, after 1 hr-post transfusion

Problems

HLA aBs in pt (if not matched)

Continued plt consumption at bleeding sites

Marrow Failure - Leucopenia

***Neutrophil count !!!

<1.0 = pyogenic infection
<0.5 = severe risk

FNEs (Febrile Neutropenic Episodes)

Temp = 38.5 x1 or 38x2 w/i 1hr

Ix
Clin exam - severe infection poss from minor inj
Blood M,C&S
Throat sub

MSU

Tx
BSp ABs + change according to sensitivities/if unresponsive to BSpectrum ABs
Continuing fever after ABs = admin of IV anti-fungal agents (amphotericin)

Prophylaxis in Np patients

Barrier Isolation (filtered air & sterile food) = Severely Immunocompromised
Alternatives = Compromise isolation/Home
Compromise isolation = xVisitors with active infections, xFood with bacteria eg cheese, glove & gown

Oral anti-fungals eg nystatin/amphotericin (against oral candida)
x prophylactic ABs except poss LD co-trimoxazole for post-transplant and AIDs pts (against PCP)

Leucocyte Transfusion - from - normal donor treated with G-CSF/pts with chronic granulocytic leukaemia (due to higher no of circulating Nps)


Lymphopenia
Increased risk of viral infections/pneumocystis

Prophylactic aciclovir (against herpes) until T-lymphocyte count > 0.2
Marrow transplant causes immunosuppression * with GVHD
CTx (nucleoside analogues eg fludarabine) also cause immunosuppression

Marrow Failure - Anaemia

Symptoms
Tiredness
Dyspnoea
Angina

Ex
Pale mucous membranes eg eyes

Tx
Transfusion = Packed cells/plasma reduced red cells (NB vol overload)
Adult = 1 unit of blood : 1g/dl in Hb
Aim in-patient = Hb 9-10g/dl
Severe An (Hcrit<.30) = Prolonged BT & can worsen Tbcytopenia

Transfusion reactions
Prev transfusions = antibodies against blood components
eg
- HLA Ag (found on WC & plts)
therefore can = NHFTRs (non-haemolytic febrile transfusion reactions) - from dead WC&Plts in red cells units

Immunocompromised
Require CMV-ve (found dormant in lymphocytes) blood
40% UK donors CMV-ve
Patient CMV aB+ve status useful to establish

Cx
Heart failure

Bone Marrow Failure

Marrow Failure
=
Pancytopenia i.e.
Anaemia
Leucopenia

Thrombocytopenia

2 types

- Hypocellular (empty)

- Infiltrated (competes with normal marrow & normal haemopoetic cells)

Hypocellular
Aplastic Anaemia
Myelodysplasia (can be cellular)
CTx
RTx

Infiltrated
2ry causes (lung/prostate/breast/thyroid/kidney)
Acute leukaemias
Lymphomas
Myeloma

Differentials of Chest Pain

Cardiac
- Angina
- MI
- Myocarditis/Pericarditis (pleuritic)
Pulmonary
- Pneumonia
- Pleurisy
- PE
- Pneumothorax
Gastrointestinal
- GORD
- Oesophageal Spasm
- Peptic Ulcer Disease
Musculoskeletal
- Muscular Strain
- Costochondritis
- Rib Fracture
Other
Anxiety

Infectious Diseases - Empirical Therapies

Skin

Cellulitis

Strep. pyogenes
± Staph. aureus

Mild/Moderate (oral)
Penicillin V + flucloxacillin
or Co-amoxyclav alone
or Erythromycin alone (if penicillin allergic)

Severe (IV)
Benzylpenicillin + flucloxacillin
or Co-amoxyclav alone

Bones & Joints

Osteomyelitis & Septic Arthritis
Staph. Aureus

Streptococci

Staph Epidermidis

ALL CASES ARE SEVERE
IV Flucloxacillin (+ fusidic acid for osteomyelitis)
or Clindamycin alone

ENT Infections

Sinusitis & Otitis Media

Viruses
Strep. pneumoniae

Haemophilus influenzae

Nothing
or Amoxycillin
or Erythromycin

Throat Infections

Viruses

Strep. pyogenes

Nothing

or Penicillin V

or Erythromycin

Respiratory Infections

Community Acquired Pneumonia
Pneumococcus (Strep. pneumoniae)
‘Atypicals’

