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1 COUNSELLING STATIONS.........................................................................................................................................................3 1.1 MRSA INFO GIVING (2009) ............................................................................................................................................................3 1.2 EXPLAIN PEAK FLOW AND TTO (2009 (TTO 2006))........................................................................................................................5 1.3 SURGICAL OPTIONS FOR AAA (2005, 2009).....................................................................................................................................8 1.4 SMOKING CESSATION (2005 & 2009)...............................................................................................................................................9 1.5 COMPLAINTS PROCEDURE (2005, 2007, 2008, 2009)......................................................................................................................11 1.6 BREAST CANCER HX (PAIR WITH COUNSELLING) (2008).....................................................................................................................13 1.7 BREAST CANCER COUNSELLING (PAIR WITH BREAST CA HISTORY) (2008)..............................................................................................14 1.8 EPILEPSY EXPLANATION (2006, 2008)............................................................................................................................................16 1.9 POST MI & INFORMED CONSENT (2008)..........................................................................................................................................18 1.10 EXPLAIN POST MI DRUGS & TTO (2008)....................................................................................................................................20 1.11 BREAKING BAD NEWS (2005).......................................................................................................................................................22 1.12 HYPERTENSION MED NON ADHERENCE (12 MIN).......................................................................................................................................23 1.13 DIABETES COUNSELLING TYPE 1 (6 MIN).....................................................................................................................................26 1.14 TYPE II DIABETES........................................................................................................................................................................30 1.15 DO NOT RESUSCITATE (2005).....................................................................................................................................................33 1.16 INHALER TECHNIQUE NEWLY DIAGNOSED ASTHMATIC (2007).............................................................................................................35 1.17 EXPLAIN GASTROSCOPY/SIGMOIDOSCOPY PROCEDURE (2006; 12 MIN)...............................................................................................39 1.18 EXPLAIN SIGMOIDOSCOPY RESULTS = CROHNS DISEASE (2007 - 6 MIN).............................................................................................42 1.19 GORD (2006, 12 MIN).............................................................................................................................................................44 1.20 EXPLAIN AF AND INITIATE WARFARIN THERAPY (2009) .................................................................................................................46 1.21 CYSTIC FIBROSIS COUNSELLING (2006) .........................................................................................................................................48 2 CLINICAL SKILLS......................................................................................................................................................................50 2.1 BLOOD GAS & INTERPRETATION (2008, 2009)................................................................................................................................50 2.2 BLOOD CULTURES, INTERPRET, PRESCRIBE ANTIBIOTICS (2005, 2009)..................................................................................................53 2.3 MANAGING HANDOVER & PRIORITISING............................................................................................................................................55 2.4 PRESCRIBING IN RENAL FAILURE (2009)...........................................................................................................................................56 2.5 CANNULATION AND FLUID MANAGEMENT (2008, 2009).....................................................................................................................58 2.6 PRE-OP ASSESSMENT (2006)...........................................................................................................................................................62 2.7 INTERPRET BLOOD TEST RESULTS ADDISONS (2007) .......................................................................................................................64 2.8 CREMATION FORM (2005, 2007) ...................................................................................................................................................65 2.9 TTO FORM TRANSCRIBE FROM DRUG CHART (2006)..........................................................................................................................66 2.10 CATHETERISATION.......................................................................................................................................................................67 2.11 VIDEO OF WARD ROUND WRITE NOTES (2006, 2008) ......................................................................................................................68 2.12 NEEDLESTICK INJURY...................................................................................................................................................................69 2.13 ADVERSE REACTION TO BLOOD TRANSFUSION...................................................................................................................................71 2.14 BLOOD TRANSFUSION: EXPLAIN , TAKE BLOOD, FILL IN FORM (2006, 2008).........................................................................................72 ECG -PERFORM AND INTERPRET II.......................................................................................................................................................74 2.14.1 Atrial Fibrillation potential examiners questions........................................................................................................78 2.15 URINALYSIS, PRESCRIBING (PENICILLIN ALLERGY) ............................................................................................................................80 2.16 ALS (2005, 2007)...................................................................................................................................................................81 2.17 ANAPHYLACTIC DRUG REACTION, TREAT & BLS (2007).................................................................................................................83 2.18 DRUG CHART POST GI BLEED (2008)............................................................................................................................................84 2.19 CONFIRM DEATH AND DOCUMENT (2008).......................................................................................................................................86 2.20 CHEST X-RAY & PRESCRIBE.........................................................................................................................................................89
............................................................................................................................................................................................................91 HISTORIES......................................................................................................................................................................................92 2.21 TIA, MANAGEMENT, GUIDELINES (2009).......................................................................................................................................92 2.22 GI HX IBD (2009)...................................................................................................................................................................96 2.23 RENAL CALCULI HX (2007, 2009)...............................................................................................................................................97 2.24 THYROTOXICOSIS (2005).............................................................................................................................................................99 2.25 PVD - INTERMITTENT CLAUDICATION (2006 12 MIN) ...................................................................................................................101 2.26 BACK PAIN (RENAL CAUSE, 2007) ..............................................................................................................................................103 2.27 FATIGUE - CHRONIC RENAL FAILURE (2008).................................................................................................................................105 2.28 BPH & INTERPRET BLOODS (2005, RENAL FAILURE).....................................................................................................................107 2.29 DIARRHOEA - HYPERTHYROID (2006, 12 MIN).............................................................................................................................108 2.30 ELDERLY PT COLLAPSE (2007)..................................................................................................................................................109 2.31 PAINLESS JAUNDICE - PANCREATIC CANCER (2008)........................................................................................................................111 2.32 POLYMYALGIA RHEUMATICA (2005)............................................................................................................................................113 2.33 SLE (2006: YR 4 STATION)......................................................................................................................................................115 2.34 CYSTIC FIBROSIS (2006, 12 MIN)...............................................................................................................................................117 2.35 PSEUDOMEMBRANOUS COLITIS (2007) .........................................................................................................................................119 2.36 GORD (2005).......................................................................................................................................................................121 2.37 DISCHARGE PLANNING (2006)...................................................................................................................................................123 2.38 ASSESSMENT POST OVERDOSE (2007).........................................................................................................................................125 3 EXAMINATIONS........................................................................................................................................................................126 3.1 GAIT (2005, 2007 PREVIOUS YR 4 STATION).................................................................................................................................126 3.1.1 Abnormal Gaits with video links.....................................................................................................................................127 3.2 HAND ((RHEUM ARTHRITIS) 2005 (YR 5), 2006, 2008 (YR 4))......................................................................................................128 3.3 KNEE (2007, 2008: YR 4).........................................................................................................................................................130 3.4 HIP (2005, 2006 PREVIOUS YR 4 STATION)...................................................................................................................................132 3.5 SHOULDER (HASNT COME UP PREVIOUSLY).....................................................................................................................................134 3.6 GALS (HASNT COME UP PREVIOUSLY)..........................................................................................................................................136 3.7 SPINE (HASNT COME UP BEFORE)..................................................................................................................................................137 3.8 GI EXAM (2005, 06, 07, 08, 09)................................................................................................................................................139 3.9 CVS - IDENTIFY MURMUR (2005, 06, 07, 08, 09)........................................................................................................................142 3.10 RESPIRATORY (BRONCHIECTASIS 05, 07, 08, LOBECTOMY 06, ? 09)................................................................................................145 3.11 LOWER PERIPHERAL VASCULAR EXAMINATION................................................................................................................................147 3.12 LOWER PERIPHERAL ARTERIAL EXAMINATION ................................................................................................................................150 3.13 CRANIAL NERVES II, III, IV, & VI AND FUNDOSCOPY (2005, 2006, 2007, 2008).........................................................................151 3.14 CAPACITY AND CONSENT............................................................................................................................................................154 3.15 NEURO EXAM - LEGS - PERIPH NEUROPATHY (6 MIN) .....................................................................................................................156 3.16 NEURO EXAM ARMS................................................................................................................................................................158 ....................................................................................................................................................................................................159 3.17 DERMATOMES...........................................................................................................................................................................160 4 FORMULARY.............................................................................................................................................................................161 5 BMJ LEARNING MODULES....................................................................................................................................................174 5.1 COUNSELLING.............................................................................................................................................................................174 5.2 CLINICAL SKILLS.........................................................................................................................................................................174 5.3 HISTORIES..................................................................................................................................................................................174 5.4 EXAMINATIONS...........................................................................................................................................................................175
1 Counselling stations
1.1 MRSA info giving (2009)
Wash hands, introduce self, check ID, get consent, summarise patients presenting symptoms Determine how much the patient already knows, and check they want to know more. Elicit main concerns What is MRSA? The SA stands for Staphylococcus aureus - usually harmless germ often found on skin/nose of healthy people SA sometimes invades skin causing infection. More likely if cut or graze. Cause of boils, pimples, impetigo, skin abscesses and common cause of wound infections. May get into bloodstream to cause more serious infections. More likely in people already unwell. Most SA infections can be treated with commonly used antibiotics MR stands for methicillin-resistant - some healthy people are carriers of MRSA some get infections. MRSA infections resistant to antibiotic called methicillin and also other types i.e. they dont kill the bacteria Infections with MRSA can sometimes become more severe. Who gets MRSA? Most common in people already in hospital, esp. if very ill or have wounds or open sores Catheters and tubes going into veins or other parts of the body ('drips' etc) can be contaminated by MRSA. You can be a carrier or have an infection caused by MRSA If you know you are a carrier you should let the hospital know before you go in (e.g. for an operation). You can then be offered treatment (e.g. ointment to put in the nose or antiseptic washes) MRSA infections usually associated with high fevers, boils, abscesses, can cause pneumonia and urine infections. How is MRSA diagnosed? Sample of blood, urine, body fluid or a swab of a wound can be sent to laboratory. MRSA identified by seeing which antibiotics kill the bacteria How is MRSA spread? Usually by direct skin-to-skin contact, usually in hospitals. Also sheets, towels, clothes, dressings, etc. How can it be avoided? Wash hands regularly (e.g. alcohol), cover cuts, wear gloves if in contact, avoid sharing towels etc. Patients with an MRSA infection may be put in a single bed room Is MRSA screened for in the UK? No universal screening but recommended for: hospital transfers, ICU, orthopaedic and vascular surgery wards. If you are undergoing planned surgery you will be screened for MRSA before you go in (unless emergency) What is the treatment? Usually treated with antibiotics. Limited choice. May need to be IV. Often several weeks, side-effects Summarise, Check Understanding, Ask Questions, offer Leaflet, arrange Follow Up Possible examiners questions: Q. What are the infection screening procedures for MRSA for: i) elective admissions? ii) Emergency admissions? (March 09: http://www.leedsth.nhs.uk/sites/infection_control/documents/LTHT-MRSAscreening-policy.doc ) Screen in pre-operative assessment clinics. Elective admissions to hospitals unless: day case opthalmology, dental, endoscopy; minor derm (eg warts), paeds unless high risk group, 3
maternity/obstetrics unless elective caesareans or high-risk. Swab both sides, separate swabs: anterior nares, groin, axilla, Children < 1 month old umbilicus, sites likely to be colonised. Put in a single specimen bag and send to lab labelled MRSA screening elective admission. Documented in notes. Swabs for sites thought to be clinically infected need separate request forms & specimen bag. Q. What are the eradication and treatment procedures for patients with MRSA? Letter to GP & patient info leaflet to patient. Chlorhexidine gluconate 4% in a surfactant solution 500ml all over body wash to be used 5 days before surgery. Wash hair day 1 and 5. Mupirocin 2% nasal ointment 3g to inner surface of both nostrils three times daily for the 5 days prior to surgery. Alternative is Naseptin but avoid in nut allergy. Another alternative is Prontoderm.
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The Yorkshire and Humberside Independent Complaints Advocacy Service (ICAS) can provide independent, free information, advice, support and representation to people wanting to make a complaint about NHS treatment. Tel: 0300 456 8349 Advocacy Network Leeds can provide information about other specialist advocacy services. Tel: (0113) 244 9045. Click on Useful Contacts below for more detail. Summarise, Check Understanding, Ask Questions, offer Leaflet, arrange Follow Up
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Presenting Complaint & History or presenting complaint Use open questions Ask specifically about pain, lumps, nipple discharge If pain SOCRATES Associated symptoms: o Lump; site, size, onset, duration, cyclicity, associated symptoms o Nipple discharge; amount, colour, unilateral/bilateral, one duct or several, spontaneous or not o Skin changes, nipple retraction/inversion Systemic symptoms: tiredness, fever, night sweats, weight loss, chest or back pain Cyclicity (i.e. menstrual cycle) Similar symptoms in the past? Any other changes? Past medical history Age at menarche/menopause Children? Ages? Breastfed? Current past and childhood illnesses Surgery Previous breast investigations Recent visits to the doctor Drug History Prescribed meds, esp OCP, HRT, antipsychotics (some can cause hyperprolactinaemia/galactorrhoea) Over the counter medications Recreational drug use Allergies Family history Parents, siblings and children. Specifically breast problems and cancers Social History Smoking, alcohol, employment (past and present), housing, recreational activities Systems enquiry S Summarise Follow up C - Check understanding, A Ask questions, L Leaflet, F arrange a
Possible examiners questions Q. What investigations might you order? A. Mammogram, ultrasound scan, fine-needle aspiration cytology (FNAC) Q. Differential diagnoses? A. Fibroadenoma, Fibrocystic disease, Mastitis, Breast abscess, Mammary duct ectasia, intraductal papilloma (See overleaf for breast cancer counselling) 13
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Potential examiners questions Q. What is the first line drug treatment? Carbamazepine 100mg/12h Q. Toxic effects? Rash, nausea, diplopia, dizziness, fluid retention, hyponatraemia, blood dyscrasias Q. What is the 2nd line drug treatment? Sodium valproate 300mg/12h 16
Q. Toxic effects? Sedation, tremor, weight gain, hair thinning, ankle swelling, hyperammonaemia, liver failure. Q. What is status epilepticus? One continuous seizure > 30 minutes, or recurrent seizures without regaining consciousness between seizures for > 30 minutes.
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Q. What Troponin value is considered elevated? A. Troponin T >0.1 ng/mL, Troponin I > 1ng/ml Q. What specific type of Troponin is most informative? A. In renal impairment, even against second generation cTnT assays, cTnI is superior. In muscle damage, cTnI is as least as useful as cTnT. Q. What other cardiac markers are there? Creatine Kinase (CK) Q. What else may raise cardiac markers? Troponin CRF, PE, septicaemia; CK: rhabdomyolysis (check kidneys), exercise, surgery, hypothyroidism. Q. What is informed consent? Individual's ability to make an informed decision. Q. What is capacity? Ability to retain and understand information and weigh up risks and benefits Q. What is competence? Degree of mental soundness necessary to make decisions about a specific issue or to carry out a specific act.
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Additional points for Establishing and maintaining rapport Active listening. Demonstrating interest, concern and empathy Pauses. Appropriate pacing allowing patient to express feelings freely 20
Potential interview questions BP should be treated post MI if over what? 140/90 What is Dresslers syndrome? Persistent low-grade fever, chest pain (usually pleuritic), pericardial rub, and/or pericardial effusion. Tends to occur a few weeks or even months after MI and tends to subside in a few days. Associated with an elevated ESR.
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Drug therapy shoud be offered to? Persistently >= 160/100 mmHg or CVD risk >= 140/90 mmHg. First line drug for >=55 or black patients of any age? calcium-channel blocker or a thiazide-type diuretic. First line drug < 55s? ACE inhibitor (or an angiotensin-II receptor antagonist if ACEI not tolerated). When would you refer? BP>= 180/110 mmHg, suspected phaeochromocytoma (e.g. postural hypotension, headache, palpitations, pallor and diaphoresis), fall in systolic when standing of >=20 mmHg). What investigations might you wish to do? FBC, U&Es, creatinine, lipids, GGT (alch), ECG, Echo (LVH) See over for guidelines
BETA-BLOCKERS Beta-blockers are no longer preferred as a routine initial therapy for hypertension. But consider them for younger people, particularly: women of childbearing potential patients with evidence of increased sympathetic drive patients with intolerance of or contraindications to ACE inhibitors and angiotensin-II receptor antagonists. If a patient taking a beta-blocker needs a second drug, add a calcium-channel blocker rather than a thiazide-type diuretic, to reduce the patients risk of developing diabetes. If a patients blood pressure is not controlled by a regimen that includes a beta-blocker (that is, it is still above 140/90 mmHg), change their treatment by following the flow chart above. If a patients blood pressure is well controlled (that is,140/90 mmHg or less) by a regimen that includes a beta-blocker, consider long-term management at their routine review. There is no absolute need to replace the beta-blocker in this case. When withdrawing a beta-blocker, step down the dose gradually. 24
Beta-blockers should not usually be withdrawn if a patient has a compelling indication for being treated with one, such as symptomatic angina or a previous myocardial infarction.
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Kidney function, Foot checks - prevent foot ulcers; Coeliac and thyroid disorders more common Immunisation against 'flu (each autumn) and pneumococcus (once).
Further info: www.diabetes.org.uk Summarise, Check Understanding, Ask Questions, offer Leaflet, arrange Follow Up
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Potential examiners questions Q1. If someone has not appointed an agent to act on their behalf in the event of them being unable to make decisions about their treatment, who is ultimately responsible for decisions about their care the most immediate relative, or the consultant in charge of their care? A: The doctor in charge of their care. Q2. Can proxy decision makers (i.e. those appointed by the patient) over-rule decisions made by a doctor regarding a patients treatment ? A: Proxy decision makers can not demand treatment that is judged to be against a patients best interests.
