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APPENDIX OSCE Scenario Answers
481
1. Describe how you will manage this patient’s warfarin prior to surgery.
With elective surgery the best option is to stop the warfarin; aer 3–5 days the INR should be below 2 and therapeu­tic low-molecular-weight heparin (LMWH) can be given instead. On the night before surgery a DVT prophylaxis dose can be given. Following the operation, full anticoagu­lation can be commenced when clinically safe to do so (i.e. risk of post-op bleeding). An alternative is using i.v. hepa­rin; the anticoagulant eect will be gone aer stopping the infusion aer 60–90 min. e patient would need to be in hospital, however, receiving the infusion.
2. On the evening before the operation the INR has come
back as 1.9; you tell your consultant who says it must be below 1.5 and asks if you will kindly sort this out. Describe what you can do to lower the INR and why it will work given the method of action of warfarin.
e patient could be given vitamin K – a dose of 2 mg i.v. would likely be satisfactory but could be repeated. Warfarin acts as a vitamin K antagonist and interferes with the pro­duction by the liver of vitamin K dependent clotting factors II, VII, IX and X. It is important not to give too high a dose of vitamin K as you may nd it dicult to re-warfarinize the patient post-op.
3. Imagine the patient has presented with an INR of 6 and
has small bowel obstruction and needs urgent surgery; describe what options you have to reverse the action of warfarin.
In an emergency it is not appropriate to wait for the INR to fall by omitting warfarin; vitamin K takes sev­eral hours to take eect and may need several doses. A patient can be given FFP, which is rich in all clotting fac­tors, or a prothrombin concentrate complex can be used (e.g. Beriplex), which will reverse the eects of warfarin in under 30 min.
OSCE SCENARIO ANSWER 21.1
A 37-year-old male attends A&E, complaining bitterly of pain in his le groin. On examination the skin appears red and cellulitic. He is in severe pain when it is touched, and he has a tachycardia of 133 beats/min and a temperature of
38.8°C.
1. Given the above information, what broad dierential diagnoses are you considering?
• Likely:
• necrotizing fasciitis
• cellulitis
• infected femoral injection site +/− pseudo­aneurysm.
• Less likely:
• strangulated inguinal/femoral hernia.
2. What questions would you like to ask this patient to get
a rapid idea of the diagnosis? Important points to elicit would include:
• history of trauma, particularly intravenous drug abuse
• course of illness and spread of erythema
• loss of sensation of skin over groin
• systemic illness, e.g. anorexia, rigors
• predisposing factors, e.g. diabetes, immunological compromise.
3. What investigations and management plan would you
initiate?
Investigations
• Blood tests: FBC/U&Es/LFT/CRP/ESR/blood cultures.
• Arterial blood gas.
• Wound swabs.
• If time permits, X-rays may show gas in tissues.
Management
• Surgical debridement is urgently needed as a life­saving measure.
• Prepare for theatre immediately.
• Resuscitate using i.v. uids.
• Start high-dose i.v. antibiotics aer discussion with a senior microbiologist regarding the antibiotic protocol in your hospital for suspected necrotizing infections.
• Contact senior anaesthetist and request help with lines/monitoring, etc.
• Send multiple tissue cultures for microbiology at time of surgery.
e patient rapidly becomes haemodynamically unstable and a diagnosis of septic shock due to severe so tissue infection is assumed. He is taken to theatre where extensive debridement of infected and necrotic tissue is performed along the fascial planes of his leg.
4. What are the diagnosis and prognosis, and which
organisms are commonly associated with this condition?
• Diagnosis: necrotizing fasciitis.
• High mortality rate: 15–40% quoted for treated cases, and much higher if untreated.
• Common organisms include clostridia, group A streptococci and anaerobes; but increasingly com­binations of aerobes and anaerobes are possible, including MRSA.
OSCE SCENARIO ANSWER 21.2
A 68-year-old male patient develops acute retention of urine aer repair of a right inguinal hernia. An indwelling urethral catheter was inserted and he has now developed a urinary tract infection. He was started on appropriate broad-spectrum
482
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SECTION IV Appendix
antibiotics and is now systemically much better. He has asked to speak to one of the surgical team as he is upset about devel­oping a hospital-acquired infection (HAI).
1. Answer the patient’s questions about HAI. e tone of this conversation should be considerate to this man’s feelings and to provide him with information about the condition in language he can understand. Important things to mention would include:
• e need for a catheter when a patient develops post­operative retention, to avoid renal failure.
• The risk of developing an infection at the time of catheter insertion (despite this risk being reduced by the use of aseptic technique) or from organ­isms that can travel up the catheter whilst it is indwelling.
