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Question 1-3 of 147
Theme: Chest pain
A. Pulmonary embolism
B. Acute exacerbation asthma
C. Physiological
D. Mitral valve stenosis
E. Aortic dissection
F. Mitral regurgitation
G. Bronchopneumonia
H. Tuberculosis
I. None of the above What is the most likely diagnosis for the scenario given? Each option may be used once, more than once or not at all.
1. A 28 year old Indian woman, who is 18 weeks pregnant, presents with increasing shortness
of breath, chest pain and coughing clear sputum. She is apyrexial, blood pressure is 140/80
mmHg, heart rate 130 bpm and saturations 94% on 15L oxygen. On examination there is a
mid diastolic murmur, there are bibasal crepitations and mild pedal oedema. She suddenly
deteriorates and has a respiratory arrest. Her chest x-ray shows a whiteout of both of her
lungs.
You answered Pulmonary embolism
The correct answer is Mitral valve stenosis
Mitral stenosis is the commonest cause of cardiac abnormality occurring in pregnant
women. Mitral stenosis is becoming less common in the UK population, however should be
considered in women from countries where there is a higher incidence of rheumatic heart
disease. Mitral stenosis causes a mid diastolic murmur which may be difficult to auscultate
unless the patient is placed into the left lateral position. These patients are at risk of atrial
fibrillation (up to 40%), which can also contribute to rapid decompensation such as
pulmonary oedema (hence cxr 'whiteout' of lungs). Physiological changes in pregnancy may
cause an otherwise asymptomatic patient to suddenly deteriorate. Balloon valvuloplasty is
the treatment of choice.
2. A 28 year old woman, who is 30 weeks pregnant, presents with sudden onset chest pain
associated with loss of consciousness. Her blood pressure is 170/90 mmHg, saturations on
15L oxygen 93%, heart rate 120 bpm and she is apyrexial. On examination there is an early
diastolic murmur, occasional bibasal creptitations and mild peal oedema. An ECG shows
ST elevation in leads II, III and aVF.
You answered Pulmonary embolism
The correct answer is Aortic dissection
Aortic dissection is associated with the 3rd trimester of pregnancy, connective tissue
disorders (Marfan's, Ehlers- Danlos) and bicuspid valve. Patients may complain of a tearing
chest pain or syncope. Clinically they may be hypertensive. The right coronary artery may
become involved in the dissection, causing myocardial infarct in up to 2% cases (hence ST
elevation in the inferior leads). An aortic regurgitant murmur may be auscultated.
3. A 28 year old woman, who is 18 weeks pregnant, presents with sudden chest pain. Her
blood pressure is 150/70 mmHg, saturations are 92% on 15L oxygen and her heart rate is
130 bpm. There are no murmurs and her chest is clear. There is signs of thrombophlebit is in
the left leg.
Pulmonary embolism
Chest pain, hypoxia and clear chest on auscultation in pregnancy should lead to a high
suspicion of pulmonary embolism.
Theme question in September 2011 exam Pregnant women can decompensate rapidly from cardiac compromise.
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Chest pain in pregnancy
Aortic dissection
Predisposing factors in pregnancy are hypertension, congenital heart disease and Marfan's syndrome
Mainly Stanford type A dissections Sudden tearing chest pain, transient syncope Patient may be cold and clammy, hypertensive and have an aortic regurgitation murmur Involvement of the right coronary artery may cause inferior myocardial infarction
Surgical management
Gestational timeframe Management
< 28/40 Aortic repair with the fetus kept in utero
28-32/40 Dependent on fetal condition
> 32/40 Primary Cesarean section followed by aortic repair at the same operation
Mitral stenosis
Most cases associated with rheumatic heart disease Becoming less common in British women; suspect in Immigrant women Commonest cardiac condition in pregnancy Commonly associated with mortality
Valve surgery; balloon valvuloplasty preferable
Pulmonary embolism
Leading cause of mortality in pregnancy Half dose scintigraphy; CT chest if underlying lung disease, should aid diagnosis
Treatment with low molecular weight heparin throughout pregnancy and 4-6 weeks after childbirth
Warfarin is contra indicated in pregnancy (though may be continued in women with mechanical heart valves due to the significant risk of thromboembolism)
References 1. Bates S.M. and Ginsberg J.S. How we manage venous thromboembolism during pregnancy. Blood2002 (100): 3470-3478. 2. Scarsbrook A.Fand Gleeson V. Investigating suspected pulmonary embolism in pregnancy. BMJ2007 (326) : 1135 doi: 10.1136/bmj.7399.1135. 3. Morley C. A. and Lim B. A. Lesson of the Week: The risks of delay in diagnosis of breathlessness in pregnancy. BMJ 1995 (311) : 1083.
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Question 4 of 147
A 67 year old man is investigated for biliary colic and a 4.8 cm abdominal aortic aneurysm is identified. Which of the following statements relating to this condition is untrue?
The wall will be composed of dense fibrous tissue only
The majority are located inferior to the renal arteries
They occur most often in current or former smokers
He should initially be managed by a process of active surveillance
Aortoduodenal fistula is a recognised complication following repair.
They are true aneurysms and have all 3 layers of arterial wall. Please rate this question:
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Abdominal aorta aneurysm
Abdominal aortic aneurysms are a common problem in vascular surgery. They may occur as either true or false aneurysm. With the former all 3 layers of the arterial
wall are involved, in the latter only a single layer of fibrous tissue forms the aneurysm wall.
True abdominal aortic aneurysms have an approximate incidence of 0.06 per 1000 people. They are commonest in elderly men and for this reason the UK is now introducing the aneurysm screening program with the aim of performing an abdominal aortic ultrasound measurement in all men aged 65 years.
Causes
Several different groups of patients suffer from aneurysmal disease.
The commonest group is those who suffer from standard arterial disease, i.e. Those who arehypertensive, have diabetes and have been or are smokers.
Other patients such as those suffering from connective tissue diseases such as Marfan's may also develop aneurysms. In patients with abdominal aortic aneurysms the extracellular matrix becomes disrupted with a change in the balance of collagen and elastic fibres.
Management
Most abdominal aortic aneurysms are an incidental finding.
Symptoms most often relate to rupture or impending rupture. 20% rupture anteriorly into the peritoneal cavity. Very poor prognosis. 80% rupture posteriorly into the retroperitoneal space The risk of rupture is related to aneurysm size, only 2% of aneurysms measuring less than
4cm in diameter will rupture over a 5 year period. This contrasts with 75% of aneurysms measuring over 7cm in diameter.
This is well explained by Laplaces' law which relates size to transmural pressure. For this reason most vascular surgeons will subject patients with an aneurysm size of 5cm or
greater to CT scanning of the chest, abdomen and pelvis with the aim of delineating anatomy and planning treatment. Depending upon co-morbidities, surgery is generally offered once the aneurysm is between 5.5cm and 6cm.
A CT reconstruction showing an infrarenal abdominal aortic aneurysm. The walls of the sac are
calcified which may facilitate identification on plain x-rays
Image sourced from Wikipedia
Indications for surgery
Symptomatic aneurysms (80% annual mortality if untreated)
Increasing size above 5.5cm if asymptomatic Rupture (100% mortality without surgery)
Surgical procedures Abdominal aortic aneurysm repair Procedure: GA Invasive monitoring (A-line, CVP, catheter) Incision: Midline or transverse Bowel and distal duodenum mobilised to access aorta. Aneurysm neck and base dissected out and prepared for cross clamp Systemic heparinisation Cross clamp (proximal first) Longitudinal aortotomy Atherectomy Deal with back bleeding from lumbar vessels and inferior mesenteric artery Insert graft either tube or bifurcated depending upon anatomy Suture using Prolene (3/0 for proximal , distal anastomosis suture varies according to site) Clamps off: End tidal CO2 will rise owing to effects of reperfusion, at this point major risk of myocardial events. Haemostasis Closure of aneurysm sac to minimise risk of aorto-enteric fistula Closure: Loop 1 PDS or Prolene to abdominal wall Skin- surgeons preference Post operatively: ITU (Almost all) Greatest risk of complications following emergency repair Complications: Embolic- gut and foot infarcts Cardiac - owing to premorbid states, re-perfusion injury and effects of cross clamp Wound problems Later risks related to graft- infection and aorto-enteric fistula Special groups
Supra renal AAA These patients will require a supra renal clamp and this carries a far higher risk of complications and risk of renal failure. Ruptured AAA
Pre-operatively the management depends upon haemodynamic instability. In patients with symptoms of rupture (typical pain, haemodynamic compromise and risk factors) then ideally prompt laparotomy. In those with vague symptoms and haemodynamic stability the ideal test is CT scan to determine whether rupture has occurred or not. Most common rupture site is retroperitoneal 80%. These patients will tend to develop retroperitoneal haematoma. This can be disrupted if Bp is allowed to rise too high so aim for Bp 100mmHg. Operative details are similar to elective repair although surgery should be swift, blind rushing often makes the situation worse. Plunging vascular clamps blindly into a pool of blood at the aneurysm neck carries the risk of injury the vena cava that these patients do not withstand. Occasionally a supracoeliac clamp is needed to effect temporary control, although leaving this applied for more than 20 minutes tends to carry a dismal outcome.
EVAR Increasingly patients are now being offered endovascular aortic aneurysm repair. This is undertaken by surgeons and radiologists working jointly. The morphology of the aneurysm is important and not all are suitable. Here is a typical list of those features favoring a suitable aneurysm:
Long neck Straight iliac vessels Healthy groin vessels
Clearly few AAA patients possess the above and compromise has to be made. The use of fenestrated grafts can allow supra renal AAA to be treated. Procedure: GA Radiology or theatre Bilateral groin incisions Common femoral artery dissected out Heparinisation Arteriotomy and insertion of guide wire Dilation of arteriotomy Insertion of EVAR Device Once in satisfactory position it is released Arteriotomy closed once check angiogram shows good position and no endoleak Complications: Endoleaks depending upon site are either Type I or 2. These may necessitate re-intervention and all EVAR patients require follow up . Details are not needed for MRCS. References A reasonable review is provided by: Sakalihasan N, Limet R, Defawe O. Abdominal aortic aneurysm. Lancet 2005 (365):1577- 1589
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Question 5 of 147
Which of the following statements in relation to the p53 tumour suppressor protein is false?
It may induce necrosis of cells with non repairable DNA damage
It is affected in Li Fraumeni syndrome
It can induce DNA repair
It can halt the cell cycle
It may inhibit angiogenesis
When DNA cannot be repaired it will induce cellular apoptosis (not necrosis) Please rate this question:
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Genetics and surgical disease
Some of the more commonly occurring genetic conditions occurring in surgical patients are presented here. Li-Fraumeni Syndrome
Autosomal dominant
Consists of germline mutations to p53 tumour suppressor gene High incidence of malignancies particularly sarcomas and leukaemias Diagnosed when:
*Individual develops sarcoma under 45 years *First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age BRCA 1 and 2
Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2) Linked to developing breast cancer (60%) risk. Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).
Lynch Syndrome
Autosomal dominant Develop colonic cancer and endometrial cancer at young age 80% of affected individuals will get colonic and/ or endometrial cancer
High risk individuals may be identified using the Amsterdam criteria
Amsterdam criteria
Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent, child, sibling) relative of the other two. Two successive affected generations. One or more colon cancers diagnosed under age 50 years. Familial adenomatous polyposis (FAP) has been excluded. Gardners syndrome
Autosomal dominant familial colorectal polyposis
Multiple colonic polyps Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts Desmoid tumours are seen in 15% Mutation of APC gene located on chromosome 5 Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal
cancer
Now considered a variant of familial adenomatous polyposis coli
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Question 6 of 147
Which of the following cell types is most likely to be identified in the wall of a fistula in ano?
Squamous cells
Goblet cells
Columnar cells
Ciliated columnar cells
None of the above
A fistula is an abnormal connection between two epithelial lined surfaces, in the case of a fistula in ano it will be lined by squamous cells. Please rate this question:
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Fistulas
A fistula is defined as an abnormal connection between two epithelial surfaces. There are many types ranging from Branchial fistulae in the neck to entero-cutaneous
fistulae abdominally.
In general surgical practice the abdominal cavity generates the majority and most of these arise from diverticular disease and Crohn's.
As a general rule all fistulae will resolve spontaneously as long as there is no distal obstruction. This is particularly true of intestinal fistulae.