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See also: http://www.nhs.uk/video/pages/medialibrary.aspx? Tag=Children+and+babies+&Page=4 See over for BTS 2009 guidelines
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Sigmoidoscopy. Introduction: Introduce self. Elicit name, age, occupation. Establish rapport. Understanding: Find out what the patient knows so far. Concerns: Find out if the patient has any particular concerns. Explanation: Sigmoidoscopy is a procedure where a doctor or nurse looks into your back passage (the rectum) and the part of the bowel before this (the sigmoid colon) using an instrument called a sigmoidoscope. Definitions: The sigmoid colon is the final portion of bowel joined to the rectum. A sigmoidoscope is a small tube with an attached light source about the thickness of your finger. A doctor or nurse inserts the sigmoidoscope into the anus and pushes it slowly into the rectum and sigmoid colon. This allows the doctor or nurse to see the lining of the rectum and sigmoid colon. The procedure should not be painful but it may be a little uncomfortable. Preparation: In order for us to get a clear view, your rectum and lower bowel need to be empty of faeces (stools or motions). You may be asked to clear your bowel by taking laxatives for a day or two, or by using one or two enemas prior to the procedure. A commonly used laxative to clear the bowel is called Picolax. A common plan is: For three days before the procedure - eat a light diet. On the day before the procedure - take one Picolax sachet (by mouth) at 8am and one at 6 pm. Read the instructions carefully on the Picolax sachet on how much water to add. For 12 hours before the procedure - have fluids only. You may be given an enema on arrival in the hospital to clear the very bottom of the bowel of faeces. The test itself: It usually takes 15-20 minutes. Usually you do not need an anaesthetic or sedation. Youll wear a hospital gown so that the lower half of your body is exposed. You will be asked to lie on your left side with your knees drawn up toward your chest. First the doctor or nurse will gently insert a gloved and lubricated finger into the rectum to check for blockage and to widen the anus. Then the sigmoidoscope will be inserted and gently pushed further into the rectum and colon. Air is gently pumped through the sigmoidoscope to help viewing. This can cause you to feel bloated and uncomfortable, and give you an urge to defecate ('move your bowels'). As the sigmoidoscope is slowly removed, the lining of the bowel is carefully examined. You may pass this air as wind when the sigmoidscope is being removed. A small sample (biopsy) of bowel lining may be taken during the procedure. (A channel in the sigmoidoscope allows the doctor or nurse to pass forceps or other instruments to take biopsies, or for therapy.) The sample is sent to the laboratory to be looked at under the microscope. It may also be tested for various conditions that can affect the bowel. SCALF: Summarise. Check understanding, any Concerns? up. Ask questions. Leaflet. Follow-
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Preventing flare-ups?: case by case basis: Regular mesalazine, immunomodulators, biological therapy. BUT do not always work. Steroid medication is not generally used longterm to prevent flare-ups. Giving up smoking may reduce number and severity Pregnancy: Discuss in advance with doctor. May need extra folate, and certain drugs must not be used. Prognosis? Variable. Without treatment ~3 in 20 have frequent flare-ups. Sometimes flare-ups life-threatening. 15/20 remain in work 10 years after diagnosis. Majority of cases disease is manageable enough to maintain a near normal life. Up to 8/10 require surgery at some stage. Half within the first 10 years. Commonly to remove stricture. Young adultsexpect to have 2-4 operations in life. Inflammatory bowel disease? Crohn's or ulcerative colitis. Similar. But UC inner lining of gut, Crohn's can spread through whole wall. UC only affects colon and rectum. Features of both = indeterminate colitis. SCALF: Summarise. Check understanding, any Concerns? Ask questions. Leaflet. Follow-up.
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Surgery: 'tighten' lower oesophagus. May be an option if drug treatment not working well or not wanted long-term. Are there any complications from oesophagitis? Stricture (scarring and narrowing) uncommon. Barrett's oesophagus - changed cells more prone to cancer (1-2%). Most people do not develop these complications. Tell doc if you have pain or difficulty (food 'sticking') swallowing - may be complication. SCALF: Summarise. Check understanding, any Concerns? up. Ask questions. Leaflet. Follow-
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Counselling Check knowledge of atrial fibrillation and explain diagnosis Check knowledge of treatment and explain cardioversion Explain need for need for anticoagulant (stroke, limb ischaemia, kidney failure) Check knowledge of warfarin tablet, explain what it does in simple terms Any questions so far? Explain risk of excessive bleeding though need for careful monitoring (INR) Explain need to visit warfarin clinic to get dose at right level. Stress compliance. Check with pharmacist before starting any new drugs (warfarin interactions). This includes over the counter tables and herbal remedies Avoid NSAIDS (ibuprofen, aspirin, diclofenac) and changes in levels of consumption of alcohol, cranberry juice , Vit K rich foods such as green leafy vegetables, herbal remedies eg. Ginseng, St Johns Wort, Cod liver oil Avoid cuts and bruises (sewing, shaving, contact sports) Screen for contraindications: stomach ulcer, bleeding disorder, high blood pressure, kidney disease, pregnant, trying for a baby or breastfeeding Youll be given a yellow warfarin therapy book check your details and read this You will be given a warfarin card or medic alert bracelet keep with you at all times Tell GP, dentist and other HCPs you are on Warfarin Not recommended in pregnancy, periods may be heavier. SEs = bleeding, bruising, diarrhoea, purple toes (3-8 weeks)
Prescribing warfarin Use Fennertys Protocol: o Young/healthy patients - 10mg at 18:00 daily for 3 days with adjustments based on daily INR at 09:00. Elderly 5mg at 18:00 daily for 3 days with adjustments based on daily INR at 09:00
Possible questions What drugs might you wish to stop before commencing warfarin? What is the target INR; 46
o o o
In this case (i.e. AF)? (INR of 3.0 for up to 4 weeks before procedure) For treatment of DVT & PE? (2.5, unless recurrent then 3.5) For mechanical valves? (3.0 for aortic, 3.5 for mitral)
How would you manage the situation if Mrs Smith had been given 50mg of warfarin initially by accident? (stop warfarin, if INR >12 5mg VitK PO/IV, if bleeding seek senior help urgently) How does warfarin work? (inhibits vitamin K-dependent clotting factors)
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OTHER TREATMENTS: Salt supplements, specialist liver treatments, insulin (diabetes), nasal steroids (polyps), antacids, laxatives, routine immunisations, lung or heart/lung transplantation. FUTURE: Gene therapy, What is the outlook (prognosis)? People now living into their 40s Genetic counselling: People with family history may wish to have genetic counselling and testing Further help and information: Cystic Fibrosis Trust www.cftrust.org.uk
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2 Clinical Skills
2.1 Blood Gas & interpretation (2008, 2009)
You are the medical house office on call. Mr Gower was admitted under yoiur care two days ago for infective exacerbation of COPD. The nurse in charge has bleeped you stating that he is deteriorating. Demonstarte how you would take an arterial blood gas on the manikin provided. Explain what youre doing as you go. Orientation: Establish location of nearest blood gas analyser, and if not one nearby, what procedure is Introduction: Introduce self. Elicit name and age. Establish rapport Explain: I understand you are having some difficulty breathing. In order to check how things are progressing, I need ot take some blood from your wrist. Although this procedure is quite painful, I can reassure you that it is a quick procedure that is essential for us to help you get better. Do you have any questions? Consent: Obtain consent and re-check ID Position: Ensure patient is sitting or lying comfortably Equipment: Clean trolley and gather relevant equipment: pre-heparinised syringe, (optional local anaesthetic), alcohol swabs, cotton wool/gauze, 23G arterial gas needle, pair of non-sterile gloves, sharps box. Preparation: Wash hands and don gloves Position: Have patient lying down or sitting with arm well supported. Hyper extend wrist on rolled up towel. Locate radial pulse, noting size, depth and direction Clean skin with alcohol swab (and infiltrate with local anaesthetic if necessary) and drape the area Attach 23G ABG needle to pre-heparinised syringe. Expel excess heparin. Hold in dominant hand like a dart. Fix chosen area on skin between index and middle fingers of non-dominant hand (do not repalpate area) Warn patient to expect a sharp scratch Insert needle at 30 against the direction of arterial flow (i.e. towards the elbow) When a flash of blood appears in the hub of the needle stop advancing. The blood should fill the syringe under arterial pressure. Gentle aspiration may be required in some cases (eg manikins). Obtain 2ml blood Withdraw needle and press firmly on puncture site with a gauze for 5 minutes (check for haematoma). Immediately place needle in sharps bin Expel bubbles from syringe and immediately cap it State that you would immediately label the specimen and take it to the blood gas analyser, or if it needs to be sent to the lab, label the specimen and arrange immediate transport Case 2.
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Case 1: Elderly patient breathing room air Q1. Outline the abnormalities in this ABG Q2. What are the likely causes for these abnormalities? Case 2: 68 yr old man, 40 pack years, SOB, productive cough, green sputum. Tachypnoeic and using accessory muscles. Widespread expiratory wheeze with bibasal coarse crepitations. On 28% oxygen. Q1. Outline the abnormalities and give a likely diagnosis Q2. What type of ventilation could be considered in this case? Answers to case 1 and 2: Case 1: A1. PaO2, pH (alkalosis), PaC02 normal, HCO3. Therefore uncompensated metabolic alkalosis A2. Common causes of poor oxygenation are pulmonary oedema or pneumonia. Causes of metabolic alkalosis: vomiting, 1 or 2 hyperaldosteronism, hypercalcaemia, diuretics, bicarbonate ingestion. Case 2: A1. pH, PaO2, PaCO2, HCO3, BE. Therefore partially compensated respiratory acidosis. Type 2 respiratory failure (i.e. both PaO2 and PaCO2 are abnormal). Likely to be COPD. A2. Bi-level positive airway pressure ventilation. If more serious intubation might be considered. Case 3. Case 4.
Case 5.
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Case 3: A 27 year old student with SOB and tingling in hands. RR 28. Chest exam unremarkable. CXR and bloods normal. ECG sinus tachycardia. ABG taken on 35% O2. Q1. Outline the abnormalities in this ECG Q2. What is the likely cause? Q3. Outline treatment. Case 4: A 32 year old. Generally unwell. No history available. Appears dehydrated. RR 22, ABG on room air. Q1. Outline the abnormalities seen Q2. What tests should you request Q3. Which drugs or substances taken in overdose could give similar findings? Case 5: 57 year old former shipyard worker. Exercise tolerance now 10 metres on flat. Life long non smoker. CT shows diffuse bibasal interstitial changes. ABG on room air Q1. Outline the abnormalities seen Q2. What are the likely causes? Q3. What long term therapy might be considered? Blood Gas Answers Case3: A1. pH, PaO2~ (should be roughly 10% less than inspired i.e. 35-10=25%), PaCO2, HCO3, BE. Therefore partially compensated respiratory alkalosis. A2. Probably caused by hyperventilation. May also occur due to stroke or SAH affecting respiratory centre. A3. Remove oxygen. Reassure and encourage to breathe slowly into a paper bag. Case 4: A1. pH, PaO2 normal, PaCO2, HCO3, BE. Therefore metabolic acidosis with partial respiratory compensation. Na+, K+ normal, urea, creatinine normal, Cl- normal, HCO3. Anion gap = (131 + 4.5) (96.1 + 12.6) = 26.8. Thus raised anion gap metabolic acidosis. The anion gap is an 'artificial' and calculated measure that is representative of the unmeasured ions in plasma or serum. Metabolic acidosis with normal ion gap < 16mmol/L = HCO3 loss from gut, e.g. diarrhoea, renal tubular acidosis Metabolic acidosis with raised ion gap > 16mmol/L = ketoacidosis, rneal failure, lactic acidosis, salicylate toxicity, methanol, antifreeze ingestion A2. Urinalysis for ketones, plasma lactate levels, salicylate levels. A3. Aspirin, methanol or ethylene glycol. Case 5: A1. pH normal, PaO2, PaCO2 normal, HCO3 normal, BE normal to high A2. Type 1 respiratory failure (i.e. O2 low but CO2 normal). Possible causes include pulmonary fibrosis (most likely), pulmonary oedema, pneumonia, pulmonary embolism. A3. Long Term O2 Therapy (LTOT) may be considered, however strict guidelines for this must be met.
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N.B. These are the most recent Leeds guidelines Wash hands with soap and water, then dry hands and put on disposable apron. Prepare equipment (2 culture bottles, butterfly needle and vaccutainer (or needle and 20ml syringe), sharps bin, chlorhexidine/isopropyl alcohol, cotton wool, sterile gloves, disposable tourniquet Disinfect the rubber tops of culture bottles using a wipe containing 2% chlorhexidine in 70% isopropyl alcohol. Identify patient e.g. double check name band and verbally confirm identity Select venepuncture site and clean visibly soiled skin with soap and water then dry. Apply tourniquet if required. Clean site using a 2% chlorhexidine in 70% isopropyl alcohol wipe - press swab in centre of chosen venepuncture site. Then apply the disinfectant with a spiral outward motion from the centre of the venepuncture covering 1-2 finger breadth to each side. Allow to air dry (the drying process kills the bacteria). Put on sterile gloves while skin disinfectants dry. Sterile examination gloves allow for repalpation if necessary Attach a butterfly needle (needle-safe if available) to the needle-safe bottle-filling device. Perform venepuncture ensuring asepsis is maintained. Collect blood sample by placing needle-safe bottle-filling device onto blood culture bottles (aerobic followed by anaerobic). Remove bottles once 10ml has been obtained in each. Remove tourniquet. Place cotton wool over site and apply gentle pressure while removing needle. Press firmly over site until bleeding has stopped (the patient can be asked to do this if appropriate). Discard needle and blood bottle filling device into a point of use sharps bin. Write patient details and clinical information on blood culture bottles according to Trust policy. Wash hands with soap and water, then dry hands Arrange transport of the sample to the laboratory. Ensure that sampling details and any subsequent positive results communicated by the microbiology department are accurately documented in the patients notes and advice is acted on. If using needle and syringe follow the same procedure and do not change needle between venepuncture and inoculation, or between bottles.
Possible examiners questions Q1. How long might it take to get the results back from microbiology? A1. Depends on the bacteria, but can take up to 72 hours. Q2. The lab has grown E.Coli from your blood cultures. What can e.coli in the blood cause? A2. Neonatal meningitis, septicaemia Q3. The patient is allergic to penicillin which of the following would you use to treat?: Gentamicin - ok 53
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A1. Acute Renal Failure A2. Ramipril: (1.25 10mg max daily) Mild to moderate hypertension, congestive heart failure Furosemide: (20-40mg daily) Oedema, resistant hypertension Spironolactone: (100-200mg daily up to 400mg) Oedema and ascites in cirrhosis of the liver, nephritic syndrome, CHF, primary hyperaldosteronism Metformin: (500mg 2g daily max) diabetes mellitus, polycystic ovary syndrome Aspirin: (300-900mg every 4-6 hrs, max 4g) analgesia, angina, MI (75mg daily), post-TIA Voltarol: (75-150mg daily in 2-3 divided doses) Pain and inflammation in rheumatic disease, gout, postoperative pain Pilocarpine eye drops: (1-2 drops max 4x daily) glaucoma, dry mouth Paracetamol: (0.5-1g every 4-6 hours max 4g daily) pain, pyrexia A3. Estimated Creatinine Clearance in mL/min = (140 84) x 65 x 1.04 403 = 56 x 65 x 1.04 / 403 = 3785.6/403 = 9.39 A4. Degree of renal failure eGFR mL/min/1.73m2 Normal stage 1 > 90 with other evidence of kidney damage Mild Stage 2 60-89 with other evidence of kidney damage Moderate Stage 3 30-59 Severe Stage 4 15-29 Established Stage 5 < 15 Therefore Mrs Reiter is in Stage 5 Renal failure. A5. Drugs I would wish to cross off; Spironolactone Avoid in severe renal impairment Metformin contraindicated in patients with severe renal impairment Aspirin oral anticoagulants should be avoided if creatinine clearance is < 10mL/min Voltarol - should be avoided if creatinine clearance is < 10mL/min Other things to note; Ramipril max initial dose 1.25mg once daily (dont exceed 2.5mg daily if eGFR < 10mL/min Furosemide may need higher doses. Deafness may follow IV injection Pilocarpine eye drops manufacturers advise caution Paracetamol OK but may need infusion A6. If her eGFR improved, some of the drugs could be re-started cautiously, such as Aspirin and Voltarol A8. > 400mL/24 hr
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Ensure patient is comfortable. Apply insertion date sticker, with the date and time Document insertion using cannula documentation record. Dispose of waste appropriately
Stop at this point and ask questions about choice of fluid (see over) 2. Fluid challenge: choice of fluid Q. What are the two main types of fluids and give examples of each? A. Crystalloids (Saline, Dextrose, Hartmans) and Colloids (gelofusine, volplex, blood) Q. What is the main disadvantage of crystalloids? A. When used to replace massive loss of fluid, they cause peripheral oedema and occasionally pulmonary oedema. Q. Describe how saline redistributes within the body? About 75% redistributes within extracellular compartment and about 25% remains in the intravascular compartment. Q. Name 3 disadvantages of colloids? Risk of pulmonary oedema/respiratory failure, interference with coagulation, risk of anaphylactic or transfusion reactions, cost Q. What types of fluid loss are crystalloids better for (give specific examples)? severe vomiting, diarrhoea, diabetic ketoacidosis, bowel obstruction Q. What is the advantage of Hartmann's? Less likely than normal saline to cause a hyperchloraemic acidosis. Q. What type of fluid loss are colloids better for (give examples)? Severe acute volume depletion: haemorrhage, burns, severe sepsis. Talk/walk through how you would set up an IV infusion Gather appropriate equipment: fluid bag, giving set, extension tubing if necessary, drip stand Explain to the patient what you are going to do and gain consent Check fluid prescription chart (type of fluid, volume ot be infused, period of time for infusion to run) Check bag with a colleague: expiry date, clarity of solution, presence/absence of additives Close wheel clamp on giving set line Pierce outlet port on bag with spike of giving set Squeeze fluid chamber and release repeat until chamber about half full Slowly open wheel clamp and run through fluid, removing air from tube Secure giving set to arm making sure there are no potential snags with clothing or bedding Check drip runs freely when opened and adjust drip rate according to prescription Sign fluid chart, noting start time.