• at you have sent o a sample of his urine to try to identify the particular bug causing the infection, so that the antibiotics can be tailored to this.
• Explain that you understand he is feeling upset, and that you regret he suered a complication of the treatment.
He is satised with your explanation and feels much hap­pier now; however, he is worried about the possibility of getting an MRSA infection whilst he is in hospital, as he has read so much about it in the newspapers.
2. Explain what MRSA is, the dierent sources of infec- tion and methods of spread.
• MRSA is a type of bacteria that normally lives on
people’s skin, particularly around the nose, armpits and groin.
• e reason that MRSA is dierent from the normal
type of this bug is that it has developed resistance to the more common types of antibiotics used to treat it.
• It can be a very serious infection, and MRSA infec-
tion risk is increased in the elderly, those who have been in hospital for a long time, or have been in and out of hospital a lot, and those who have been on lots of antibiotics and have wounds.
• It is most commonly spread by touch.
3. Explain the methods employed in hospitals for preven- tion and control of HAI.
e methods employed by hospitals to reduce HAI include:
• Sta and patient/visitor education and awareness,
e.g. handwashing teaching, posters.
• Good sterile techniques before examinations or
procedures.
• Sterilization and disinfection of equipment.
• Protective clothing and barrier nursing when treat-
ing those infected.
• Careful tracking of hospital/ward infection rates.
OSCE SCENARIO ANSWER 21.3
A 31-year-old male patient who admits to regular intrave­nous drug use is admitted with cellulitis of his right groin, which began 48 h aer repeated attempts to inject his femo­ral vessels. He saw his GP and was started on oral antibiotics but tells you the redness is increasing, though he is systemi­cally well. On examination, the area is warm, pink and swol­len but there is no evidence of abscess.
1. Which two bacterial species are the most likely to be the
cause of this patient’s infection?
Staphylococcus and Streptococcus.
Microbiology culture results of a wound swab taken by the patient’s GP report that a resistant organism has been isolated.
2. Explain how organisms develop and spread resistance
to antimicrobials. Resistance can be:
• Intrinsic (innate) – e.g. when the organism lacks the target site for the agent or is impermeable to the antibiotic.
• Acquired – resistance develops in organisms that were previously susceptible to the antibiotic by:
• altering the target site of the antibiotic
• altering antibiotic uptake (by changing cell per-
meability or actively pumping drug out of the cell)
• antibiotic-inactivating enzymes, e.g. β-lactamase.
Resistance is spread by:
• Chromosomal mutations causing altered protein expression.
• Genes on transmissible plasmids.
• Transposons.
e antibiotics are changed, but as the erythema settles, the patient develops a uctuant area in the skin, consistent with an abscess. e patient is prepped for theatre.
3. What considerations and precautions should be taken
when operating on this patient?
Special precautions should be taken when operating on a patient who is high risk for a blood-borne virus. ese measures include:
• Informing personnel involved in patient care of the potential/actual risk.
• Arrangements for disposal of contaminated material.
• Minimizing theatre sta present to essential person­nel only.
• Removal of all but essential equipment.
• Disposable drapes and gowns.
• Double-gloving and indicator gloves.
• Visors to prevent splash injuries.
• Blunt suture needles or staples.
• Use of kidney dishes to pass all instruments.
APPENDIX OSCE Scenario Answers
483
• orough post-operative cleansing of theatre. In addition, an ultrasound scan of this man’s groin would help to reassure the surgeon that the abscess did not com­municate with a false aneurysm.
OSCE SCENARIO ANSWER 21.4
A 67-year-old male patient was admitted with perforated duodenal ulcer that necessitated laparotomy and repair. Postoperatively, he recovered on the high-dependency unit and was stepped down to the ward and deemed medically t for discharge. He was commenced on H. pylori eradica­tion therapy and was awaiting a social package. However, he developed severe diarrhoea a few days later along with abdominal pain and distension. He had T of 39.5°C, PR of 140/min, RR of 25/min and his blood tests showed WBC count of 35,000 × 106/dL. Abdominal X-ray showed very dilated colon.
1. What is the most likely diagnosis and responsible
microorganism?
e diagnosis is consistent with colitis due to Clostridium dicile, which is a gram-positive spore-forming anaer-
obic bacillus. It is present in the gut of 3% of healthy adults and remains the most common cause of hospital­acquired infectious diarrhoea. It can cause a spectrum of illnesses ranging from mild diarrhoea to life-threatening pseudomembranous colitis, paralytic ileus, peritonitis and death.
2. What are the predisposing risk factors for acquiring
this infection in this context?
Risk factors for C. dicile colonization/ infection include:
• Antibiotic use, especially broad-spectrum antibiotics.
• Acid-suppressing medication (especially proton
pump inhibitors).
