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CHAPTER 22 System-Specific Pathology
421
Gall Bladder
Gallstones (cholelithiasis)
Gallstones are common, found in 10–15% of patients.
Aetiology
Predisposing factors include:
• sex: more common in females; multiple pregnancies
may also increase predisposition
• age: incidence increases with age
• diet/obesity: possibly related to increased cholesterol
secretion from liver
• gastrointestinal disease: aecting terminal ileum, which
interferes with enterohepatic circulation of bile salts –
Crohn’s disease; intestinal resection
• drugs: clobrate and oestrogens
• geographical: high incidence in developed countries,
e.g. Europe, North America
• haemolytic disease: increased incidence of pigment
stones – sickle cell disease, thalassaemia, hereditary
spherocytosis.
Types of stone
• Mixed:
• 80% are mixed
• predominantly cholesterol with small amounts of
calcium and bile pigments
• characteristically multiple with faceted surface and
laminated on cross-section.
• Pure cholesterol stones:
• 10% of stones
• usually solitary
• up to 5 cm in diameter
• radial arrangement of crystals on cross-section
• usually form in bile, which is supersaturated with
cholesterol.
• Pigment stones:
• 10% of stones
• composed of calcium bilirubinate
• usually multiple, small and black in colour.
Pathological consequences of gallstones
ese are:
• inammation of gall bladder: acute cholecystitis,
chronic cholecystitis, acute-on-chronic cholecystitis
• obstructive jaundice due to impaction of a stone at the
lower end of the common bile duct; secondary biliary
cirrhosis may result
• ascending cholangitis
• empyema of the gall bladder
• mucocoele
• gallstone ileus: a stula occurs between the gall bladder and duodenum, and a large stone enters the small
bowel, causing obstruction usually at the terminal ileum
• acute pancreatitis, usually associated with multiple
small stones
• carcinoma of the gall bladder
• perforation of the gall bladder.
Acute cholecystitis
• Usually associated with stones.
• Occasionally occurs without stones, i.e. acalculous
cholecystitis.
• Acalculous cholecystitis may be due to infection with E.
coli, clostridia or rarely Salmonella typhi.
• Acalculous cholecystitis may occur aer prolonged starvation or TPN; stasis is probably a contributing factor.
• Gall bladder becomes oedematous with mucosal ulceration and bropurulent exudate.
• Cystic artery may thrombose but gangrene is rare, as
gall bladder gains a second blood supply from the liver
directly via the gall bladder.
• Occasionally gangrene does occur with perforation.
• Suppuration may occur with formation of empyema.
• Occasionally gall bladder may stulate into second part
of duodenum.
Chronic cholecystitis
• Invariably associated with gallstones.
• May develop aer several episodes of acute cholecystitis.
• More oen develops insidiously without any preceding
clinically evident acute attacks.
• Gall bladder wall becomes thickened, brotic and relatively indistensible.
• Glandular outpouchings are formed by the lining of the
mucosa and are known as Rokitansky–Ascho sinuses.
• Obstructive jaundice may occur if stone impacts in
common bile duct.
• Gall bladder does not usually distend as the wall is
relatively rigid due to brosis consequent on chronic
cholecystitis.
Mucocoele
• Due to impaction of stone in neck of gall bladder or cystic duct without super-added infection.
• Bile absorbed from gall bladder and mucus is secreted
into it from mucus-secreting cells of epithelium.
• Lack of inammation in wall allows gall bladder to distend to several times its normal size.
Empyema
• Due to impaction of stone in neck of gall bladder or cystic duct with super-added infection.
• Gall bladder full of pus.
• In 50% of cases organisms cannot be cultured from
the pus.
• May result from:
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SECTION III Pathology
• acute cholecystitis
• infection of mucocoele.
Cholesterolosis
• Lipid-laden macrophages accumulate in gall bladder
wall, producing yellowish ecks in red mucosa – ‘strawberry’ gall bladder.
• Oen asymptomatic but may accompany or predispose
to cholesterol stones.
Pancreatitis
Acute pancreatitis
Acute pancreatitis is an acute inammatory process caused
by the eects of enzymes released from the pancreatic acini.