Q. How do you calculate the drip rate? Drops per minute = volume to be infused (ml) x drops per ml (standard set is 20 drops/ml) / time in minutes - e.g. drops per minute = 1000 x 20 / 480 (8 hours) = 42 drops per minute Q. What are the average fluid requirements of an adult? A. 30-35ml/kg/24hr Q. Name three types of fluid loss? 1. Recordable (polyuria, NG aspirate, diarrhoea, vomiting, drains), 2. Insensible (wound leakage, pyrexia, tachypnoea, burns), 3. Third space (e.g. pancreatitis, post-op) Q. Estimate the fluid deficit for each of the following (in an adult): - HR < 100, BP normal, Urine output > 30ml/hr = < 750ml - HR >100, BP normal, urine output < 30ml/hr = 750-1500ml - HR > 120, BP reduced, urine output < 17ml/hr = 1500-2000ml Q. How might you gain a more accurate estimation of fluid requirements? A. Fluid balance chart Q. What are the average Na+ requirements? A. 2mmol/kg/24hrs ~ 140mmol/day Q. What are the average K+ requirements? A. 0.5-1mmol/kg/24hr ~40-60mmol/day Q. What are the U+Es reference ranges for Na+ and K+? Na+ 135-145 mmol/L, K+ 3.55 mmol/L 59
Q. What might be the best fluid to use in a patient with liver failure and ascites? A. 5% dextrose it containes no Na+ and excess Na+ causes ascities in chronic liver failure. Q. What might be the best fluid to use in a patient with acute renal failure? A. Colloid or saline but avoid K+ Q. What may be required in severe renal failure? A. restriction of Na+, K+ and fluid.
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Q. Which of the following would you use for cardiothroacic surgery if the patient had a penicillin allergy? Flucloxacillin, gentamicin, vancomycin, amoxicillin, co-amoxiclav Q. Which of the following would you use for ENT surgery if the patient had a penicillin allergy? Flucloxacillin, gentamicin, amoxicillin, clarithromycin, co-amoxiclav
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Blood Glucose is 4.2. You order some more blood tests and they come back with the following; Na+ 125 (135-145mmol/L) K+ 6.2 (3.5-5mmol/L) Urea 7.2 (2.5-6.7 mmol/L) Calcium 3.4 (2.12-2.65) TSH 11 (< 10 mU/L) Q. Give a possible diagnosis A. Addisons disease Potential examiners questions Q. What is Addisons disease? Endocrine disorder where the adrenal glands produce insufficient steroid hormones (glucocorticoids (e.g. cortisol) and often mineralocorticoids (e.g. aldosterone)). Q. How is it diagnosed? Short ACTH stimulation test Q. Name some symptoms of Addisons disease: A. fatigue, loss of appetite, weight loss, nausea, abdominal pain, myalgia, salt craving Q. Name some signs of Addisons disease: Areas of hyperpigmentation on skin and mucous membranes. Low BP. Q. How is Addisons diagnosed? Short ACTH stimulation test (Synacthen test): Do plasma cortisol before and 30 minutes after giving 250g Synacthen IM. Addison's excluded if 2nd cortisol >550nmol/L. Q. How is it treated? ~15-25mg hydrocortisone daily, in 2-3 divided doses eg 10mg on waking, 5mg lunchtime. Can cause insomnia. Mineralocorticoid replacement may be needed eg if postural hypotension, Na+, K+ or plasma renin: fludrocortisone PO from 50-200g daily. Adjust both on clinical grounds. If poor response to treatment, suspect associated autoimmune disease (check thyroid, do coeliac serology). Q. What should you tell the patient about their treatment? Warn against abruptly stopping steroids. Inform Doctors/dentists/surgeons of steroid use: give steroid card, advise wearing a bracelet declaring steroid use. Add 5-10mg hydrocortisone to daily intake before strenuous activity/exercise. Double steroids in febrile illness, injury or stress. Patients should be given syringes and in-date IM hydrocortisone, and shown how to inject themselves in case vomiting prevents oral intake. If vomiting, take hydrocortisone 100mg IM, and seek medical help. Q. How might an addisonian crisis present? Patient acutely ill, hypotension (esp postural), weakness, confusion, feeble rapid pulse and soft heart sounds, pyrexia common, 64
anorexia, nausea, vomiting, severe abdominal pain, increased motor activity progressing to delirium or seizures. Q. What is the treatment for an Addisonian crisis? Hydrocortisone 100mg IV stat, cefuroxime 1.5g IV, give IV fluids (i.e. treat shock)
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2.10 Catheterisation
You are a FY1 in urology. Mr Johnson has presented with acute urinary retention. You decide he needs a urinary catheter. Explain to the patient what you would like to do, then insert the catheter talking through each step as you go. Introduce self. Elicit name, age and occupation. Establish rapport. Because of the problems you are having I would like to insert a flexible plastic tube through your penis and into your bladder to relieve the pressure. It should not be painful but may feel a little uncomfortable. Ill just need to go and get someone else to help me with this. Do you have any questions? Obtain consent and get a chaperone Gather: Catherisation pack, catheter bag, sterile gloves, lignocaine gel, Foley Catheter 16 or 18 (male), antiseptic solution, 10ml sterile water filled syringe, adhesive tape, 10ml saline solution. Wash hands, put on an apron and clean the trolley Ask the patient to undress from the waist and ask him to retract his foreskin Drop the catheter pack on to the trolley and unwrap it, touching only the outside of the packaging. Drop the equipment that is wrapped from its wrapping on to the sterile area. Pour sterile water into small bowl with cotton wool. Don sterile goves Open LA jelly and stick catheter tip into it Make hole in drape and place on patient so that penis passes through the hole. Wrap gauze around penis using left (or non dominant) hand. Clean the penis using the wet swabs and a pair of tweezers. Alternatively use dominant hand being extremely careful not to touch the penis with the hand. If in any doubt, change gloves. Still holding penis with left hand, insert the tip of the syringe and put in 5ml of the local anaesthetic. Hold for 3-5 minutes. Talk about the weather/politics/holiday! Put catheter in kidney dish and place kidney dish between patients legs Holding the penis vertically, insert the catheter into the urethra. Keep the end of the catheter over the tray to catch any urine. If resistance is encountered, lower the penis to a horizontal position to negotiate the prostate. When the catheter is fully inserted, inflate the balloon with 1ml sterile water and ask patient to let you know if they feel any pain. If not, continue with remaining 9ml. Tug on catheter to ensure balloon lodged in neck of baldder. Attach drainage bag to end of catheter and REPLACE THE FORESKIN or ask the patient to do so (paraphimosis) Document in notes, writing in size of catheter, lot numbers and residual volume of urine collected. Dispose of waste appropriately. Thank the patient and ask them to let someone know if they experience any pain or discomfort
Potential examiners questions Q. What are the indications for catheterization? A. Monitoring of urine output, acute urinary retention, chronic obstruction, irrigation of the bladder, imaging Q. What are the contraindications? A. Pelvic trauma, previous stricture, previous failure to catheterize, severe phimosis Q. What are the potential complications? A. Paraphimosis, urethral perforation/trauma, bleeding, infection, urethral strictures 67
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A. < 0.5%, < 0.5%, , 0.1% respectively Q. What is the transmission risk of Hep B, C and HIV? (Hep B if not vaccinated) A. 1 in 3, 1 in 50, 1 in 300 respectively Q. What is triple therapy? A. combination of three drugs including either a protease inhibitor or a non-nucleoside analogue reverse transcriptase inhibitor (NNRTI) and two nucleoside analogue reverse transcriptase inhibitors (NRTIs)
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Potential examiners questions: Q. What type of blood may be used if crossmatch not available? A. Rh O Negative Q. When giving blood, what should you monitor? A. HR, BP, RR, Temp Q. What might you use to correct anaemia or blood loss? A. Packed red cells See also notes/OHCM
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2.14 Blood transfusion: explain, take blood, fill in form (2006, 2008)
Mr David Doolan has had shortness of breath on exertion for two weeks. A recent blood test revealed a haemoglobin of 8g/dL. He needs 2 units of blood. Explain the procedure to him, take a blood sample, and fill in the form to request 2 units of blood. Introduce self. Elicit name, age and occupation. Establish rapport. Establish level of understanding: e.g. Hello Mr Doolan, I understand you have been experiencing shortness of breath over the last couple of weeks. pause, he may help you out, if not Has anyone spoken to you about what might be causing this?
EXPLANATION We have done some tests and have found that you are low on red blood cells. These are the cells that carry oxygen around your body, and this is most likely why you have been feeling short of breath. Normally your own body would make more of these cells but for some reason at the minute it is not doing this. We feel that the best way to treat this is to give you a blood transfusion that is to put blood from someone else into your veins Elicit concerns: Im going to go on and explain this in a bit more depth, but before I do, do you have any concerns. acknowledge these and let her know you will address them. Safety: Like all medical procedures, there are some risks involved with receiving a blood transfusion, but these risks are very low. They include; o Being given the wrong blood but there are procedures in place which makes this very unlikely (If we decide to go ahead, wed need to take a sample of your blood, to check what your blood type is) o Getting an infection from the blood or equipment again, risk is very low. Blood donors are carefully screened. E.g. Risk of Hep B is 1 in 500,000, Hep C 1 in 30 million, HIV 1 in 5 million o There is a very small risk of CJD, but donated blood has the white cells removed to reduce this risk Practicalities: Usually given through little tube directly into a vein in arm. Bag of blood can take up to 4 hours. You may need three bags so this could take a while. How will you feel during transfusion?: Most people do not feel anything. A nurse or doctor will observe you at regular intervals to check that you are feeling well. If you do start to feel unwell you should let a member of staff know straight away. o You might develop a temperature, chills or a rash. These reactions are usually mild and are easily treated with paracetamol, or by slowing the transfusion. Severe reactions to blood are extremely rare, but staff are trained to recognise and treat these. Time to think: How does that all sound so far? Offer an information leaflet, and time to think if time allows. Consent: Obtain written consent. Before we go any further I just need to check that you agree that it is OK for us to go ahead with giving you a blood transfusion (LTHT policy is that written consent should be obtained wherever possible; www.leedsth.nhs.uk/sites/board_meetings/agenda.../TransfusionPolicy.doc ). VENEPUNCTURE Explain: Id like to take some blood so that we can find out what your blood type and give you the correct blood. This would involve putting a band round your arm and inserting a thin needle into one of your veins. You may feel a sharp scratch as the needle is inserted. Its a simple and quick routine procedure. Do you have any questions? Double check patients ID (first & last name & date of birth) verbally and match with wristband. Ensure patient is sitting comfortably. Collect equiptment: Kidney dish, gloves, green needle, tourniquet, vaccutainer, blood bottle (below), chloraprep, cotton wool, micropore
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Wash hands Apply tourniquet Find vein (mention techniques that may help) Clean with chloraprep in crosshatch & let dry Stabilize vein and insert needle at 15-30 Fill bottle appropriately and remove bottle Release tourniquet Remove needle and place cotton wool over wound site. Dispose of sharp immediately in sharps bin, dispose of other waste appropriately Label the blood bottle at bedside with surname, first name, date of birth, hospital number, date, and sign. Complete the relevant form (see below) FORM COMPLETION Fill in the form as shown below
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Procedure Explain that upper half of clothing will need to be removed, including bra if female. Explain need for chaperone Advise patient to remove watches and jewellery Provide patient with something to cover themselves Allow patient privacy to undress and get chaperone Advise to lay flat and keep limbs relaxed Plug ECG machine in an apply electrodes as shown Connect limb wires Connect chest wires working from V1 V6 Start machine Allow paper to run through Remove wires and pads Give pt privacy to dress Advise when/where results will be available
Interpretation Intro - Confirm patients name, age, and ECG date Rate (usual paper speed = 25mm/s) divide 300 by the number of big squares per R-R interval (e.g. 3 big squares = 100 bpm). Each big square is 0.2 seconds. Whole page = 10sec so x6 Rhythm mark position of 3 R waves on a piece of card and slide along Axis roughly speaking, if o I and II are positive, axis is normal. o I is ve = Right axis deviation o II, III ve = Left axis deviation P-wave absent = AF, sinoatrial block, disassociated with QRS = complete heart block, bifed = left atrial hypertrophy, peaked = right atrial hypertrophy P-R interval (start of P wave to start of QRS) normal range 3-5 small squares (0.12-0.2 sec). Prolonged = delayed AV conduction (1st degree HB). Short may be congenital, WPW. QRS normal = < 0.12s (3 small squares). If greater suggests ventricular conduction defects (eg BBB). Large QRS suggest ventricular hypertrophy. QT Measure from start Q to end T. Varies with rate. QTC = QT / sqrtR-R. Normal QTC = 0.38 - 0.42. Prolonged QT acute myocardial ischaemia, myocarditis, bradycardia, head injury, hypothermia, U&E imbalance, drugs etc. ST usually isoelectric. Elevation > 1mm = infarction, or depression < 0.5 = ischemia T abnormal if inverted in I, II, V4, V5, V6. Peaked in hyperkalaemia and flattened in hypokalaemia.
Potential Examiners Questions Q. What is atrial fibrillation? Supraventricular arrhythmia characterised by complete absence of coordinated atrial contractions. 74
Q. Interpret the following ECGs (overleaf) 1. Normal, 2. Anteroseptal MI, 3. Atrial Fibrilation, 4. Atrial Flutter, 5. Paroxysmal supraventricular tachycardia, 6. Atrial flutter, 7: VF
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ECG 1:
ECG 2:
ECG 3:
ECG 4:
ECG 5: 76
ECG 6:
ECG 7:
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2.14.1
Q. How would you diagnose AF? Regularly irregular pulse, ECG - absent P waves Q. What is atrial flutter? More organised and regular form of atrial activation = sawtooth pattern on ECG. Q. What are the symptoms of AF? May be asymptomatic, palpitations, dizziness, chest pain, anxiety, SOB Q. How is AF classified? (4 categories) 1) First detected AF = first clinical presentation, 2) Paroxysmal AF = recurrent episodes (not more than 7 days) that eventually self-terminate (within 48 hours), 3) Persistent AF = > 7 days, not self terminating. 4) Permanent AF = All attempts to restore sinus rhythm abandoned. Q. Name some causes or risk factors for AF Acute: Binge drinking, surgery, myocarditis or pericarditis, hyperthyroidism, drugs Cardiovascular disease: Hypertension, CHF, Valvular disease (esp mitral) , atrial septal defects, sick sinus. Pulmonary disease: COPD, emphysema, pulmonary hypertension, pneumonia, bronchiectasis, PE, lung cancer Other: Obesity, sleep apnoea, diabetes mellitus Q. What is the CHADS2 score? Clinical prediction rule for estimating the risk of stroke in patients with non-rheumatic atrial fibrillation (AF). C Congestive heart failure 1 , H Hypertension more than 160 Hg (or treated hypertension) 1 , A Age >75 years 1 D Diabetes Mellitus 1, S2 Prior Stroke or TIA 2; Annual Stroke Risk: 0=1.9%, 1=2.8%, 2=4.0, 3=5.9, 4=8.5, 5=12.5, 6=18.2 Q. What are the key principles of management for atrial fibrillation? Restore sinus rhythm, control ventricular rate, prevent recurrence, preventing thromboembolic events Q. When is immediate electrical cardioversion indicated? If rapid ventricular rate & either haemodynamically unstable or evidence of acute ischaemia or heart failure that doesnt respond to pharmacological measures. Q. What INR should you aim for before cardioconversion? If stable & rate controlled 2.0-3.0 three weeks before, if urgent & duration > 48 hours arrange transoesophageal echocardiography to prove absence of thrombus Q. Is cardioversion appropriate for the elderly? Ventricular rate control may be as effective as rythm control Q. What is the first line choice for pharmacological cardioversion? Propafenone, flecainide, or amiodarone. Q. What is commonly used to prevent recurrences? Side effects? Sotalol and amiodarone. Can prolong the QT interval, polymorphic ventricular arrhythmias. (esp sotalol). Q. What other drugs might you consider? In selected pts; beta blockers, calcium channel blockers, and digoxin Q. Whch drugs should be avoided in patients with heart failure? Flecainide and propafenone (risk of ventricular proarrhythmia and sudden cardiac death). Q. Which drugs should be avoided in patients with hypertension and left ventricular hypertrophy Sotalol (increased risk of QT prolongation). Use Amiodarone instead. Q. What is considered adequate rate control? 60-80 bpm at rest and 90-115 bpm during exercise. 78
Q. What drugs are comonly used for rate control? Beta blockers (e.g. atenolol, propranolol), non-dihydropyridine calcium channel blockers (verapamil and diltiazem), Digoxin (restrict to sedentary, less active pts). Q. When should aspirin be considered? When <65, no hypertension, no diabetes mellitus, no previous cerebrovascular accidents, no left ventricular dysfunction, no co-existent ischaemic or valvular heart disease, no hyperthyroidism, and no presence of prosthetic valves. Otherwise Warfarin. Q. If Warfarin is being used, what is the target INR? 2.0 - 3.0.
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You notice that you have given penicillin to this patient, but they have a penicillin allergy. Speak to the patients granddaughter to explain what has happened and what to do from here. See section 1.5
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Potential examiners questions Q. Discuss reversible causes of respiratory/cardiac arrest A. see above Q. Which rhythms are shockable? Whats PEA? Pulseless electrical activity In VF/VT, defibrillation must occur without delay: 360J (150-360J biphasic). Asystole and electromechanical dissociation (synonymous with pulseless electrical activity) are rhythms with a poorer prognosis than VF/VT, but potentially remediable. 81
Obtain IV access and intubation if possible. Look for reversible causes of cardiac arrest, and treat accordingly. Check for pulse if ECG rhythm compatible with a cardiac output. Reassess ECG rhythm. Repeat defibrillation if still VF/VT. All shocks are 360J. Send someone to find the patient's notes and usual doctor. If IV access fails, adrenaline, atropine, and lidocaine may be given down the tracheal tube but absorption is unpredictable. Give 2-3 times the IV dose diluted in 10mL 0.9% saline followed by 5 ventilations to assist absorption. Intracardiac injection is not recommended.