• Signicant co-morbidity e.g. chronic renal failure,
pre-existing bowel pathology, malignancy.
• Naso-gastric feeding.
• Alteration in gut motility, e.g. by laxatives.
• Age over 65.
• Recent healthcare intervention/stay in care facility. e above patient had recent surgery and hospitalization, was commenced on broad-spectrum antibiotics and PPI and likely had postoperative NG feeding. Although the big­gest risk factor for C. dicile is prior exposure to antibiot- ics, cases have been associated with no obvious antibiotic exposure. Almost all antibiotics have been implicated as they all cause disruption of commensal microbiota includ­ing paradoxically metronidazole and vancomycin, which are antibiotics used for treatment of C. dicile. However, the highest-risk antibiotics are broad-spectrum antibiot­ics such as penicillins, cephalosporins and clindamycin.
Quinolones are high risk for the 027 strain of C. dicile, which is hyper virulent and hyper transmissible.
3. How do you conrm the diagnosis? is requires sending a stool sample immediately to test for C. dicile. If C. dicile toxin is detected; this means the patient has C. dicile and should be treated in the context of symptoms. e case would be also subject to mandatory reporting to the Department of Health. Occasionally C. dicile toxin is not detected, but C. di- cile toxin gene is detected. is indicates that the patient is likely colonized with C. dicile. ey should be reviewed and assessed for treatment, but it does not trigger manda­tory reporting to the Department of Health.
4. How do you manage this condition? Suspected infectious diarrhoea must be managed by apply­ing the SIGHT mnemonic.
S Suspect that a case may be infective where there is
no clear alternative cause for diarrhoea.
I Isolate the patient and consult with the infection
prevention and control team while determining the cause of diarrhoea.
G Gloves and aprons must be used for all contacts
with the patient and their environment.
H Hand washing with soap and water should be
carried out before and after each contact with the patient and the patient’s environment.
T Test the stool for C. difficile by sending a specimen
immediately.
5. What are the precautions required to prevent this
infection from occurring and spreading in hospitals?
Ward staff must isolate symptomatic patients on first suspicion of C. difficile at the onset of symptoms in a single room, preferably with en suite toilet facilities. Isolation can be discontinued when the patient has been symptom-free for at least 72 h and has passed formed stool or stool is normal for the patient within that time. There is no requirement to submit further faeces sam­ples for toxin detection, as toxin may be present in the gut for some time after the patient has become asymp­tomatic. All staff and visitors on entering an isolation room should put on disposable gloves and aprons. PPE must be removed, and hands washed with soap and water before leaving the isolation room. Alcohol-based hand sanitizers are not effective against C. difficile. Stool chart should be commenced and hospital’s antibiotic policy for treating C. difficile should be consulted. Generally, this is based on the severity of symptoms and includes oral or i.v. metronidazole and oral vancomycin.
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SECTION IV Appendix
OSCE SCENARIO ANSWER 21.5
You attend the minor operation room to perform excision of skin lesions under local anaesthesia. Your consultant reminds you of using the pink disinfectant for skin preparation and performing the procedures under strict sterile measures using sterile instruments, gloves and gowns.
1. What disinfection agents are used on skin? ere are several available skin disinfectants. e com­monest are alcohol, chlorhexidine and povidine–iodine.
• Alcohol: eective against Gram-positive and Gram­negative organisms and has some antiviral activity; however, it is relatively inactive against spores and fungi. Avoid pooling as it is inammable. It can also irritate sensitive areas.
• Chlorhexidine: non-toxic to skin and mucous membranes in aqueous solution (0.5%), while 4% solution is used as surgical scrub. It is more eective against Gram-positive, but has moderate activity against Gram-negative; hence, 0.5% concentration is frequently mixed with 70% alcohol for local anti­sepsis as it is more eective than aqueous prepara­tions, but caution should be taken with diathermy to avoid re.
• Povidine–iodine: broad spectrum against bacteria, spores, fungi, viruses (hepatitis B and HIV). In addi­tion to skin disinfection, it is used for wound anti­sepsis, but can get inactivated by organic material such as pus, blood and faeces.
2. What is the dierence between cleaning, disinfection,
and sterilization?
• Cleaning is the process of physically removing contamination, but it does not inactivate micro­organisms.
• Disinfection is the process of reducing the number of viable microorganisms; however, bacterial spores and viruses may survive.
• Sterilization is the process of complete eradication of all microorganisms including spores and viruses.
3. What are the four main methods of sterilization?
• Heat:
• moist heat (autoclave): most used in hospitals:
121°C for 15 min or 134°C for 3 min
• dry heat: higher heat; hence, not suitable for plas-
tics and other material that cannot withstand such heat: 160°C for 2 h
• Irradiation: for heat labile articles, such as lines, catheters, syringes.