- Mycoplasma pneumoniae

- Chlamydia pneumoniae

- Legionella

Mild/Moderate (oral)
Amoxycillin 

+ Erythromycin (if ‘atypical suspected’)

or Erythromycin alone

Severe (IV)
Co-amoxiclav

or 2nd/3rdgen. cephalosporin + Macrolide

Pulmonary tuberculosis

Mycobacterium tuberculosis

Rifampicin + Isoniazid + Pyrazinamide + Ethambutol (2 months)
Rifampicin + Isoniazid (4 months)

Acute Exacerbations of COPD
Pneumococcus (Strep. pneumoniae)

Haemophilus influenzae

Moraxella catarrhalis

Amoxycillin + Clarithromycin

or Tetracycline (if penicillin allergic)

Urinary Tract

Urinary Tract Infection
E. Coli (60-90%)
Proteus (10%)
Klebsiella

Mild/Moderate (oral)
Trimethoprim (unless pregnant)
or Amoxycillin

or Nitrofurantoin

or Ciprofloxacin
(A 3-day course is usually sufficient)

Severe (IV)

Co-amoxiclav

or 2nd/3rd gen. cephalosporin ± gentamicin

GI Tract Infections

Gastro-enteritis
Often viral and self-limiting
No antibiotic usually indicated

Campylobacter
Ciprofloxacin

Salmonella
Ciprofloxacin

Typhoid fever
Ciprofloxacin

Pseudomembranous colitis
Oral metronidazole

or Oral Vancomycin

GI Tract Surgery & Peritonitis - Antibiotic Prophylaxis and Treatment

Staph. aureus (wounds)
Mixed faecal flora including anaerobe

2nd/3rd gen. cephalosporin + metronidazole

or Co-amoxyclav alone

Meningitis

Meningococcus (N. meningitidis)

Pneumococcus (Strep. pneumoniae)

Haemophilus influenzae

ALL CASES ARE SEVERE

Ceftriaxone IV

Prophylaxis for Meningococcal contacts

Rifampicin

or Ciprofloxacin

Septicaemia

Many possible causes

‘Blind therapy’ is broad spectrum + additional cover for strong clinical suspicion
Definitive therapy based on culture results

Community Acquired

Ceftriaxone ± gentamicin
Add Metronidazole if anaerobes suspected
Add Flucloxacillin is Staph. aureus suspected
Add Vancomycin if MRSA suspected

Infectious Diseases - Antibiotics Profiles

General Principles

Empirical Therapy

Likely organisms

Severity of infection

Investigations
Microbiological:
Swabs
Fluids e.g. sputum, urine, aspirates
Blood culture
Serology

Bloods

FBC

Inflammatory markers

Radiology

Review Progress

Clinical

Cultures & Sensitivity

Adverse Effects

Penicillins
Inhibit bacterial cell wall synthesis
Well tolerated:

Rash (common)

Anaphylaxis (rare)
Excreted in urine
‘Safe’ in pregnancy
Destroyed by beta-lactamase (S. aureus and some anaerobes)

Except:

Flucloxacillin - beta-lactamase resistant

Amoxycillin & clavulinic acid - beta-lactamase inhibitor, may cause jaundice

Benzylpenicillin (IV) or Penicillin V (oral)
Gram +ve (strep)
Meningococcos
Gram +ve Clostridia species of Anaerobes

Ampicillin/Amoxycillin
Gram +ve (strep)
Gram -ve

Flucloxacillin

1st choice - S. aureus

Co-amoxyclav (amox & clavulinic acid)
Gram +ve (strep)
S. aureus
Gram -ve
Anaerobes

Cephalosporins

Inhibit bacterial cell wall synthesis
Broad spectrum
Well tolerated, though 10% cross-over with penicillin allergy
Excreted in urine
‘Safe’ in pregnancy
Resistant to beta-lactamase (S. aureus and some anaerobes)
x cover Enterococci

Cefuroxime (‘2nd generation’)
Gram +ve
S. aureus (not 1st choice)
Gram -ve

Ceftriaxone (‘3rd generation’)
Gram +ve
S. aureus (not 1st choice)
Meningococcus
Gram -ve