When to stop resuscitation No general rule. In patients without myocardial disease, do not stop until core temperature is >33C and pH and potassium are normal. Consider stopping after 20min if refractory asystole or electromechanical dissociation. After successful resuscitation: Investigations 12-lead ECG; CXR, U&Es, glucose, blood gases, FBC, CK/troponin. Transfer to coronary care unit/ITU. Monitor vital signs. Whatever the outcome, explain to relatives what has happened. When do not resuscitate may be a valid decision (UK DoH guidelines) If a patient's condition is such that resuscitation is unlikely to succeed. If mentally competent patient has consistently stated or recorded DNR request. If the patient has signed an advanced directive forbidding resuscitation. If resuscitation is not in a patient's interest as it would lead to a poor quality of life (often a great imponderable!). Involve patients and relatives in decision before emergency. When in doubt, resuscitate. Should be competent to: Initiate appropriate action o See ALS logarithm Prescribe appropriately, basic knowledge of the doses of COMMON & EMERGENCY drugs o Adrenaline 1mg in 10ml o Atropine 3mg in 10ml (muscarinic receptor antagonist) o Amiodarone 300mg in 10ml (antiarrythmic) o Always give 20ml saline flush to encourage into central circulation Atropine is muscarinic receptor antagonist used to inhibit the effects of excessive vagal activation on heart. Can temporarily revert sinus bradycardia to normal sinus rhythm and reverse AV nodal blocks.
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Potential examiners questions Q. What is Anaphylaxis? A. Type I IgE-mediated hypersensitivity reaction. Release of histamine and other agents causes: capillary leak; wheeze; cyanosis; oedema (larynx, lids, tongue, lips); urticaria. More common in atopic individuals. Q. Common precipitants? Drugs: eg penicillin, and contrast media in radiology, latex, stings, eggs, fish, peanuts, strawberries, semen Q. Signs and symptoms? Itching, erythema, urticaria, oedema, wheeze, laryngeal obstruction, cyanosis tachycardia, hypotension 83
Possible examiners questions overleaf Well done. He is now haemodynamically stable and has had an endoscopy. 84
What would you want to do next? - Check his drug chart and stop NSAIDs if possible - Give omeprazole 40 mg IV after endoscopy (reduces risk of rebleeding and need for surgery). - Check FBC, U&E, LFT, and clotting daily. - Keep nil by mouth for 24h. Allow clear fluids after 24h and light diet after 48h, if no rebleeding How is risk assessed in cases of GI bleeds? The Rockall Score
Indications for surgery? - Severe bleeding or bleeding despite transfusing 6U if >60yrs (8U if <60yrs) - Rebleeding - Active or uncontrollable bleeding at endoscopy - Initial Rockall score >=3 or final Rockall score >6. Common causes of GI Bleeding? Mallory-Weiss tear, Oesophagitis, Oesophageal varices, Peptic ulcers, Gastritis/gastric erosions, Duodenitis, Malignancy, Drugs (NSAIDs, aspirin, steroids, thrombolytics, anticoagulants), Rarer causes of GI Bleeding? Bleeding disorders, Portal hypertensive gastropathy, Aorto-enteric fistula, Angiodysplasia, Haemobilia (bleeding in biliary tree), Dieulafoy lesion (arteriole in stomache erodes and bleeds), Meckel's diverticulum, Peutz-Jeghers' syndrome (hereditary intestinal polyposis), Osler-Weber-Rendu syndrome (hereditary hemorrhagic telangiectasia (HHT)) 85
Offer to complete a death certificate, inform the patients GP and the next of kin. Offer to inform the coroner if relevant
Potential examiners questions Q. When does rigor mortis set in? A. 3 hours after death Q. Legally, when can you fill in a death certificate? A. If I have seen patient in last 14 days and cause of death does not require referral to coroner. Q. When would you need to inform the coroner? A. Within 24 hours of admission, 86
suspicious, accidental, violent (including RTAs), suicide, operation, anaesthetic or procedure in last year (including endoscopy, chest drain, central lines etc.), alcohol or drugs, cause of death uncertain, due to industrial disease. Not seen by doctor in last 14 days. See over for death certification DEATH CERTIFICATION John Smith was a 85 year old retired teacher. Two years ago he was diagnosed with multi-infarct dementia. He has had hypertension and diabetes for the last 15 years. One evening his wife found him collapsed on the floor unable to move his right side. He was brought into hospital and admitted under your team with a diagnosis of stroke. Despite the efforts of your team he died 6 days later. You last saw him the day before he died and there was no sign of pneumonia or heart failure. Complete the death certificate as accurately as possible. See sample death certificate overleaf Use black ink Enter: o patients name, date of death, the age at death, place of death o Date last seen alive by you In this case there is no need for a post-mortem, so you would ring 3 and a I (a) Disease of condition directly leading to death: Cerebrovascular accident (b) Other disease or condition, if any, leading to I (a): Atherosclerosis (c) Other disease or condition, if any, leading to I (b): Hypertension(I checked & hypertension is thought to cause atherosclerosis). Employment: The disease or condition was not thought to be related to employment in this case. Your details: Sign, print full name, medical qualification (e.g. MBChB), date. Consultant: Enter the name of the consultant in charge of the patients care Notice to informant: Complete notice to informant, sign and date Coroner: There are no indications for referring to the coroner in this case.
Potential examiners questions: Q. What are the reasons for referring a patients death to the coroner? A. Within 24 hours of admission, suspicious, accidental, violent (including RTAs), suicide, operation, anaesthetic or procedure in last year (including endoscopy, chest drain, central lines etc.), alcohol or drugs, cause of death uncertain, due to industrial disease. Q. Can you fill in a death certificate if one of your colleagues (but not you) has seen the deceased in the last 14 days? A. No See death certificate overleaf.
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Q1. What is the likely diagnosis and what would your initial management be? Q2. What further investigations would you like to carry out? Start simple! Q3. How would you assess how severe her pneumonia is? Q4. What is the MEWS score? Q5. Assume this is community acquired pneumonia talk through the drug treatment you would prescribe depending on severity Q6. Assume this is hospital acquired pneumonia talk through the drug treatment you would prescribe depending on severity Q7. What else may be required? Q8. What is the commonest cause of community acquired pneumonia? Q9. What is the commonest cause of hospital acquired pneumonia? Q10. What are the potential complications of pneumonia? Answers 89
A1. Right middle lobe pneumonia. Her SaO2 is < 92% so she should be given high flow oxygen. A2. Further investigations: - Simple obs: Respiratory Rate, Blood Pressure, - Bloods: FBC, U&Es, LFT, CRP, atypical serology - pleural fluid maybe aspirated for culture - Bronchoscopy or bronchoaveloar lavage if patient immunocompromised A3. CURB65 score. If urea >7, CURB65 >=3 (confused, urea>7, age>=65), so manage in hospital. Describe as below A4. Modified early warning Score (see overleaf) used to determine risk of death and hence level of intervention reqd A5 & A6. Drug treatment for community acquired pneumonia depends on CURB65 score (see below). Drug treatment for hospital acquired different see Leeds Guidelines below (September 2009 guidelines). A7. If her BP is low (systolic<90 = shock) or dropping, she will require fluid resuscitation. She may need analgesia for chest pain (e.g. paracetamol 1g/6h or NSAID). She may require intubation or ventilatory support. She should be offered Pneumococcal vaccine in future. A8. Streptococcus pneumonia, haemophilus influenzae, mycoplasma pneumoniae in that order A9. Gram negative enterobacteria or staph aureus. A10. Pleural effusion, empyema, lung abscess, respiratory failure, septacemia, brain abscess, pericarditis, myocarditis, cholestatic jaundice
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2.21 TIA, management, guidelines (2009)
You are a FY1 working in A&E. Mr George presents having had a funny turn. Take a history, suggest a diagnosis, and outline the management. Instructions to actor: You are Mr George and are 55 years old. Yesterday, you experienced a weakness in your right arm and your wife noticed that you slurred speech at the same time. It lasted 30 minutes and now you are fine. You have not had anything like this before. You are a taxi driver. You have not been to your doctor for many years. You didnt fall. Fill in the blanks, but stick to what would be a TIA diagnosis. Introduction and establish rapport. Confirm name, age, occupation Explain that you would like to ask them some questions about the problem theyve experienced HPC: Site of problem Onset of symptoms (sudden or gradual?) Character of problem (deteriorating or improving?) Radiation (did it go anywhere else?) Associated symptoms Timing (how long did it last?) Exacerbating/Relieving factors/Predisposing events (any history of trauma?) Specific questions Was the arm weakness associated with any sort of fit / jerking motion? (no) Did anyone witness the event? (yes, wife) What happened before and afterwards? (sudden onset & resolved quickly) Did the patient fall? (no) Other neurological symptoms o Headache, change in consciousness, Drowsiness / sleeping (no) o Changes in smell/vision/hearing, sensory disturbances, parasthesiae (no) Features of anterior cerebral artery involvement: Paralysis of opposite leg, sensory deficits, gait apraxia Middle cerebral artery As above + hemianopsia, amaurosis fugax, aphasia, agnosia Posterior cerebral artery Hemianopsia, visual agnosia, cortical blindness Vertebrobasilar Vertigo or nystagmus, facial numbness, dysarthria, loss of pain and temp, diplopia & visual field defects, bilateral spasticity PMH: Investigations and treatment to date, Previous stroke/TIA, BP, IHD, AF, PVD, Diabetes, cholesterol. DH: Including over the counter, Allergies FH: First degree relatives with a history of CVA, TIA etc SH: Occupation, smoking, alcohol, marital status, living accommodation, ADLs Review of systems: Cardio, Respiratory, GI, Urogenital, Metabolic Possible examiner questions Q1. What are your differential diagnoses? Q2. What is a TIA? Q3. What investigations would you like to do and why? Q4. How would you assess the risk of stroke in this patient? Q5. What features would suggest a carotid Doppler is NOT required? Q6. How would you treat this patient? Q7. What advice would you want to give this patient? Q8. What is the prognosis? (combined risk of stroke & MI?) (See also 2008 SIGN guidelines on following pages) 92
TIA Management A1. TIA, focal epilepsy, migraine aura, MS, peripheral neuropathy, hypoglycaemia A2. Sudden focal CNS phenomenon due to temporary occlusion lasting <24 h A3. Investigations based on Leeds guidelines; http://www.leedsteachinghospitals.com/sites/emibank/LGICDUProtocolTIA-13.07.swf o Obs: temp, BP, pulse o Examination: Full examination including a neurological examination o Investigations: FBC, U&Es, Glucose, Cholesterol, ECG, CXR (if smoker or chest complaint), urinalysis A4. Assess risk of stroke using ABCD2; * A Age: 60 years of age or older, 1 point. * B Blood pressure at presentation: 140/90 mmHg or greater, 1 point. * C Clinical features: unilateral weakness, 2 points; speech disturbance without weakness, 1 point. * D Duration of symptoms: 60 minutes or longer, 2 points; 1059 minutes, 1 point. * D Diabetic: 1 point. People with a score of 4 or more are regarded as being at high risk of an early stroke. A5. According to Leeds guidelines, a carotid Doppler is not required if symptoms are confined to those characteristic of posterior cerebral artery or vertebrobasilar artery involvement. A6. Treatment depends on risk assessment: o o If symptoms present during examination, refer to medicine (<65 years) or stroke unit (>65 years) If ABCD2 score >=4 aspirin (300 mg daily) started immediately specialist assessment and investigation within 24 hours of onset of symptoms secondary prevention measures introduced as soon as diagnosis confirmed If ABCD2 score < 4 as above, but specialist investigation should be within 1 week rather than 24 hours Secondary prevention: smoking cessation, antihypertensive, statin If AF, mitral stenosis, septal MI consider warfarin Carotid endarterectomy in carotid TIA if operative risk is good Further treatment details on following pages
o o o o o
A7. Avoid driving for >=1 month. Inform DVLA if multiple attacks or residual deficit. A8. Combined risk of stroke and MI following a TIA is ~9%/year (See also 2008 SIGN guidelines on following pages)
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Instructions to Candidate: Below are some test results. What is the likely diagnosis? Hb ESR CRP WCC Albumin 11.5g/dL (13-18) 25 mm/L (<20) 15 mg/L (<10) 15 x 109/L (4-11) 20 g/L (35-50)
Instructions to Candidate: The diagnosis is Crohns, how is it managed? Mild attacks are treated with Prednisolone 30mg/d PO for 1 week, the 20mg/d for 1 month. 2-4 week follow ups, reducing prednisolone by 5mg every 2-4 weeks with aim of stopping when parameters normal. Severe attacks: admit for IV steroids, nil by mouth and IV hydration (e.g. 1 L saline = 2L dextro-saline /24h + 20 mmol K+), then hydrocortisone 100mg/6h IV, topical steroids for rectal disease, metronizadole 400mg/8h. If improving after 5d transfer to oral prednisolone 40mg/d Additional therapies include: Azathioprine, Methotrexate, Surgery (50-80% need =>1 op in life), Infliximab effective at reducing remissions. 96
Instructions to Candidate: Explain probable diagnosis, investigations & management to the patient (see 1.17 & 1.18)
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Ultrasound to look for hydronephrosis or hydroureter Q5. How would you manage this lady? Analgesia (diclofenac 75mg IV or IM). IV fluids if unable to tolerate orally, antibiotics (e.g. cefuroxime 1.5g/8h) if infection, seek urological help urgently if evidence of obstruction: extracorporeal shockwave lithotripsy (ESWL), or percutaneous nephrolithotomy (PCNL). If no obstruction: fluids & sieve urine, <5mm pass spontaneously.
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2.24 Thyrotoxicosis(2005)
Instructions to candidate: You are an FY1 on a general medical firm. Please take a history off this 48 year old female who has presented with weight loss. Instructions to actor: I am a 48 year old (female) hairdresser. I have lost over a stone in the last three months but I have not been trying to lose weight. My appetite has changed I am eating more than I used to but still losing weight. I am concerned because this happened to my mum before she died of cancer. My husband says that I am crabby and irritable lately. He also says that I am unable to sit still. My muscles ache a bit recently. Ive noticed my hand trembles slightly when Im drinking a cup of tea. I have some palpitations (Ive got AF). Im hot all the time and I sweat more than I used to. My stools are a bit loose than they used to be. My son says my eyes look a bit goggley. I get a bit of double vision when Im tired. My periods have become infrequent, but I put this down to the change. Introduction and establish rapport. Confirm name, age, occupation PC/HPC: Confirm weight loss and ask about onset, duration, amount & if intentional. Also ask about; o change in appetite o difficulty concentrating o muscle weakness o heat intolerance, excessive sweating o agitation or restlessness o diarrhoea/changes in bowel habit o eye changes/changes in vision o palpitations o tremor o difficulty swallowing or breathing o pretibial myxoedema o changes in periods PMH: Other autoimmune disorders: diabetes, Addisions, vitiligo, myasthenia gravis, cancer, thyroid problems, previous surgery DH: e.g. thyroxine SH: Alcohol, tobacco, exercise, diet, social circumstances, employment FH: Any FH of autoimmune disorders? Allergies
Potential examiners questions Q. What are the common causes of hyperthyroidism? Graves disease (due to autoantibodies directed at the TSH receptor. Also toxic multinodular goitre, toxic adenoma (Plummers disease), Iatrogenic, drug induced (lithium, amiodarone), transient thyroiditis (e.g. de Quervains). Q. What treatment options are available? Anti-thyroid drugs: Carbimazole (methimazole), propylthiouracil, or methimazole. Side effects: nausea, bitter taste, hepatotoxiciy, vasculities, agranulocytosis: warn patients to come for FBC if they develop sore throat etc. (0.5% of patients). Radioiodine: given as drink (not if pregnant or breast feeding females or planning to get pregnant in next 4 months), may worsen eye disease in Graves'. Avoid close contact with children and pregnant women. Sleep alone for a week. Surgical: Sub-total or near total thyroidectomy (98% cure rate). Complications: haemorrhage, hypoparathyroidism, vocal cord paralysis, hypothyroidism. Q. What is a thyroid storm? Exxagerated manifestation of hyperthyroidism precipitated by major stressors (20-50% mortality). Symptoms: palpitations, tachycardia, tachyarrythmia, cardiac failure, anxiety, agitation, high fever. Jaundice is a late and ominous sign.
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Q. What is the immediate management of a suspected thyroid storm? ABC, IV infusion, beta blocker infusion, cooling blankets, paracetamol, propylthiouracil (blocks T4 production), iodine (blocks release of t4)
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Potential examiner questions: Q1. What investigations would you like to do? ABPI, Buergers test (<20 and filling < 15sec = severe ischaemia) Bloods: FBC (anaemia/infection),Glucose (diabetes), ESR/CRP (exclude arteritis), U&E (renal disease contrast contraindicated), lipids, ECG (cardiac ischaemia). Contrast arteriography or colour duplex imagining to assess extent and location of stenoses. Q2. What drug should you stop before doing angiography? Metformin to prevent metabolic acidosis Q3. How would you interpret ABPI results? >=1 normal, 0.9-0.6 = claudication, 0.3-0.6 = rest pain, <=0.3 = impending gangrene. Q4. What are the signs of peripheral arterial disease? 6 Ps Pain, pallor, pulseless, parasthesia, paralysis, perishing cold Q5. How would you manage this patient? Quit smoking, weight, supervised exercise programme, blood glucose control if diabetic, treat hypertension and high cholesterol (avoid B blockers). Percutaneous transluminal angioplasty, surgical reconstruction (arterial bypass graft (femoral-popliteal, femoro-femoral, aorto-bifemoral bypass grafts). Aspirin and warfarin help grafts remain patent. Sympathectomy (interruption of nerve supply), amputation. Q6. What is the treatment for acute limb ischaemia? Open surgery, angioplasty, surgical embolectomy (fogarty catheter), thrombolysis (e.g. tissue plasminogen activator 101
(tPa)), anticoagulate with heparin after either procedure. Be aware of reperfusion injury and subsequent compartment syndrome. Q7. How can you classify the severity of PV disease? Fontaine classification: I: Asymptomatic, II: Intermittent claudication, II-a: Pain free, claudication walking more than 200 metres, II-b: Pain free, claudication walking less than 200 metres, III: Rest or nocturnal pain, IV: Necrosis or gangrene.
