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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_1093_Библиотеки_им_академика_М_И_Перельмана.pdf
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
RISK FACTORS
● Smoking.
● Alcohol.
● Achalasia.
● Barrett’s oesophagus (for adenocarcinoma).
● Oesophageal web.
CLINICAL FEATURES (MAY BE ASYMPTOMATIC UNTIL LATE IN DISEASE)
● Progressive dysphagia from solids to liquids.
● Weight loss, loss of appetite.
● Regurgitation +/– cough.
● Few physical signs – cachexia +/– enlarged supraclavicular lymph node.
DIAGNOSIS Made with OGD and biopsy (although can be seen with barium
swallow). Further imaging: CT scanning for staging.
MANAGEMENT
● Treatment: surgical resection +/– radiotherapy or chemotherapy.
● Palliative options include endoscopic dilation and stenting.
Overall prognosis is poor ≈ 5% survival rate at fi ve years.
Barrett’s oesophagus
Transformation of the lower squamous epithelium of the oesophagus to columnar
gastric epithelium. This is a premalignant condition. Predisposing factors: gastrooesophageal refl ux. Presentation: often with dyspepsia or as an incidental fi nding
at endoscopy. Management: regular screening OGD and biopsy for malignant
change.
Hiatus hernia
Abnormal protrusion of the the stomach through the oesophageal opening in the
diaphragm, leading to a more proximally placed oesophageal-gastric (O-G) junction.
≈ 3/4 are sliding (i.e. the O-G junction and stomach pass through the opening) and
1/4 are rolling (i.e. the O-G junction remains below the opening, with the cardia
of the stomach only passing through it). Incidence: very common. Predisposes to
gastro-oesophageal reflux. Diagnosis: made on OGD or barium swallow.
Achalasia
An oesophageal disorder characterised by failure of normal peristalsis, failure of
relaxation of the lower oesophageal sphincter (LOS) and an increased LOS resting
tone; caused by an abnormality of the myenteric plexus.
PRESENTATION Can occur at any age; initial symptom is typically dysphagia
(usually to liquids earlier than solids); other symptoms include regurgitation and
chest pain.
INVESTIGATIONS Barium swallow shows a dilated tapering oesophagus; oesophageal
manometry shows a high LOS resting tone.
MANAGEMENT Conservative unless symptoms are severe. Treatment options
include: botox injection; endoscopic LOS dilatation and surgery, e.g. Heller’s
myotomy.
54
GASTROENTEROLOGY
Gastro-oesophageal reflux disease (GORD)
Caused by failure of the normal anti-reflux mechanisms, e.g. in hiatus hernia. Risk
factors: alcohol or caffeine intake, obesity, smoking, pregnancy.
CLINICAL FEATURES
● Retrosternal chest pain (‘heartburn’) typically worse on lying down.
● Regurgitation of acid/water.
DIAGNOSIS Made with oesophageal pH monitoring.
MANAGEMENT
● Lifestyle modification: avoid alcohol, stop smoking, weight loss, dietary
changes.
If symptoms persist: H
●
Surgery (Nissen fundoplication) in select cases.
●
antagonist or PPI and investigate with OGD.
2
Oesophageal web (Plummer-Vinson syndrome)
Premalignant condition. More common in women and associated with iron
deficiency. Gives rise to symptoms of dysphagia. Management is with iron
replacement and endoscopic dilation in select cases.
Oesophageal stricture
Narrowing of the oesophagus, normally presenting with dysphagia. Causes:
oesophageal carcinoma, chronic GORD, chemical ingestion. Management: treat
underlying cause; consider endoscopic dilatation.
Pharyngeal pouch
Diverticulum of the pharyngeal muscosa through a weakness in the wall between the
thryopharyngeus and cricopharyngeus. Presentation: typically with abnormal fetor
and dysphagia or complications such as aspiration. Diagnosis is confi rmed with
barium swallow. Management: pouch can be excised surgically if problematic.