Ceftazidime (‘anti-pseudomonal’)
Gram +ve
S. aureus
Gram -ve
Some Pseudomonas

Aminoglycosides

e.g. Gentamicin

Inhibit bacterial protein synthesis
Reserved for severe Gram –ve infections
IV only
Excreted in urine
Important adverse effects:

Nephrotoxic

Ototoxic
Monitor blood levels
Only use in pregnancy if benefit outweighs risk

Aminoglycosides
Gram -ve

Pseudomonas
Mycobacteria - some, not 1st line

Macrolides

e.g. erythromycin, clarithromycin

Inhibit bacterial protein synthesis
Atypical pneumonias
Patients allergic to penicillins
Well tolerated

GI upset (common)

Jaundice (rare)
Erythromycin inhibits cytochrome P450

Macrolides
Gram +ve

S. aureus

Atypicals

Tetracyclines

Inhibit bacterial protein synthesis
Broad spectrum including most atypicals
Over-used in the ‘60s and ‘70s - widespread resistance
Deposits in bone and teeth - grey staining
Avoid in pregnancy and children < 12 years
May exacerbate renal impairment

Tetracyclines

Gram +ve (Used as empirical alternatives to penicillin in mild/moderate URTI, also used for acne)
Gram -ve
Atypicals (Treatment of choice for microbiologically proven Chlamydia, Rickettsia, Brucella, Borrelia)

Trimethoprim

Bacterial dihydrofolate reductase inhibitor
Broad spectrum, some resistance
Well tolerated
Excreted in urine
Avoid in pregnancy
Useful for empirical treatment of UTI and respiratory infections

Trimethoprim

Gram +ve
Gram -ve

Quinolones

e.g. ciprofloxacin

Inhibits DNA gyrase

Mainly Gram –ve aerobes inc some pseudomonas
Over-used in the ‘80s - widespread resistance
Rarely = seizures or tendon inflammation/rupture
Excreted in urine
Avoid in pregnancy

Quinolones

Meningococcus - Prophylaxis only
Gram -ve
Some Pseudomonas

Glycopeptides

e.g. vancomycin, teicoplanin

Inhibit cell wall synthesis

Severe Gram +ve infections resistant to penicillins
Inc. MRSA (resistant to flucloxacillin)
Vancomycin:

Nephrotoxicity

Ototoxicity

‘Red man’ syndrome
Requires blood levels

Glycopeptides

Gram +ve
S. aureus
Anaerobes - Clostridia species

Metronidazole

Inhibits bacterial DNA synthesis
Anaerobic bacteria and protozoal infections only
Very low resistance
Well tolerated but can cause metallic taste
Avoid if possible in pregnancy

Metronidazole

Anaerobes

Chronic Kidney Disease

Chronic Kidney Disease

Not that you can possibly care...
GFR (ml/min/1.73 m2) = 186* x
{[Serum creatinine (mmol/l)/88.4] -1.154}
x age (years) -0.203
x 0.742 if female
x 1.21 if African American
(* correction factor depends on creatinine assay)

Stages of Chronic Kidney Disease & GFR (ml/min)

Stage 1
Normal GFR with another abnormality
> 90

Stage 2
Mild reduction in GFR with another abnormality
60-89

Stage 3
Moderate reduction in GFR
30-59

Stage 4
Severe reduction in GFR
15-29

Stage 5
End-stage renal disease
<15 or dialysis

Kidney Damage
•Proteinuria (albuminuria)
•Haematuria (microscopic, macroscopic)
•Abnormalities on imaging studies
•Histological abnormalities on biopsy

Causes of Chronic Kidney Disease
•Diabetes mellitus
•Glomerulonephritis
•Chronic pyelonephritis
•Prostatic hypertrophy
•Renovascular disease

•Multisystem diseases
•Genetic diseases

Management of CKD
Establish a diagnosis
Avoid nephrotoxic drugs
Treat hypertension
Treat complications
Monitor kidney function
Prepare for dialysis and transplantation

The “Uraemic Emergency”
•Pulmonary Oedema
•Peripheral Oedema
•Metabolic acidosis
•Hyperkalaemia
•Uraemic Pericarditis