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What helps prevent renal stones? fluid intake, if hypercalciuria, thiazide diuretic calcium excretion. If oxalate intake (tea, chocolate, nuts, strawberries, rhubarb, spinach, beans, beetroot). If urate urine alkalinization may help.
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Differential diagnoses? Renal failure, DM, DI. Others: DM, cancer, depression, anxiety, alcohol, recreational drugs, anaemia, hypothyroid, infections, menopause, insomnia, heart failure, antihistamines, sedatives, chronic fatigue. Investigations? FBC (Hb; normochromic, normocytic), ESR, U&E (urea, creatinine), glucose (DM), if Ca, PO, Alk phos - renal osteodystrophy, PTH hyperparathyroidism, Urine MC&S, urine PCI or 24 hr protein. Imaging renal US may be larger in CRF with DM (> 9cm), polycystic kidney, amyloidosis, myeloma, systemic sclerosis, asymmetric renal vascular disease. Consider DTPA scan. CXR cardiomegaly, pleural pericardial effusions or pulmonary oedema. Bone X-Rays may show osteodystrophy. Renal biopsy if cause unclear and normal sized kidneys. Causes of chronic renal failure? Common: Glomerulonephritis, DM, renovascular disease, BP, pyelonephritis, polycystic disease. Rarer: Myeloma, amyloidosis, SLE, scleroderma, vasculitis, haemolytic uraemic syndrome, nephrocalcinosis, gout, renal tumour. Tests? Hb (normochromic, normocytic), ESR, U&E (urea, creatinine), glucose (DM); Ca2+, PO, alk phos (renal osteodystrophy); PTH. Urine: MC&S, dipstick, urine PCI or 24h urinary protein. Imaging: Renal ultrasound to exclude obstruction and check renal size (usually small, eg <9cm, but may be normal or large with CRF in DM, polycystic kidney disease, amyloidosis, myeloma, systemic sclerosis, asymmetric renal vascular disease). Consider DTPA scan. CXR: Cardiomegaly, pleural/pericardial effusions or pulmonary oedema. 105
Bone X-rays may show renal osteodystrophy. Renal biopsy should be considered if the cause is unclear and there are normal-sized kidneys. Treatment? Refer early to nephrologist. Treat reversible causes: relieve obstruction, stop nephrotoxic drugs, deal with Ca2+ and cardiovascular risk: Treat BP, oedema, anaemia, diet restrictions as deemed necessary
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Q. Present your history back to examiner. Q. Comment on the following U&Es sodium 135-145 normal potassium 3.5-5 raised urea 2.5-6.7 raised creatinine 70-150 raised Cl- 95-105 slightly low HCO3 22-30 normal 24 hr urine output 400-3000 normal A plasma creatinine > 300 suggests sever renal failure Q. How could you classify the degree of this patients renal impairment? Using the Cockcroft Gault formula it could be classified into stages 1 5, with 1 being normal and 5 being established renal failure. Q. List some possible causes of chronic renal failure. In this case previous renal damage as a child. Common: Glomerulonephritis, DM, renovascular disease, BP, pyelonephritis, polycystic disease. Rarer: Myeloma, amyloidosis, SLE, scleroderma, vasculitis, haemolytic uraemic syndrome, nephrocalcinosis, gout, renal tumour. Q. Is there anything you would like to change about the way this patient is being managed? Take him off NSAIDS as they exacerbate renal failure. Get his BPH under control. Contact the renal physician. Q. Treatments for BPH? Assess impact on life. PR exam. Tests: MSU; U&E; ultrasound. Rule out cancer: PSA, transrectal ultrasound biopsy. Consider: Transurethral resection of the 107
prostate (TURP). Transurethral incision of the prostate (TUIP), Transurethral laser-induced prostatectomy (TULIP). Drugs: blockers: eg tamsulosin 400g/d. 5 reductase inhibitors: finasteride 5mg/d PO. Saw palmetto said to help.
Potential examiners questions Q. What are the common causes of hyperthyroidism? Graves disease (due to autoantibodies directed at the TSH receptor. Also toxic multinodular goitre, toxic adenoma (Plummers disease), Iatrogenic, drug induced (lithium, amiodarone), transient thyroiditis (e.g. de Quervains). Q. What treatment options are available? Anti-thyroid drugs: Carbimazole (methimazole), propylthiouracil, or methimazole. Side effects: nausea, bitter taste, hepatotoxiciy, vasculities, agranulocytosis: warn patients to come for FBC if they develop sore throat etc. (0.5% of patients). Radioiodine: given as drink (not if pregnant or breast feeding females or planning to get pregnant in next 4 months), may worsen eye disease in Graves'. Avoid close contact with children and pregnant women. Sleep alone for a week. Surgical: Sub-total or near total thyroidectomy (98% cure rate). Complications: haemorrhage, hypoparathyroidism, vocal cord paralysis, hypothyroidism. 108
Q. What is a thyroid storm? Exxagerated manifestation of hyperthyroidism precipitated by major stressors (20-50% mortality). Symptoms: palpitations, tachycardia, tachyarrythmia, cardiac failure, anxiety, agitation, high fever. Jaundice is a late and ominous sign. Q. What is the immediate management of a suspected thyroid storm? ABC, IV infusion, beta blocker infusion, cooling blankets, paracetamol, propylthiouracil (blocks T4 production), iodine (blocks release of t4)
Potential questions: Q1. Suggest some differential diagnoses. A. Recently started on beta blockers, hypoglycaemia, alcohol intoxication, vasovagal/situational/cough/micturition/carotid sinus syncope, epilepsy, stokes-adams attack, cardiac cause.... Q2. What investigations would you want to do and why? Obs temp, HR, lying and standing BP, glucose, GC, sats, RR. neuro exam, Investigations: look for injuries, ECG (consider 24hr monitor), FBC, U&Es, CRP, troponin at 12h, CT if focal neurology, GCS or head injury, X-Ray if fracture suspected, echo, ABG if GCS diminished, LFTs.
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Potential examiners questions: Q. What are your differential diagnoses? Most likely to be cancer of the head of the pancreas. Courvousiers law: in the presence of a palpable gall bladder, painless jaundice is unlikely to be caused by gall stones. Could also be; Pre-hepatic: haemolysis, Crigler Najjar syndrome, Gilbert syndrome Hepatocellular: Hepatitis A, B, C, D, E. alcohol, leptospirosis, autoimmune, cirrhosis Post-hepatic: intrahepatic: primary biliar cirrhosis, primary sclerosing cholangitis, cholangiocarcinoma, sepsis, hepatocellular disease. Extrahepatic: gallstones, benign stricture of CBD, lymphoma. Q. What investigations would you like to do? urine: MSU, bilirubin, urobilinogen. Bloods: FBC, reticulocytes, blood film, clotting, U&Es, LFTs, amylase, lipase, LDH, paracetamol levels, hepatitis serology (ABC), EBV and CMV serology, bld cultures,. Urgent USS abdo (dilated bile ducts, cirrhosis, mets). CT or MRI if abdominal malignancy suspected. Q. How is Ca head of the pancreas treated? < 10% suitable for radical surgery (pancreatoduodenectomy (Whipples)). Endoscopic or percutaneous stent may help jaundice and anorexia. Opiates may be required in large quantities, radiotherapy may help. Referral to palliative care is essential. 111
Q. What is the prognosis like? Mean survival < 6 months. 5 year survival < 2%.
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Q. What investigations would you like to do? ESR (in PMR), FBC (normochromic normocytic anaemia), CRP (), LFTs, autoantibody screen negative. Temporal artery biopsy (can confirm but not exclude), DEXA scan (assess need for osteoporosis prophylaxis). Q. How would you treat this patient? Initially high dose prednisolone (40-80mg od) for 46 weeks. Reduce by 5mg every 2-4 weeks. When 15mg reached, reduce by 1-2mg month. Most patients require 1-2 years of steroids. Azathioprine and methotrexate may also be used if steroids do not control disease Q. Difference between PMR and Fibromyalgia? Both=muscle pain. PMR is inflammatory, FM is not (abnormal sensory processing) FM chronic, PMR usually resolves. PMR associated with GCA, FM not.
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Q. What investigations would you like to do? FBC (Hb/WCC/plts), C3+C4, ESR (but CRP normal), ANA +ve (95%), Xray (periarticular osteoporosis), U&Es (check for renal disease), urinalysis (protein, blood, casts) Q. How would you treat this patient? Refer to rheumatologist? High factor sun block. NSAIDS for arthritis. Hydroxychloroquine 00-400mg od if NSAIDs ineffective. Low dose steroids in chronic disease. High dose prednisolone + IV cyclophosphamide in severe flares. Q. What might be making this patients condition worse? OCP (also sulfonamides) Drugs that may cause SLE? include isoniazid, hydrazaline, chlorpromazine, phenytoin, procainamide, minocyline. Q. What is antiphospholipid syndrome and what are the features of it? occurs secondary to SLE in 20-30%. Caused by antiphospholipid antibodies. CLOT Coagulation 115
defect, Livedo reticularis (mottled skin), Obstetric: recurrent miscarriage, Thrombocytopenia (platelets). Rx = low dose aspirin or warfarin (INR 2-3)
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Potential examiners questions. Q1. What are your differential diagnoses? CF, pneumonia, bronchiectasis, Kartageners syndrome, TB Q2. What is the pathogenesis of CF? autosomal recessive (1:2000 live births) affecting Caucasians. Caused by mutations in the CF transmembrane conductance regulator (CFTR) gene on chromosome 7. chloride secretion and sodium absorption across airway epithelium. Predisposes to chronic pulmonary infections and bronchiectasis. Q3. How is it diagnosed? Sweat test: sweat sodium and chloride >60mmol/L; chloride usually > sodium. Genetics: screening for known common CF mutations should be considered. Faecal elastase is a simple and useful screening test for exocrine pancreatic dysfunction. Q4. What other investigations would you like to do? Blood: FBC, U&E, LFTs; clotting; vitamin A, D, E levels; annual glucose tolerance test. Bacteriology: cough swab, sputum culture. Radiology: CXR; hyperinflation; bronchiectasis. Abdominal ultrasound: fatty liver; cirrhosis; chronic pancreatitis; Spirometry: obstructive defect. Aspergillus serology/skin test (20% develop ABPA, p160). Biochemistry: faecal fat analysis. Q5. How would you manage this patient? Best managed by a multidisciplinary team. Chest: Physiotherapy, antibiotics, mucolytics (eg DNase, ie Dornase alfa, 2.5mg daily nebulized). Bronchodilators. Gastrointestinal: Pancreatic enzyme replacement; vitamin supplements (A, D, E, K); ursodeoxycholic acid for impaired liver function; liver 117
transplantation, Other: Treatment of CF-related diabetes; screening for and treatment of osteoporosis; treatment of arthritis, sinusitis, and vasculitis; fertility and genetic counselling. Advanced lung disease: Oxygen, diuretics (cor pulmonale); non-invasive ventilation; lung or heart/lung transplantation. Q6. Prognosis? Median survival now >30yrs. Many live into 40s Q7. Counsel this patient on CF. See 1.2.1
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Potential examiners questions Q1. Differential diagnoses? Pseudomembranous colitis, gastroenteritis, IBD, IBS, Malabsorption, Bowel cancer, Diverticular disease, pancreatitis, drugs, hyperthyroidism. Q2. What investigations would you like to do? Obs, U&Es, FBC, glucose, MC&S (C.diff toxin?), LFTs, Ca2+ (in malabsorption), TFTs, CRP, Blood cultures, AXR (obstruction, faecal impaction), sigmoidoscopy if not improving, colonscopy/barium enema if cancer suspected, coeliac screen. Q3. What might you look for on examination? volume satus, cachexia, mouth ulcers, clubbing, jaundice, rashes, pallor, thyroid mass, abdo tenderness, (+/- peritonitis, masses, distention, surgical scars), PR faecal impaction, pain, masses, stool colour, consistency. 119
Q4. How would you treat pseudomembranous colitis? Oral metronizadole 400mg tds (vancomycin 125mg qds). Q5. What complications may occur? Toxic megacolon, performation, high risk of spread to others.
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Q1. What are your differentials? Benign stricture secondary to long term GORD ; - Mechanical: malignant stricture, benign stricture, extrinsic pressure (cancer, lymph nodes, aortic aneurysm, goitre, pharyngeal pouch. - Motility: Achalasia, oesophageal spasm, systemic sclerosis, myasthenia gravis, bulbar palsy, Chagas disease. - Others: Oesophagitis, Globus hystericus. Q2. What investigations would you like to do? FBC (anaemia), U&E (dehydration), CXR (mediastinal fluid level), barium swallow (oesophageal stricture) +/- video fluroscopy, upper GI endoscopy and biopsy. ENT opinion if suspected pharyngeal cause. Q3.How are Achalasia and Benign oesophageal stricture treated? Endoscopic baloon dilitation or botox (Achalasia only). Q4. What is Barretts oespohagus? In chronic reflux oesophagitis, columnar gastric epithelium extends upwards replacing normal oesophageal squamous epithelium. Intestinal metaplasia occurs in these cells. Changes visible on endoscopy. There is a 40-fold risk of oesophageal adenocarcinoma. Management: If pre-malignant oesophageal resection generally advocated, especially in younger, fit patients; endoscopic mucosal ablation by epithelial laser or photodynamic ablation is used in others.
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(2007)
You are a junior doctor in A&E and have been asked to see this 26-year-old female who took an overdose, was treated and is about to be discharged. Please take a focused history including a self harm/ suicide risk assessment. Introduce self and establish rapport Elicit patients name age and occupation Set the scene: I understand you took some tablets is that right? About the overdose sorry to go through this all again but... How do you feel about it all now? How long had you been thinking of it/planning beforehand? What tablets? How many? When? All at once/ staggered? With alcohol? What did you expect would happen? Did you go out to buy the tablets or have them in your house already? Did you take all that were available to you? Where were you? On your own? What had happened in the day? i.e. why then? Triggers e.g. arguments? Did you leave a note/ call anyone/ tell anyone what you were going to do? What happened? i.e. how did they come to hospital? Did you expect to be found? Want to be? Wish you hadnt been? What are the chances of you doing it again? If now unlikely, why? Has anything changed? Original triggers been resolved? Is there anything that might stop you? (protective factors) Are there tablets still at home? Is there anyone at home / any friends / family? assess level of social support Screen for depression: o Early morning waking/sleep disturbance o Loss of appetite/weight o Loss of energy and enthusiasm o View of environment, self and future o previous self harm/suicidal intentions o symptoms: mood, anhedonia, sleep, appetite, libido etc. duration. Family or personal history of mental illness Premorbid personality Drug, alcohol and smoking history Appropriate non verbal behaviour, appropriate questioning technique Summarises history back to patient, makes explicit empathic statements Systematic organized approach Ideas Concerns Expectations Summarise C - Check understanding, A Ask questions, L Leaflet, F arrange a Follow up Q. How might you assess if this patient needs psychiatric assessment? Modified SAD PERSONS scale Sex: Male = 1 , Age <19 >45yrs = 1, Depression or hopelessness = 2, Previous suicide attempts or Psychiatric care = 1, Excessive alcohol or drug use = 1, Rational thinking loss (psych or organic) = 2, Separated, widowed, divorced = 1, organised or serious attempt = 2, No social support = 1, Stated future intent (determined to repeat or ambivalent) = 2 Interpretation of Score < 6 may be safe to discharge (depending on circumstances) 6-8 probably requires psychiatirc consultation >8 probably requires hospital admission
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3 Examinations
3.1 Gait (2005, 2007 previous Yr 4 station)
Examine this patients gait. Present your findings to the examiner as you go along. (Play one of the videos overleaf and ask the candidate to describe the gait). Introduction: Elicit name, age, occupation. Establish rapport Consent: Explain the examination to the patient and seek consent Exposure: Position and expose the patients arms and legs adequately Sitting: First observe the patient whilst sitting and note any postural abnormality or instability Rising: First ask if pt able to stand and walk. Ask patient to stand up. Note any difficulty standing up (e.g. truncal ataxia = lack of co-ordination of muscle movements in the trunk). Offer support if unsteady. Walking: ask patient to walk to end of room, turn round and return. Permit use of an aid if needed. Observe each stage of gait cycle and comment on start, rate, type of gait, arm swinging and how they turn around. Heel to Toe: ask patient to walk in straight line, putting heel of one foot directly in front of toe of the other. Observe if pt veers to one side (cerebellar lesion) or has wide based gait and loss of balance (truncal ataxia) Rombergs test: Ask pt to stand with feet together and arms by side. Explain you will catch them if they fall. Ask them to close their eyes. Negative if less stable with eyes open (Cerebellar disease), positive if less stable with eyes closed (posterior column disease).
Additional tests if appropriate Tiptoe walking: S1 lesion makes this difficult, Heel walking: L4 / L5 lesion makes this difficult If appropriate asking patient to run may accentuate findings The pattern of wear on the shoes provides information about symmetry and nature of abnormalities Excessive lateral wear = genu varum, Excessive medial wear = genu valgum 1. 2. 3. 4. 5. 6. 7.