• Filtration: used to sterilize drugs for injection.
• Chemicals:
• ethylene oxide: used for electrical equipment,
sutures
• glutaraldehyde: used for endoscopes, needs 3 h to kill all microbes
• formaldehyde: for heat labile instruments.
OSCE SCENARIO ANSWER 22.1
A 28-year-old right-handed female attends A&E with a wound on the radial and volar border of her right index n­ger, just proximal to the PIPJ. She explains that she cut it last night with a knife whilst washing dishes, and complains of radial numbness distal to the wound.
1. Outline how you would examine the patient’s nger to
establish what structures have been injured other than the digital nerve.
• Need to elicit numbness distal to the wound with loss of light touch sensation.
• Establish that the nger is well vascularized by test­ing capillary rell.
• Examine the tendons of the nger to ensure that extensor digitorum communis (EDC), exor digito­rum supercialis (FDS), and exor digitorum pro­fundus (FDP) are intact.
2. Explain to the examiners what would happen patho-
logically and clinically if the nerve injury was le untreated.
Histopathologically
• Wallerian degeneration would occur: degeneration of the axons and myelin distal to the wound.
• Regeneration would start to occur 3–4 days post­injury and the axons would grow at 1–2 mm/day.
• Schwann cells would perform remyelination.
• However, if the perineurium has been disrupted, then the regeneration may not be successful.
Clinically
• Permanent loss of sensation is likely if the nerve has been transected.
• A painful neuroma may form.
3. Explain your management plan to the patient and answer any questions she may have.
• It is likely that the nerve has been cut, and to ensure
that no neuroma occurs and to have the best chance of sensation returning, surgical repair is advised.
• If we repair it, there is a chance that the sensation will
return, but this is not always the case and is oen not exactly the same as before the injury.
• Nerves grow very slowly, so there will be a long wait
to see how much recovery the nerve will get.
• e most important reason for repairing the nerve is to
try to avoid a neuroma, which is uncontrolled re-growth of the nerve endings that can be painful and irritating.
• e side of the index nger you have injured is one
that you use to grasp objects (e.g. pens) against your
APPENDIX OSCE Scenario Answers
485
thumb, so we consider this even more important to try to keep your hand functioning well.
OSCE SCENARIO ANSWER 22.2
A 19-year-old male attends your outpatient clinic with a 3-month history of right knee pain and swelling. e pain and swelling are worsening, waking him at night, and he now walks with a limp. He denies any traumatic injury, is otherwise t and well, and on no medications. An X-ray arranged by his GP whilst waiting for his referral is shown below (Fig. 22.2Q).
1. Describe the pathological signs on the X-ray (Fig.
22.2A).
• Bone destruction.
• So tissue invasion.
• Growth of bone outside of the cortex and elevating periosteum.
• Deposition of periosteal bone (Codman’s triangle) – single arrow.
• Spicules of radiating bone (‘sunray’ spicules) –double ar row.
2. What is the likely diagnosis, given the history and the
X-ray?
Osteosarcoma (osteogenic sarcoma) of the lower femur.
3. What other investigations could you arrange?
• Alkaline phosphatase.
• ESR.
• CT.
• MRI.
• CXR/CT chest.
• Bone biopsy.
4. What are the management options?
Medical
• Neo-adjuvant chemotherapy to shrink the tumour and/or lung metastases.
• Post-operative chemotherapy.
Surgical
• Wide local excision with chemotherapy.
• Amputation.
• Resection of pulmonary metastases if appropriate.
OSCE SCENARIO ANSWER 22.3
A 45-year-old female has presented in A&E aer falling down some steps. She is alert and her pulse and blood pres­sure are normal, though her oxygen saturations are only 80% on high-ow oxygen. She is complaining bitterly of pain down her right chest wall, though only grazes are present.
1. How will you approach the assessment of this patient? Using ATLS principles:
• Airway with C-spine control
• Breathing
• Circulation.
2. Her chest X-ray is shown below (Fig. 22.3Q). What is
the condition shown? What is the likely cause?
• A right-sided closed pneumothorax (Fig. 22.3A).
• ough rib fractures cannot be seen, it is possible that this is the cause, given the history.
3. How would you treat this condition?
• If oxygenation is severely compromised, needle decompression of the pneumothorax in the 2nd inter­costal space in the midclavicular line is appropriate.
• Denitive treatment is with insertion of a chest drain connected to an underwater seal.
4. Explain to the examiners the classication of causes
and types of this condition, and how you would have treated the patient if she had presented with tracheal deviation and haemodynamic instability.
Types of pneumothorax
• Open.
• Closed.