Acute Kidney Injury

Acute Kidney Injury

3 Types:

1) Pre-renal i.e. renal hypoperfusion

- Dehydration

- Haemorrhage
- Clamps

- “Shock”
- Low cardiac output

2) Intrinsic renal i.e. tubular, glomerular or interstitial injury
 - Acute tubular necrosis
 - Acute glomerulonephritis
 - Acute interstitial nephritis

3) Post-renal

 - Renal tract obstruction
 - Ureteric stone(s)
 - Bladder outflow problems

 - Surgical ties
 - Retroperitoneal disease

Pre-renal:

•Urinary sodium < 20 mmol/l
•Urinary plasma:urea ratio > 10:1

Intrinsic renal:
•Urinary sodium > 20 mmol/l
•Urinary plasma:urea ratio < 10:1

US scan:
Are there two kidneys?
How big are they?
Are they “bright”?
Are they obstructed?

Management of AKI
- Fluid: Match urine output + 500 ml
- Nutrition: Restrict only potassium
- Monitor and treat sepsis
- Reduce gastric acid production
- DVT prophylaxis

Renal Failure

Kidney Functions

- Produces EPO - acts on bone marrow - which produces RBCs
- Vitamin D absorbed from skin/gut (cholecalciferol) - converted in liver to 25(OH)2D3 - converted in kidney to 1,25(OH)2D3 (calcitriol)

Dysfunction results in accumulation of toxic waste products:
- Fluid retention
- Hypertension
- Metabolic acidosis
- Hormonal disturbances

- Normochromic normocytic anaemia
- Secondary hyperparathyroidism and bone disease
(high phosphate & low calcium & low 1,25(OH)2D3 stims PTH)

Biomarkers of “kidney failure”
•Elevated blood urea and creatinine
•Reduced estimated GFR (eGFR)
•High blood potassium and phosphate
•Reduced blood pH and low bicarbonate
•Normochromic normocytic anaemia
•Reduced blood 1,25(OH)2vitamin D3
•Elevated blood parathyroid hormone levels

Prescribing Safely

• Know a lot about drugs
• Only prescribe for a narrow list of drugs that you know really well
• Use more established drugs, and avoid new drugs unless they really are an advance
• Be careful prescribing drugs to young women
• Use low doses in the elderly
• Double check with the BNF if you are prescribing a drug

–For the first time
–To someone on lots of other drugs
–To someone with liver or kidney disease

ALWAYS WRITE
–Name

–Date of birth

–Hospital Identity number

–Allergies

–Date of admission

–Consultant’s name

–Prescriber’s name and bleep no.

Avoid decimal points

Units

–g: grams

–mg: milligrams

–mcg: micrograms

–ng: nanograms

–U: units

Formulation of the drugs:

-tabs (tablets)

-caps (capsules)

Frequency:

–od–once a day

–bd–twice a day

–tds–three times a day

–qds–four times a day

–PRN(still need to give maximum dose)

–1º-1 hourly

Route of Administration

–po-orally

–iv -intravenously

–im-intramuscularly

–top–topical (state where)

–s/c-subcutaneously

Special instructions

e.g. take before food

Finally

SIGN and DATE

Ultimate Finals List - Clinical Skills, Prescribing & Pharmacology

Clinical Skills, Prescribing & Pharmacology

• Fluid balance – standard every year station. Mention looking around bed for drugs, drips, lines, catheters in situ, cannulae, central lines. Then feel peripheries (?warm), cap refill (examiner asked for normal time <2s), check pulse. There is a blood pressure cuff, he asks you to measure the BP, so do it fast, other students spent ages fiddling with the cuff and wasted time, the examiner will not let you proceed until you get the BP. Then check JVP, examiner asks for normal height (=2cm). Then assess skin turgor, auscultate heart and lungs especially lung bases for crackles (?pulmonary oedema), check for sacral and ankle oedema // I asked if patient had had a fever, recent surgry, diarrhoea or vomitting // How to do a lying and standing BP and the time interval between measuring both. // Examiner then wants to know what else, so mention all of your charts: 

- fluid balance chart, examiner asks what is on it so you say: inputs (IV fluids, oral intake) and outputs (urine, stool, drains, stoma bags etc)
- obs chart (temperature, BP, O2 sats, pulse, RR).
- Urine output chart.
- Drug chart – is patient on any diuretics?
- Further Ix i.e. U&Es, FBC, central line monitoring