The four types of fistulae are: Enterocutaneous These link the intestine to the skin. They may be high (>500ml) or low output (<250ml) depending upon source. Duodenal /jejunal fistulae will tend to produce high volume, electrolyte rich secretions which can lead to severe excoriation of the skin. Colo-cutaneous fistulae will tend to leak faeculent material. Both fistulae may result from the spontaneous rupture of an abscess cavity onto the skin (such as following perianal abscess drainage) or may occur as a result of iatrogenic input. In some
cases it may even be surgically desirable e.g. mucous fistula following sub total colectomy for colitis. Suspect if there is excess fluid in the drain. Enteroenteric or Enterocolic
This is a fistula that involves the large or small intestine. They may originate in a similar manner to enterocutaneous fistulae. A particular problem with this fistula type is that bacterial overgrowth may precipitate malabsorption syndromes. This may be particularly serious in inflammatory bowel disease. Enterovaginal Aetiology as above. Enterovesicular This type of fistula goes to the bladder. These fistulas may result in frequent urinary tract infections, or the passage of gas from the urethra during urination. Management
Some rules relating to fistula management:
They will heal provided there is no underlying inflammatory bowel disease and no distal obstruction, so conservative measures may be the best option
Where there is skin involvement, protect the overlying skin, often using a well fitted stoma bag- skin damage is difficult to treat
A high output fistula may be rendered more easily managed by the use of octreotide, this will tend to reduce the volume of pancreatic secretions.
Nutritional complications are common especially with high fistula (e.g. high jejunal or duodenal) these may necessitate the use of TPN to provide nutritional support together with the concomitant use of octreotide to reduce volume and protect skin.
When managing perianal fistulae surgeons should avoid probing the fistula where acute inflammation is present, this almost always worsens outcomes.
When perianal fistulae occur secondary to Crohn's disease the best management option is often to drain acute sepsis and maintain that drainage through the judicious use of setons whilst medical management is implemented.
Always attempt to delineate the fistula anatomy, for abscesses and fistulae that have an intra abdominal source the use of barium and CT studies should show a track. For perianal fistulae surgeons should recall Goodsall's rule in relation to internal and external openings.
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Question 7 of 147
A 22 year old man is referred to the surgical clinic. He has been complaining of varicose veins for many years. On examination he has extensive varicosities of the right leg, there are areas of marked port wine staining. The saphenofemoral junction is competent on doppler assessment. The most likely underlying diagnosis is:
Deep vein thrombosis
Klippel-Trenaunay syndrome
Varicose veins due to sapheno-popliteal junction incompetence
Sturge - Weber syndrome
Angiosarcoma
Sturge - Weber syndrome is a an arteriovenous malformation affecting the face and CNS, the peripheral vessels are not affected. Simple varicose veins should not typically be associated with port wine staining, nor should a DVT or angiosarcoma. Please rate this question:
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Klippel-Trenaunay syndrome
Klippel-Trenaunay-Weber syndrome generally affects a single extremity, although cases of multiple affected limbs have been reported. The leg is the most common site followed by the arms, the trunk, and rarely the head and the neck Signs and symptoms The birth defect is diagnosed by the presence of a combination of these symptoms:
One or more distinctive port-wine stains with sharp borders
Varicose veins Hypertrophy of bony and soft tissues, that may lead to local gigantism or shrinking. An improperly developed lymphatic system
In some cases, port-wine stains (capillary port wine type) may be absent. Such cases are very rare and may be classified as "atypical Klippel-Trenaunay syndrome". KTS can either affect blood vessels, lymph vessels, or both. The condition most commonly presents with a mixture of the two. Those with venous involvement experience increased pain and complications.
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Question 8 of 147
A 68 year old man presents with an ulcerated lesion on his right cheek. It is excised and on histological assessment a squamous cell carcinoma is diagnosed. It measures 25mm in diameter and is 4mm deep. Which of the following statements relating to this condition is false?
In this particular case margins of at least 6mm are required
Use of cryosurgery to treat this patients lesion would have been unsafe
Use of radiotherapy to treat this lesion would have been unsafe
This patients local recurrence rate may approach 15%
The disease usually spreads via lymphatics
Poor prognostic factors in SCC:
Size >20mm (local recurrence rate of up to 15%) Depth greater than 4mm (risk of metastasis up to 30%)
This man has an SCC with significant risk of metastasis. Although cryotherapy may be used to treat SCC it would be most unsafe in this setting as the lesion extends deeply. However, radiotherapy is a safe treatment modality for SCC and may be used in selected cases. It is unwise to use radiotherapy in areas prone to radionecrosis e.g. the nose. Please rate this question:
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Squamous cell carcinoma of the skin
Second most common skin malignancy Derived from epidermal keratinocytes Commonest in fair skinned individuals in sun exposed sites May occur in perianal and genital skin especially in association with Human Papilloma Virus
16 and 18 infections.
Groups at high risk
Renal transplant and on immunosuppression
Individuals with HIV
Those who have received psoralen UVA therapy
Chronic wounds (Marjolins ulcer)
Xeroderma pigmentosum
Oculocutaneous albinism
Prognosis
Good Prognosis Poor prognosis
Well differentiated tumours Poorly differentiated tumours
<20mm diameter >20mm in diameter
<2mm deep >4mm deep
No associated diseases Immunosupression for whatever reason
Treatment Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins should be 6mm. Squamous cell carcinomas of the skin typically arise in areas of sun exposure as shown here
Image sourced from Wikipedia
References The British Association of Dermatology provides guidelines for the diagnosis and treatment of SCC. http://www. bad.org.uk
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Question 9 of 147
A 23 year old man presents with weight loss fatigue and lymphadenopathy. He is diagnosed with
tuberculosis. Which of the following processes most closely matches the underlying pathological
process?
Type 1 hypersensitivity reaction
Type 2 hypersensitivity reaction
Type 3 hypersensitivity reaction
Type 4 hypersensitivity reaction
None of the above
Granulomas (which occur in tuberculosis) are a feature of Type 4 hypersensitivity reactions.
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Hypersensitivity reactions
The Gell and Coombs classification divides hypersensitivity reactions into 4 types
Type I Type II Type III Type IV
Type I Type II Type III Type IV
Description Anaphylactic Cytotoxic Immune
complex
Delayed type
Mediator IgE IgG, IgM IgG, Ig A, IgM T-cells
Antigen Exogenous Cell surface Soluble Tissues
Response
time
Minutes Hours Hours 2-3 days
Examples Asthma
Hay fever
Autoimmune haemolytic
anaemia
Pemphigus
Goodpasture's
Serum sickness
SLE
Aspergillosis
Graft versus host
disease
Contact dermatitis
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Question 10 of 147
A 73 year old man undergoes an emergency amputation for severe lower limb sepsis and gangrene. Post operatively he develops disseminated intravascular coagulation. Which of the following clotting factors will be most rapidly consumed in this process?
Factor V and VIII
Factor I
Factor I and III
Factor III and VII
Factor VI and VIII
D-I-S-S-E-M-I-N-A-T-E-D D-Dx: D dimer I-Immune complexes S-Snakebite, shock, heatstroke S-SLE E-Eclampsia, HELLP syndrome M-Massive tissue damage I-Infections: viral and bacterial N-Neoplasms A-Acute promyelocytic leukemia T-Tumor products: Tissue Factor (TF) and TF-like factors released by carcinomas of pancreas, prostate, lung, colon, stomach E-Endotoxins (bacterial) D-Dead fetus (retained)
DIC Will tend to consume factors five and eight intially (and platelets). Please rate this question:
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Disseminated intravascular coagulation
Simultaneous coagulation and haemorrhage caused by initially formation of thrombi which consume clotting factors (factors 5,8) and platelets, ultimately leading to bleeding Causes include:
Infection Malignancy Trauma e.g. major surgery, burns, shock, dissecting aortic aneurysm Liver disease
Obstetric complications
Key points
Clinically bleeding is usually a dominant feature, bruising, ischaemia and organ failure Blood tests: prolonged clotting times, thrombocytopenia, decreased fibrinogen, increased
fibrinogen degradation products Treat the underlying cause and supportive management
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Question 11 of 147
A pregnant women suddenly develops bilateral leg swelling. Her mother and aunt were troubled by the same problem. What is the most likely underlying abnormality?
Anti endomysial antibodies
Anti nuclear antibodies
Anti cardiolipin antibodies
Anti thyroid antibodies
Anti mitochondrial antibodies
Anti phospholipid syndrome= following antibodies
Lupus anticoagulant
Anti-cardiolipin Anti-β2-glycoprotein
Theme from September 2014 Exam Antiphospholipid syndrome, is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS provokes blood clots (thrombosis) in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, or severe preeclampsia. The diagnostic criteria requires one clinical event, i.e. thrombosis or pregnancy complication, and two positive blood tests spaced at least 3 months apart. These antibodies are: lupus anticoagulant, anti-cardiolipin and anti-β2-glycoprotein. Antiphospholipid syndrome can be primary or secondary. Primary antiphospholipid syndrome occurs in the absence of any other related disease. Secondary antiphospholipid syndrome occurs with other autoimmune diseases, such as systemic lupus erythematosus (SLE). In rare cases, APS leads to rapid organ failure due to generalised thrombosis; this is termed "catastrophic antiphospholipid syndrome" (CAPS) and is associated with a high risk of death. Antiphospholipid syndrome often requires treatment with anticoagulant medication such as heparin to reduce the risk of further episodes of thrombosis and improve the prognosis of pregnancy. Warfarin is not used during pregnancy because it can cross the placenta, unlike heparin, and is teratogenic. Please rate this question:
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Hypercoagulability
Type of thrombophilia Features
Antithrombin deficiency Antithrombin inactivates thrombin and factor XII a, XIa, IXa and Xa
Rare defect, inherited in autosomal dominant fashion
10x increase in risk of thrombotic events Heparin may be ineffective because it works via antithrombin
Protein C and S
deficiency
These are natural anticoagulants (vitamin K dependent synthesis)
Protein C produced by liver
Protein S produced by liver, megakaryocytes, Leydig cells and
endothelial cells
Protein C and S bind to form activated complex which binds to factor
V Deficiency accounts for up to 5% of thrombotic episodes
Factor V Leiden Resistance to anticoagulant effect of activated protein C
May account for up to 20% or more of thrombotic episodes
Prevalence of 7% in Europe
Most common genetic defect accounting for DVT
Antiphospholipid syndrome
Multi organ disease
Pregnancy involvement common
Arterial and venous thromboses
Either Lupus anticoagulant or Anti cardiolipin antibodies
APTT usually prolonged
Antibodies may be elevated following surgery, drugs or malignancy
Need anticoagulation with INR between 3 and 4
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Question 12 of 147
A 63 year old Japanese man presents with epigastric discomfort and iron deficiency anaemia. He undergoes an upper GI endoscopy, where the following appearances are found:
Image sourced from Wikipedia
The most likely diagnosis is:
Squamous cell carcinoma
Linitis plastica
Leiomyosarcoma
Gastric varices
None of the above
During upper GI endoscopy, a linitis plastica lesion may prevent gastric distension.
Linitis plastica produces a diffuse infiltrating lesion, the stomach is fibrotic and rigid and will not typically distend. This may be described as a 'leather bottle stomach'. Diagnosis is made with a combination of pathology examination with endoscopy, radiological or surgical assessment. Pathologically signet-ring cell proliferation occurs. Please rate this question:
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Gastric cancer
Overview
There are 700,000 new cases of gastric cancer worldwide each year. It is most common in Japan and less common in western countries. It is more common in men and incidence rises with increasing age. The exact cause of many sporadic cancer is not known, however, familial cases do occur in HNPCC families. In addition, smoking and smoked or preserved foods increase the risk. Japanese migrants retain their increased risk (decreased in subsequent generations). The distribution of the disease in western countries is changing towards a more proximal location (perhaps due to rising obesity). Pathology There is some evidence of support a stepwise progression of the disease through intestinal metaplasia progressing to atrophic gastritis and subsequent dysplasia, through to cancer. The favoured staging system is TNM. The risk of lymph node involvement is related to size and depth of invasion; early cancers confined to submucosa have a 20% incidence of lymph node metastasis. Tumours of the gastro-oesophageal junction are classified as below:
Type
1
True oesophageal cancers and may be associated with Barrett's oesophagus.
Type
2
Carcinoma of the cardia, arising from cardiac type epithelium or short segments with intestinal metaplasia at the oesophagogastric junction.
Type
3
Sub cardial cancers that spread across the junction. Involve similar nodal stations to gastric cancer.
Groups for close endoscopic monitoring
Intestinal metaplasia of columnar type
Atrophic gastritis Low to medium grade dysplasia Patients who have previously undergone resections for benign peptic ulcer disease (except
highly selective vagotomy).