Aetiological factors include:
• gallstone disease
• chronic alcoholism
• infection, e.g. mumps, Coxsackie virus, typhoid
• hypercalcaemia, e.g. hyperparathyroidism
• trauma
• post-operative, e.g. aer upper GI operations where
pancreas is handled
• hyperlipidaemia
• drugs: corticosteroids, oestrogen-containing contraceptives, azathioprine, thiazide diuretics
• hypothermia
• vascular insuciency, e.g. shock, polyarteritis nodosa
• scorpion bites
• iatrogenic, e.g. aer ERCP.
Pathogenesis
• Duct obstruction: may lead to reux of bile into the pancreatic ducts causing injury; increased intraductal pressure may damage pancreatic acini, leading to leakage of
pancreatic enzymes with further damage to pancreas.
• Direct acinar damage: due to viruses, bacteria, drugs or
trauma.
• Protease release causes widespread destruction of pancreas and increases further enzyme release with consequent further damage.
• Lipase causes fat necrosis, resulting in characteristic
yellowish-white ecks on the pancreas, mesentery and
omentum, oen with calcium deposition (fat necrosis).
• Elastase destroys blood vessels, leading to haemorrhage
within the pancreas and haemorrhagic exudate into the
peritoneum.
• Haemorrhage may be extensive, leading to acute haemorrhagic pancreatitis.
Biochemical changes
• Increased serum amylase: released from damaged acini
into bloodstream.
• Hypocalcaemia: arises because of deposition of calcium
in areas of fat necrosis.
• Hyperglycaemia: occurs because of associated damage
to pancreatic islets.
• Abnormal liver function tests, especially raised bilirubin and alkaline phosphatase, due to mild obstruction
of bile ducts by oedema.
Complications
ese include:
• pancreatic pseudocyst: localized collection of uid in
lesser sac of peritoneum
• pancreatic abscess
• stress-induced gastric erosions with haematemesis or
melaena
• acute renal failure
• toxic psychosis
• multiple organ failure
• chronic pancreatitis.
Prognosis
• Overall mortality 10–20%.
• Severe haemorrhagic pancreatitis has mortality rate of
50%.
• Usual cause of mortality is multiple organ failure.
Chronic pancreatitis
Chronic pancreatitis is a relapsing disorder which may
arise insidiously or follow repeated attacks of acute pancreatitis. Aetiological factors include:
• Chronic alcoholism (70–85%).
• Biliary tract disease.
• Cystic brosis.
• Rare familial pancreatitis inherited as an autosomal
dominant.
• Pathological changes include parenchymal destruction,
brosis, loss of acini and duct stenosis with dilatation
behind the stenosis.
• Calcication may be seen on plain abdominal X-ray.
• Clinical eects include:
• abdominal pain
• malabsorption resulting in steatorrhoea, hypoalbu-
minaemia and weight loss
• diabetes mellitus
• jaundice
• pancreatic calcication.
Carcinoma of the Pancreas
Pancreatic cancer is increasing in incidence in many countries.
It accounts for about 5% of deaths from cancer in the UK.
Aetiology
Factors include:
• cigarette smoking
• high-fat diet
• diabetes mellitus
• familial pancreatitis.
CHAPTER 22 System-Specific Pathology
423
Clinical features
• About two-thirds arise in the head of the pancreas.
• Carcinomas of the head of the pancreas may present
with obstructive jaundice.
• Carcinomas at other sites may be symptomless until
they invade local organs, e.g. vertebral column, stomach, colon.
• Weight loss.
• rombophlebitis migrans, i.e. Trousseau’s sign.
Prognosis
• Poor: 5-year survival 2%.
Portal Hypertension
Cirrhosis is the commonest cause of portal hypertension in
the UK. Worldwide, schistosomiasis is the commonest cause.
e causes of portal hypertension are shown in Box 22.6.
Intestinal Fistulae
Small bowel fistulae
Fistulae involving the small bowel may be external, where
the stula opens onto the skin; or internal, between two
pieces of bowel. e result of a stula is:
• loss of absorptive surface
• loss of nutrients
• loss of water
• loss of electrolytes.