4.2. Disorders of the stomach
Peptic ulcer disease (gastric and duodenal ulcers)
Aetiology: due to acid oversecretion. More common in men (3:1).
RISK FACTORS
● Helicobacter pylori infection.
Smoking.
●
● Drugs (NSAIDs, corticosteroids).
● Stressful scenarios, e.g. major surgery.
CLINICAL FEATURES
● Dyspepsia, i.e. epigastric pain (classically: gastric ulcers – pain is worse with
eating; duodenal ulcers – pain is worse at night/hours after eating).
Complications: upper GI bleeding (see below) and perforation.
●
INVESTIGATIONS
● In the younger person investigate for H. pylori status (e.g. H.pylori breath test)
with eradication treatment is all that is normally required.
If >55 years and symptoms are new or persistent +/– associated warning
●
symptoms, e.g. weight loss/anaemia, urgent referral for investigation for
55
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
possible gastric carcinoma is necessary (OGD + biopsy + CLO test for H. pylori
status).
MANAGEMENT
● Remove any precipitating factors.
● Eradicate H. pylori if present: triple therapy with a PPI + two antibiotics (e.g.
amoxicillin and clarithromycin).
Consider longer term treatment with PPI.
●
Gastric carcinoma
More common in males (2:1), aged >50 years old. Usually adenocarcinoma, with
the pylorus/antrum being the most commonly affected sites.
RISK FACTORS Chronic gastric infl ammation, H. pylori infection, smoking.
CLINICAL FEATURES
● Dyspepsia.
● Weight loss, anorexia.
● Complications: upper GI bleeding or perforation.
INVESTIGATIONS
● OGD + biopsy.
● Staging CT scan.
MANAGEMENT
● Multi-disciplinary approach involving surgeons, oncologists, pain and
McMillan teams.
Surgery (partial or total gastrectomy) – curative if early stage. May also be
●
indicated for palliation in later stages.
Palliation – if advanced disease.
●
4.3. Upper gastrointestinal bleed
This refers to haemorrhage arising from the upper gastrointestinal tract proximal
to the ligament of Treitz. Usually this is a medical emergency, presenting with
haematemesis, coffee-ground vomiting or melaena.
Causes of upper GI bleeding
❍
Peptic ulcer disease
❍
Oesophageal varices
❍
Mallory-Weiss tear
PRESENTATION May be mild, e.g. Mallory-Weiss tear but often bleeding is severe
❍
Gastritis/oesophagitis
❍
Gastric/oesophageal tumours
leading to hypovolaemia and shock.
MANAGEMENT
● ABC – high flow oxygen, insert two large bore IV cannulae and fl uid resuscitate.
● Send urgent bloods for FBC, U&Es, LFTs, clotting and crossmatch six units
blood; transfuse as appropriate.
Catheterise +/– insert CVP line and monitor closely.
●
● Give IV PPI +/– vasoactive drug, e.g. vasopressin or octreotide.
● OGD for diagnosis of source of bleeding, +/– intervention: banding/
sclerotherapy of oesophageal varices; injection of ulcers with adrenaline.
56
GASTROENTEROLOGY
● Consider balloon tamponade (Sengstaken-Blakemore tube) – can provide
temporary haemostasis in variceal bleeding.
Involve ITU and general surgical teams if bleeding is severe/uncontrolled.
●
4.4. Coeliac disease (gluten-sensitive enteropathy)
Aetiology: gluten intolerance (Note: gluten is found in rye, wheat and barley) leading
to villous atrophy in the proximal small bowel and consequently malabsorption.
Common and often undiagnosed for several years. Associations: increased incidence
among those of Irish descent and with certain HLA types, e.g. HLA-B8.
CLINICAL FEATURES
● Diarrhoea/steatorrhoea.
● Weight loss, general malaise.
● Abdominal discomfort +/– nausea/vomiting.
● Anaemia.
● Complications: increased risk of malignancy particularly small bowel
lymphoma, dermatitis herpetiformis, peripheral neuropathy.