Referral to endoscopy
Patients of any age with
dyspepsia and any of the
following
Patients without
dyspepsia
Worsening dyspepsia
Chronic gastrointestinal bleeding Dysphagia Barretts oesophagus
Dysphagia Unexplained abdominal
pain or weight loss
Intestinal metaplasia
Weight loss Vomiting Dysplasia
Iron deficiency anaemia Upper abdominal mass Atrophic gastritis
Upper abdominal mass Jaundice Patient aged over 55 years with
unexplained or persistent dyspepsia
Upper GI endoscopy performed for dyspepsia. The addition of dye spraying (as shown in the bottom
right) may facilitate identification of smaller tumours
Image sourced from Wikipedia
Staging
CT scanning of the chest abdomen and pelvis is the routine first line staging investigation in most centres.
Laparoscopy to identify occult peritoneal disease PET CT (particularly for junctional tumours)
Treatment
Proximally sited disease greater than 5-10cm from the OG junction may be treated by sub total gastrectomy
Total gastrectomy if tumour is <5cm from OG junction For type 2 junctional tumours (extending into oesophagus) oesophagogastrectomy is usual Endoscopic sub mucosal resection may play a role in early gastric cancer confined to the
mucosa and perhaps the sub mucosa (this is debated) Lymphadenectomy should be performed. A D2 lymphadenectomy is widely advocated by the
Japanese, the survival advantages of extended lymphadenectomy have been debated. However, the overall recommendation is that a D2 nodal dissection be undertaken.
Most patients will receive chemotherapy either pre or post operatively.
Prognosis
UK Data
Disease extent Percentage 5 year survival
All RO resections 54%
Early gastric cancer 91%
Stage 1 87%
Stage 2 65%
Stage 3 18%
Operative procedure Total Gastrectomy , lymphadenectomy and Roux en Y anastomosis General anaesthesia Prophylactic intravenous antibiotics Incision: Rooftop. Perform a thorough laparotomy to identify any occult disease. Mobilise the left lobe of the liver off the diaphragm and place a large pack over it. Insert a large self retaining retractor e.g. omnitract or Balfour (take time with this, the set up should be perfect). Pack the small bowel away. Begin by mobilising the omentum off the transverse colon. Proceed to detach the short gastric vessels. Mobilise the pylorus and divide it at least 2cm distally using a linear cutter stapling device. Continue the dissection into the lesser sac taking the lesser omentum and left gastric artery flush at its origin. The lymph nodes should be removed en bloc with the specimen where possible. Place 2 stay sutures either side of the distal oesophagus. Ask the anaesthetist to pull back on the nasogastric tube. Divide the distal oesophagus and remove the stomach. The oesphago jejunal anastomosis should be constructed. Identify the DJ flexure and bring a loop of jejunum up to the oesophagus (to check it will reach). Divide the jejunum at this point. Bring the divided jejunum either retrocolic or antecolic to the oesophagus. Anastamose the oesophagus to the jejunum, using either interrupted 3/0 vicryl or a stapling device. Then create the remainder of the Roux en Y reconstruction distally. Place a jejunostomy feeding tube. Wash out the abdomen and insert drains (usually the anastomosis and duodenal stump). Help the anaesthetist insert the nasogastric tube (carefully!) Close the abdomen and skin.
Enteral feeding may commence on the first post-operative day. However, most surgeons will leave patients on free NG drainage for several days and keep them nil by mouth.
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0 / 3 Question 13-15 of 147
Theme: Genetics and cancer
A. Multiple endocrine neoplasia type I
B. Multiple endocrine neoplasia type II
C. Gardner's syndrome
D. Lynch Syndrome
E. Kartagener's syndrome
F. Neurofibromatosis Type I
G. Neurofibromatosis Type II Please select the most likely condition for the disease process described. Each option may be used once, more than once or not at all.
13. A 40 year old male is found to have multiple colonic polyps during a colonoscopy. He
mentions that he has extra teeth.
You answered Multiple endocrine neoplasia type I
The correct answer is Gardner's syndrome
Gardner's syndrome is an AD disorder, characterised by: Colonic polyps, supernumerary
teeth, jaw osteomas, congenital hypertrophy of retinal pigment. osteomas of the skull,
thyroid cancer, epidermoid cysts, fibromas and sebaceous cysts.
14. A 10 year old boy who has learning difficulties, reports a difference in size between his
two legs.
You answered Multiple endocrine neoplasia type I
The correct answer is Neurofibromatosis Type I
Neurofibromatosis type I. A hallmark finding is a plexiform neurofibroma, which is a
sheet of neurofibromatosis tissue which encases major nerves. In children this attracts
extra blood circulation, which can accelerate growth of the affected limb.
Other features include:
Schwannoma, > 6
Cafe au lait spots, axillary freckling, Lisch nodules, Optic glioma. Meningiomas, Glioma,
or Schwannoma.
15. A 22 year old is found to have bilateral acoustic neuromas.
You answered Multiple endocrine neoplasia type I
The correct answer is Neurofibromatosis Type II
In NF2 bilateral acoustic neuromas are characteristic with a family history of
Neurofibroma,
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Genetics and surgical disease
Some of the more commonly occurring genetic conditions occurring in surgical patients are presented here. Li-Fraumeni Syndrome
Autosomal dominant Consists of germline mutations to p53 tumour suppressor gene High incidence of malignancies particularly sarcomas and leukaemias Diagnosed when:
*Individual develops sarcoma under 45 years *First degree relative diagnosed with any cancer below age 45 years and another family member develops malignancy under 45 years or sarcoma at any age BRCA 1 and 2
Carried on chromosome 17 (BRCA 1) and Chromosome 13 (BRCA 2)
Linked to developing breast cancer (60%) risk. Associated risk of developing ovarian cancer (55% with BRCA 1 and 25% with BRCA 2).
Lynch Syndrome
Autosomal dominant
Develop colonic cancer and endometrial cancer at young age 80% of affected individuals will get colonic and/ or endometrial cancer High risk individuals may be identified using the Amsterdam criteria
Amsterdam criteria
Three or more family members with a confirmed diagnosis of colorectal cancer, one of whom is a first degree (parent, child, sibling) relative of the other two. Two successive affected generations. One or more colon cancers diagnosed under age 50 years. Familial adenomatous polyposis (FAP) has been excluded. Gardners syndrome
Autosomal dominant familial colorectal polyposis
Multiple colonic polyps Extra colonic diseases include: skull osteoma, thyroid cancer and epidermoid cysts Desmoid tumours are seen in 15% Mutation of APC gene located on chromosome 5 Due to colonic polyps most patients will undergo colectomy to reduce risk of colorectal
cancer
Now considered a variant of familial adenomatous polyposis coli
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Question 16 of 147
A 52 year old lady is referred to the breast clinic with symptoms of nipple discharge. The discharge is usually thick and green. Which of the following statements relating to the most likely underlying diagnosis is untrue?
The majority of patients will be smokers
Typically produces blood stained nipple discharge
It is not associated with increased risk of breast cancer
May result in development of mammary duct fistula
May require total duct excision (Hadfields operation) if it fails to resolve
Blood stained nipple discharge should always be investigated. Nipple fluid cytology is generally unhelpful.
Discharge of this type of material is most likely to be due to duct ectasia. Green or brown discharge is most common. Blood stained discharge should raise concern of intraductal papilloma or cancer. Please rate this question:
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Nipple discharge
Causes of nipple discharge
Physiological During breast feeding
Galactorrhoea Commonest cause may be response to emotional events, drugs such as histamine receptor antagonists are also implicated
Hyperprolactinaemia Commonest type of pituitary tumour
Microadenomas <1cm in diameter
Macroadenomas >1cm in diameter
Pressure on optic chiasm may cause bitemporal hemianopia
Mammary duct
ectasia
Dilatation breast ducts.
Most common in menopausal women
Discharge typically thick and green in colour
Most common in smokers
Carcinoma Often blood stained
May be underlying mass or axillary lymphadenopathy
Intraductal papilloma Commoner in younger patients
May cause blood stained discharge
There is usually no palpable lump
Assessment of patients
Examine breast and determine whether there is mass lesion present
All mass lesions should undergo Triple assessment.
Reporting of investigations Where a mass lesion is suspected or investigations are requested these are prefixed using a system that denotes the investigation type e.g. M for mammography, followed by a numerical code as shown below:
1 No abnormality
2 Abnormality with benign features
3 Indeterminate probably benign
4 Indeterminate probably malignant
5 Malignant
Management of non malignant nipple discharge
Exclude endocrine disease Nipple cytology unhelpful
Smoking cessation advice for duct ectasia For duct ectasia with severe symptoms, total duct excision may be warranted.
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Question 17 of 147
Which of the following statements relating to gas gangrene is untrue?
There is necrosis with putrefaction
The causative pathogens may be detected on normal perineal skin
Treatment with low dose penicillin is indicated
Hyperbaric oxygen may be beneficial
Clostridium perfringens is a recognised cause
Rapid surgery and high dose antibiotics are indicated in the treatment of gas gangrene. Please rate this question:
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Meleney's Gangrene and Necrotising Fasciitis
Necrotising fasciitis
Advancing soft tissue infection associated with fascial necrosis
Uncommon, but can be fatal In many cases there is underlying background immunosuppression e.g. Diabetes Caused by polymicrobial flora (aerobic and anaerobic) and MRSA is seen increasingly in
cases of necrotising fasciitis
Streptococcus is the commonest organism in isolated pathogen infection (15%)
Meleneys gangrene
Meleneys is a similar principle but the infection is more superficially sited than necrotising fasciitis and often confined to the trunk
Fournier gangrene
Necrotising fasciitis affecting the perineum Polymicrobial with E-coli and Bacteroides acting in synergy
Clinical features
Fever Pain Cellulitis Oedema Induration Numbness Late findings Purple/black skin discolouration Blistering Haemorrhagic bullae Crepitus Dirty Dishwater fluid discharge Septic shock A typical case of gas gangrene presenting late demonstrating some of the features described above
Image sourced from Wikipedia
Diagnosis is mainly clinical Management
Radical surgical debridement forms the cornerstone of management Sterile dressing is used to dress the wound Reconstructive surgery is considered once the infection is completely treated
Reference Hasham S, Matteucci P, Stanley PR, Hart NB. Necrotising fasciitis. BMJ 2005;330:830-833.
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Question 18 of 147
A 30 year old man presents with abdominal distension, a laparotomy is performed, at operation the abdomen is filled with a large amount of gelatinous fluid. What is the most likely underlying diagnosis?
Infection with entamoeba histolytica
Pseudomxyoma peritonei
Metastatic colonic cancer
Chylous ascites
None of the above
Pseudomyxoma is associated with the deposition of large amounts of gelatinous material. The appendix is the commonest organ or origin. Please rate this question:
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Pseudomyxoma Peritonei
Rare mucinous tumour Most commonly arising from the appendix (other abdominal viscera are also recognised as
primary sites) Incidence of 1-2/1,000,000 per year The disease is characterised by the accumulation of large amounts of mucinous material in
the abdominal cavity
Treatment Is usually surgical and consists of cytoreductive surgery (and often peritonectomy c.f Sugarbaker procedure) combined with intra peritoneal chemotherapy with mitomycin C. Survival is related to the quality of primary treatment and in Sugarbakers own centre 5 year survival rates of 75% have been quoted. Patients with disseminated intraperitoneal malignancy from another
source fare far worse. In selected patients a second look laparotomy is advocated and some practice this routinely.
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Question 19 of 147
A 30 year old man is suspected of having appendicitis. At operation an inflamed Meckels diverticulum is found. Which of the following vessels is responsible for the blood supply to a Meckels diverticulum?
Right colic artery
Vitelline artery
Appendicular artery
Internal iliac artery
External iliac artery
The vitelline arteries supply a Meckels these are usually derived from the ileal arcades. Please rate this question:
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Meckel's diverticulum
Congenital abnormality resulting in incomplete obliteration of the vitello-intestinal duct
Normally, in the foetus, there is an attachment between the vitello-intestinal duct and the yolk sac.This disappears at 6 weeks gestation.
The tip is free in majority of cases. Associated with enterocystomas, umbilical sinuses, and omphaloileal fistulas. Arterial supply: omphalomesenteric artery. 2% of population, 2 inches long, 2 feet from the ileocaecal valve.
Typically lined by ileal mucosa but ectopic gastric mucosa can occur, with the risk of peptic ulceration. Pancreatic and jejunal mucosa can also occur.