Fistulae may have high output or low output, depending
on the site:
• high-output stulae: upper small bowel, e.g. duodenal
stula
• low-output stulae: ileum.
High-output fistulae
• Approximately 3–4 L of uid lost per day.
• Derived from gastric juice, bile, pancreatic juice or duodenal secretions.
• Depletion of intravascular and interstitial volume;
requires replacement with isotonic saline.
• Loss of alkaline pancreatic juice and bile gives rise to a
metabolic acidosis.
• Skin protection required with external stula because of
activated pancreatic trypsin digesting the keratin of the
skin, causing excoriation.
• Treatment requires:
• intravenous administration of water and electrolytes
commensurate with losses
• total parenteral nutrition until stula closes or is sur-
gically closed.
Low-output fistulae
• May put out initially up to 1.5 L per day.
• Low-output small bowel stula similar to ileostomy.
• Proximal ileum can gradually adapt to loss of any
colonic surface distal to it, and more uid and electrolytes are absorbed.
• Fluid loss less in low-output stulae because there is still
a large proximal surface for absorption.
• Loss of nutrients less, because most have already been
absorbed in the proximal small bowel.
• In initial stages, uid and electrolyte management is
important, but nutrition may be maintained by elemental diets.
Disorders of Colon and Rectum
Polyps
ese are a heterogeneous group of protuberant growths
into the bowel lumen. ey may be:
• sessile or pedunculated
• benign or malignant.
Polyposis is a term reserved for hundreds of polyps occurring in the large bowel. e most common forms of polyps
are shown in Box 22.7.
Adenomas
• Tubular, tubulovillous or villous.
• May give rise to adenocarcinoma.
• Malignant potential of an adenoma depends on:
BOX 22.6 Causes of portal hypertension
Prehepatic (obstruction of portal vein)
Congenital atresia or stenosis
Portal vein thrombosis
Extrinsic compression, e.g. tumour
Hepatic (obstruction to portal flow within liver)
Cirrhosis
Hepatoportal sclerosis
Schistosomiasis
Sarcoidosis
Post-hepatic
Budd–Chiari syndrome
Idiopathic hepatic venous thrombosis, e.g. due to polycythaemia, contraceptive pill, congenital obliteration,
tumour invasion of hepatic veins
Constrictive pericarditis
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SECTION III Pathology
BOX 22.7 Polyps of the large intestine
Type Histology
Neoplastic Benign
Adenoma
Tubular
Tubulovillous
Villous
Malignant
Polypoid adenocarcinomas
Carcinoid polyps
Inflammatory Pseudopolyp (ulcerative
colitis)
Hamartomatous Peutz–Jegher’s polyp
Juvenile polyp
Unclassified Metaplastic (hyperplastic)
Others Mesenchymal in origin
Benign
Lipoma
Fibroma
Leiomyoma
Haemangiomas
Malignant
Sarcomas
Lymphomatous polyps
• size
• growth pattern
• degree of epithelial dysplasia.
• Malignant change is found in:
• 1% of adenomas <1 cm in diameter
• 10% of adenomas 1–2 cm in diameter
• up to 40% >2 cm in diameter.
• Malignant potential depends upon type of adenoma: 5%
of tubular adenomas, 20% of tubulovillous adenomas
and 40% of villous adenomas become malignant.
• Sessile lesions are more likely to become malignant than
pedunculated ones.
Inflammatory polyps (pseudopolyps)
• Associated with ulcerative colitis; result from mucosal
ulceration.
Hamartomas
• Rare.
• May be solitary, e.g. juvenile polyps.
• May be present throughout the gastrointestinal tract,
e.g. Peutz–Jegher’s syndrome.
Metaplastic polyps
• Not neoplastic, therefore no malignant potential.
• Origin unknown.
Malignant epithelial polyps
• Vast majority arise within pre-existing adenomas.
• Small number may be carcinoid tumours of low malignant potential.
• Complete local excision is usually curative.
Familial adenomatous polyposis (FAP) – (aka familial
polyposis coli)
• Rare condition inherited as autosomal dominant.