INVESTIGATIONS AND MANAGEMENT
● Micro- or macrocytic anaemia due to iron or folate deficiency (may have both).
● Autoantibodies: anti-gliadin, anti-endomysial, anti-tissue transglutaminase.
● OGD + jejunal biopsy.
● Management – strict adherence to a gluten-free diet.
4.5. Malabsorption
Usually causes diarrhoea and non-specific symptoms such as weight loss and
lethargy.
Causes of malabsorption
❍
Coeliac disease
❍
Other causes of villous atrophy, e.g. Whipple’s disease
❍
Small bowel resection
❍
Bacterial overgrowth
❍
Chronic GI infections, e.g. giardiasis
❍
Chronic pancreatitis
❍
Cystic fibrosis
4.6. Diarrhoea
Multiple definitions: increased amount, increased frequency or decreased consistency
of stool.
Causes of diarrhoea
❍
GI infections – see ID section
❍
Colorectal cancer
❍
Diverticular disease
❍
Inflammation, e.g. inflammatory bowel disease
❍
Malabsorption – see above
❍
Irritable bowel syndrome – see below
❍
Ischaemic colitis
❍
Drug reactions
❍
Autonomic neuropathy
❍
Laxatives
57
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
Causes of bloody diarrhoea: inflammatory bowel disease, GI infections (dysentery),
colorectal cancer, ischaemic colitis.
4.7. Constipation
Multiple definitions: decreased amount, decreased frequency, or harder stools.
Causes of constipation
❍
Obstruction, e.g. colorectal cancer, diverticular disease
❍
Decreased motility, e.g. neurological disorders
❍
Drugs, e.g. opiates, anticholinergics
❍
IBS (a diagnosis of exclusion)
❍
Low-fi bre diet
Investigation and treatment of the underlying cause is necessary; laxatives can be
useful for symptomatic relief. Types of laxatives include: bulk-forming agents, faecal
softeners, stimulants (e.g. senna), or osmotics (e.g. lactulose).
4.8. Inflammatory bowel disease (IBD)
Peak incidence is between the ages of 20 to 40 years. Two disorders cause chronic
inflammation and although there is overlap they have distinct features:
Crohn’s disease
●
Ulcerative Colitis (UC).
●
.
Both conditions are associated with HLA-B27 and ankylosing spondylitis. In addition,
there is an increased risk of colorectal cancer (more for UC than Crohn’s).
Crohn’s disease
Incidence M=F. Can affect any area of the GI tract from the mouth to the anus. The
terminal ileum is the most commonly affected site. Different areas of bowel can be
affected at the same time with normal bowel intervening, i.e. skip lesions.
HISTOLOGICALLY Transmural disease (i.e. whole thickness of the bowel is affected)
with non-caeseating granuloma.
CLINICAL FEATURES
● Abdominal pain (often right iliac fossa).
● Weight loss.
● Diarrhoea (may be bloody).
● Fever, malaise and anorexia in acute episodes (‘fl are-ups’).
● Aphthous ulcers (mouth/anus).
● Perianal skin tags, abscesses and fi stulae.
● Malabsorption (e.g. of vitamin B12 due to terminal ileal disease).
● Anaemia (which can be due to iron or B12 defi ciency).
● Extra-intestinal disease:
◗ clubbing
◗ arthritis
◗ nephrolithiasis
◗ eye problems (e.g. uveitis)
◗ skin disorders (e.g. erythema nodosum).
INVESTIGATIONS
● Barium follow-through (to image small intestine) or barium enema (to
58
GASTROENTEROLOGY
image large intestine) – for strictures or ulceration (so-called ‘cobblestone’
appearance).
Upper GI endoscopy/colonoscopy (depending on symptoms) +/– biopsy.
●
Ulcerative colitis (UC)
Involves the large bowel only (although the terminal ileum can also be affected
in a ‘backwash ileitis’). The rectum is always involved and the disease progresses
proximally.
HISTOLOGICALLY Only the mucosa and submucosa are involved with ulceration
and the presence of crypt abscesses, pseudopolyps and goblet cell depletion.