• Spacer - Explain spacer and demonstrate its use with a MDT. Woman was on bd inhaler of salbutamol, I don’t know why it wasn’t prn. I started discussing this before the bell went. Asked about why should use a spacer, had to assemble and demonstrate technique. Should have been a very straightforward station. Actress was very pleasant and trying to help. // Inhaler with spacer – advise newly diagnosed asthmatic woman on how to use it. Assemble it in front of her and tell her to rinse it with warm water and leave to dry without drying manually. Replace spacers every 6 months or so for optimum delivery of drugs. I offered to explain other things like side effects of salbutamol, but she stated that she already knew these things and only wanted to know about the spacer device and its advantages over using only an inhaler.// make sure you check his actual technique with the spacer and inhaler provided! 

• Certifying death. Nurse bleeps you, says thinks pt has died, you come on over and do your thing. Look at the notes, signs of death (look, listen, pupils etc). // Told patient died expectantly. Had to demonstrate what would do on a very dead plastic dummy! eg. Test pain, check pupils, listen to heart sounds and lung sounds. Then had to document appropriate things in the notes. the examiner asked if there was anything else I’d like to write that I missed things out. Hmm, maybe I forgot to write down about pacemakers? // do the basics: check for pain, shine light in eyes to check pupils r dilated...no response to pain..no breath sounds...no heart sounds...apnoeic....CHECK for PACEMAKER!!! then write ur finding in notes... // Write the date and time etc and who is doing the ward round, then mention findings and I also wrote a management plan, which included: a) fill out death certificate, b) contact family, c) arrange for patient to be moved to morgue etc 

• Bladder catheterisation - No one expected this to come up as we all thought UCL would be too stingy to provide catheters for everyone! We were right about them being stingy - the catheters were reused. This was to test our comm skills and catheterisation, there was a guy sitting on a bed with a plastic penis between his legs - hilarious 

• Insert cannula 

• Suturing - double station. Was my last station, by which time I was a blithering idiot and managed to take 3 minutes to discuss a sterile field! The examiner kept asking me what I needed to do to clean the wound, and I just said sterile water and lignocaine 5 times till he pointed at the green sheet and I got the message! The girl pretending to be drunk saw I was a wreck and didn’t even chat to me, which I think they were meant to do to put you off. I did my stitches competently enough. Chuck sharps! Questions on advice to patient re wound care and max dose of lignocaine. // suturing...10 min station!!! u had to suture wound of an alcoholic n I had this annoying patient who was acting drunk and completely overacting and trying to disturb me...which was the whole point of the station since it was a mixed communication skills station // she kept asking things like do u love ur job??? r u happy being a doc???? and she wouldn’t be quiet...so after about 6 minutes I thought lets put her out of her misery and I replied " yes I love myself, and I love my job and my university is the best university in the world. being a doctor is the best job in the world and I wouldn’t trade it for anything" and hooray I made the examiner smile! // apparently on the second day they asked people what kind of dressing they would use // Remember your lignocaine dose, 3mg/kg maximum, I was asked this. Also remember to arrange a safety et, tell the patient to attend GP if any worries (red, oozing wound, stitches come out etc) and to attend GP in about 7-10 days time for stitches removal. // Consent, check wound, tetanus, allergy, LA etc then x3 // I think marks may have been given for attempting to make small talk. Also patient had fear of needles so had to give counselling prior. // Examiner was nice enough but a bit annoying as kept saying ‘pretend I’m not here’ and then proceeded to talk to me or to keep telling me to ‘pretend’ he wasn’t there. 

• Written station (true/false mcqs), fluid balance chart, massive haematemesis 

• Venepuncture

• IV drugs administration (2 stations)- one to prepare the drugs and the second one to adminster it. Have to talk through what one would look for in the drug information leaflet and drug chart // Look at drugs chart for pt with severe asthma – need to give IV Hydrocortisone 100mg Look at drug chart- cherk allergies, correct drug, dose, route, time,date, not yet given and that it has been signed for (IT WASN’T SIGNED) // explain how u calculate drug dose- look @ sheet to see how slow to give as IV - glove up and go to next station to give the drug Give the drug having checked pt name, dob etc ad that no signs inflammation- flush, give according to sheet, flush and discuss re what would do if anaphylaxis

• Filling in crossmatch form, checks before administering blood - asked what ANTT stood for and no one could work it out!! Aseptic Non-Touch Technique!! What you would do if you dropped a syringe before taking blood // most of the marks for this section seemed to be concerned with triplechecking the identity of the patient and filling in forms and blood bottle labels to send correct bloods off for the right tests. // The examiner gives the candidate a set of labels with the patients details on to use on the blood form but this is a trick!!! You have to hand write the patient's details on the blood form!! 