• Tension.
Causes
• Spontaneous (primary and secondary).
• Traumatic (open and closed).
• Iatrogenic.
Treatment
• If the patient had presented with tracheal deviation and haemodynamic instability with clinical signs of a pneu­mothorax, you would suspect a tension pneumothorax.Fig. 22.2A X-ray of the patient’s right knee.
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Fig. 22.3A The patient’s chest X-ray. A pneumotho-
rax is visible on the right side. The lung edge is vis­ible (arrow).
• As this is a life-threatening condition which can rapidly cause death, a swi needle decompression WITHOUT waiting for a chest X-ray would be the appropriate management.
SECTION IV Appendix
OSCE SCENARIO ANSWER 22.4
A 14-year-old boy attends your clinic with his mother, who is concerned that her son seems to be developing breasts. e boy is overweight, with a BMI of 29, but both he and his mother state that he has lost weight recently and his breasts are still enlarging. His examination reveals enlarged nipples with small rm breast bud development.
1. What is the likely diagnosis? What questions would
you like to ask to conrm this?
• Pubertal physiological gynaecomastia.
Relevant points to elicit would include:
• A full drug history to exclude drug-induced gyn­aecomastia; note that the patient’s mother is in the room and therefore answers regarding cannabis and anabolic steroid use may have to be asked at a con­dential time, e.g. during examination.
• Anything to suggest hypogonadism, i.e. unde­scended testes, lack of body hair, bilateral torsion, Kleinfelter’s syndrome.
• Any testicular swellings (testicular tumour).
• Any visual disturbance/lactation (pituitary cause).
• Anything to suggest male breast carcinoma (nipple dis­charge or retraction, hard lump, lymphadenopathy).
• Family history of gynaecomastia or hypogonadism.
2. Explain the diagnosis and its causes in layman’s
terms, and outline the options for investigation and management.
Important to perform this very sensitively as the patient is likely to be embarrassed and confused. Points to raise would include:
• All men have some breast tissue, and in some men this tissue can grow – we call this gynaecomastia and it can happen to babies, teenagers or older men and it’s actually not that rare.
• is is dierent to just being ‘overweight’ as it is breast tissue and not just fat causing the swelling, though weight loss may help.
• is can happen at puberty because of hormonal imbalances, but oen we don’t really know why it happens.
• Sometimes there are specic causes such as certain drugs, which can reduce your male hormones or increase female hormones, or medical conditions.
• If we aren’t sure of the cause then certain blood tests, X-rays and even taking a tissue sample can help, though oen we don’t need to do this if we think the cause is puberty.
• General options for treatment include:
• removing the cause (i.e. stop any medications
causing it)
• nothing – 90% of physiological gynaecomastia
goes away by itself, though it can take a few weeks or a couple of years
• medication to reduce oestrogen or increase
testosterone
• surgery to remove the breast tissue – but this will
leave scarring.
OSCE SCENARIO ANSWER 22.5
A 62-year-old male attends A&E with acute onset of severe abdominal pain radiating to the back. He is pale and sweaty with a tense, distended, tender abdomen. A CT of his abdo­men is shown below (Fig. 22.5Q).
1. What pathology is shown? A leaking abdominal aortic aneurysm (Fig. 22.5A).
e patient is still in the radiology department and his
blood pressure is stable at 90 mmHg systolic.
2. Outline the immediate management of this patient.
• Immediate surgery is needed to try to save this man’s life.
Fig. 22.5A CT scan of the patient’s abdomen. There is
a large leaking abdominal aortic aneurysm (arrow).
• Explain the diagnosis to the patient and the urgent need for surgery.
• Arrange for immediate transfer to theatre.
• Alert the senior anaesthetist on call, the on-call the­atre team and the senior surgeon.
• Ensure that the patient has had FBC/U&Es/LFT/ clotting screen taken and is cross-matched for 10 units of blood.
3. What risk factors exist for this condition?
• Smoking.
• Hypertension.
• Male sex.
• Family history.
4. What is the operative mortality risk for this condition? 30–50%.
5. Explain to the examiners the dierent types of this con- dition, their classication and their aetiology.
• Can be classied in the following ways:
• true: where the wall of the aneurysm contains all three elements of intima, media and adventitia (can be subdivided by shape into fusiform and saccular)
• false: pulsating haematoma with a cavity in conti­nuity with the lumen.
• Or as:
• congenital: ‘berry’ aneurysms around the circle of Willis
APPENDIX OSCE Scenario Answers
• acquired: aneurysms which develop in life for various reasons (listed below).
• Or by cause:
• atheromatous
• mycotic
• syphilitic
• dissecting
• arteriovenous aneurysms (aneurysmal varices associated with A/V stulae).