Clinical
Normally asymptomatic and an incidental finding.
Complications are the result of obstruction, ectopic tissue, or inflammation.
Removal if narrow neck or symptomatic. Options are between wedge excision or formal small bowel resection and anastomosis.
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Question 20 of 147
Which of the following associations are incorrect?
Afro-Caribbean skin and keloid scarring
Extensive third degree burns and wound contraction
Chemotherapy and dehisence of healed wounds
Poor healing at the site of previous radiotherapy
Zinc deficiency and delayed healing
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Wound healing
Surgical wounds are either incisional or excisional and either clean, clean contaminated or dirty. Although the stages of wound healing are broadly similar their contributions will vary according to the wound type. The main stages of wound healing include: Haemostasis
Minutes to hours following injury Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.
Inflammation
Typically days 1-5 Neutrophils migrate into wound (function impaired in diabetes).
Growth factors released, including basic fibroblast growth factor and vascular endothelial growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound.
Macrophages and fibroblasts couple matrix regeneration and clot substitution.
Regeneration
Typically days 7 to 56
Platelet derived growth factor and transformation growth factors stimulate fibroblasts and epithelial cells.
Fibroblasts produce a collagen network. Angiogenesis occurs and wound resembles granulation tissue.
Remodeling
From 6 weeks to 1 year Longest phase of the healing process and may last up to one year (or longer). During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate
wound contraction.
Collagen fibres are remodeled. Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may distort this process. Neovascularisation is an important early process. Endothelial cells may proliferate in the wound bed and recanalise to form a vessel. Vascular disease, shock and sepsis can all compromise microvascular flow and impair healing. Conditions such as jaundice will impair fibroblast synthetic function and immunity with a detrimental effect in most parts of the healing process. Problems with scars: Hypertrophic scars Excessive amounts of collagen within a scar. Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on to develop contractures. Image of hypertrophic scarring. Note that it remains confined to the boundaries of the original wound:
Image sourced from Wikipedia
Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries of the original injury. They do not contain nodules and may occur following even trivial injury. They do not regress over time and may recur following removal. Image of a keloid scar. Note the extension beyond the boundaries of the original incision:
Image sourced from Wikipedia
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs Steroids Immunosupressive agents Anti neoplastic drugs
Closure
Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue becomes macroscopically evident. Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.
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Question 21 of 147
A 45 year old women is identified as having a gastric gastro-intestinal stromal tumour. What is the
usual cell of origin of these lesions?
Brunners glands
Interstitial cells of Cajal
Primitive stem cells of the gut wall
Fundic glands
Antral goblet cells
GIST's are derived from the interstitial pacemaker cells of Cajal. This means that they are often
located extramucosally and macroscopically, demonstrate little mucosal disruption.
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Gastrointestinal stromal tumour
GIST's are not common tumours (10 per million) and originate primarily from the interstitial
pacemaker cells (of Cajal). Up to 70% occur in the stomach, the remainder occurring in the small
intestine (20%) and the colon and rectum (5%). Up to 95% are solitary lesions and most are
sporadic. The vast majority express CD117 which is a transmembrane tyrosine kinase receptor and
in these there is a mutation of the c-KIT gene.
The goal of surgery is resection of the tumour with a 1-2cm margin of normal tissue. As a result
extensive resections are not required. Unfortunately there is a high local recurrence rate, the risk of
which is related to site, incomplete resections and high mitotic count. Salvage surgery for recurrent
disease is associated with a median survival of 15 months.
The prognosis in high risk patients is greatly improved through the use of imatinib, which in the
ACOSOG trial (imatinib vs placebo) improved relapse rates from 17% to 2%.
In the UK it is advocated by NICE for use in patients with metastatic disease or locally unresectable
disease.
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Question 22 of 147
A 23 year old man fractures his right tibia in a sporting accident. At which point in the healing process is fracture callus most likely to be visible radiologically?
1 day
7 days
8 weeks
6 weeks
3 weeks
Fracture callus is composed of fibroblasts and chondroblasts and the synthesis of fibrocartilage. It is typically visible on radiographs approximately 3 weeks following injury. If delayed then there may be risk of non union. Please rate this question:
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Fracture healing
Bone fracture - Bleeding vessels in the bone and periosteum - Clot and haematoma formation - The clot organises over a week (improved structure and collagen) - The periosteum contains osteoblasts which produce new bone - Mesenchymal cells produce cartilage (fibrocartilage and hyaline cartilage) in the soft tissue around the fracture - Connective tissue + hyaline cartilage = callus - As the new bone approaches the new cartilage, endochondral ossification occurs to bridge the gap - Trabecular bone forms - Trabecular bone is resorbed by osteoclasts and replaced with compact bone Factors affecting fracture healing
Age Malnutrition Bone disorders: osteoporosis Systemic disorders: diabetes, Marfan's syndrome and Ehlers-Danlos syndrome cause
abnormal musculoskeletal healing. Drugs: steroids, non steroidal anti inflammatory agents. Type of bone: Cancellous (spongy) bone fractures are usually more stable, involve greater
surface areas, and have a better blood supply than cortical (compact) bone fractures.
Degree of Trauma: The more extensive the injury to bone and surrounding soft tissue, the poorer the outcome.
Vascular Injury: Especially the femoral head, talus, and scaphoid bones. Degree of Immobilization Intra-articular Fractures: These fractures communicate with synovial fluid, which contains
collagenases that retard bone healing. Separation of Bone Ends: Normal apposition of fracture fragments is needed for union to
occur. Inadequate reduction, excessive traction, or interposition of soft tissue will prevent healing.
Infection
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Question 23 of 147
Of the options below, which does not cause lymphadenopathy?
Kawasaki disease
Systemic Lupus Erthematosus
Phenytoin
Hydrallazine
Amiodarone
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Lymphadenopathy
Lymphadenopathy in the neck, axillae, groins and abdomen
Need to note: solitary/multiple, defined/indistinct, hard/rubbery/soft, tender/painless
Causes of lymphadenopathy
Mnemonic: Hodgkins disease H aematological: Hodgkins lymphoma, NHL, Leukaemia O ncological: metastases D ermatopathic lympadenitis G aucher's disease K awasaki disease I nfections: TB, glandular fever, Syphilis N iemann Pick disease S erum sickness D rug reaction (phenytoin) I mmunological (SLE) S arcoidosis
E ndocrinological (Hyperthyroidism) A ngioimmunoplastic lymphadenopathy S LE E osinophilic granulomatosis
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Question 24 of 147
A 23 year old man is reviewed on the ward 10 days following a laparotomy. The wound is inspected and is healing well. Which of the following processes is least likely to be occurring in the wound at this stage?
Angiogenesis
Synthesis of collagen
Necrosis of fibroblasts
Secretion of matrix metalloproteinases by fibroblasts
Proliferation of fibroblasts
Vasculogenesis vs Angiogenesis Vascu is new. Angi is pre Vasculogenesis is new vessels developing in situ from existing mesenchyme. Angiogenesis is vessels develop from sprouting off pre-existing arteries.
Fibroblasts are an important cell type in healing wounds. They typically proliferate in the early phases of wound healing. They release matrix metalloproteinases and these facilitate in the remodelling of the matrix within the healing wound. Necrosis in a healing wound would be unusual as wounds will tend to show clinical evidence of angiognesis by this time. Please rate this question:
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Wound healing
Surgical wounds are either incisional or excisional and either clean, clean contaminated or dirty. Although the stages of wound healing are broadly similar their contributions will vary according to the wound type. The main stages of wound healing include:
Haemostasis
Minutes to hours following injury Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.
Inflammation
Typically days 1-5 Neutrophils migrate into wound (function impaired in diabetes). Growth factors released, including basic fibroblast growth factor and vascular endothelial
growth factor.
Fibroblasts replicate within the adjacent matrix and migrate into wound. Macrophages and fibroblasts couple matrix regeneration and clot substitution.
Regeneration
Typically days 7 to 56
Platelet derived growth factor and transformation growth factors stimulate fibroblasts and epithelial cells.
Fibroblasts produce a collagen network. Angiogenesis occurs and wound resembles granulation tissue.
Remodeling
From 6 weeks to 1 year Longest phase of the healing process and may last up to one year (or longer). During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate
wound contraction. Collagen fibres are remodeled. Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may distort this process. Neovascularisation is an important early process. Endothelial cells may proliferate in the wound bed and recanalise to form a vessel. Vascular disease, shock and sepsis can all compromise microvascular flow and impair healing. Conditions such as jaundice will impair fibroblast synthetic function and immunity with a detrimental effect in most parts of the healing process. Problems with scars:
Hypertrophic scars Excessive amounts of collagen within a scar. Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the
extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on to develop contractures. Image of hypertrophic scarring. Note that it remains confined to the boundaries of the original wound:
Image sourced from Wikipedia
Keloid scars
Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries of the original injury. They do not contain nodules and may occur following even trivial injury. They do not regress over time and may recur following removal. Image of a keloid scar. Note the extension beyond the boundaries of the original incision:
Image sourced from Wikipedia
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids Immunosupressive agents Anti neoplastic drugs
Closure Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue becomes macroscopically evident. Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.
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Question 25 of 147
A 25 year old women presents with a slowly enlarging mass on the side of the face. Clinical examination demonstrates that the mass is located in the tail of the parotid gland. There is no evidence of facial nerve involvement. What is the most likely cause?
Sialolithiasis
Adenocarcinoma
Warthins tumour
Oncocytoma
Pleomorphic adenoma
Pleomorphic adenomas are the commonest tumours of the parotid gland and are often slow growing, smooth and mobile. Warthins tumours are typically found in elderly males and are composed of multiple cysts and solid components consisting of lymphoid tissue. Warthins tumours are most often found in the tail of the parotid gland, but not in 25 year old females, where a pleomorphic adenoma remains the most likely lesion. Please rate this question:
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Parotid gland clinical
Benign neoplasms Up to 80% of all salivary gland tumours occur in the parotid gland and up to 80% of these are benign. There is no consistent correlation between the rate of growth and the malignant potential of the lesion. However, benign tumours should not invade structures such as the facial nerve. With the exception of Warthins tumours, they are commoner in women than men. The median age of developing a lesion is in the 5th decade of life. Benign tumour types
Tumour type Features
Tumour type Features
Benign pleomorphic adenoma or
benign mixed tumor
Most common parotid neoplasm (80%)
Proliferation of epithelial and myoepithelial cells of the ducts
and an increase in stromal components
Slow growing, lobular, and not well encapsulated
Recurrence rate of 1-5% with appropriate excision
(parotidectomy)
Recurrence possibly secondary to capsular disruption during
surgery
Malignant degeneration occurring in 2-10% of adenomas
observed for long periods, with carcinoma ex-pleomorphic adenoma occurring most frequently as adenocarcinoma
Warthin tumor (papillary
cystadenoma lymphoma or adenolymphoma)
Second most common benign parotid tumor (5%)
Most common bilateral benign neoplasm of the parotid
Marked male as compared to female predominance
Occurs later in life (sixth and seventh decades)
Presents as a lymphocytic infiltrate and cystic epithelial
proliferation
May represent heterotopic salivary gland epithelial tissue
trapped within intraparotid lymph nodes
Incidence of bilaterality and multicentricity of 10%
Malignant transformation rare (almost unheard of)
Monomorphic adenoma Account for less than 5% of tumours
Slow growing
Consist of only one morphological cell type (hence term
mono)
Include; basal cell adenoma, canalicular adenoma, oncocytoma, myoepitheliomas
Haemangioma Should be considered in the differential of a parotid mass in a
child
Accounts for 90% of parotid tumours in children less than 1
year of age
Hypervascular on imaging
Spontaneous regression may occur and malignant transformation is almost unheard of
Malignant salivary gland tumours
Types of malignancy
Mucoepidermoid
carcinoma
30% of all parotid malignancies
Usually low potential for local invasiveness and metastasis (depends
mainly on grade)
Adenoid cystic
carcinoma
Unpredictable growth pattern
Tendency for perineural spread
Nerve growth may display skip lesions resulting in incomplete excision
Distant metastasis more common (visceral rather than nodal spread)
5 year survival 35%
Mixed tumours Often a malignancy occurring in a previously benign parotid lesion
Acinic cell carcinoma Intermediate grade malignancy
May show perineural invasion
Low potential for distant metastasis
5 year survival 80%
Adenocarcinoma Develops from secretory portion of gland
Risk of regional nodal and distant metastasis
5 year survival depends upon stage at presentation, may be up to 75% with small lesions with no nodal involvement
Lymphoma Large rubbery lesion, may occur in association with Warthins tumours
Diagnosis should be based on regional nodal biopsy rather than parotid
resection
Treatment is with chemotherapy (and radiotherapy)
Diagnostic evaluation
Plain x-rays may be used to exclude calculi Sialography may be used to delineate ductal anatomy FNAC is used in most cases
Superficial parotidectomy may be either diagnostic of therapeutic depending upon the nature of the lesion
Where malignancy is suspected the primary approach should be definitive resection rather than excisional biopsy
CT/ MRI may be used in cases of malignancy for staging primary disease
Treatment
For nearly all lesions this consists of surgical resection, for benign disease this will usually consist of a superficial parotidectomy. For malignant disease a radical or extended radical parotidectomy is performed. The facial nerve is included in the resection if involved. The need for neck dissection is determined by the potential for nodal involvement. Other parotid disorders HIV infection
Lymphoepithelial cysts associated with HIV occur almost exclusively in the parotid
Typically presents as bilateral, multicystic, symmetrical swelling Risk of malignant transformation is low and management usually conservative
Sjogren syndrome
Autoimmune disorder characterised by parotid enlargement, xerostomia and keratoconjunctivitis sicca
90% of cases occur in females Second most common connective tissue disorder Bilateral, non tender enlargement of the gland is usual Histologically, the usual findings are of a lymphocytic infiltrate in acinar units and
epimyoepithelial islands surrounded by lymphoid stroma Treatment is supportive There is an increased risk of subsequent lymphoma
Sarcoid
Parotid involvement occurs in 6% of patients with sarcoid
Bilateral in most cases Gland is not tender Xerostomia may occur Management of isolated parotid disease is usually conservative
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Question 26 of 147
Beta-naphthalamine is associated with which of the following malignancies?