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= = = =
Thank patient and ask if they have any questions State that you would also wish to do a full neurological examination
Possible questions: 1. Causes of cerebellar disease? MS, stroke, alcohol, space occupying lesions, anticonvulsants 2. Signs and symptoms of ? DANISH dysdiadochokinesia, ataxic gait, nystagmus, intention 126
tremor, slurred speech and hypotonia 3. Cerebellar versus vermis lesions? Cerebellar worse on ipsilateral side, vermis usually bilateral eg truncal ataxia 3.1.1 Abnormal Gaits with video links Abnormalit y Antalgic gait: Trendelenbe rg gait: Bow legs (genu varum) Knock knees (genu valgum) Flat feet (pes planus) In-toeing Out-toeing Toe-walking Hemiplegic gait Diplegic gait Neuropathic gait Myopathic gait Choreiform gait Ataxic gait Parkinsonian gait Foot drop Causes altered to reduce pain. Treat the cause. Contralateral pelvis falls when weight bearing. Polio, paresis of superior gluteal nerve after hip replacement, congenital dislocation of the hip, pain eg osteoarthritis Bowing of tibia up to 3 years (seldom needs treatment). Rickets or Blounts disease. Orthoses or surgical correction may be required. Bilateral common usually physiological cause. Unilateral: often pathological (eg fibrous dysplasia). Usually resolves before the age of 6 Toddlers have flat arch and fat pad usually disappears. May be due to collagen disorder (Ehlers-Danlos synd). Arch support provides symptomatic relief Metatarsus varus (big toes point in no treatment usually required unless > 5 years). Medial tibial torsion (usually self corrects), 3. Persistent anteversion of femoral neck (usually self corrects) . Usually age 6-12 months. Lateral rotation of hips. Usually resolves spontaneously. Common 1-3 years. Cerebral palsy, Achilles t. tight, Duchennes muscular dystrophy. http://library.med.utah.edu/neurologicexam/movies/gait_ab_08.mov Usually due to spastic cerebral palsy, stroke, demyelination http://library.med.utah.edu/neurologicexam/movies/gait_ab_09.mov Usually cerebral palsy http://library.med.utah.edu/neurologicexam/movies/gait_ab_10.mov Diabetes, Alcoholism, HIV, Toxin exposure, Metabolic abnormalities, Vitamin deficiency, Adverse effects of certain drugs http://library.med.utah.edu/neurologicexam/movies/gait_ab_11.mov pelvic girdle weakness, e.g. muscular dystrophy http://library.med.utah.edu/neurologicexam/movies/gait_ab_13.mov Huntingtons disease, antipsychotics, infections http://library.med.utah.edu/neurologicexam/movies/gait_ab_14.mov Trauma, stroke, TIA, Cerebral palsy, MS, chickenpox, Paraneoplastic syndromes, Tumor, Toxic reaction http://library.med.utah.edu/neurologicexam/movies/gait_ab_12.mov aka Festinating gait treatments include L-Dopa with dopa decarboxylase inhibitors, eg Carbidopa and benserazide High stepping gait may be caused by peroneal nerve palsy
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3.2 Hand ((Rheum arthritis) 2005 (yr 5), 2006, 2008 (Yr 4))
Introduction: Wash hands Introduce self. Elicit name, age and occupation. Establish rapport. Consent: Explain what you would like to do and get consent. Expose: Ask the patient to expose their hands and arms to above the elbows. Pillow: Put a pillow on the patients lap and ask them to rest their hands on it.
LOOK Start with the elbows, and behind the ears in case you forget later (psoriatic arthritis). Examine both the dorsal and plantar surfaces of the hands, then examine from side with palms outstretched. Note any of the following o Nails: nail fold infarcts, clubbing, pitting, onycholysis o Skin: Rashes, thinning, bruising, palmar erythema, dupuytrens contracture, rheumatoid nodules o Muscle: wasting (dorsal interossei, thenar, hypothenar eminences) o Joints: Heberdens (DIPJ) & Bouchards (PIPJ) nodes. Swan neck or boutionnere deformities, z shaped thumb o Wrists: swelling, ganglion, vertical carpal tunnel release scars o Elbows: Psoriatic plaques, gouty trophy, rheumatoid nodules FEEL ASK: Before doing anything check if the patient has any pain! Peripheral pulses, muscle bulk, tendon thickening Skin: Assess temperature over forearm, hands and fingers. Sensation: Test light touch over index finder (median nerve), lateral aspect of thumb (radial nerve) and little finger (ulnar nerve). Request to formally assess pain using pin. Compare both sides. Joints: squeeze carpal and metacarpal joints, then each PIP and DIP in turn. Also anatomical snuff box (scaphoid #), tip of styloid process (de Quervains disease), head of ulna dorsally (exstensor carpi ulnaris tendonitis) MOVE Fingers: o Ask to spread fingers out & test power of extension and abduction o Hold each joint (MCP & IP) between thumb and forefinger flex and extend each joint separately. o Test precision grip strength (finger and thumb) and full grip strength (squeeze finger). Compare sides Thumb o Palms facing upwards test thumb abduction (median nerve) by asking pt to keep it pointing to ceiling against resistance, test opposition asking pt to touch thumb and little finger and trying to pull apart. Then test adduction (thumb across palm) and extension (thumb out to side) Wrist o Active & passive flexion (80) and extension (80). Radial (40) and ulnar (10) deviation, plus pronation and supination. FUNCTION Assess ability to perform tasks such as buttoning a shirt, writing a sentence, picking up a coin etc. SPECIAL TESTS 128
Tinels test tap over median nerve at wrist to reproduce symptoms of Carpal tunnel Phalens test hold wrists hyperflexed for 2 minutes to reproduce Carpal tunnel Froments sign ask pt to hold piece of paper between thumb and index finger. Thumb IPJ will flex if ulnar nerve compression Thank the patient and ask if they have any questions
Possible examiners questions overleaf Q. Name some signs of rheumatoid arthritis? Ulnar deviation, swan neck and boutionnieres, sub cutaneous nodules, Z thumb, metacarpal subluxation Q. Osteoarthritis? Heberden's nodes (DIP), Bouchard's nodes (PIP), squaring of hand Q. Psoriatic arthritis? Inflammation of PIPs and DIPs, nail pitting, onycholysis, hyperkeratosis, ridging, discoloration. Q. Treatments for each? RA: DMARDS (mtx, sulfasalazine, steroids, anti TNF, NSAIDS), OA (NSAIDS, steroid injections, glucosamine, chondroitin) PA: as with RA. Also education, physio, surgery etc. Q. What joints are typically affected by RA? MCPs & PIPs Q. What is carpal tunnel syndrome- causes, signs, symptoms? Entrapment of median nerve in carpal tunnel due to pressure. Usually idiopathic but causes include: hypothyroidism, diabetes, pregnancy, obesity, RA, acromegaly. Burning pain and tingling felt in thumb, index, middle and medial half of ring finger. Usually worse at night, relieved by shaking hand. (Wake + shake) Loss of sensation, wasting of thenar eminance, power of abductor pollicis brevis. Q. What is trigger finger? causes signs symptoms? Flexor tendor gets trapped in opening of its sheath. Middle and ring most commonly affected. Clicking noise when other fingers extended. Q. What is De Quervains disease (stenosing tenovaginitis?) Caused by repetitive abduction and adduction of thumb, e.g. gardening. causes pain at radial side of wrist.
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Thank patient and ask if they would like help re-dressing. Ask patient if they have any questions
Potential examiner question Q1. How can you differentiate a Bakers cyst from a popliteal aneurysm? A = absence of pulse
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LOOK General: Clues in surrounding area. Ask patient to stand examine alignment of shoulders, hips, ASIS and patella. Look from behind for scoliosis and gluteal wasting. Inspect from side for lumbar lordosis. Gait: ask patient to walk to end of room and return. Comment on use of walking aids, speed, heel strike, stance, push off and swing, stride length, arms swing. Gait eg. Trendenburg (hip drops on non weight bearing side). Trendelenburgs test ask patient to stand on one leg, resting their outstretched hands in yours. Positive if hip drops on non-weight bearing side. Lying down: observe the following; o Skin: scars, sinuses, pigmentation, skin creases o Muscle: wasting fasiculations o Swelling: Effusions o Position: shortened, rotated, fixed flexion deformity Measure: Apparent limb length (xiphisternum to medial malleolus) and true limb length (ASIS to medial malleolus). Apparent limb length discrepancies could be due to fixed adduction deformity of the hip. FEEL Palpate hip feel for temperature effusions and bony landmarks MOVE Note any limited range of movement or the reporting of pain. Normal flexion 130 Thomas test: Patient lying on back, place hand below lumbar lordosis. Ask patient to hold one knee flexed then try to straighten other leg. If unable to fully straighten, theres a fixed flexion deformity of hip on that side. Rotation knee flexed, internal rotation (move foot laterally) and external rotation (move foot medially) Abduction 45 Adduction - 30 END PIECES State that youd also like to examine the back and the knee. State that youd like to test for neurovascular deficits. Dorsalis pedis and posterior tibial. Compare sensation and proprioception. Thank patient and offer to help them re-dress. Ask the patient if they have any questions Potential examiners questions Q. What can osteoarthritis on the hip be secondary to? A: Perthes, Pagets, Rheumatoid Q. What causes Trendelenbergs sign? A: Deficient hip abductor function (ie gluteals) Q. What are the symptoms of Trochanteric bursitis? A: Pain over greater trochanter, worse when lying on affected side Q. What are the signs of an inferiorly anteriorly dislocated femur? A: Hip flexed, abducted and internally rotated. 132
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Q1. What is impingement syndrome? IMpingement of rotator cuff muscles against coracoacromial ligament. Due to repetitive overhead activities eg swimming, occupational. Pain exacerbated by overhead activities, and at night when lying on affected side. Painful arc between 60 and 120 (but not if arm in full external rotation) Q2. What muscles make up the rotator cuff? Supraspinatus, infraspinatus and subscapularis. Q3. How can you tell a rotator cuff tear from impingement? Cant actively go beyond 60 but passively move arm to 90 abduction and patient will be able to hold it and continue above this level. Q4. What is frozen shoulder? Aka adhesive capsulitis. Pain loss of motion, stiffness. Thickening and contracture of capsule. More common in women aged 40-60. May subside after 9-12 months. Full ROM return by 18 months. Q5. How does shoulder normally dislocate? 95% anteriorly. What nerve is commonly injured and how do you test for this? Axillary test sensation in regimental badge area.
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Possible examiners questions Q. What may cause cerebellar disease? MS, stroke, alcohol, space occupying lesions (tumour, aneurysm, abscess, granuloma, cyst), and anti convulsant medications. Q. What are the signs and symptoms of cerebellar disease? DANISH D Dysdiadochokinesia, A Ataxic gait, N Nystagmus (worse in direction of lesion), I Intention tremor, S Slurred speech, H Hypotonia. Cerebellar lesion causes symptoms worse on ipsilateral side, vermis lesion causes bilateral signs and symptoms.
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Q. What are the symptoms? L4/L5 weakness of hallux extension and sensation to outer aspect of leg and dorsum of foot; L5/S1 pain in the calf, weakness to plantarflexion and eversion of the foot, sensationover later aspect of foot and depressed ankle reflexes.
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Go back towards and beyond midline. Fluid thrill: patient places hand in middle of abdomen. Flick one flank and feel for thrill on opposite side. AUSCULTATION: Bowel sounds, aorta for bruits, renal for bruits. END PIECES: SHRUG I would also like to send off a stool sample if clinically relevant, check for hernias, perform a rectal examination, urinanalysis and examine the external genetalia. Thank the patient and let them know they can get dressed
In previous years this has been: kidney transplant 2007, 2008, 2009; dialysis, 2006; abdo pain 2005 Potential examiners questions overleaf Q. Name some potential causes for hepatomegaly. Large, smooth and tender: hepatitis, chronic heart failure, sarcoidosis, early alcoholic cirrhosis, tricuspid incompetence Large, hard and craggy: primary hepatoma or secondary tumours Large, smooth and non-tender: cirrhosis and lymphoma (n.b. small liver typical in late cirrhosis) Q. Name some potential causes for splenomegaly. Chronic myeloid leukaemia, myelofibrosis, lymphoma, infective (TB, Malaria), Glandular fever. Q. Name some causes of hepatosplenomegaly. Viral hepatitis, infectious monnucleosis, CMV, leukaemia, myeloproliferative disease, lymphoma, amyloidosis, acromegaly, SLE Q. Name some causes of enlarged kidney(s). Polycystic kidney disease, perinephritic abscess, hydronephrosis, malignancy Q. Name some causes of ascites. Transudate (protein < 30g/L): liver cirrhosis, constrictive pericarditis, cardiac failure, nephrotic syndrome. Exudate (protein > 30g/L): malignancy, acute pancreatitis, infective (TB, pneumococcal), Budd-Chari syndrome (caused by occlusion of the hepatic veins. Presents with classical triad of abdominal pain, ascites and hepatomegaly.) Q. Describe this patients abdomen
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The patient has a large midline scar and a stoma in the left iliac fossa. This would be consistent with having had a Hartmanns procedure. However the bag on the patients left is not collecting solid matter and is therefore not a colostomy. It appears to be collecting urine and is therefore most likely a urostomy. The bag on the patients right appears to be collecting liquid faeces and its location is most consistent with a ileostomy (although a spout can not be seen). Q. What is Hartmans procedure? Excision of lesion in descending or sigmoid colon, over sewing of rectum and creation of a colostomy. Q. What is a loop ileostomy and what is it used for? A type of stoma where both proximal and distal segments of bowel drain on to the skin. May be used to protect and anterior resection (typically reversed after 6 weeks) Q. Complications of stomas? Fluid loss, odour, ulceration, leakage, stenosis, herniation or prolapse, ischaemia, poor B12 absorption, sexual and psychological problems.
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Intensity: 1-6; 1=faint and hard to hear, 2=easily heard with steth, 3=loud with steth, no thrill, 4=easily heard with thrill, 5=heard over wide area and thrill, 6=audible without steth. o Site, Character: rumbling (MS), blowing (MR), harsh (AS), Pitch: high (AS), low (MR), Radiation: carotids (AS), lse (AR), back (PDA), Respiration: RILE: Right Inspiration, Left Expiration. Position (AR, MR) o Manoeuvres: valsava increases mitral regurg, squatting increases aortic stenosis Lung Bases: Crepitations, pleural effusion (left ventricular failure). Palpate for sacral oedema and ankle oedema. Pitting = heart failure, nephrotic syndrome, cirrhosis, malnutrition, severe anaemia. Non pitting = lymphatic obstruction, DVT, myxoedema End pieces: Palpate for peripheral pulses, ECG, CXR, dipstick uine, fundoscopy (hypertension), sats and temp Thank the patient and let them know they can get dressed Potential examiners questions overleaf Q. What causes S1 and S2? S1 = mitral and tricuspid valves closing, S2 = aortic and pulmonary valves closing. o Q. What causes a 4th heart sound? Atrial contraction into hypertrophied or non compliant ventricle; heart failure, MI,cardiomyopathy, hypertension. Q. What causes a 3rd heart sound? Normal in chldren/young adults or stiff dilated ventricle; heart failure, MI, cardiomyopathy, hypertension, mitral/aortic regurg, constrictive pericarditis. Q. Name the five signs of endocarditis? clubbing, splinter haemorrhages, murmurs, splenomegaly, microscopic haematuria, oslers nodes, roth spots, janeways lesions. Q. What are the causes of AF? Ischaemic Heart Disease, Rheumatic Heart Disease, thyrotoxicosis Q. What are the two causes of an irregularily irregular pulse and how could you distinguish between them without an ECG? AF or ectopics. Excercise the patient and ectopics will Q. Why does the radial and ventricular rate sometimes differ? Pulse deficit (i.e. some radial beats not palpable). Q. Whats the target INR for AF? for prosthetic valve? 2-3, 3-4 Q. How could you assess the risk of a stroke in a patient with AF? CHADS2 C Congestive heart failure 1 , H Hypertension more than 160 Hg (or treated hypertension) 1 , A Age >75 years 1 D Diabetes Mellitus 1, S2 Prior Stroke or TIA 2. If 0=Low Aspirin daily, If 1=Moderate - Aspirin or Warfarin Aspirin daily or raise INR to 2.0-3.0, if =>2 - Moderate or High Risk - Warfarin -Raise INR to 2.0-3.0, unless contraindicated. Q. What are the signs of mitral stenosis? malar flush, AF, Apex beat not displaced, Tapping Apex beat, LUB! de derrrr. Prominent left atrium on CXR Q. What are the signs of mitral regurguitation? Apex beat usually displaced, quiet 1st heart sound, pansystolic murmur, radiates loudly to axilla, 2nd heart sound not heard separately. Q. What are the signs and common causes of aortic regurgitation? Collapsing pulse, apex beat displaced, diastolic murmur follows second sound lub taaaarr. Causes: rheumatic heart disease, tertiary syphilis, endocarditis, connective tissue disease (Marfans etc).