487
OSCE SCENARIO ANSWER 22.6
A 37-year-old female attends your clinic having been referred by her GP with excessive sweating, diarrhoea and neck swelling.
1. Ask this patient about her symptoms and give the examiners your dierential diagnosis.
• Elicit goitre features:
• How long present for? Is it enlarging?
• Painful?
• Problems swallowing?
• Problems breathing in?
• Change in voice?
• Enlarging?
• Elicit features of hyperthyroidism:
• excessive sweating/heat intolerance
• weight loss; check not intentional, i.e. not dieting
• anxiety/irritability
• palpitations/tremor
• insomnia
• diarrhoea
• menorrhagia.
• Dierential diagnosis is thyrotoxicosis, secondary to:
• a toxic goitre (single/multinodular)
• Graves’ disease
• functioning adenoma.
2. What physical signs may you expect to see on
examination?
• Clubbing.
• Wet palms/excessive sweating.
• Tachycardia/irregular heart rate/AF.
• Eye signs (exophthalmos/lid lag).
• Tremor.
• Pretibial myxoedema/hyper-reexia.
• Proximal myopathy.
3. What investigations might you arrange?
• FBC/ESR/TFTs.
• USS (ultrasound scan) of goitre.
• Radioisotope scan of goitre.
• FNA of goitre.
e results of your investigations suggest a benign toxic goitre with a dominant nodule.
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SECTION IV Appendix
4. What treatment options are available?
• Medical treatment for symptoms (e.g. beta-blockers).
• Medical treatment to block thyroid hormone pro­duction (e.g. carbimazole).
• Radioactive iodine treatment.
• Surgical removal (e.g. total/subtotal thyroidectomy – will need thyroxine treatment aerwards).
5. If the patient opts for surgery, which nerves are at risk
of intra-operative damage?
• Recurrent laryngeal nerve (related to the inferior thyroid artery).
• External branch of the superior laryngeal nerve (related to the superior thyroid artery).
OSCE SCENARIO ANSWER 22.7
e blood results displayed below are those taken from a 49-year-old male ex-alcoholic, feeling generally unwell with vague abdominal pain, whose GP has referred him to your clinic.
Bilirubin 57 µmol/L Albumin 22 g/L Total protein 64 g/L Alkaline phosphatase (ALP) 152 IU/L Alanine aminotransferase (ALT) 188 IU/L Aspartate aminotransferase (AST) 220 IU/L Gamma glutamyltransferase (GGT) 129 IU/L
1. What biochemical abnormalities are shown?
• Raised levels of bilirubin, AST/ALT/GGT, and to a lesser extent ALP.
• Reduced levels of albumin.
2. Explain to the examiners the dierent types of jaundice
and give examples of the causes of each type.
Pre-hepatic jaundice
is is due to intravascular haemolysis and some causes include:
• Congenital defects, e.g. Gilbert’s disease.
• Congenital red cell defects, e.g. sickle cell, hereditary spherocytosis.
• Acquired red cell defects, e.g. malaria, autoimmune disease, hypersplenism.
Hepatic jaundice
is is due to intrinsic liver pathology and some causes include:
• Acute hepatocellular disease due to:
• infections, e.g. hepatitis, CMV, leptospirosis
• drugs, e.g. paracetamol, anaesthetics
• autoimmune disease.
• Chronic hepatocellular disease due to:
• infections, e.g. chronic viral hepatitis
• chronic autoimmune disease
• end-stage liver disease, e.g. alcohol, cirrhosis,
Wilson’s disease.
Post-hepatic/cholestatic jaundice
is is due to either intrahepatic cholestasis or post-hepatic biliary obstruction and some causes include:
• Intrahepatic causes due to:
• pregnancy
• drugs/nutrition, e.g. chlorpromazine; TPN
• primary biliary cirrhosis.
• Extrahepatic causes due to obstruction in:
• lumen, e.g. gallstones or parasite infestation (schistosomiasis)
• wall, e.g. strictures, cholangitis, cholangiocar­cinoma
• outside of wall, e.g. tumour in head of pancreas, nodes in porta hepatis, chronic pancreatitis.
3. Which type is this patient’s likely to be from the blood
results?
Blood results suggest a chronic hepatocellular form of jaundice, possibly due to alcoholic cirrhosis. Chronic ele­ment is suggested due to low levels of albumin.
4. Closer questioning reveals that the patient has devel-
oped abnormal stools which are pale, oat, and are dif­cult to ush away. What other condition is the patient likely to have developed?
Chronic pancreatitis due to chronic alcoholism.
OSCE SCENARIO ANSWER 22.8
An 82-year-old male is brought into the emergency depart­ment with an acutely painful right leg. e symptoms include the leg feeling cold, looking very pale and pins and needles. e patient’s ECG is shown below (Fig. 22.8Q).