CLINICAL FEATURES
● Bloody diarrhoea with mucus.
● Abdominal pain.
● Weight loss.
● Anaemia (usually due to iron defi ciency).
● Extra-intestinal disease: skin disorders (e.g. pyoderma gangrenosum), increased
incidence of primary sclerosing cholangitis.
Complications: toxic megacolon in acute presentations +/– perforation.
●
INVESTIGATIONS
● Sigmoidoscopy or colonoscopy + biopsy.
● Barium enema: shows loss of haustra (‘lead pipe’ colon), pseudopolyps.
● If suspect toxic megacolon then serial abdominal x-rays should be performed
to monitor progression/resolution.
MANAGEMENT: SIMILAR FOR BOTH CROHN’S DISEASE AND UC
● Hospital admission may be required for acute ‘fl are-ups’: fl uid resuscitation
and steroids +/– antibiotics +/– serial AXR if toxic megacolon; and surgery may
form part of the management.
Medical treatment options:
●
◗ aminosalicylates, e.g. mesalazine and olsalazine
◗ steroids, e.g. oral prednisolone or topical for proctitis
◗ steroid-sparing agents, e.g. azathioprine
◗ newer agents, e.g. infl iximab (anti-TNF-alpha).
● Surgery: indicated if recurrent obstructive symptoms and fi stulae.
Irritable bowel syndrome (IBS)
Functional bowel disorder. Diagnosis of exclusion. More common in women.
CLINICAL FEATURES
● Abdominal pain +/– bloating typically relieved by defaecation or the passage of
wind.
Alternating bouts of constipation and diarrhoea.
●
MANAGEMENT
● Exclude other bowel pathology then reassure.
● Advise dietary modifications, e.g. high fibre diet and antispasmodics, e.g.
mebeverine.
59
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
4.9. Jaundice
Yellow pigmentation of the skin, sclera and mucous membranes due to an
accumulation of unconjugated or conjugated bilirubin. Observed clinically when
the serum bilirubin is >30 µmol/l. Can be classified as pre-hepatic, hepatic or posthepatic (cholestatic or obstructive)
Pre-hepatic jaundice
Occurs due to excess bilirubin production from any cause. Plasma bilirubin is
predominantly unconjugated.
Causes of pre-hepatic jaundice
❍
Haemolysis, e.g. haemolytic anaemia (see Haematology section for causes)
❍
Neonatal jaundice
Hepatic jaundice
Occurs due to hepatocellular damage. Normally both unconjugated and conjugated
bilirubin are present in the plasma.
Causes of hepatic jaundice
❍
Viral hepatitis (hepatitis A, B, C, D and E, CMV, EBV)
❍
Alcohol
❍
Liver metastases
❍
Cirrhosis (see below)
❍
Drugs, e.g. paracetamol
❍
Metabolic, e.g. Wilson’s disease, haemochromatosis, alpha-1-antitrypsin deficiency
❍
Autoimmune, e.g. autoimmune hepatitis
Post-hepatic jaundice
Due to obstruction of the bile ducts either intra- or extrahepatically (cholestasis)
(see Obstructive jaundice section under General Surgery). Primarily conjugated
bilirubin found in the plasma.
Note there are a number of congenital disorders that cause jaundice: Gilbert’s syndrome
(relatively common and otherwise asymptomatic, jaundice may only appear during
intercurrent illness), Crigler-Najjar syndrome, Dubin-Johnson syndrome, Rotor’s
syndrome.
CLINICAL FEATURES
● Yellow pigmentation of the sclera, skin and mucous membranes.
● Take a detailed history for: recent blood transfusion, body piercing, intravenous
drug abuse, jaundiced contacts, sexual history, recent travel abroad, excess
alcohol intake, drug use (including non-prescription).
Look for signs of underlying disease causing jaundice, e.g. chronic liver disease.
●
INVESTIGATIONS Initial investigations.