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Q. What are the signs and common causes of aortic stenosis? Slow rising pulse, low volume pulse, low pulse pressure, JVP not elevated, apex beat forceful but not displaced, ejection systolic murmur. Causes: degenerative calcification, rheumatic heart disease, can be congenital. Q. What are the different types of heart vale replacements? Biological (eg porcine xenograft) or mechanical prosthetic: ball and cage (eg Starr Edwards) or bi-leaflet (St Jude) Q. What are the complications of an MI? Sudden death of PRAED sudden death, pump failure, rupture of papillary muscle or septum, aneurysm or arrythmias, embolism, Dresslers syndrome (pericarditis that develops 2 to 10 weeks after MI) Q. What are the signs and symptoms of acute LVF? Patient will look ill, cold clammy peripheries, frothy blood stained sputum, orthopnoea, wheeze, tachycardia or AF, systolic hypotension, cardiomegaly, 3rd & 4th heart sounds, right sided or bilateral pleural effusions. Q. What might you use if a standard echo did not give you a good view of the mitral and aortic valves in suspected endocarditis? transoesophageal echo Q. How would you treat an acute MI? MORE GAS Morphine, Oxygen, Reassurance, Explanation, GTN, Anti-platelets, Streptokinase or PCI
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INSPECTION: General: O2 masks, nebulizers, sputum pots etc. Breathing at rest, cough, wheeze, stridor. Scars: e.g. thoracotomy, Shape: barrel chest, pectus excavatum, pectus carinatum. Use of accessory muscles, intercostal recession (asthma, COPD), pursed lips, RR (normal = 16-25) tachypnoea > 25. Hands: Temperature (warm and well perfused?), Tremor (beta agonist salbutamol), peripheral cyanosis, tar staining, CO2 retention flap, clubbing. o Causes of clubbing: ABCDEF: Asbestosis, Bronchiectasis/Bronchial Carcinoma, Cystic fibrosis, Decreased O2, Empyema, Fibrosing alveolitis Pulse: rate and rhythm of radial pulse (bounding pulse = CO2 retention) Arms: Indicate you would like to measure BP sitting and standing Face and Neck: anaemia, cyanosis, JVP (cor pulmonale = right ventricle damage due to pulmonary pressure) PALPATION: Lymph nodes: Enlarged cervical/supraclavicualr lymph nodes = TB bronchial cancer Trachea: warn patient, look for tracheal deviation. Apex beat: normally 5th intercostal space mid clavicular line (displaced = pleural effusion, pneumothorax) Expansion: normal chest expansion > 5cm PERCUSSION: Chest: Upper, middle and lower, axillae and apices. Compare sides. o Stony dull = pleural effusion; dull = consolidation, fibrosis, collapse; hyper-resonant = COPD, pneumothx Vocal fremitus: ask pateint to say 99 and use ulnar border of hand. in consolidation & fibrosis, in pneumothorax, COPD, absent in collapse or effusion. AUSCULTATION: Chest: request pt breathe through mouth. Listen in all areas for breath sounds/added sounds; o wheeze (asthma, bronchitis); crackles (fine: heart failure, fibrosing alveolitis; coarse: bronchietasis, pneumonia, bronchitis) pleural rub: pneumonia, pulmonary embolism. o Vocal resonance 99 see vocal fremitus above o Repeat on back Examine for sacral oedema and ankle oedema. Check no pain when pressing. END PIECES: peak flow, CXR, sats, temp chart, sputum MC&S. Thank the patient and let them know they can get dressed Potential examiners questions Q. What might the following colours of sputum suggest: a) Black, b) Frothy pink, c) Rusty golden? a) aspergillosis, b) acute pulmonary oedema, c) pneumococcal pneumonia. Q. What signs might you expect in pulmonary fibrosis? chest expansion , vocal fremitus , Percussion dull, bronchial breath sounds, coarse crepitations. Q. What are the causes of a pleural effusion? Transudates (<25g/L) and exudates (>35g/L). - Transudates may be due to venous pressure (cardiac failure, constrictive pericarditis, fluid overload), hypoproteinaemia (cirrhosis, nephrotic syndrome, malabsorption), hypothyroidism, Meigs' syndrome (right pleural effusion and ovarian fibroma). 145
- Exudates mostly due to leakiness of pleural capillaries secondary to infection, inflammation, or malignancy. Causes: pneumonia; TB; pulmonary infarction; rheumatoid arthritis; SLE; bronchogenic carcinoma; malignant metastases; lymphoma; mesothelioma; lymphangitis carcinomatosis. See OHCM for more possible questions!
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INSPECTION Shape: swelling suggestive of oedema and venous compromise Varicose veins: location, distribution. Long saphenous (groin to medial malleolus), short saphenous (popliteal to lateral malleolus) Gaiter area: skin changes in lower third of leg just above medial malleolus o Venous stars: dilitation of superficial venules spreading from ankle o Eczema: above medial malleolus and lower calf o Ulcers: especially over medial malleolus o Ankle swelling o Pigmentation: brown discolouration = haemosiderin o Lipodermatosclerosis: fibrosis of skin and subcutaneous fat o Scars: previous vascular surgery? PALPATION: Temperature: note any temperature changes Veins: Feel along long saphenous and short saphenous for tenderness (ask first) or hardness (thrombosis) Junctions: feel saphenofemoral junction (4cm below& lateral to pubic tubercle) for a saphena varix (dilitation in saphenous vein as it joints femoral vein). Ask patient to cough, Impulse = saphenopopliteal incompetence. Peripheral pulses: Examine peripheral pulses to assess arterial blood supply SPECIAL TESTS: Tap test: Place one finger at bottom of long varicose vein and tap above this site. Impulse demonstrates superficial vein incompetence. Trendelenburgs: Ask pt to lie flat. Raise and milk leg. Occlude saphenofemoral junction and ask patient to stand. Remove fingers. If superficial veins refill = incompetence at saphenofemoral junction. Tourniquet test: Do as above but use tourniquet at different levels until veins below tourniquet remain collapsed (incompetent perforators lie above tourniquet) Perthes test: With patient standing and veins filled, place tourniquet around mid thigh and ask pt to stand up and down on the spot x10. If superficial veins collapse the deep veins are patent and communicatuing veins competent. If unchanged, both saphenous and communicating veins are incompetent. If the veins become more prominent, then the deep veins are occluded. Hand held doppler: Place the doppler on the vein. Squeeze the calf, blood will flow up through vein. Release the calf. Retrograde flow > 1 sec suggests valve incompetence. END PIECES 147
Request to perform an abdominal and pelvic exam (PV in females, genitalia in males masses may cause IVC obstruction). Thank the patient and cover legs. Acknowledge patients concerns. Summarise findings to examiner.
see over for questions Potential examiners questions Q. What are varicose veins? Dilated, tortuous, and prominent veins of the superficial venous system. Q. How common are they? Around 25% of women and 15% of men will get them. Q. What are the risk factors? Most varicose veins are primary - they have no identifiable cause. Incompetent valves play a role. Increasing age, prolonged standing, pregnancy, obesity, family history and the Pill all increase the risk. Pelvic masses, trauma, and previous deep venous thrombosis are also recognised causes. Q. What are the symptoms? Pain, cramps, tingling, heaviness and restless legs slightly commoner. Q. Name some complications of varicose veins. Haemorrhage, ulceration, lipodermatosclerosis, phlebitis, eczema, calcification. Q. Where is the saphenofemoral junction? It can be found by first locating the femoral artery between the anterior superior iliac spine and the pubic tubercle. The vein is medial to the artery and the saphenofemoral junction about two fingers' breadths below the inguinal ligament. Q. What is venous claudication? Acute, bursting pain on walking that is relieved by rest and leg elevation. This is called venous claudication. Q. What causes lipodermatosclerosis and what does it result in? Chronic venous hypertension when fibrin deposition results in progressive sclerosis of the skin and subcutaneous fat. Q. What are the treatment options? - Education: avoid prolonged standing; support stockings, lose weight, regular exercise - Injection sclerotherapy ethanolamine is injected and vein compressed ot avoid thrombosis. UNsuitable for perforation sites. - Laser coagulation especially for small varicosities and thread veins - Surgery is still the gold standard e.g. saphenofemoral ligation Q. How should thrombophlebitis be treated? With NSAIDs, not antibiotics. A hard, inflamed area above the ankle in the presence of varicose veins may well be inflammatory liposclerosis - not thrombophlebitis Q. What are reticular veins? Dilated non-palpable subdermal veins smaller than 4 mm in diameter. Q. How should lipodermatosclerosis be managed? Use of well fitted, below knee, graduated compression hosiery (normally Class 2) and a moisturiser (once or twice a day) and/or referral for treatment of varicose veins. Analgesic and anti-inflammatory medication may help the symptoms. Antibiotic treatment is unnecessary. Early referral to a vascular specialist is indicated to consider treatment for the underlying venous hypertension. Q. Hard, tender varicose veins indicate... thrombophlebitis. 148
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INSPECTION Note colour, shiny skin, hair loss, ulcers, thinning of skin, gangrenous patches, oedema, amputations, loss of subctuaneous fat. Pressure points: check heel, malleoli, head of first metatarsl, lateral side of foot, toes, dorsum of foot for ulcers (if found describe size, shape, depth, edge, base) PALPATION Temperature: run back of hand along both limbs and soles of feet. Compare sides. Signs/symptoms of acute limb ischaemia; 6 Ps Painful, Pulseless, Pallor, paralysis, Parathesia, Perishing cold. Capillary refill: < 2 secs normal Pulses: posterior tibial, dorsalis pedis, popliteal, femoral. Compare sides. SPECIAL TESTS Guttering: elevate patients legs about 15 and look for venous guttering (arterial insufficiency) Buergers test: elevate the leg further and look for the angle at which it becomes pale (Buergers angle) < 30 indicates severe ischaemia. Sit patient up and hang legs over bed. Note time taken to return to normal colour. Reactive hyperaemia 2-3 mins suggests chronic lower limb ischaemia ABPI: ankle/brachial blood pressure using doppler. >=1 normal, 0.9-0.6 = claudication, 0.3-0.6 = rest pain, <=0.3 = impending gangrene. END PIECES Indicate that you would like to examine the rest of the peripheral vascular system (radial and carotid pulses, radio-femoral delay (coarctation of aorta), carotid bruit. State that you would like to perform a full cardiovascular examination and an abdominal examination (AAA). Thank the patient and cover their legs Potential examiners questions Q. What is the cause of intermittent claudication? Due to narrowing of the vessels due to atherosclerosis. Q. What is critical ischaemia? Continuous and aching pain in the leg at rest. Due to gross narrowing of vessels due to atheroclerosis. May be eased by hanging leg down. Q. Name some features of ischaemic (aterial) ulcers. Usually painful. Absenceof peripheral pulses. Deep with punched out edge. Found at pressure points or over tips of toes. Surrounding tissue cold. Discharge is serous or pus. Q. Name some features of venous ulcers. Found especially above medial malleolus. May be associated with lipodermatosclerosis and haemosiderin pigmentation. Shallow and flat with irregular pale purple or blue sloping edge. Base usually contains either fibrous or granulation tissue. Discharge often seropurulent in nature. See also OHCM!
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3.13 Cranial nerves II, III, IV, & VI and Fundoscopy (2005, 2006, 2007, 2008)
Wash hands. Introduction. Elicit name, age, and occupation. Establish rapport. Explain and seek consent. Ask patient if their have any problems with vision and if they wear glasses /contacts (leave on/in). INSPECTION Eyelids: symmetrical? Eyelashes ingrowing (trichiasis)or loss/thining. Skin around eyes: any scars, inflammation, crusting, swelling. Drooping eyelid? Eyes: Any jaundice, redness of the eye, any foreign objects in the eye? Pupils of equal size? Strabismus? If yes, try the cover test. II OPTIC NERVE (Very Very Big Fat People Are Squidgey) Visual acuity: Use a Snellen chart or alternatively record smallest type that can be read at 30cm. If patient cannot read Snellen chart, bring to 3m. If patient cannot read at 3m ask to count fingers at 1m. If unsuccessful, test if they can see hand movements and if still unsuccessful ask if they can see the light from a pen torch at 1m. Mention that youd also like to test near sightedness using a book. Assess colour vision using Ishihara plates. Visual fields: test one eye at a time by confrontation using a white hat pin. Blind spot: test using the red hat pin Fundoscopy (save this for later) Pupillary light reflex: Direct and consensual one eye at a time. Relevant afferent pupillary defect. Accomodation reflex: Ask patient to look at object in distance then quickly focus on near object. Sensory inattention: hold fingers out to side and waggle one or both. Which moved? Occulomotor (III), Trochlear (IV), & Abducens (VI) nerves Ask pt to keep head fixed whilst following your finger. Make an H shape. Any pain, double vision? Nystagmus? If double vision are the images up and down or side by side? FUNDOSCOPY Explain: I would like to check your vision by having a look in your eyes. I will be using an opthalmoscope, which is really just a torch with a magnifying glass that will let me look a the back of your eye. It will not be painful, but I will need to get close up to your face to be able to do this. Would the be OK? Check the fundoscope is working and set to zero. Use right hand to view right eye and finger to focus. Ask the patient to focus on a distant object Red reflex: Focus on the pupil 12 inches form the patients eyes. Absence suggests presence of cataract. Let patient know you are going to get close to them and remind them to breathe and blink normally. Keep the beam pointing nasally to help focus on optic disc. Follow blood vessels from optic disc to periphery (or vice versa to find it first). Then look at all four quadrants. Look for microaneurysms, venous beading, arteriolar narrowing, AV nipping, copper or silver wiring, haemorrhages or exudates. Ask patient to look directly into the light to visualise the macula. Note its colour. Repeat for the other eye. Thank the patient. Acknowledge any concerns. Summarise findings to the examiner. Potential examiners questions Q. What might cause inflammation, crusting, and/or swelling around the eyelids? A. belpharitis, cysts, chalazions, styes). 151
Q. What might cause a drooping eyelid? A. 3rd nerve palsy, Horners Q. What are the different types of strabismus, and how would you test for them? A. Esotropia: eye turns inwards, Exotropia: outwards, Hypertropia: upwards, Hypotropia: downwards). In the cover test, the affected eye will readjust and look forward when the unaffected eye is covered. Q. When reporting the results from a Snellen chart, which number do you report first? A. The first figure is distance in metres, second is the number on line. 6/6 is normal. If patient can read line 9 at 6m then this would be 6/9. Q. What is the best thing to use when testing peripheral vision at the bedside and why? A. A white hat pin. peripheral vision is monochrome and central vision is colour. P.T.O. Q. Describe the location of the lesion for the following; (1) Unilateral vision loss, (2) Bitemporal hemianopia, (3) Right homonymous hemianopia, (4) Upper right quadrantanopia, (5) Lower quadrantanopia, (6) Right homonymous hemianopia with sparing of the macula.
(1) Unilateral vision loss, (2) Bitemporal hemianopia (compression of optic chiasm), (3) Right homonymous hemianopia (optic tract lesion), (4) Upper right quadrantanopia (lesion- lower fibres of the optic radiation) (5) Lower quadrantanopia (lesion- upper fibres of optic radiation), (6) Right homonymous hemianopia with sparing of the macula due to lesion of the optic radiation in the posterior part of the parietal lobe. Q. What would cause the blind spot to be enlarged? Give some possible conditions? A. A central scotoma. Possible causes; multiple sclerosis, methyl alcohol, nutritional causes -e.g. B12 deficiency, vascular lesions, glioma of optic nerve, glaucoma. Q. What is a Marcus Gunn pupil, what causes it, and what condition might it be associated with?
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A relative afferent pupillary defect can be tested for by moving a torch quickly from pupil to pupil. If incomplete damage to afferent pathway (eg due to optic neuritis in multiple sclerosis), affected pupil will paradoxically dilate when light is moved from normal eye to abnormal eye. Due to reduced afferent input from the affected eye - the consensual pupillary relaxation response from the normal eye predominates. This phenomenon is also known as the Marcus Gunn sign. Q. Which nerves are involved in the accommodation reflex and in actual pupil constriction? A. a. II and III, b. III Q. How is diabetic retinopathy classified? Background retinopathy: Microaneurysms (dots), haemorrhages (blots), and hard exudates (lipid deposits). Pre-proliferative retinopathy: Cotton wool spots (infarcts), haemorrhages, venous beading. Proliferative retinopathy: New vessels form. Maculopathy: often not visible at early stage. Suspect if visual acuity.
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Q. What does the Court of Protection do? It is part of the Office of the Public Guardian and has the power to decide whether a person has capacity to make a particular decision for themselves Q. Difference between dementia and delerium? Delerium is an acute confusional state, dementia is a chronic condition and entails progressive deficits in several cognitive domains.