GET AN AF ECG
1. What is the likely diagnosis? e likely diagnosis given the symptoms and ECG ndings are an acute arterial embolism leading to acute ischaemia of the right leg. e ECG shows the classic signs of Atrial Fibrillation (AF) - irregularly irregular pulse and lack of P waves.
2. What are the causes? Causes of acute ischaemia can be divided broadly into luminal and extra-luminal causes.
• Luminal causes include embolism, thrombosis (including clotting disorders), arterial dissection.
• Extra-luminal causes include trauma, external com­pression, popliteal entrapment, and cystic adventitial disease (the last two rarely present acutely).
3. What other symptoms can occur and which are the
most clinically important?
e classic symptoms of an acutely ischaemic limb are the 6 P’s: Pain, Pulseless, Perishingly cold, Paralysis, Paraesthesia, and Pallor. e most clinically important of these are the
APPENDIX OSCE Scenario Answers
489
degree of paraesthesia and paralysis; nerves are very sensi­tive to ischaemia. It is very common to have mild pins and needles or a mild dierence in sensation; paralysis is oen absent in the early stages. However, as ischaemia persists, a limb which is paralysed and insensate may not be salvage­able. e 6 P’s does not draw attention to the importance of pain on muscle squeezing; a patient with pain on com­pression of the gastrocnemius or anterior compartment has severe limb ischaemia and is at high risk of compartment syndrome.
4. What investigations would you perform? Bit of a trick question this one – it may be none. In a patient in AF with no previous vascular surgery/interventions and normal pulses on the opposite side and severe symptoms, the patient may be taken to theatre for an urgent embolectomy. If, however, the diagnosis is not so clear cut then a CT angiogram or duplex ultrasound will give the required information.
5. Are you aware of any classication systems for this
condition?
e most widely used classication system is by Rutherford; it divides the severity into viable, threatened and irrevers­ible on the grounds of capillary return, degree of paralysis and sensory loss and whether there are audible arterial and venous Doppler signals.
6. If the patient had a paralysed and insensate leg with
a purple discolouration which did not blanch under pressure, what would be the likely management plan?
is sadly sounds like a Rutherford stage 3 ischaemia; the leg is irreversibly ischaemic; the classic sign is the deep pur­ple discolouration of the leg does not blanch aer digital pressure. e only treatment is primary amputation or in patients where this would be inappropriate then palliation.
OSCE SCENARIO ANSWER 22.9
A 56-year-old male is admitted with severe dehydration and vomiting, his urea and creatinine are raised at 15 mmol/L and 215 μmol/L. A blood gas shows the following abnormali- ties: pH 7.55, PO2 10.9 kPa, CO2 6.9 kPa and HCO3 is 21.
1. What type of metabolic abnormality is this patient
displaying?
e patient has a metabolic alkalosis – this is indicated by the pH showing alkalosis. e fact that is it metabolic in nature is indicated by the raised CO2 (compensatory hypoventilation) and the low HCO3 (compensatory loss by the kidneys). e fact that the HCO3 is low would suggest the cause of the alka­losis is loss of H ions rather than excess HCO3.
2. How has it occurred? Vomiting results in a loss of H ions and thus a metabolic alkalosis.
3. e patient has a ‘succussion splash’ on examination –
what is the diagnosis?
A ‘succussion splash’ is a characteristic nding in gastric outlet obstruction which leads to severe vomiting. It is an examination nding where you literally shake the patient’s abdomen from side to side and can hear the uid in the stomach moving.
4. How would you manage this condition? e management of this condition would fall into –
• Resuscitation and correction of electrolyte abnorma­lities.
• Investigation as to the cause – OGD and or CT scan.
• Management of the cause – the commonest causes are peptic ulcer disease or malignancy. If due to malignancy then surgical resection of the tumour or palliative gastro-jejunostomy would be appropri­ate. If due to peptic ulcer disease then initial medical management with i.v. PPI is appropriate for 48–72 h. If there is no improvement then surgical resection may be deemed appropriate.
OSCE SCENARIO ANSWER 22.11
A 62-year-old male is in the A&E department and is com­plaining of epigastric pain. is feels like his normal heart­burn but has not been relieved by antacids. In addition he is sweating and has a bradycardia. An ECG is performed and shows raised ST segments.
1. From the history, what type of myocardial infarction is
the patient having and in what leads would you expect to see the ST segment rises?
e symptoms are suggestive of an inferior MI – this is an oen overlooked dierential diagnosis for acute epigastric pain and explains why an ECG is essential in patients present­ing with upper abdominal pain. Classically the leads showing raised ST segment changes are leads II, III and aVF.