Lung cancer
Bowel cancer
Bladder cancer
Liver cancer
Renal cancer
Beta-naphthalamine is used in the rubber industry. The following factors are associated with the development of bladder cancer:
smoking occupational: aniline dyes used in printing and textile industry, rubber manufacture
schistosomiasis drugs: cyclophosphamide
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Occupational cancers
Occupational cancers accounted for 5.3% cancer deaths in 2005. In men the main cancers include:
Mesothelioma Bladder cancer
Non melanoma skin cancer Lung cancer
Sino nasal cancer
Occupations with high levels of occupational tumours include:
Construction industry
Working with coal tar and pitch Mining Metalworkers Working with asbestos (accounts for 98% of all mesotheliomas)
Working in rubber industry
Shift work has been linked to breast cancer in women (Health and safety executive report RR595). The latency between exposure and disease is typically 15 years for solid tumours and 20 for leukaemia. Many occupational cancers are otherwise rare. For example sino nasal cancer is an uncommon tumour, 50% will be SCC. They are linked to conditions such as wood dust exposure and unlike lung cancer is not strongly linked to cigarette smoking. Another typical occupational tumour is angiosarcoma of the liver which is linked to working with vinyl chloride. Again in the non occupational context this is an extremely rare sporadic tumour.
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Question 27 of 147
A 56 year old man with Wilsons disease presents with right upper quadrant discomfort. An ultrasound scan is performed and this demonstrates a mass lesion in the right lobe of the liver. What is the most appropriate method of establishing the underlying diagnosis?
PET CT scan
Ultrasound guided biopsy
Measurement of serum alpha feto protein
MRI scan of the liver
CT scan of the liver
High AFP + chronic liver inflammation = Hepatocellular carcinoma.
This is likely to be a hepatocellulcar carcinoma. Diagnosis is usually made by AFP measurement (with further imaging depending on the result). Biopsy should not be performed as it may seed the tumour. Chronic liver diseases such as Wilsons disease (Hepato-lenticular degeneration) increase the risk. Please rate this question:
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Liver tumours
Primary liver tumours
The most common primary tumours are cholangiocarcinoma and hepatocellular carcinoma. Overall metastatic disease accounts for 95% of all liver malignancies making the primary liver tumours comparatively rare. Primary liver tumours include:
Cholangiocarcinoma
Hepatocellular carcinoma Hepatoblastoma
Sarcomas (Rare) Lymphomas Carcinoids (most often secondary although primary may occur)
Hepatocellular carcinoma These account for the bulk of primary liver tumours (75% cases). Its worldwide incidence reflects its propensity to occur on a background of chronic inflammatory activity. Most cases arise in cirrhotic livers or those with chronic hepatitis B infection, especially where viral replication is actively occurring. In the UK it accounts for less than 5% of all cancers, although in parts of Asia its incidence is 100 per 100,000. The majority of patients (80%) present with existing liver cirrhosis, with a mass discovered on screening ultrasound. Diagnosis
CT/ MRI (usually both) are the imaging modalities of choice a-fetoprotein is elevated in almost all cases Biopsy should be avoided as it seeds tumours cells through a resection plane. In cases of diagnostic doubt serial CT and αFP measurements are the preferred strategy.
Treatment
Patients should be staged with liver MRI and chest, abdomen and pelvic CT scan. The testis should be examined in males (testicular tumours may cause raised AFP). PET CT
may be used to identify occult nodal disease.
Surgical resection is the mainstay of treatment in operable cases. In patients with a small primary tumour in a cirrhotic liver whose primary disease process is controlled, consideration may be given to primary whole liver resection and transplantation.
Liver resections are an option but since most cases occur in an already diseased liver the operative risks and post-operative hepatic dysfunction are far greater than is seen following metastectomy.
These tumours are not particularly chemo or radiosensitive however, both may be used in a palliative setting. Tumour ablation is a more popular strategy.
Survival
Poor, overall survival is 15% at 5 years. Cholangiocarcinoma
This is the second most common type of primary liver malignancy. As its name suggests these tumours arise in the bile ducts. Up to 80% of tumours arise in the extra hepatic biliary tree. Most patients present with jaundice and by this stage the majority will have disease that is not resectable. Primary sclerosing cholangitis is the main risk factor. In deprived countries typhoid and liver flukes are also major risk factors. Diagnosis
Patients will typically have an obstructive picture on liver function tests. CA 19-9, CEA and CA 125 are often elevated CT/ MRI and MRCP are the imaging methods of choice.
Treatment
Surgical resection offers the best chance of cure. Local invasion of peri hilar tumours is a particular problem and this coupled with lobar atrophy will often contra indicate surgical resection.
Palliation of jaundice is important, although metallic stents should be avoided in those considered for resection.
Survival Is poor, approximately 5-10% 5 year survival.
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Question 28 of 147
A 55 year old man has suffered from reflux oesophagitis for many years. During a recent endoscopy a biopsy is taken from the distal oesophagus. The histopathology report indicates that cells are identified with features of coarse chromatin and abnormal mitoses. The cells are confined to the superficial epithelial layer only. Which of the following accounts for this process?
Metaplasia
Apoptosis
Autoimmune oesophagitis
Dysplasia
Infection with Helicobacter pylori
Dysplasia = pre cancerous
Dysplasia tends to develop as a result of prolonged stimulation by precipitants. Removal of these precipitants may possibly reverse these changes. Replacement of differentiated cells with another cell type describes metaplasia rather than dysplasia. The absence of invasion distinguishes this from malignancy. Please rate this question:
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Dysplasia
Premalignant condition Disordered growth and differentiation of cells Alteration in size, shape, and organization of cells Features increased abnormal cell growth (increased number of mitoses/abnormal mitoses
and cellular differentiation)
Underlying connective tissue is not invaded Causes include smoking, Helicobacter pylori, Human papilloma virus Main differences to metaplasia is that dysplasia is considered to be part of carcinogenesis
(pre cancerous) and is associated with a delay in maturation of cells rather than differentiated cells replacing one another
The absence of invasion differentiates dysplasia from invasive malignancy Severe dysplasia with foci of invasion are well recognised
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Question 29 of 147
Which one of the following confers the least risk of developing osteoporosis?
Obesity
Long term unfractionated heparin therapy
Gastrectomy
Osteogenesis imperfecta
Diabetes
Low body weight is a risk factor for osteoporosis. Please rate this question:
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Osteoporosis
Risk factors
Family history
Female sex Increasing age Deficient diet Sedentary lifestyle
Smoking Premature menopause Low body weight Caucasians and Asians
Diseases which predispose
Endocrine: glucocorticoid excess (e.g. Cushing's, steroid therapy), hyperthyroidism, hypogonadism (e.g. Turner's, testosterone deficiency), growth hormone deficiency, hyperparathyroidism, diabetes mellitus
Multiple myeloma, lymphoma Gastrointestinal problems: inflammatory bowel disease, malabsorption (e.g. Coeliacs),
gastrectomy, liver disease Rheumatoid arthritis
Long term heparin therapy Chronic renal failure Osteogenesis imperfecta, homocystinuria
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Question 30 of 147
A 63 year old man has a history of claudication that has been present for many years. He is recently
evaluated in the clinic and a duplex scan shows that he has an 85% stenosis of the superficial
femoral artery. Two weeks later he presents with a 1 hour history of severe pain in his leg. On
examination he has absent pulses in the affected limb and it is much cooler than the contra-lateral
limb. Which process best accounts for this presentation?
Thrombosis
Embolus
Atheroma growth
Sub intimal dissection
Anaemia
Theme from April 2012 Exam
In an existing lesion a complication such as thrombosis is more likely than embolus. These patients
should receive heparin and imaging with duplex scanning. Whilst an early surgical bypass or intra-
arterial thrombolysis may be indicated, an embolectomy should not generally be performed as the
lesion is not an embolus and the operation therefore ineffective.
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Claudication
Claudication is a condition in which patients develop pain in a limb during periods of exercise. The
underlying disorder is usually that of arterial insufficiency. Atheroma develops in the arterial wall and
once this occludes >50-75% of the lumenal diameter the supply to metabolising tissues distally may
become compromised. The typical claudicant complains of calf pain that is worse on exercise and
relieved by rest. This typical description assumes that the SFA is the site of disease, more proximal
disease may present with other symptoms such as buttock claudication and impotence.
The history is usually a progressive one, patients presenting as an emergency with severe pain,
diminished sensation, pallor and absent pulses have critical limb ischaemia. This may complicate
claudication and usually indicates a plaque related complication, such as thrombosis.
Risk factors
Risk factors for claudication include smoking, diabetes and hyperlipidaemia.
Diagnosis
Diagnostic work -up includes measurement of ankle- brachial pressure indices, duplex scanning and
formal angiography.
Treatment
Those with long claudication distances, no ulceration or gangrene may be managed conservatively.
Patients with rest pain, ulceration or gangrene will almost always require intervention. All patients
should receive an antiplatelet agent and a statin unless there are compelling contra-indications.
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Question 31 of 147
The following are true of carcinoid tumours except:
When present in the appendix tip and measure less than 2 cm have an excellent prognosis
Even when metastatic disease is present it tends to follow a protracted course
When present in the appendix body tend to present with carcinoid syndrome even when
liver metastases are not present
May be imaged using 5 HIAA radionucleotide scanning
Advanced appendiceal carcinoids may require right hemicolectomy
Rule of thirds: 1/3 multiple 1/3 small bowel 1/3 metastasize 1/3 second tumour
Liver metastases are necessary for the presence of carcinoid syndrome. Please rate this question:
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Carcinoid syndrome
Carcinoid tumours secrete serotonin Originate in neuroendocrine cells mainly in the intestine (midgut-distal ileum/appendix)
Can occur in the rectum, bronchi Hormonal symptoms mainly occur when disease spreads outside the bowel
Clinical features
Onset: insidious over many years
Flushing face Palpitations Pulmonary valve stenosis and tricuspid regurgitation causing dyspnoea Asthma
Severe diarrhoea (secretory, persists despite fasting)
Investigation
5-HIAA in a 24-hour urine collection
Somatostatin receptor scintigraphy CT scan Blood testing for chromogranin A
Treatment
Octreotide
Surgical removal
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Question 32 of 147
During a difficult femoro-popliteal bypass operation the surgeon inadvertently places a clamp across the femoral nerve. It remains there for most of the procedure. At the end of the operation the nerve is inspected, it is in continuity but has evidence of being crushed. Which of the following is most likely to occur over the following months?
Wallerian degeneration
Rapid restoration of neuronal function because the axon itself is intact
Normal but delayed neuronal transmission due to disruption of the myelin
Absence of neuroma formation
None of the above
A neuronal injury such as this will result in Wallerian degeneration even though the nerve remains in continuity. Neuromas may well form. Please rate this question:
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Nerve injury
There are 3 types of nerve injury:
Neuropraxia Nerve intact but electrical conduction is affected
Full recovery
Autonomic function preserved
Wallerian degeneration does not occur
Axonotmesis Axon is damaged and the myelin sheath is preserved. The connective tissue
framework is not affected.