• Equal sex incidence.
• Hundreds of polyps carpet colon and rectum.
• Cancer develops before age of 40 years in almost all
patients.
• Gene responsible for FAP is on the long arm of chromosome 5.
Gardner’s syndrome
• FAP-associated.
• Desmoid tumours, osteomas of the mandible, sebaceous
cysts.
Rectal Cancer
In Western countries, colorectal cancer ranks second only
to lung cancer in incidence and mortality rates. Multiple
synchronous colonic cancers, i.e. two more carcinomas
occurring simultaneously, are found in 5% of patients.
Metachronous cancer is a new primary lesion in a patient
who has had a previous resection for cancer. e risk of
metachronous tumours reaches 25% aer 20 years of
follow-up.
Progression of adenoma to carcinoma (see Fig. 18.1)
ere is considerable evidence that most colorectal cancers
develop from adenomas:
• colorectal cancers develop in familial adenomatous
polyposis
• adenomas and carcinomas frequently occur together
in the resected specimen of bowel; such patients have
an increased risk of developing a metachronous cancer
compared with those having carcinoma alone in the
resected specimen
• marked geographical variation in the prevalence of adenomas: there is a strong correlation with the incidence
of colorectal cancer in the same geographical areas.
Aetiology
• Inherited genetic factors:
• familial adenomatous polyposis
• autosomal dominant hereditary non-polyposis
colorectal cancer (HNPCC). ere are two types:
• cancer family syndrome (CFS: Lynch syndrome
2; early onset – age 20–30 years) and associated
CHAPTER 22 System-Specific Pathology
25%
%
425
with other adenocarcinomas, especially endometrial carcinoma
• hereditary site-specic colon cancer (HSSCC:
Lynch syndrome 1): shows same characteristics except for extracolonic carcinomas; in the
absence of the above syndromes, rst-degree relatives of patients with colorectal cancer have 2- to
3-fold increased risk of the disease.
• Environmental factors:
• low-bre/high-fat diets: high fat leads to an increase in
bile acid production; bile acids are promoters of carcinogenesis. Dietary bre contains plant lignans, which
are converted to human lignans by bacterial action in
the colon; lignans may protect against cancer.
• Inammatory bowel disease: greater risk in ulcerative
colitis than Crohn’s disease.
• Colorectal polyps.
• Schistosomal colitis.
• Exposure to radiation.
• Presence of a ureterocolostomy – this operation is rarely
performed nowadays.
Molecular basis for development of colorectal cancer
• Activation of ras oncogene:
• c-Ki-ras is aected in 80% of cases.
• Abnormalities of long arm of chromosome 5:
• 5q deletion (FAP gene).
• Deletions on long arm of chromosome 18:
• 18q deletion
• seen in 70% of carcinomas and 50% of large adenomas.
• Deletions on short arm of chromosome 17:
• inactivation of p53 in 75% of colorectal cancers.
Site
See Fig. 22.3.
Spread
• Direct:
• encircles bowel lumen
• longitudinal submucosal spread occurs, but rarely
more than 2 cm from edge of tumour
• to bowel wall and into neighbouring structures, e.g.
liver, greater curvature of stomach, duodenum, small
bowel, pancreas, kidneys, bladder, ureters or vagina.
Carcinoma of the rectum may invade the bladder,
prostate or sacrum.
• Lymphatic: regional nodes along vessels are involved
but not necessarily in a progressive or orderly fashion.
Positive nodes may be found at some distance from the
primary intervening nodes, which are normal.
• Blood:
• liver
• lungs.
• Transcoelomic: seedlings on serosal surface with ascites.
10%
15
20%
30%
Fig. 22.3 The distribution of colorectal cancer.
Complications
ese include:
• obstruction
• perforation
• perforation of the caecum in closed loop obstruction
with competent ileocaecal valve
• perforation into an adjacent organ with stula formation, e.g. colovesical, ileocolic, colovaginal
• symptoms relating to direct extension.