LFTs: raised bilirubin (check if unconjugated or conjugated). If ALT and
●
AST high, then likely hepatic jaundice; if ALP and GGT raised, then likely
obstructive jaundice.
Urinalysis: pre-hepatic – increased urobilinogen but no bilirubin; obstructive –
●
no urobilinogen but positive for bilirubin.
Abdominal ultrasound for cholelithiasis, hepatomegally etc.
●
60
GASTROENTEROLOGY
Further investigations are guided by findings on initial investigation.
Pre-hepatic: investigate for haemolysis: see Haematology section.
●
Hepatic: ‘Liver screen’: viral serology (A, B, C, CMV, EBV), serum ferritin/iron
●
studies (for haemochromatosis), copper/caeruloplasmin (for Wilson’s disease),
autoantibodies (ANA, anti-mitochondrial, anti-smooth muscle), AFP (raised in
hepatocellular carcinoma); consider liver biopsy.
Post-hepatic: depends on ultrasound findings: if evidence of duct dilation,
●
patient will need MRCP +/– ERCP; Consider CT abdomen if no gallstones seen
and cancer of the pancreas suspected; if no duct dilation consider liver biopsy.
4.10. Ascites
Accumulation of free fluid within the peritoneal cavity. Can be classified as either a
transudate (<30 g/l) or an exudate (>30 g/l) depending on protein content.
Causes of ascites
❍
Exudate (mnemonic is IMP ): Infection (bacterial or TB), Malignancy, Pancreatitis
❍
Transudate (mnemonic is PRINT ): Portal hypertension (e.g. due to cirrhosis), Right-
sided heart failure, IVC obstruction, Nephrotic syndrome, Thrombosis of the portal
vein (Budd-Chiari syndrome)
On examination: there is abdominal distension with evidence of shifting dullness.
INVESTIGATIONS Investigate for underlying cause: perform diagnostic ascitic tap
(for albumin, total protein, amylase, blood, WCC, MC&S and cytology).
MANAGEMENT Treat underlying cause. Consider paracentesis (+/– IV albumin
replacement) for tense ascites. For transudates: fluid restriction, low salt intake and
diuretics, e.g. spironolactone, may be helpful.
4.11. Cirrhosis
This is irreversible liver damage, characterised and defined histologically by loss of
normal liver architecture, fibrosis and nodular regeneration and represents the fi nal
pathway for a number of chronic liver diseases.
Causes of cirrhosis
❍
Alcohol
❍
Hepatitis B, B and D, or C
❍
Autoimmune hepatitis
❍
Cryptogenic (idiopathic)
❍
Metabolic: haemochromatosis, Wilson’s disease, alpha-1 anti-trypsin deficiency
❍
Primary biliary cirrhosis
CLINICAL FEATURES There may be signs of chronic liver disease (although some
patients will have no signs).
Jaundice.
●
● Hands: clubbing, leuconychia, Dupuytren’s contracture, palmar erythema.
● Asterixis (‘liver fl ap’).
● Foetor hepaticus.
● Over upper body: spider naevi (>5 is abnormal), gynaecomastia, loss of axillary
hair, caput medusae (distended abdominal veins).
On abdominal and genital exam: ascites, liver is usually small and not palpable,
●
testicular atrophy, loss of pubic hair.
61
ESSENTIAL NOTES FOR MEDICAL AND SURGICAL FINALS
COMPLICATIONS Portal hypertension (see below), hepatic encephalopathy,
hepatorenal syndrome, hepatocellular carcinoma, ascites.
Portal hypertension
Commonly due to cirrhosis but other causes include portal vein thrombosis, Budd-Chiari
syndrome and heart disease (right-sided heart failure, constrictive pericarditis). May be
asymptomatic or present with:
❍
varices with a risk of subsequent upper GI bleeding
❍
ascites
❍
splenomegaly
INVESTIGATIONS
● Blood tests: abnormal LFTs, hypoalbuminaemia, abnormal clotting.
● Tests to identify the cause.