Wallerian degeneration occurs.
Neurotmesis Disruption of the axon, myelin sheath and surrounding connective tissue.
Wallerian degeneration occurs.
Wallerian Degeneration
Axonal degeneration distal to the site of injury.
Typically begins 24-36 hours following injury. Axons are excitable prior to degeneration occurring. Myelin sheath degenerates and is phagocytosed by tissue macrophages.
Nerve repair
Neuronal repair may only occur physiologically where nerves are in direct contact. Where a large defect is present, the process of nerve regeneration is hampered. It may not occur at all or result in the formation of a neuroma. Where nerve regrowth occurs it is typically at a rate of 1mm per day.
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Question 33 of 147
A 38 year old lady who smokes heavily presents with recurrent episodes of infection in the right
breast. On examination she has an indurated area at the lateral aspect of the nipple areaolar
complex. Imaging shows no mass lesions. What is the most likely diagnosis?
Duct ectasia
Periductal mastitis
Pagets disease of the nipple
Mondors disease of the breast
Radial scar
Periductal mastitis is common in smokers and may present with recurrent infections. Treatment is
with co-amoxyclav. Mondors disease of the breast is a localised thrombophlebitis of a breast vein.
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Duct ectasia
Duct ectasia is a dilatation and shortening of the terminal breast ducts within 3cm of the nipple. It is
common and the incidence increases with age. It typically presents with nipple retraction and
occasionally creamy nipple discharge. It may be confused with periductal mastitis, which presents in
younger women, the vast majority of which are smokers. Periductal mastitis typically presents with
periareolar or sub areolar infections and may be recurrent.
Patients with troublesome nipple discharge may be treated by microdochectomy (if young) or total
duct excision (if older).
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Question 34 of 147
Which of the following statements relating to chronic inflammation is true?
Chronic inflammation is mainly secondary to acute inflammation
Neutrophils are the predominant cells involved
Growth factors are not involved in the process
Appendicitis is mainly a form of chronic inflammation
Fibrosis is a macroscopic feature
Macroscopic features include:
Ulcers
Fibrosis Granulomatous process
It most commonly occurs as a primary event rather than as a result of acute inflammation. Please rate this question:
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Chronic inflammation
Overview Chronic inflammation may occur secondary to acute inflammation.In most cases chronic inflammation occurs as a primary process. These may be broadly viewed as being one of three main processes:
Persisting infection with certain organisms such as Mycobacterium tuberculosis which results in delayed type hypersensitivity reactions and inflammation.
Prolonged exposure to non-biodegradable substances such as silica or suture materials which may induce an inflammatory response.
Autoimmune conditions involving antibodies formed against host antigens.
Acute vs. Chronic inflammation
Acute inflammation Chronic inflammation
Changes to existing vascular structure and increased
permeability of endothelial cells
Angiogenesis predominates
Infiltration of neutrophils Macrophages, plasma cells and lymphocytes predominate
Process may resolve with:
Suppuration
Complete resolution
Abscess formation
Progression to chronic inflammation
Healing by fibrosis
Healing by fibrosis is the main result
Granulomatous inflammation
A granuloma consists of a microscopic aggregation of macrophages (with epithelial type arrangement =epitheliod). Large giant cells may be found at the periphery of granulomas. Mediators Growth factors released by activated macrophages include agents such as interferon and fibroblast growth factor (plus many more). Some of these such as interferons may have systemic features resulting in systemic symptoms and signs, which may be present in individuals with long standing chronic inflammation. The finding of granulomas is pathognomonic of chronic inflammation, as illustrated in this biopsy
from a patient with colonic Crohns disease
Image sourced from Wikipedia
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1 / 3
Question 35-37 of 147
Theme: Paediatric ano-rectal disorders
A. Ulcerative colitis
B. Juvenile polyps
C. Haemorroids
D. Intussceception
E. Rectal cancer
F. Anal fissure
G. Arteriovenous malformation
Please select the most likely cause for the condition described. Each option may be used once,
more than once or not at all.
35. A 4 year old boy is brought to the clinic. He gives a history of difficult, painful defecation with
bright red rectal bleeding.
You answered Ulcerative colitis
The correct answer is Anal fissure
Theme from April 2012 Exam
Painful rectal bleeding in this age group is typically due to a fissure. Treatment should include
stool softeners and lifestyle advice.
36. A 2 year old has a history of rectal bleeding. The parents notice that post defecation, a cherry red
lesion is present at the anal verge.
You answered Ulcerative colitis
The correct answer is Juvenile polyps
Theme from September 2012 Exam
These lesions are usually hamartomas and this accounts for the colour of the lesions. Although
the lesions are not themselves malignant they serve as a marker of an underlying polyposis
disorder.
37. A 12 year old is brought to the colorectal clinic with a history of rectal bleeding, altered bowel
habit, weight loss and malaise. Abdominal examination is normal.
Ulcerative colitis
The systemic features in the history are strongly suggestive of inflammatory bowel disease rather
than the other causes.
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Paediatric proctology
Children may present with altered bowel habit and/ or rectal bleeding. Classical haemorroidal
disease is relatively rare in children. Painful bright red rectal bleeding is much more common since
constipation is a relatively common childhood disorder. The hard stool causes a tear of the ano-
rectal mucosa with subsequent fissure. The pain from the fissure must be addressed promptly or the
child will delay defecation and this fissure will worsen.
Inflammatory bowel disease may present in a similar pattern in paediatric practice with altered bowel
habit (usually diarrhoea) and bleeding. Systemic features may be present and investigation with an
endoscopy may be required.
Children with intussceception usually present at a relatively young age and the history is usually one
of colicky abdominal pain, together with a mass on clinical examination.The often cited red current
jelly type stool is a rare but classical feature.
Juvenile polyps may occur as part of the familial polyposis coli syndromes. The lesions, which are
hamartomas, are often cherry red if they protrude externally.
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Question 38 of 147
You review a 42-year-old woman 8 months following a renal transplant for focal segmental glomerulosclerosis. She is on a combination of tacrolimus, mycophenolate, and prednisolone. She has now presented with a five day history of feeling generally unwell with jaundice, fatigue and arthralgia. On examination she has jaundice, widespread lymphadenopathy and hepatomegaly. What is the most likely diagnosis?
Hepatitis C
Epstein-Barr virus
HIV
Hepatitis B
Cytomegalovirus
Post transplant complications CMV: 4 weeks to 6 months post transplant EBV: post transplant lymphoproliferative disease. > 6 months post transplant
Post transplant lymphoproliferative disorder is most commonly associated with Epstein-Barr virus. It typically occurs 6 months post transplant and is associated with high dose immunosupressant therapy. Remember cytomegalovirus presents within the first 4 weeks to 6 months post transplant. Please rate this question:
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Renal transplant:HLA typing and graft failure
The human leucocyte antigen (HLA) system is the name given to the major histocompatibility complex (MHC) in humans. It is coded for on chromosome 6. Some basic points on the HLA system
Class 1 antigens include A, B and C. Class 2 antigens include DP,DQ and DR When HLA matching for a renal transplant the relative importance of the HLA antigens are as
follows DR > B > A
Graft survival
1 year = 90%, 10 years = 60% for cadaveric transplants 1 year = 95%, 10 years = 70% for living-donor transplants
Post-op problems
ATN of graft Vascular thrombosis Urine leakage
UTI
Hyperacute acute rejection
Due to antibodies against donor HLA type 1 antigens
Rarely seen due to HLA matching
Acute graft failure (< 6 months)
Usually due to mismatched HLA Other causes include cytomegalovirus infection
Management: give steroids, if resistant use monoclonal antibodies
Causes of chronic graft failure (> 6 months)
Chronic allograft nephropathy
Ureteric obstruction Recurrence of original renal disease (MCGN > IgA > FSGS)
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Question 39 of 147
Which of the following processes facilitates phagocytosis?
Apoptosis
Opsonisation
Proteolysis
Angiogenesis
Necrosis
Theme from September 2014 Exam Opsonisation will facilitate phagocytosis. The micro-organism becomes coated with antibody, C3b and certain acute phase proteins. The macrophages and neutrophils have up regulation of phagocytic cell surface receptors in these circumstances, a process mediated by pro-inflammatory cytokines. These cells then engulf the micro organism. Please rate this question:
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Phagocytosis
Ingestion of pathogens or foreign materials by cells First step is opsonisation whereby the organism is coated by antibody Second step is adhesion to cell surface Third step is pseudopodial extension to form a phagocytic vacuole
Lysosomes fuse with vacuole and degrade contents
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Question 40 of 147
Features which are evaluated for the grading of breast cancer include all the following, except:
Tubule formation
Mitoses
Nuclear pleomorphism
Tumour necrosis
Coarse chromatin
The necrosis of a tumour may be suggestive of a high grade tumour which has out grown its blood
supply. However, the grading of breast cancer which classically follows the Bloom -Richardson
grading model will tend to favor nuclear appearances (which include mitoses, coarse chromatin and
pleomorphism). Tubule formation is an important marker of the degree of differentiation with
formation of tubular structures being associated with well differentiated tumours.
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Tumour grading
Tumours may be graded according to their degree of differentiation, mitotic activity and other
features. Grade 1 tumours are the most differentiated and grade 3 or 4 the least. The assessment is
subjective, in most cases high grade equates to poor prognosis, or at least rapid growth.
Tumours of glandular epithelium will tend to arrange themselves into acinar type structures
containing a central lumen. Well differentiated tumours may show excellent acinar formation and
poorly differentiated tumours simply clumps of cells around a desmoplastic stroma. Sometimes
tumours demonstrate mucous production without evidence of acinar formation. Since mucous
production is evidence of a glandular function such tumours are often termed mucinous
adenocarcinoma.
Squamous cell tumours will typically produce structures resembling epithelial cell components. Well
differentiated tumours may also produce keratin (depending upon tissue of origin).
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Question 41 of 147
A 34 year old man is diagnosed with an aggressive caecal adenocarcinoma. His sister died from the
same disease at 38 years of age. His mother died from endometrial cancer at the age of 41. What is
the most likely underlying abnormality?
Familial adenopolypomatosis coli
Gardeners syndrome
Mutation of mismatch repair genes
Deletion of chromosome 6
MYH gene mutation
Lynch syndrome which is characterised by aggressive right sided colonic malignancy and
endometrial cancer is caused by microsatellite instability of DNA repair genes.
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Genetics of colorectal cancer
The lifetime risk of colorectal cancer in the UK population is 5%. Up to 5% of newly diagnosed bowel
cancers will be in those individuals who have a high genetically acquired risk of bowel cancer.
Cancers arising in the low-moderate genetic risk group comprise approximately 30% of newly
diagnosed bowel cancer.
Genetics of inherited colorectal cancer syndromes
Syndrome Features Genes implicated
FAP More than 100 adenomatous polyps affecting the colon and
rectum. Duodenal and fundic glandular polyps
APC (over 90%)
Gardner
syndrome
As FAP but with desmoid tumours and mandibular osteomas APC
Turcots syndrome Polyposis and colonic tumours and CNS tumours APC +MLH1 and
PMS2
HNPCC Colorectal cancer without extensive polyposis. Endometrial
cancer, renal and CNS
MSH2, MLH1, PMS2
and GTBP
Peutz-Jeghers
syndrome
Hamartomatous polyps in GI tract and increased risk of GI
malignancy
LKB1 andSTK11 (in
up to 70%)
Cowden disease Multiple hamartomas (see below) PTEN (85%)
MYH associated
polyposis
Autosomal recessive, multiple adenomatous polyps in GI tract,
those in colon having somatic KRAS mutations
MYH
FAP
Autosomal dominant condition, affects 1 in 12,000. Accounts for 0.5% of all CRCs. Lifetime
incidence of colorectal cancer in untreated FAP =100%. Up to 25% cases are caused by de-novo
germ line mutations and show no prior family history. The APC tumour suppressor gene is affected
in most cases.
APC in non inherited colorectal cancer
Up to 80% of sporadic colorectal cancers will have somatic mutations that inactivate APC[1]. Both
alleles are usually affected. Although the APC protein more than likely has multiple critical cellular
functions, the best-established role for APC in the cancer process is as a major binding partner and
regulator of the β- catenin protein in the so-called canonical or β- catenin dependent Wnt signaling
pathway.