Prognosis
is depends on:
• degree of dierentiation of tumour
• completeness of excision degree of spread
• examination of resection margins (proximal, distal and
circumferential needed to assess completeness of excision)
• extent of spread is given by Dukes' classication, which
also relates to prognosis (Table 22.2).
Carcinoid Tumours
• Arise from enterochroman cells throughout the gut.
• May be associated with multiple endocrine neoplasia
(MEN type I and type II).
• Commonest in the midgut, the appendix being the most
common site.
• Firm, yellowish, subcutaneous nodules.
• In the appendix they are oen an incidental nding at
appendicectomy.
• Approximately 30% of small bowel carcinoids cause
symptoms such as obstruction, pain, bleeding or carcinoid syndrome.
Carcinoid syndrome
• Extensive metastases, particularly in the liver, result in
carcinoid syndrome.
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SECTION III Pathology
TABLE 22.2 Staging of Colorectal
Carcinoma Based on Dukes’ Classification,
With Survival Rates after Surgery
Dukes’
Grade Spread
A Confined to the
bowel wall
B Spread through the
bowel wall
C Spread to lymph
nodes
Stage D was added to Dukes’ classification later, based on
clinical rather than pathological evidence. Stage D implies
distant metastases.
5-Year
Survival (%)
90
70
30
• Syndrome consists of cutaneous ushing, diarrhoea,
bronchoconstriction with wheezing and right-sided cardiac valvular disease (usually pulmonary stenosis) due to
collagen deposition.
• Principal cause of symptoms and signs is 5-hydroxytryptamine (5-HT, serotonin).
• 5-HT in circulation is degraded to 5-hydroxyindoleacetic
acid (5-HIAA), which is measured in the urine as a diagnostic marker.
Inflammatory Bowel Disease
Crohn’s Disease
Crohn’s disease is a chronic inammatory granulomatous
disorder that may occur anywhere in the alimentary canal
from the mouth to the anus. It is most common in temperate climates and among those of European origin.
Aetiology
e aetiology is largely unknown. Hypotheses include:
• infection, e.g. mycobacteria and viruses
• abnormal immune mechanisms
• environmental factors, e.g. cigarette smoking and intake
of rened sugars
• family history of disease in 15–20% of patients.
Appearances
Macroscopic
• Classically segmental with areas of normal bowel separating areas of involved bowel – ‘skip’ lesions.
• ickening of wall, which becomes rm and rigid.
• Encroachment on mesenteric fat.
• Linear mucosal ulceration.
• A ‘cobble-stone’ pattern of islands of surviving mucosa.
• Deep linear ulceration.
Microscopic
• Transmural inammation from mucosa to serosa.
• Marked oedema of submucosa.
• Lymphoid aggregates.
• Patchy mucosal ulceration and ssuring.
• Presence of non-caseating granulomas (found in only
60% of cases).
Complications
• Intestinal obstruction.
• Fistula formation.
• Abscess formation.
• Malabsorption syndrome.
• Malignancy (increased risk of adenocarcinoma).
• Toxic dilatation.
• Haemorrhage.
• Perianal complications.
• Gallstones (reduction of enterohepatic circulation of
bile in terminal ileum).
Extragastrointestinal manifestations
• Eyes: conjunctivitis, episcleritis, uveitis.
• Joints: sacroiliitis, arthritis, ankylosing spondylitis.
• Skin: erythema nodosum, pyoderma gangrenosum.
• Liver: sclerosing cholangitis (rare).
Ulcerative Colitis
Ulcerative colitis is a chronic inammatory disease that
involves the whole or part of the colon. Inammation is
initially conned to the mucosa and nearly always involves
the rectum, extending to involve the distal or whole colon.
Aetiology
• Abnormal immune response to gut micro-organisms.
• Autoimmunity against colonic epithelial cells.
• Genetic factors:
• familial clustering occurs
• association with HLA-DR2
• higher concordance rate in monozygotic twins.
• Geographic factors: much commoner in Western countries than in developing world.
Appearances
Macroscopic
ere may be:
• Proctitis: inammation limited to rectum.
• Varying extent of colitis extending for a variable distance proximally from the rectum.
• Total colitis with or without backwash ileitis.