● Abdominal ultrasound.
● Liver biopsy – required for defi nitive diagnosis.
MANAGEMENT
● Treat the underlying cause (e.g. alcohol cessation) and complications.
● Refer to a specialist for consideration for liver transplantation in select cases.
4.12. Chronic hepatitis
Inflammation of the liver lasting longer than six months. Often classified into two
types:
Chronic persistent hepatitis
Relatively benign and patients normally recover spontaneously over months to
years. Patients are generally asymptomatic without signs of chronic liver disease.
Blood tests: show raised ALT and AST. Cause in the majority of cases is viral hepatitis
(B, B+D or C).
Chronic active hepatitis
Normally progresses to cirrhosis and liver failure. Histologically, piecemeal and
bridging necrosis of the liver with later fibrosis seen. Blood tests: show raised ALT
and AST. Causes include: alcohol, hepatitis B, B+D or C, autoimmune hepatitis,
haemochromatosis, Wilson’s disease, alpha-1 anti-trypsin defi ciency.
4.13. Alcoholic liver disease (ALD)
Alcohol may cause a number of problems of increasing severity in the liver:
Alcoholic steatosis – fatty change, reversible if patient stops drinking.
●
● Alcoholic hepatitis – may present acutely with jaundice, tender hepatomegaly,
vomiting, fever and general malaise.
Alcoholic cirrhosis.
●
INVESTIGATIONS
● Abnormal LFTs: raised bilirubin, AST >ALT, GGT; raised serum ferritin.
● Liver biopsy.
MANAGEMENT
● Abstinence from alcohol (and if acute presentation, treatment of withdrawal).
● Treatment of complications of cirrhosis.
● Surgery: consider liver transplantation in select cases.
62
GASTROENTEROLOGY
4.14. Autoimmune hepatitis
More common in women (3:1), and presents from a young age. Associated with
other autoimmune conditions, e.g. Hashimoto’s thyroiditis, Sjögren’s syndrome and
ulcerative colitis. Presentation: produces a chronic active hepatitis with insidious
onset of features of chronic liver disease. A minority of patients present with an
acute hepatitis.
INVESTIGATIONS
● Signs of inflammation: raised ESR/CRP.
● Abnormal LFTs: raised bilirubin, AST and ALT (and later on low albumin).
● Raised serum IgG.
● ANA and anti-smooth muscle antibodies present in the majority of cases, anti-
liver and kidney microsomal (LKM) antibodies may also be present.
Liver biopsy may show signs of chronic active hepatitis.
●
MANAGEMENT
● Medical therapy: prednisolone +/– azathioprine.
● Treat complications of cirrhosis.
● Surgical: consider liver transplantation.
4.15. Metabolic liver disease
Wilson’s disease
Rare, inherited autosomal recessive disorder of copper metabolism (ATP 7B on
chromosome 13), leading to the accumulation of copper, e.g. liver, basal ganglia.
CLINICAL FEATURES
● Liver disease: acute or chronic active hepatitis, cirrhosis.
● Neurological disease: extrapyramidal syndrome most common presentation.
● Eyes: Kayser-Fleischer rings (deposition of copper in Descemet’s membrane).
INVESTIGATIONS AND MANAGEMENT
● Abnormal LFTs.
● Reduced serum caeruloplasmin (and usually reduced serum copper).
● 24 hour urine collection: excess urinary copper excretion.
● Liver biopsy demonstrates copper deposition.
● Medical therapy: penicillamine is fi rst line.
● Treat complications of cirrhosis.
● Surgery: consider liver transplantation.
Haemochromatosis
An inherited autosomal recessive disorder of iron uptake (HFE on chromosome 6),
leading to excess iron deposition.
CLINICAL FEATURES
● Liver disease.
● Skin: bronze pigmentation.
● Pancreas: diabetes.
● Heart: cardiomyopathy.
● Joints: arthritis.
INVESTIGATIONS AND MANAGEMENT
● Abnormal LFTs; raised serum ferritin and iron.
63