HNPCC (Lynch syndrome)
HNPCC cancers differ from conventional tumours in a number of respects. In the colon the tumours
are more likely to be right sided, histologically they are more likely to be mucinous and have dense
lymphocytic infiltrates. To be diagnosed as having HNPCC individuals must show typically HNPCC
tumours in at least three individuals, (one of whom must be a first degree relative to the other two).
In at least two successive generations. At least one cancer must be diagnosed under the age of 50.
FAP must be excluded and tumours should be verified by pathological identification (Amsterdam
criteria). The genetic changes in HNPCC stem primarily from microsatellite instability affecting DNA
mismatch repair genes. In HNPCC the mismatch repair genes most commonly implicated include;
MSH2 and MLH1 and these occur in up to 70% of people with HNPCC. The finding of microsatellite
instability is unusual in sporadic colorectal cancers. Approximately 60% of individuals who fulfill the
Amsterdam criteria will not be found to have evidence of mismatch repair gene defects on genetic
testing. The risk of developing colorectal cancer in those who have not demonstrated mutation of the
mis match repair genes is increased if they fulfill the Amsterdam criteria, but not
the extent that it is increased in those who fulfill the criteria AND have evidence of mis match repair
gene defects.
KRAS Mutations
The RAS family of small G proteins act as molecular switches downstream of growth factor
receptors. KRAS and the other two members of the family; HRAS and NRAS, are the site of
mutation in approximately 40% of colorectal cancers. When adenomas are examined the proportion
of adenomas less than 1cm showing KRAS mutations was only 10% which contrasts with 50% in
those lesions greater than 1cm.
p53 mutations
The p53 protein functions as a key transcriptional regulator of genes that encode proteins with
functions in cell-cycle checkpoints at the G1/S and G2/M boundaries, in promoting apoptosis, and in
restricting angiogenesis . As such, selection for p53 defects at the adenoma-carcinoma transition
may reflect the fact that stresses on tumor cells activate cell-cycle arrest, apoptotic, and
antiangiogenic pathways in cells with wild-type p53 function. Many colonic tumours will demonstrate
changes in the p53 gene that may facilitate tumour progression through from adenoma to
carcinoma.
Cowden syndrome
Also known as multiple hamartoma syndrome. Rare autosomal dominant condition with incidence of
1 in 200,000.. It is characterised by multiple mucocutaneous lesions, trichilemmomas, oral
papillomas and acral keratosis. Most often diagnosed in third decade of life. Breast carcinoma may
occur in up to 50% of patients and conditions such as fibrocystic disease of the breast may occur in
75% of women. Thyroid disease occurs in 75% and may include malignancy. Endoscopic screening
will identify disease in up to 85% although the small bowel is rarely involved. There is a 15-20% risk
of developing colorectal cancer and regular colonoscopic screening from age 45 is recommended.
Terminology
Oncogene Oncogenes are genes which have the potential to induce cellular proliferation and avoid
apoptosis. Oncogene mutations are general gain of function and are therefore
dominant. Increased expression of oncogenes are found in most tumours
Tumour
suppressor
gene
These genes generally inhibit cellular proliferation or induce apoptosis. Mutations in
tumour suppressor genes are generally loss of function mutations, and are therefore
recessive. Mutations in both tumour suppressor gene alleles allow cells to proliferate
without restraint
References
1. Fearon, E.R. and B. Vogelstein, A genetic model for colorectal tumorigenesis. Cell, 1990. 61(5): p.
759-67.
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Question 42 of 147
Which of the following is associated with poor wound healing?
Jaundice
Patients taking carbamazepine
General anaesthesia using thiopentone
General anaesthesia using ketamine
Multiple sclerosis
Mnemonic to remember factors affecting wound healing: DID NOT HEAL D iabetes I nfection, irradiation D rugs eg steroids, chemotherapy N utritional deficiencies (vitamin A, C & zinc, manganese), Neoplasia O bject (foreign material) T issue necrosis H ypoxia E xcess tension on wound A nother wound L ow temperature, Liver jaundice
Multiple sclerosis is associated with pressure sores, however the cellular healing process is not affected. Please rate this question:
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Wound healing
Surgical wounds are either incisional or excisional and either clean, clean contaminated or dirty. Although the stages of wound healing are broadly similar their contributions will vary according to the
wound type. The main stages of wound healing include: Haemostasis
Minutes to hours following injury Vasospasm in adjacent vessels, platelet plug formation and generation of fibrin rich clot.
Inflammation
Typically days 1-5 Neutrophils migrate into wound (function impaired in diabetes). Growth factors released, including basic fibroblast growth factor and vascular endothelial
growth factor. Fibroblasts replicate within the adjacent matrix and migrate into wound. Macrophages and fibroblasts couple matrix regeneration and clot substitution.
Regeneration
Typically days 7 to 56
Platelet derived growth factor and transformation growth factors stimulate fibroblasts and epithelial cells.
Fibroblasts produce a collagen network.
Angiogenesis occurs and wound resembles granulation tissue.
Remodeling
From 6 weeks to 1 year
Longest phase of the healing process and may last up to one year (or longer). During this phase fibroblasts become differentiated (myofibroblasts) and these facilitate
wound contraction. Collagen fibres are remodeled. Microvessels regress leaving a pale scar.
The above description represents an idealised scenario. A number of diseases may distort this process. Neovascularisation is an important early process. Endothelial cells may proliferate in the wound bed and recanalise to form a vessel. Vascular disease, shock and sepsis can all compromise microvascular flow and impair healing. Conditions such as jaundice will impair fibroblast synthetic function and immunity with a detrimental effect in most parts of the healing process. Problems with scars:
Hypertrophic scars
Excessive amounts of collagen within a scar. Nodules may be present histologically containing randomly arranged fibrils within and parallel fibres on the surface. The tissue itself is confined to the extent of the wound itself and is usually the result of a full thickness dermal injury. They may go on to develop contractures. Image of hypertrophic scarring. Note that it remains confined to the boundaries of the original wound:
Image sourced from Wikipedia
Keloid scars Excessive amounts of collagen within a scar. Typically a keloid scar will pass beyond the boundaries of the original injury. They do not contain nodules and may occur following even trivial injury. They do not regress over time and may recur following removal. Image of a keloid scar. Note the extension beyond the boundaries of the original incision:
Image sourced from Wikipedia
Drugs which impair wound healing:
Non steroidal anti inflammatory drugs
Steroids Immunosupressive agents Anti neoplastic drugs
Closure Delayed primary closure is the anatomically precise closure that is delayed for a few days but before granulation tissue becomes macroscopically evident. Secondary closure refers to either spontaneous closure or to surgical closure after granulation tissue has formed.
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Question 43 of 147
A 55 year old man undergoes a colonoscopy and a colonic polyp is identified. It has a lobular
appearance and is located on a stalk in the sigmoid colon. Which of the processes below best
accounts for this disease?
Apoptosis
Metaplasia
Dysplasia
Calcification
Degeneration
Theme from April 2012 Exam
Most colonic polyps described above are adenomas. These may have associated dysplasia. The
more high grade the dysplasia the greater the level of clinical concern.
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Colonic polyps
Colonic Polyps
May occur in isolation, or greater numbers as part of the polyposis syndromes. In FAP greater than
100 polyps are typically present. The risk of malignancy in association with adenomas is related to
size, and is the order of 10% in a 1cm adenoma. Isolated adenomas seldom give risk of symptoms
(unless large and distal). Distally sited villous lesions may produce mucous and if very large,
electrolyte disturbances may occur.
Follow up of colonic polyps
Group Features Action
Low risk 1 or 2 adenomas less than 1cm No follow up or re-colonoscopy
at 5 years
Moderate
risk
3 or 4 small adenomas or 1 adenoma greater than 1cm Re-scope at 3 years
High risk More than 5 small adenomas or more than 3 with 1 of
them greater than 1cm
Re scope at 1 year
From Atkins and Saunders Gut 2002 51 (suppl V:V6-V9). It is important to stratify patients
appropriately and ensure that a complete colonoscopy with good views was performed.
Segmental resection or complete colectomy should be considered when:
1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.
Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.
References
Cairns S et al. Guidelines for colorectal cancer screening and surveillance in moderate and high risk
groups (update from 2002). Gut 2010;59:666-690.
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Question 44 of 147
A 56 year old lady has just undergone a colonoscopy and a 1.5cm lesion was identified in the
caecum. The histology report states that biopsies have been taken from a sessile serrated polyp with
traditional features. What is the best management option?
Perform a right hemicolectomy
List the patient for colonoscopic polypectomy
Discharge the patient
Re scope the patient in 6 months
Re scope the patient at 3 years
These polyps represent an alternative pathway to progression to carcinoma and may be
diagnostically confused with hyperplastic polyps. Hyperplastic polyps are more common in the left
colon and confer no increased risk. SSA's are more common in the right colon and are usually
larger. Those with "traditional features" on histology have dysplasia with increased risk of malignant
transformation.
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Colonic polyps
Colonic Polyps
May occur in isolation, or greater numbers as part of the polyposis syndromes. In FAP greater than
100 polyps are typically present. The risk of malignancy in association with adenomas is related to
size, and is the order of 10% in a 1cm adenoma. Isolated adenomas seldom give risk of symptoms
(unless large and distal). Distally sited villous lesions may produce mucous and if very large,
electrolyte disturbances may occur.
Follow up of colonic polyps
Group Features Action
Low risk 1 or 2 adenomas less than 1cm No follow up or re-colonoscopy
at 5 years
Moderate
risk
3 or 4 small adenomas or 1 adenoma greater than 1cm Re-scope at 3 years
High risk More than 5 small adenomas or more than 3 with 1 of
them greater than 1cm
Re scope at 1 year
From Atkins and Saunders Gut 2002 51 (suppl V:V6-V9). It is important to stratify patients
appropriately and ensure that a complete colonoscopy with good views was performed.
Segmental resection or complete colectomy should be considered when:
1. Incomplete excision of malignant polyp
2. Malignant sessile polyp
3. Malignant pedunculated polyp with submucosal invasion
4. Polyps with poorly differentiated carcinoma
5. Familial polyposis coli
-Screening from teenager up to 40 years by 2 yearly sigmoidoscopy/colonoscopy
-Panproctocolectomy and Ileostomy or Restorative Panproctocolectomy.
Rectal polypoidal lesions may be amenable to trans anal endoscopic microsurgery.
References
Cairns S et al. Guidelines for colorectal cancer screening and surveillance in moderate and high risk
groups (update from 2002). Gut 2010;59:666-690.
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Question 45 of 147
A 30 year old male presents with gynaecomastia. Clinically, he is noted to have a nodule in the left testis. What is the most likely diagnosis?
Oestrogen abuse
Seminoma with syncytiotrophoblast giant cells
Teratoma
Choriocarcinoma
Leydig cell tumour
Leydig cell tumours are rare testicular sex cord stromal tumours (which also include sertoli cell tumours) which are associated with hormonal activity.
Patients with Leydig cell tumours may present with gynaecomastia before they notice testicular enlargement.
Majority are benign Histology: eosinophilic cells in columns
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Testicular disorders
Testicular cancer Testicular cancer is the most common malignancy in men aged 20-30 years. Around 95% of cases of testicular cancer are germ-cell tumours. Germ cell tumours may essentially be divided into:
Tumour type Key features
Tumour
markers Pathology
Tumour type Key features
Tumour
markers Pathology
Seminoma Commonest
subtype (50%)
Average age at
diagnosis = 40
Even advanced
disease associated
with 5 year
survival of 73%
AFP usually
normal
HCG elevated
in 10%
seminomas
Lactate
dehydrogenase;
elevated in 10-
20% seminomas
(but also in many
other conditions)
Sheet like lobular
patterns of cells
with substantial
fibrous
component.
Fibrous septa
contain
lymphocytic
inclusions and
granulomas may
be seen.
Non seminomatous germ
cell tumours (42%)
Teratoma
Yolk sac tumour
Choriocarcinoma
Mixed germ cell
tumours (10%)
Younger age at
presentation =20-30
years
Advanced disease
carries worse prognosis
(48% at 5 years)
Retroperitoneal lymph
node dissection may be
needed for residual
disease after
chemotherapy
AFP elevated
in up to 70% of
cases
HCG elevated
in up to 40% of
cases
Other markers
rarely helpful
Heterogenous
texture with
occasional ectopic
tissue such as hair
Image demonstrating a classical seminoma, these tumours are typically more uniform than
teratomas
Image sourced from Wikipedia
Risk factors for testicular cancer
Cryptorchidism Infertility
Family history Klinefelter's syndrome Mumps orchitis
Features
A painless lump is the most common presenting symptom Pain may also be present in a minority of men Other possible features include hydrocele, gynaecomastia
Diagnosis
Ultrasound is first-line CT scanning of the chest/ abdomen and pelvis is used for staging Tumour markers (see above) should be measured
Management
Orchidectomy (Inguinal approach) Chemotherapy and radiotherapy may be given depending on staging Abdominal lesions >1cm following chemotherapy may require retroperitoneal lymph node
dissection.