2. Which coronary artery is involved? e right coronary artery supplies the territory involved in an inferior MI. Occlusion of the le anterior descend­ing artery (LAD) leads to an anterior and or septal MI. Occlusion of the circumex branch of the le coronary artery leads to a lateral MI. Occlusion of the right coronary artery leads to an inferior MI (as mentioned) and also may lead to a right ventricle and atrial infarction. Occlusion of the circumex branch of the right coronary artery can occasionally cause an inferior MI but more usually a pos­terior MI.
3. Why is it common to see a bradycardia? In approximately 60% of the population the SA node is supplied by the right coronary artery and thus infarctions involving this territory may present with bradycardia and conduction problems.
ACKNOWLEDGE
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INDEX
Page numbers followed by “f” indicate gures, “t”indicate tables, and “b” indicate boxes.
A
Abdomen, 20–23
development, 20–23
mass, 325 Abdominal aorta, 30–32, 30f Abdominal aortic aneurysms, 32, 213,
406
repair, 213 Abdominal breathing, 13 Abdominal incisions, anatomy of, 25–26 Abdominal muscles
nerve supply of, 24
reex, 167t Abdominal pain, acute. See Acute
abdominal pain Abdominal reexes, 164, 167t Abdominal viscera, 38–60, 38f
anal canal, 45–46 anal sphincters, 46–47, 46f appendix, 44 bladder, 56–57 blood supply, 39 broad ligament, 59 duodenum, 42 extrahepatic biliary system, 49–51, 50f fallopian tubes, 59 gall bladder, 51 gastric mucosa, structure of, 41–42, 42f kidneys, 54–55, 54f large intestine, 43–44 liver, 47–49 microscopic structure, 39 nerve supply, 39, 41–42 oesophagus, 38–39 ovary, 60 pancreas, 53–54 portal venous system, 51–53, 52f prostate, 57 rectal examination, 47 rectum, 44–45 seminal vesicles, 57 spleen, 54 suprarenal glands, 56 sympathetic nervous system, 168
Abdominal viscera (Continued)
ureter, 55–56 uterus, 57–59, 58f vagina, 59–60 vaginal examination, 60
Abdominal wall
anterior, 23–25 muscles, 24, 25f posterior, 29–30 rectus sheath, 24, 25f supercial fascia of, 23
Abducens nerve, 159–160, 163f
VI, 155 Abduction movements, 99 Abductor pollicis brevis, thumb, 69 Abductor pollicis longus, thumb, 69 abl oncogene, 323t Abnormal temperature regulation,
172–173 ABO blood group system, 355, 355t Abscesses, 307, 370–371, 371t
antibiotic therapy, 368 chronic, 309, 370
metastatic, 370 Absorption, 220, 221t Acanthosis nigricans, 326 Accessory nerve, 138, 162, 163f
spinal, 135
surface marking of, 135 Acetabulum, 80 Acetylcholine (ACh), 271
neuromuscular transmission, 271–272 Achilles tendon reex, 274 Achondroplasia, 298 Acid-base balance, 177–180
disturbances of, 178–180, 179t
interpretation of changes, 179–180
mixed disorders of, 179 Acoustic neuroma, 389–390 Acromegaly, 252, 253f Acromioclavicular joint, 66 ACTH. See Adrenocorticotrophic
hormone (ACTH)
Actin laments, 204, 271
Actinomycosis, breast, 402 Action potential
cardiac, 204–205, 204f nerve, 265, 266f neuromuscular transmission, 271–272
Activated partial thromboplastin time
(APTT), 348 Acute abdominal pain, 185, 409–410 Acute coronary syndrome, 405 Acute inammation, 305
causes, 305 chemical mediators, 306 eects, 308 macroscopic signs and symptoms, 305 progression from, 309 recurrent episodes, 309 resolution, 308
stages, 305–306 Acute insuciency, 409 Acute osteomyelitis, 392 Acute pelvic inammatory disease, 410 Acute phase response, 255–256, 367 Acute pyogenic cellulitis, 368 Acute pyogenic mastitis, 402 Adaptive immunity, 330 Addison’s disease, 249, 250f, 409 Adduction movements, 99 Adductor canal, 90 Adductor pollicis, thumb, 69 Adenocarcinoma, 318 Adenoma, 318, 423–424 Adenoma-carcinoma sequence, 321,
322f Aδ bres, 269, 273f ADH. See Antidiuretic hormone (ADH) Adherence, 346 Adjuvant radiotherapy, 291 Adrenal cortex
actions, 247–249 disorders, 249–251 hormones, 247–249, 248f hyperfunction, 408–409 hypofunction, 409 tumours, 409
490