• Prescribing - Given drug chart. Mr X is on paracetamol post-op, has kidney failure, and is in pain, about 4/10. Prescribe him something – you’re given a BNF if you need it. Some people went with morphine, and the things that go with it: laxative and anti-emetic. I just went one step up the ladder and gave co-codamol. // Think I should have put in something in the stat section too, but I forgot and just did the regular section. I had to ask the examiner the date, he told me but looked at me like I was a muppet! Stress does curious things, I tell you //You do not write up morphine as it is too strong for pain of 4/10. Other people I spoke to wrote up NSAIDs, he was already on paracetamol so DO NOT OVERDOSE HIM by giving paracetamol as well. I wrote up co-codamol and mentioned that I would stop the existing paracetamol. Remember to fill in the patient details, ward, consultant, date etc first as these are the main marks. // Had renal failure too so went with co-codamol // in the end I wrote up paracetamol, NSAIDS regularly and some opiates and metoclopramide in the PRN section. 

• Prescribing - Given ABGs for acute exacerbation of COPD. Asked to write up meds on a prescription chart. 
• then...TTA Letter - I found this station very confusing we had to fill out a TTA form for a lady who had had an exacerbation of COPD. There was a BNF there as well. I hardly filled anything in - it was unclear whether we had to list the drugs for the acute episode or prescribe her regular meds as written out in the scenario. 

• Discharge form - Write a discharge letter for a post-MI patient // Writing up TTOs // Explaining to a patient about drugs post MI, side effects and implications (statin, aspirin, atenolol etc.. with questions from patient about DVLA regulations on driving after an MI) - taxi driver, Heparin – explain will stop, Aspirin - lifelong, Atenolol - lifelong, Atorvastatin - lifelong nocte, Temazepam – didn’t sleep ion hosp 2 nights – not chronic used so can stop, Last Q had to explain cannot drive for a month (although examiner kept saying do I want to change my answer- though was that long but would check with colleagues, DVLA etc 

• Discharge summary - a LONG instructions page followed by a LONG history - patient had been diagnosed with temporal arteritis, needed to be placed on steroids and bisphosphanates. - needed to fill out the discharge summary form. Everything on it! 
• then... Talking to the patient whose discharge summary you filled in. She is on Prednisolone and bisphosphonate after first presentation of temporal arteritis. Explain side effects of both, steroid card. // Advise lady who needs to be on steroids because of temporal arteritis. Tell her the side effects of steroids - i couldn't remember any initially and finally blurted out 'you might go psychotic' (don't do this!)Also show her steroid card and advise her to keep it on her at all times. She asks when she can come off them - I said when her ESR was back to normal and all her symptoms had gone. 

• Read notes-style information about the admission of a man for asthma attack after exposure to a neighbour's dog. Fill in discharge summary with patient details, take home medications, instructions to the GP to review spacer technique and then sign and date form (there wasn't enough time to do all of this properly). 
• then... Meet the man (actor) whose discharge summary you've just filled out. He is worried that he was only on PRN salbutamol before admission and that now he is on 2 inhalers and oral steroids. He has heard about bad side effects for oral steroids so isn't happy about this. You needed to find out what his worries are – he thinks he has to stay on the oral pred indefinitely but is only on a 7 day course, talk to him about this, about his inhalers and demonstrate use of a spacer. // Write TTA for patient after being admitted with exacerbation of asthma - everyone found it difficult to do in 5 mins but it was easy enough, just copying info off discharge summary