Prognosis is generally excellent
5 year survival for seminomas is around 95% if Stage I
5 year survival for teratomas is around 85% if Stage I
Benign disease Epididymo-orchitis Acute epididymitis is an acute inflammation of the epididymis, often involving the testis and usually caused by bacterial infection.
Infection spreads from the urethra or bladder. In men <35 years, gonorrhoea or chlamydia are the usual infections.
Amiodarone is a recognised non infective cause of epididymitis, which resolves on stopping the drug.
Tenderness is usually confined to the epididymis, which may facilitate differentiating it from torsion where pain usually affects the entire testis.
Testicular torsion
Twist of the spermatic cord resulting in testicular ischaemia and necrosis.
Most common in males aged between 10 and 30 (peak incidence 13-15 years) Pain is usually severe and of sudden onset. Cremasteric reflex is lost and elevation of the testis does not ease the pain.
Treatment is with surgical exploration. If a torted testis is identified then both testis should be fixed as the condition of bell clapper testis is often bilateral.
Hydrocele
Presents as a mass that transilluminates, usually possible to "get above" it on examination. In younger men it should be investigated with USS to exclude tumour. In children it may occur as a result of a patent processus vaginalis.
Treatment in adults is with a Lords or Jabouley procedure. Treatment in children is with trans inguinal ligation of PPV.
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Question 46 of 147
What is the most common cause of osteolytic bone metastasis in children?
Osteosarcoma
Neuroblastoma
Leukaemia
Rhabdomyosarcoma
Nephroblastoma
Neuroblastomas are a relatively common childhood tumour and have a strong tendency to developing widespread lytic metastasis. Please rate this question:
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Secondary malignant tumours of bone
Metastatic lesions affecting bone are more common than primary bone tumours. The typical tumours that spread to bone include:
Breast
Bronchus Renal Thyroid Prostate
75% cases will affect those over the age of 50 The commonest bone sites affected are:
Vertebrae (usually thoracic) Proximal femur Ribs Sternum
Pelvis Skull
Pathological fracture Osteolytic lesions are the greatest risk for pathological fracture The risk and load required to produce fracture varies according to bone site. Bones with lesions that occupy 50% or less will be prone to fracture under loading (Harrington). When 75% of the bone is affected the process of torsion about a bony fulcrum may produce a fracture. The Mirel scoring[1] system may be used to help determine the risk of fracture and is more systematic than the Harrington system described above. Mirel Scoring system
Score
points Site
Radiographic
appearance
Width of bone
involved Pain
1 Upper extremity Blastic Less than 1/3 Mild
2 Lower extremity
Mixed 1/3 to 2/3 Moderate
3 Peritrochanteric Lytic More than 2/3 Aggravated by
function
Depending upon the score the treatment should be as follows:
Score Risk of fracture Treatment
9 or greater Impending (33%) Prophylactic fixation
8 Borderline Consider fixation
7 or less Not impending (4%) Non operative management
Where the lesion is an isolated metastatic deposit consideration should be given to excision and reconstruction as the outcome is better [2]. Non operative treatments
Hypercalcaemia- Treat with re hydration and bisphosphonates. Pain- Opiate analgesics and radiotherapy. Some tumours such as breast and prostate will benefit from chemotherapy and or hormonal agents. References 1. Mirels, H. Metastatic disease in long bones. A proposed scoring system for diagnosing impending pathologic fractures. Clin Orthop Relat Res, 1989(249): p. 256-64. 2. Mavrogenis, A.F. et al. Survival analysis of patients with femoral metastases. J Surg Oncol, 2011.
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Question 47 of 147
Which of the following features are not typical of Crohns disease?
Complex fistula in ano
Small bowel strictures
Skip lesions
'Rose thorn ulcers' on barium studies
Pseudopolyps on colonoscopy
Pseudopolyps are a feature of ulcerative colitis and occur when there is severe mucosal ulceration. The remaining islands of mucosa may then appear to be isolated and almost polypoidal. Please rate this question:
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Crohns disease
Crohns disease is a chronic transmural inflammation of a segment(s) of the gastrointestinal tract and may be associated with extra intestinal manifestations. Frequent disease patterns observed include ileal, ileocolic and colonic disease. Peri-anal disease may occur in association with any of these. The disease is often discontinuous in its distribution. Inflammation may cause ulceration, fissures, fistulas and fibrosis with stricturing. Histology reveals a chronic inflammatory infiltrate that is usually patchy and transmural. Ulcerative colitis Vs Crohns
Crohn's disease Ulcerative colitis
Distribution Mouth to anus Rectum and colon
Crohn's disease Ulcerative colitis
Macroscopic
changes
Cobblestone appearance, apthoid ulceration Contact bleeding
Depth of disease Transmural inflammation Superficial inflammation
Distribution pattern
Patchy Continuous
Histological
features
Granulomas (non caseating epithelioid cell
aggregates with Langerhans' giant cells)
Crypt abscesses, Inflammatory
cells in the lamina propria
Extraintestinal manifestations of Crohns
Related to disease extent Unrelated to disease extent
Aphthous ulcers (10%) Sacroiliiitis (10-15%)
Erythema nodosum (5-10%) Ankylosing spondylitis (1-2%)
Pyoderma gangrenosum (0.5%) Primary sclerosing cholangitis (Rare)
Acute arthropathy (6-12%) Gallstones (up to 30%)
Ocular complications (up to 10%) Renal calculi (up to 10%)
Diarrhoea in Crohns Diarrhoea in Crohns may be multifactorial since actual inflammation of the colon is not common. Causes therefore include the following:
Bile salt diarrhoea secondary to terminal ileal disease Entero-colic fistula
Short bowel due to multiple resections Bacterial overgrowth
Surgical interventions in Crohns disease
The commonest disease pattern in Crohns is stricturing terminal ileal disease and this often culminates in an ileocaecal resection. Other procedures performed include segmental small bowel resections and stricturoplasty. Colonic involvement in patients with Crohns is not common and, where found, distribution is often segmental. However, despite this distribution segmental resections of the colon in patients with Crohns disease are generally not advocated because the recurrence rate in the remaining colon is extremely high, as a result the standard options of colonic surgery in Crohns patients are generally; sub total colectomy, panproctocolectomy and staged sub total colectomy and proctectomy. Restorative procedures such as ileoanal pouch have no role in therapy. Crohns disease is notorious for the developmental of intestinal fistulae; these may form between the rectum and skin (peri anal) or the small bowel and skin. Fistulation between loops of bowel may also occur and result in bacterial overgrowth and malabsorption. Management of enterocutaneous fistulae involves controlling sepsis, optimising nutrition, imaging the disease and planning definitive surgical management.
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Question 48 of 147
At which of the following sites is the development of diverticulosis least likely?
Caecum
Ascending colon
Transverse colon
Sigmoid colon
Rectum
Rectal involvement with diverticular disease almost never occurs.
Because the rectum has a circular muscle coat (blending of of the tenia marks the recto-sigmoid junction), diverticular disease almost never occurs here. Right sided colonic diverticular disease is well recognised (though less common than left sided). Please rate this question:
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Diverticular disease
Diverticular disease is a common surgical problem. It consists of herniation of colonic mucosa through the muscular wall of the colon. The usual site is between the taenia coli where vessels pierce the muscle to supply the mucosa. For this reason, the rectum, which lacks taenia, is often spared. Symptoms
Altered bowel habit Bleeding Abdominal pain
Complications
Diverticulitis Haemorrhage
Development of fistula Perforation and faecal peritonitis Perforation and development of abscess Development of diverticular phlegmon
Diagnosis Patients presenting in clinic will typically undergo either a colonoscopy, CT cologram or barium enema as part of their diagnostic work up. All tests can identify diverticular disease. It can be far more difficult to confidently exclude cancer, particularly in diverticular strictures. Acutely unwell surgical patients should be investigated in a systematic way. Plain abdominal films and an erect chest x-ray will identify perforation. An abdominal CT scan (not a CT cologram) with oral and intravenous contrast will help to identify whether acute inflammation is present but also the presence of local complications such as abscess formation.
Severity Classification- Hinchey
I Para-colonic abscess
II Pelvic abscess
III Purulent peritonitis
IV Faecal peritonitis
Treatment
Increase dietary fibre intake.
Mild attacks of diverticulitis may be managed conservatively with antibiotics. Peri colonic abscesses should be drained either surgically or radiologically. Recurrent episodes of acute diverticulitis requiring hospitalisation are a relative indication for
a segmental resection.
Hinchey IV perforations (generalised faecal peritonitis) will require a resection and usually a stoma. This group have a very high risk of post operative complications and usually require HDU admission. Less severe perforations may be managed by laparoscopic washout and drain insertion.
Question 49 of 147
A 32 year old lady presents with a 1.5cm pigmented lesion on her back. The surgeon is concerned that this may be a melanoma. What is the most appropriate course of action?
2mm punch biopsy from the centre of the lesion
4mm punch biopsy from the centre of the lesion
Wide excision of the lesion with 3cm margins
Excisional biopsy of the lesion
Wide excision of the lesion with 1cm margins
Suspicious naevi should NOT be partially sampled as histological interpretation is severely compromised. Complete excision is mandatory where lesions fulfil diagnostic criteria. However, wide excision for margins may be deferred until definitive histology is available.
Lesions that are suspicious for melanoma should be excised with complete margins. Radical excision is not routinely undertaken for diagnostic purposes and therefore if subsequent histopathological assessment determines that the lesion is a melanoma a re-exicision of margins may be required. Incisional punch biopsies of potential melanomas makes histological interpretation difficult and is best avoided. Please rate this question:
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Malignant melanoma
The main diagnostic features (major criteria):
Change in size
Change in shape
Change in colour
Secondary features (minor criteria)
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation
Treatment
Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required (see below):
Margins of excision-Related to Breslow thickness
Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm
Marsden J et al Revised UK guidelines for management of Melanoma. Br J Dermatol 2010 163:238-256. Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applied.
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Question 50 of 147
A 50 year old male presents with painless frank haematuria. Clinical examination is unremarkable. Routine blood tests reveal a haemoglobin of 18g/dl but are otherwise normal. What is the most likely underlying diagnosis?
Squamous cell carcinoma of the bladder
Adenocarcinoma of the prostate
Adenocarcinoma of the kidney
Wilms tumour
Transitional cell carcinoma of the renal pelvis
Theme from April 2012 Exam Polycythaemia is a recognised feature of renal cell carcinoma. Wilms tumours most commonly occur in children. Please rate this question:
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Haematuria
Causes of haematuria
Trauma Injury to renal tract
Renal trauma commonly due to blunt injury (others penetrating
injuries)
Ureter trauma rare: iatrogenic
Bladder trauma: due to RTA or pelvic fractures
Infection Remember TB
Malignancy Renal cell carcinoma (remember paraneoplastic syndromes):
painful or painless
Urothelial malignancies: 90% are transitional cell carcinoma, can
occur anywhere along the urinary tract. Painless haematuria.
Squamous cell carcinoma and adenocarcinoma: rare bladder
tumours
Prostate cancer
Penile cancers: SCC
Renal disease Glomerulonephritis
Stones Microscopic haematuria common
Structural
abnormalities
Benign prostatic hyperplasia (BPH) causes haematuria due to
hypervascularity of the prostate gland
Cystic renal lesions e.g. polycystic kidney disease
Vascular malformations
Renal vein thrombosis due to renal cell carcinoma
Coagulopathy Causes bleeding of underlying lesions
Drugs Cause tubular necrosis or interstitial nephritis: aminoglycosides,
chemotherapy
Interstitial nephritis: penicillin, sulphonamides, and NSAIDs
Anticoagulants
Benign Exercise
Gynaecological Endometriosis: flank pain, dysuria, and haematuria that is cyclical
Iatrogenic Catheterisation
Radiotherapy; cystitis, severe haemorrhage, bladder necrosis
Pseudohaematuria For example following consumption of beetroot
References Http://bestpractice.bmj.com/best-practice/monograph/316/overview/aetiology.html
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