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Proprioception joint position sense Rombergs (stand feet together eyes closed proprioception) Vibration (using a tuning fork of 128Hz) 156
Observe gait If they have a particular complaint, e.g. difficulty in writing, watch them performing this task. See dermatome map 2 pages ahead
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Joint position sense Vibration (using a tuning fork of 128Hz) See dermatomes picture next page 158
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3.17 Dermatomes
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4 Formulary
Subgroup Analgesics Opiates generally Dose Fre q Rout e 24h max Common side effects Nausea, vomiting, constipation, dry mouth, biliary spasm. Larger doses; muscle rigidity, hypotension, respiratory depression. Also bradycardia, tachycardia, palpitation, oedema, postural hypotension, hallucinations, vertigo, euphoria, dysphoria, mood changes, dependence, dizziness, confusion, drowsiness, sleep disturbances, headache, sexual dysfunction, micturition difficulty, urinary retention, ureteric spasm, miosis, visual disturbances, sweating, flushing, rash, urticaria, and pruritus. see above Contraindications Acute respiratory depression, risk of paralytic ileus, raised intracranial pressure, head injury
1-2 tablets
46hr
PO
8 tablets
Codeine phosphate
30-60mg
46hr
PO/I M
see above. Caution with: hypotension, asthma and respiratory function, prostatic hypertrophy; shock; myasthenia gravis; obstructive or IBD; biliary tract disease; dose in elderly, hypothyroidism, adrenocortical insufficiency; convulsive disorders; cardiac arrhythmias; acute abdomen; gallstones; alcohol dependence See above. Caution with cardiac arrhythmias; acute abdomen; gallstones 161
Diamorphine opiate
1-5mg
14hr
n/a
see above, also anorexia, taste disturbance; syncope; asthenia, raised intracranial pressure; myocardial infarction
see above, also severe diarrhoea; toxic psychosis, CNS depression; severe cor pulmonale Contraindications NSAIDS generally; Contraindicted: previous or active peptic ulceration, pregnancy, severe heart failure, ischaemic heart disease, cerebrovascular disease, peripheral arterial disease, history of hypersensitivity to aspirin or NSAIDS, coagulation defects. Caution in: Hepatic impairment, Renal impairment, breastfeeding Diclofenac (150 mg daily) and ibuprofen increase risk of thrombotic events. see opiates above see NSAIDS above see opiates above see opiates above caution in alcohol dependence and hepatic impairment
24h Common side effects max 150mg NSAIDS generally; GI 150mg disturbance inc. discomfort, nausea, diarrhoea, bleeding, ulceration. Also hypersensitivity reactions, headache, dizziness, nervousness, depression, drowsiness, insomnia, vertigo, hearing disturbances such as tinnitus, photosensitivity, haematuria. blood disorders, fluid retention, BP 240mg see opiates above 2.4g n/a see NSAIDS above see opiates above see opiates above
Dihydrocodeine opiate Ibuprofen NSAID Morphine opiate Oramorph10mg/ opiate 5ml Paracetamol non-opioid
PO PO IV/SC
PO/IV
4g
25150mg 50100mg
prn 46hr
rare; rashes, blood disorders (thrombocytopenia, leucopenia, neutropenia); hypotension; liver damage and renal on overdose 400mg see opiates above 400mg see opiates above. also diarrhoea; fatigue; retching, gastritis, flatulence; rarely: anorexia, syncope, BP, bronchospasm, dyspnoea,
see opiates above. also phaeochromocytoma see opiates above, also: uncontrolled epilepsy; acute porphyria
162
wheezing, seizures, paraesthesia, weakness; blood disorders Anti emetics Cyclizine antihistami ne 50mg tds PO/I M/IV 150mg Anti-histamines generally; drowsiness, headache, psychomotor impairment, urinary retention, dry mouth, blurred vision, and GI disturbance. Rare: hypotension, palpitation, arrhythmias, dizziness, confusion, depression, sleep disturbance, tremor, convulsions, hypersensitivity, blood disorders, liver dysfunction, angle-closure glaucoma. 24h Common side effects max 30mg extrapyramidal effects especially in children and young adults, hyperprolactinaemia, occasionally tardive dyskinesia; also, anxiety, confusion, drowsiness, restlessness, diarrhoea, depression, neuroleptic malignant syndrome, rashes, pruritus, oedema; cardiac conduction abnormalities; rarely methaemoglobinaemia 32mg constipation; headache; flushing; injection sitereactions; hiccups, hypotension, bradycardia, chest pain, arrhythmias, movement disorders, seizures; rarely dizziness, transient Anti-histamines generally: prostatic hypertrophy, urinary retention, angle-closure glaucoma, and pyloroduodenal obstruction. Caution in: epilepsy, acute porphyria
Dose 10mg
Fre q tds
Contraindications gastro-intestinal obstruction, perforation or haemorrhage; 34 days after gastro-intestinal surgery; phaeochromocytoma
8mg
tds
PO/I M
QT interval prolongation
163
Prochlorperazine anti-emetic
5-10mg
tds
PO/I M
30mg
Fre q tds bd
Rout e PO/I M PO
visual disturbances Antipsychotics generally; Extrapyramidal, e.g. parkinsonian, dystonia, dyskinesia, akathisia, tardive dyskinesia, hypotension, interference with temperature regulation, neuroleptic malignant syndrome (hyperthermia, fluctuating consciousness, muscle rigidity, and autonomic dysfunction with pallor, tachycardia, labile blood pressure, sweating, urinary incontinence) Others; drowsiness; apathy; agitation, excitement, insomnia; convulsions; dizziness; headache; confusion; GI disturbances; nasal congestion; antimuscarinic symptoms, endocrine effects; blood dyscrasias; corneal/lens opacities, and purplish skin/eye pigmentation. Common side effects brand name for prochlorperazine brand name for prochlorperazine Drowsiness, lightheadedness; confusion, ataxia, amnesia, dependence; paradoxical aggression muscle weakness; occasionally: headache,
Antipsychotics generally; Caution in cardiovascular disease; Parkinsons disease, epilepsy, depression, myasthenia gravis, prostatic hypertrophy, angle-closure glaucoma. Respiratory disease, jaundice, blood dyscrasias, comatose states, CNS depression, and phaeochromocytoma; Hepatic impairment, renal impairment, Pregnancy, Breast-feeding
2mg 10mg
tds >4h r
PO IM/IV
30mg 30mg?
Respiratory depression; marked neuromuscular respiratory weakness including unstable myasthenia gravis; acute pulmonary insufficiency; sleep apnoea syndrome; severe hepatic 164
Temazepam anxiolytics
10-20mg
on
PO
40mg
Zopiclone anxiolytics
7.5mg
on
PO
7.5mg
vertigo, hypotension, salivation changes, GI disturbances, visual disturbances, dysarthria, tremor, changes in libido, incontinence, urinary retention; blood disorders, jaundice; skin reactions; on intravenous injection, pain, thrombophlebitis, and rarely apnoea; drowsiness and lightheadedness the next day; confusion and ataxia (especially in the elderly); amnesia may occur; dependence taste disturbance; nausea, vomiting; dizziness, drowsiness, dry mouth, headache; rarely amnesia, confusion, depression, hallucinations, nightmares; light headedness, incoordination; paradoxical effects GI irritation, nausea, epigastric pain, constipation or diarrhoea. Accidental overdose in children. nausea (can be reduced by administration with water, fruit juice or with meals), vomiting, flatulence, cramps, and abdominal discomfort
impairment; not for chronic psychosis; should not be used alone in depression or in anxiety with depression; avoid injections containing benzyl alcohol in neonates
as above
marked neuromuscular respiratory weakness including unstable myasthenia gravis, respiratory failure, severe sleep apnoea syndrome
200mg
od
PO
65mg iron
15mL
bd
PO
lactose intolerance
165
Dose 15-30mg
Fre q od
Rout e PO
24h max
Loperamide antimotility
2-4mg
prn
PO
od bd qds
PO PO IM/IV
PPIs generally; GI disturbance, headache. Dry mouth, peripheral oedema, dizziness, sleep disturbances, fatigue, paraesthesia, arthralgia, myalgia, rash, pruritus. Rarely; taste disturbance, stomatitis, hepatitis, jaundice, hypersensitivity reactions, fever, depression, hallucinations, confusion, gynaecomastia, interstitial nephritis, hyponatraemia, blood disorders, visual disturbances, sweating, photosensitivity, alopecia, Stevens-Johnson syndrome, and toxic epidermal necrolysis. May risk of GI infections (including C diff). Lanzoprazole specifically: glossitis, pancreatitis, anorexia, restlessness, tremor, impotence, petechiae, and purpura; rarely colitis, raised serum cholesterol or triglycerides 16mg abdominal cramps, dizziness, drowsiness, and skin reactions including urticaria; paralytic ileus and abdominal bloating also reported 120mg see PPIs generally, also agitation and impotence 600mg H2-RAs generally: diarrhoea, 200mg GI disturb, LFTs, headache, dizziness, rash, tiredness. Rarely: acute pancreatitis,
conditions where inhibition of peristalsis should be avoided, where abdominal distension develops, or in conditions such as active ulcerative colitis or antibiotic-associated colitis see PPIs generally might mask symptoms of gastric cancer avoid in pregnancy
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Fre q od bd od 46hr
Rout e po po po
24h max
bradycardia, AV block, confusion, depression, halluc. esp. in elderly/ v. ill, hypersensivity reactions, blood disorders, skin reactions. Common side effects Contraindications abdominal cramp; diarrhoea, hypokalaemia intestinal obstruction, shortly after bowel anastomosis. see anti-histamines above. Ceterizine is non-sedating see anti-histamines above.
Promethazine
tds
po IM IV
see anti-histamines above. Ceterizine is non-sedating 24mg see anti-histamines above; also exfoliative dermatitis and tinnitus reported; injections may cause transient hypotension or CNS stimulation and may be irritant see anti-histamines above; 100mg avoid extravasation with 100mg intravenous injection; severe coronary artery disease
75150 mg
od
po
Atorvastatin statin
10-80mg
od
po
300mg bronchospasm; gastrointestinal irritation, gastrointestinal haemorrhage (occasionally major), also other haemorrhage (e.g. subconjunctival) 80mg statins generally; rare: muscular effects, eg myositis, rhabdomyolysis. also GI disturbance, pancreatitis. LFTs, hepatitis, jaundice. Sleep disturbance, headache, dizziness, depression, paraesthesia, asthenia, peripheral neuropathy,
<16 years unless antiplatlet (Reye's syndrome), active peptic ulceration, haemophilia and other bleeding disorders, Hypersensitivity reactions to NSAIDs, breastfeeding Caution in: Hypothyroidism, history of liver disease, high alcohol intake. Risk factors for myopathy or rhabdomyolysis. Avoid in acute porphyria but rosuvastatin is thought to be safe. Avoid in pregnancy as congenital anomalies have been reported and the decreased synthesis of cholesterol 167
Clopidogrel antiplatelet
75300mg
od
po
Dipyridamole antiplatelet
300-
t/qd
po
amnesia, fatigue, sexual dysfunction, thrombocytopenia, arthralgia, visual disturbance, alopecia, and hypersensitivity reactions. Interstitial lung disease; chest pain; back pain; anorexia, malaise, weight gain, hypoglycaemia, hyperglycaemia, tinnitus; rarely cholestatic jaundice, peripheral oedema; very rarely taste disturbances, gynaecomastia, hearing loss, Stevens-Johnson Syndrome, and toxic epidermal necrolysis 300mg dyspepsia, abdominal pain, diarrhoea; bleeding disorders; less commonly nausea, vomiting, gastritis, flatulence, constipation, gastric and duodenal ulcers, headache, dizziness, paraesthesia, leucopenia, decreased platelets (very rarely severe thrombocytopenia), eosinophilia, rash, and pruritus; rarely vertigo; very rarely colitis, pancreatitis, hepatitis, acute liver failure, vasculitis, confusion, hallucinations, taste disturbance, stomatitis, bronchospasm, interstitial pneumonitis, blood disorders (including thrombocytopenic purpura, agranulocytosis and pancytopenia), and hypersensitivity-like reactions 600mg GI effects, dizziness, myalgia,
Cautions: increased risk of bleeding from trauma, surgery or other pathological conditions; concomitant use of drugs that increase risk of bleeding; Contra-indications: active bleeding, hepatic impairment, severe hepatic impairment, pregnancy
600mg
Simvastatin statin
10-80
noct
po
80mg
throbbing headache, hypotension, hot flushes and tachycardia; worsening symptoms of coronary heart disease; hypersensitivity reactions such as rash, urticaria, severe bronchospasm and angioedema; increased bleeding during or after surgery; thrombocytopenia reported see statins above also rarely anaemia
aortic stenosis, recent MI, left ventricular outflow obstruction, heart failure; may exacerbate migraine; hypotension; myasthenia gravis; coagulation disorders; concomitant use of drugs that increase risk of bleeding
Dose 200400mcg
Fre q bd
Rout e inh
Common side effects Prolonged high doses: adrenal suppression. Lower RTIs. bone mineral density, osteoporosis, growth restriction, glaucoma, cataracts, hoarseness, candidiasi, hypersensitivity reactions, Very rarely paradoxical bronchospasm, anxiety, depression, sleep disturbances, hyperactivity and irritability. Nausea, vomiting, flushing, agitation, anxiety, fear; transient BP & heart-rate; very rarely convulsions (particularly in those with epilepsy), hypersensitivity reactions including
Contraindications ?
100600mcg
IV
1mg
Cautions: short-acting (repeat doses may be necessary, benzo withdrawal symptoms. Caution in prolonged benzodiazepine therapy for epilepsy (risk of convulsions); history of panic disorders, following major surgery; head injury; elderly; 169
0.42 mg
prn
IV
10mg
40-50mg
od
po
60mg
anaphylaxis This entry for acute/severe asthma. see steroids above. Dry mouth; less commonly nausea and headache. Constipation, tachycardia, palpitation, paradoxical bronchospasm, urinary retention, blurred vision, angle-closure glaucoma, and hypersensitivity reactions including rash, urticaria, pruritus, and angioedema occur rarely. Nausea and vomiting, Sweating, tachycardia, Hyperventilation, orBP, ventricular arrhythmias, pulmonary oedema This is an emergency dose. see steroids above Common side effects fine tremor, nervous tension, headache, muscle cramps, palpitation. Tachycardia, arrhythmias, peripheral vasodilation, myocardial ischaemia, and disturbances of sleep and behaviour. Paradoxical bronchospasm, urticaria, angioedema, hypotension, and collapse. high doses hypokalaemia. haemorrhage, thrombocytopenia, rarely rebound hyperlipidaemia
children This entry for acute/severe asthma. see steroids above. Caution in patients with prostatic hyperplasia, bladder outflow obstruction, and those susceptible to angle-closure glaucoma.
Caution: physical dependence on opioids; cardiac irritability; naloxone is short-acting see steroids above
Contraindications caution in hyperthyroidism, cardiovascular disease, arrhythmias, susceptibility to QT-interval prolongation, and hypertension. caution in diabetesmonitor blood glucose (risk of ketoacidosis, especially when beta2 agonist given intravenously).
2500-
od
SC
5000 u
DVT/PE treatment Unstable angina parenteral anticoagula nts (LMWH) Enoxaparin (Clexane) DVT prophylaxis DVT/PE treatment Unstable angina
od bd
SC SC
by weight 10 000 u bd
following withdrawal, priapism, hyperkalaemia, osteoporosis, alopecia on prolonged use, injection-site reactions, skin necrosis, and hypersensitivity reactions see heparin above
haemorrhage, severe hypertension; peptic ulcer; after major trauma or recent surgery to eye or nervous system; acute bacterial endocarditis; spinal or epidural anaesthesia; hypersensitivity to heparin or to low molecular weight heparins see heparin above see heparin above see heparin above
Tinzaparin (Innohep)
20-40mg or 24000 u 1.5 mg/k g (150 u/kg ) 30 mg / 3000 unit s then 1 mg/kg OR 750mcg/ kg 3500 u
od od
SC SC
4000 u
onc e bd bd od
IV
max see heparin above 100mg 7500 mcg 4500 u see heparin above
SC SC
171
System GI
Cardiovasc ular
Type Anatacid H2 Antagonist PPI Anti-diarrhoeal agents Laxatives Loop diuretics Thiazide diuretics Potassium sparing diuretics Beta blocker Calcium antagonist ACE inhibitor AT1 blocker Nitrates Cardiac glycosides Anti-dysrhythmics Anti-platelet agents Thrombolytics Heparins Oral Anticoagulants Statins
Example Gaviscon Ranitidine Omeprazole Loperamide Mesalazine Furosemide Bendroflumethiazin e Spironolactone Atenolol Dilitiazem Ramipril Losartan Isosorbide mononitrate Digoxin Amiodarone Aspirin Clopidogrel Streptokinase Enoxaparin Warfarin Simvastatin Salbutamol Ipratropium bromide Prednisolone
System Endocrinology
Type Insulin Sulphonylureas Biguanides Thyroxine Anti-thyroid drugs Bisphosphates Calcium & Vitamin D
Pain
NSAIDs Opiates
Diclofenac Codeine, Morphine Paracetamol Amoxicillin Cephradine Doxycycline Gentamicin Erythromycin Ciprofloxacin Metronidazole
Antibiotics
Non-opioids Penicillins Cephalosporins Trimethoprim Tetracyclines Aminoglycosides Macrolides Quinolones Anaerobic antimicrobials
Respiratory
172
Antiemetics
173
5.1 Counselling
Smoking cessation - http://tinyurl.com/ycfgveo Complaints procedure - http://tinyurl.com/y9j8x57 Epilepsy - http://tinyurl.com/ykwe5sd Diabetes - http://tinyurl.com/yehvosu Breast Cancer - when to refer - http://tinyurl.com/ye8sp8t - screening - http://tinyurl.com/yd8utxx Post MI management - http://tinyurl.com/ye4kbdz MRSA - http://tinyurl.com/yb5j742 Warfarin - http://tinyurl.com/ydvaf29
5.3 Histories
Thyrotoxicosis Hyper - http://tinyurl.com/y9lctre Hypo - http://tinyurl.com/yb3bryr BPH - http://tinyurl.com/ybfadgf Polymyalgia rheumatica GCA - http://tinyurl.com/y9dpuzh Intermittent claudication - http://tinyurl.com/yc95mwx Asthma Acute - http://tinyurl.com/yhtbn2u Chronic - http://tinyurl.com/ycfl2xu Rheumatoid arthritis - http://tinyurl.com/yza5k2p Back pain Acute - http://tinyurl.com/y8p8kf4 Chronic - http://tinyurl.com/y9agds4 Collapse http://tinyurl.com/yey9879 and http://tinyurl.com/y9tb97f Pseudomembranous colitis c.diff - http://tinyurl.com/y926dqo 174
Jaundice Interpreting LFTs - http://tinyurl.com/ybghwgk and http://tinyurl.com/yck6yre TIA management guidelines - http://tinyurl.com/ykavuf6 (stroke) Chrons - http://tinyurl.com/yfsuu36 IBD management Chrons - http://tinyurl.com/yexq9la Ulcerative Colitis - http://tinyurl.com/yavmy97
5.4 Examinations
Varicose veins - http://tinyurl.com/yczavqf Bronchiectasis COPD - http://tinyurl.com/yk29cmf Pneumonia - http://tinyurl.com/yzfrosw Homonoymous/bitemporal hemianopia - http://tinyurl.com/yeufuj4 Lung cancer - http://tinyurl.com/ybfc3u9 Competence to consent - http://tinyurl.com/ycoy4kj
brian.mcmillan@doctors.org.uk
175