Ultimate Finals List - Abdominal Stations

Abdominal

• GI: multiple abdo scars // Abdo - This guy was strange. He had a long midline scar that was a bit strange (didn't look much like a laparotomy scar and yet did as well) and an incisional hernia in the scar. He also had a midline sternotomy scar (which I missed and looked like a complete idiot when I said "there are no scars in the chest." It's okay though because I passed and apparently some people also missed the hernia and they still passed! It was quite subtle). The examiner was really very nice and asked me why this man had a midline sternotomy scar (abdo station no?) and then why his laparotomy scar looked a bit strange. Apparently it was because it was the old fashioned way of performing a laparotomy. I also thought this guy had hepatomegaly, but I completely forgot to mention this when I was presenting. I was then told this man had a congenital problem. The only thing I could think of at the time was Marfan’s, with a valve replacement and aortic repair

• Gentleman with splenomegaly and anaemia, although I couldn't feel the spleen as the abdo was pretty distended! This examiner was a bit mean and told me I was digging myself a hole by examining the JVP! // Splenomegaly in a young afrocarribean girl // Abdo: Felty's RA and spleen got asked to present my findings, how I could differentiate the mass, is spleen from kidney

• Abdo - PCKD with transplant, av fistula, cushingoid from steroids & hydrocoele - Fx of Cushings // rather large woman I thought I felt fullness in flanks, I was happy with myself for noticing little scar in bellybutton, however as I presented the examiner separated a role of her fat to reveal a large flank scar! oops. asked me what I thought had gone on I said possibly kidney transplant due to pcos, he said - why else may she have this scar if she was well but her family member was ill...it was cos she had donated a kidney. this was a little mean.

• Hepatomegaly secondary to CLD, with spider naevi // Abdo - the yellowest man I've ever seen! He glowed! He also looked far too ill to be a patient for our exams and I hated moving him. No other signs apart from hepatomegaly. I think diagnosis was pancreatic cancer. // Oh and my abdominal examination pt was a gentleman with telangiectasia and a MASSIVE liver. Examiner asked for differentials, I said the 3cs : cirrhosis, congestive cardiac failure, carcinoma..then I talked about other causes: hepatitis, lymphoproliferative, myeloproliferative, endocrine etc. and time was up // Very long gentleman with pectus excavatum and palmar erythema and a whopping Mercedes scar across the abdomen – oh and two Medicalert bracelets with ‘liver transplant’ written on the back... // Guy with most of the classic liver disease signs: jaundice and yellow sclera, palmar erythema, bilateral Dupuytren's, mild ascites, spider naevi, venous engorgement, hepatomegaly. I said Alcoholic Liver Disease (alcoholic cos of the Dupytren's) and examiner was impressed. Patient also had a upper paramedian surgical scar. // Abdo - Amazing alcoholic liver disease from the ward. Ascites with old tap wound, jaundice, FLAP!!!! Hepatomegaly.

• Elderly man with anaemia. He had hepatosplenomegaly. We were expected to discuss the likely diagnosis which I think was a myeloproliferative disorder. I was asked why a person with PRV would be cyanotic and didn't have time to think about my answer and give it – really annoying as I’m sure it was a point-scorer // Abdo station - patient with bronze discolouration, duypytren's contracture and apparently hepatosplenomegaly, which I couldn't feel. I did not get the diagnosis in the exam, although when I write this all down now I can see that it was haemochromatosis, but it didn't matter anyway.

• Abdo: incisional hernia, urostomy. questions about what stoma was and why, what kind of metabolic abnormalities happen in a patient with a urostomy... i gave retroperitoneal fibrosis as a reason for needing a urostomy and was quizzed as to the potential drug causes of retroperitoneal fibrosis

• Abdo - guidance said patient had long term lyphoma but I could find no abnormailty on examination apart from subcutaneous lipomas.

• suprapubic mass - spoke about the bladder and uterus // differential, so I said fibroids, a mass in the bladder, and I would like o rule out pregnancy even though the lady was over 50... he was very impressed when I said that, he then said how would u manage someone with a fibroid, I said if it wasn’t causing any symptoms you could leave it alone, if there were symptom, there was medical management to control menorrhagia and pain, or surgical management was to remove it, and then we sat in silence, I think the examiner was very bored!// n a 50-ish year old woman with a hard pelvic mass - which really confused me, at first but just carried on my examination, presented my findings and we discussed some differentials for pelvic masses - I said fibroids, pregnancy (unlikely in a woman her age), calcified bladder, tumour and discussed how I would manage this patient (full history, basic bloods, tumour markers, dip the urine etc etc, maybe a pelvic ultrasound), then the bell went!