• Aected mucosa red, inamed, with contact bleeding
on sigmoidoscopy.
• Fistulae do not occ ur.
Microscopic
• Diuse, mixed inammatory cell inltrate.
• Crypt abscess formation.
• Distortion of glandular architecture.
• Mucosal ulceration.
Complications
• Toxic dilatation.
CHAPTER 22 System-Specific Pathology
427
• Perforation.
• Increased risk of colorectal cancer.
• Electrolyte disturbances with severe diarrhoea.
Extragastrointestinal manifestations
• Eye: iritis, uveitis, episcleritis.
• Joint: ankylosing spondylitis, arthritis.
• Skin: pigmentation, erythema nodosum, pyoderma
gangrenosum.
• Liver: fatty change, pericholangitis, sclerosing cholangitis, cirrhosis, hepatitis.
Diverticular Disease
A diverticulum is an outpouching of the colonic mucosa
through a defect in the muscular wall of the colon. is
occurs where blood vessels pierce the wall of the colon.
Diverticular disease is common in Western civilization and
is attributed to a low-bre diet.
Pathogenesis
• Formed due to increased intraluminal pressure, forcing the mucosa to herniate through weaknesses in the
muscle wall (pulsion diverticulum).
OSCE SCENARIOS
• 90% occur in the sigmoid colon, but the whole colon
may be aected.
• e term diverticular disease covers the whole spectrum, i.e. diverticulosis (presence of diverticulae but
no inammation); diverticulitis (inammation of
diverticulae).
Complications
• Diverticulitis.
• Perforation:
• into local tissues, where it becomes walled o as a
paracolic abscess
• into the general peritoneal cavity, giving rise to faecal
peritonitis
• into an adjacent viscus, e.g. colovesical stula (blad-
der), vaginocolic stula (vagina), ileocolic stula
(ileum).
• Bleeding: due to erosion into adjacent vessel.
• Intestinal obstruction: due to repeated attacks of diverticulitis causing brosis and consequent narrowing of
bowel lumen.
OSCE Scenario 22.1
A 28-year-old right-handed female attends A&E with a wound
on the radial and volar border of her right index nger, just
proximal to the Proximal Interphalangeal Joint. She explains
that she cut it last night with a knife whilst washing dishes, and
complains of radial numbness distal to the wound.
1. Outline how you would examine the patient's nger to
establish what structures have been injured other than
the digital nerve.
2. Explain to the examiners what would happen pathologi-
cally and clinically if the nerve injury was le untreated.
3. Explain your management plan to the patient and
answer any questions she may have.
OSCE Scenario 22.2
A 19-year-old male attends your outpatient clinic with a
3-month history of right knee pain and swelling. e pain
and swelling are worsening, waking him at night, and he
now walks with a limp. He denies any traumatic injury, is
otherwise t and well and on no medications. An X-ray
arranged by his GP whilst waiting for his referral is shown
in the gure (Fig. 22.2Q).
1. Describe the pathological signs on the X-ray.
2. What is the likely diagnosis, given the history and the
X-ray?
Fig. 22.2Q X-ray of the patient’s right knee.
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SECTION III Pathology
3. What other investigations could you arrange?
4. What are the management options?
OSCE Scenario 22.3
A 45-year-old female has presented in A&E aer falling
down some steps. She is alert and her pulse and blood pressure are normal, though her oxygen saturations are only 80%
on high-ow oxygen. She is complaining bitterly of pain
down her right chest wall, though only grazes are present.
1. How will you approach the assessment of this patient?
2. Her chest X-ray is shown below (Fig. 22.3Q). What is
the condition shown? What is the likely cause?
3. How would you treat this condition?
4. Explain to the examiners the classication of causes and
types of this condition, and how you would have treated
the patient if she had presented with tracheal deviation
and haemodynamic instability.
OSCE Scenario 22.4
A 14-year-old boy attends your clinic with his mother, who
is concerned that her son seems to be developing breasts.
e boy is overweight, with a BMI of 29, but both he and
his mother state that he has lost weight recently and his
breasts are still enlarging. His examination reveals enlarged
nipples with small rm breast bud development.