• Gastro-divarification of recti and a sebaceous cyst, also Dupuytren’s contracture which I missed. Asked about causes of Dupuytren’s and management. Also asked to describe the seb cyst and why I thought it was one etc.

Ultimate Finals List - Respiratory Stations

Respiratory

• Suppurative lung disease. I was asked about possible differentials. // Hyperexpanded chest, clubbing (I missed this). Empty sputum pot by bed. Coarse crackles. Bronchiectasis (I said COPD, but examiner guided me, asked for causes e.g. obstruction of bronchi, severe childhood infection like pertussis, secondary infection of tuberculosis lung, cystic fibrosis, Ix // The blindness and madness continued here. The patient had the most obvious clubbing I'd ever seen, proper drumsticks!!! He had COPD which was apparently unrelated to his clubbing I swear the left lung base was dull to percussion but again I had a moment of complete madness and said resonance was normal throughout. Afterwards the examiner made me go back and look at a plaster mark on the patient's back that revealed a needle sized hole!!! The examiner then asked me what this patient had had done, I said pleural aspiration. I was then asked why, I said pleural effusion. He then asked me if percussion was resonant and for some crazy reason I still said YES! (?!?!?!?!?!?!).

• Middle aged gentleman – ulnar deviation at MCP joints, rheumatoid nodules, hyperexpanded chest, no shortness of breath, fine inspiratory crackles more on left than right also heard at apices of lungs. Peculiar pulse. Examiner was grilling me for causes which although I said obviously secondary to rheumatoid or possibly methotrexate. he was looking for something to cause unilateral fibrosis. Only thing I could come up with was radiotherapy but with hindsight perhaps recurrent pericarditis and reactive effusions? //Peak flow at the side so use it to test peak flow // Gentleman with bilateral inspiratory crackles, decreased expansion - ?fibrosis. Asked about causes of fibrosis and then if there were any signs of any drugs patient had been on; I only noticed steroid induced "buffalo hump" when examiner pointed it out! A man with mixed connective tissue disease and lung fibrosis (I got him to do a prayer sign) // RESP- very obvious fibrosis of the lungs, I was asked about a differential but started giving causes of fibrosis..oops! she asked again about the differential, I was a little stuck, I said it may be consolidation but I would expect to hear coarse crepitations, she agreed and then said what else can we rule out, I felt a little silly saying the trachea was central so there no pneumothorax or collapse of the lung, the percussion not is resonant throughout so again rule out pneumothorax or consolidation and so on, but it what she wanted, we spent the last few minutes discussing how tired the patient must be getting, I saw her give me an A on the mark sheet

• Questions ask on different between obstructive and restrictive

• RS - Asthma - normal Examination poss! // my patient had low PEFR but normal Examination so just gave differentials - forgot to mention sputum pot I saw next to bed though!!

• Resp - lateral thoracotomy scar-lobectomy for bronchial carcinoma

• Actress with pleuritic chest pain – asked to examine her chest from behind as young female actress- 1st give 02 and reassure // followed by discussion re Diff Dx. Pneumothorax, PE, Pneumonia etc and how would treat a pneumothorax, Obs Chart with questions

• Respiratory - cryptogenic fibrosing alveolitis - questions on differentials, investigations, treatment options and criteria for home oxygen

• Respiratory: Nothing obvious on examination. Possibly hyperressonance on percussion. Peak flow was very low. When asked for differential I said COPD (hyperexpanded chest??). That was my last station, so the consultant asked the patient to stand up and made me comment on inspection. She had a marked Kyphosis and a bit of a scoliosis which was the causing a restrictive airway pattern.

• Migratory crackles in a woman with mild clubbing, no other signs, apart from dowagers hump (elderly lady with osteoporosis), I think diagnosis was bronchiectasis but I also mentioned pulmonary fibrosis.

• Resp: palmar erythema, Dupuytren’s but chest signs were not clear, end inspiratory crackles=fibrosis??, I wasn’t sure so I said its unlikely to be COPD as there was no wheeze etc, other students all came out with different differentials but the examiners was just interested in the reasoning.