1. What is the likely diagnosis? What questions would you
like to ask to conrm this?
2. Explain the diagnosis and its causes in layman’s
terms, and outline the options for investigation and
management.
OSCE Scenario 22.5
A 62-year-old male attends A&E with acute onset of severe
abdominal pain radiating to the back. He is pale and sweaty
with a tense, distended, tender abdomen. A CT of his abdomen is shown below (Fig. 22.5Q).
1. What pathology is shown? e patient is still in the radi-
ology department and his blood pressure is stable at 90
mmHg systolic.
2. Outline the management of this patient.
3. What risk factors exist for this condition?
4. What is the operative mortality risk for this condition?
5. Explain to the examiners the dierent types of this con-
dition, their classication and their aetiology.
OSCE Scenario 22.6
A 37-year-old female attends your clinic having been
referred by her GP with excessive sweating, diarrhoea and
neck swelling.
1. Ask this patient about her symptoms and give the exam-
iners your dierential diagnosis.
2. What physical signs may you expect to see on
examination?
3. What investigations might you arrange? e results of
your investigations suggest a benign toxic goitre with a
dominant nodule.
4. What treatment options are available?
Fig. 22.3Q The patient’s chest X-ray.
Fig. 22.5Q CT scan of the patient’s abdomen.
CHAPTER 22 System-Specific Pathology
429
5. If the patient opts for surgery, which nerves are at risk of
intra-operative damage?
OSCE Scenario 22.7
e blood results displayed below are those taken from a
49-year-old male ex-alcoholic, feeling generally unwell
with vague abdominal pain, whose GP has referred him to
your clinic.
Bilirubin 57 µmol/L
Albumin 22 g/L
Total protein 64 g/L
Alkaline phosphatase (ALP) 152 IU/L
Alanine aminotransferase (ALT) 188 IU/L
Aspartate aminotransferase (AST) 220 IU/L
Gamma glutamyltransferase (GGT) 129 IU/L
1. What biochemical abnormalities are shown?
2. Explain to the examiners the dierent types of jaundice
and give examples of the causes of each type.
3. Which type is this patient's likely to be from the blood
results?
4. Closer questioning reveals that the patient has devel-
oped abnormal stools which are pale, oat and are difcult to ush away. What other condition is the patient
likely to have developed?
OSCE Scenario 22.8
An 82-year-old male is brought into the emergency department with an acutely painful right leg. e symptoms
include the leg feeling cold, looking very pale and pins and
needles. e patient’s ECG is shown below (Fig. 22.8Q).
1. What is the likely diagnosis?
2. What are the causes?
3. What other symptoms can occur and which are the
most clinically important?
4. What investigations would you perform?
5. Are you aware of any classication systems for this
condition?
6. If the patient had a paralysed and insensate leg with a
purple discolouration which did not blanch under pressure, what would be the likely management plan?
OSCE Scenario 22.9
A 56-year-old male is admitted with severe dehydration
and vomiting, his urea and creatinine are raised at 15
mmol/L and creatinine at 215 μmol/L. A blood gas shows
the following abnormalities: pH 7.55, PO2 10.9 kPa, CO2
6.9 kPa and HCO3 is 21.
1. What type of metabolic abnormality is this patient
displaying?
2. How has it occurred?
3. e patient has a ‘sucsussion splash’ on examination –
what is the diagnosis?
4. How would you manage this condition?
OSCE Scenario 22.10
A 62-year-old male is in the A&E department and is complaining of epigastric pain. is feels like his normal heartburn but has not been relieved by antacids. In addition he is
sweating and has a bradycardia. An ECG is performed and
shows raised ST segments.
Fig. 22.8Q ECG from an 82-year-old patient.
1. From the history, what type of myocardial infarction is
3. Why is it common to see a bradycardia?
the patient having and in what leads would you expect
to see the ST segment rises?
2. Which coronary artery is involved?
Answers in Appendix pages 484–489
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
SECTION IV
Данная книга находится в списке для перевода на русский язык сайта https://meduniver.com/
Appendix
OSCE Scenario Answers, 431
430
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