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gast22

VIEWS: 4 PAGES: 44

									Nem’s Notes…                                                                      Phase 2 Year 2


GASTROENTEROLOGY 1 (page 1 of 4)
Oropharynx & Oesophagus

Oral Ulceration Causes: (a) Gastrointestinal           Crohn’s Disease
                                                       Ulcerative Colitis
                                                       Coeliac Disease
                                                       Lupus Erythematosus (systemic/discoid)
                                                       Behçet’s Disease
                          (b) Dermatalogical           Lichen Planus
                                                       Erythema Multiforme
                                                       Dermatitis Herpetiformis
                          (c) Viral                    HSV
                                                       Coxsackie
                          (d) Bacterial                Syphilis
                                                       TB
                          (e) Trauma                   Poorly Fitting Dentures
                                                       Harsh Brushing
                                                       Sharp Teeth


Differential     The differential diagnosis for white patches in the mouth is:
Diagnosis                 (a) Ulceration (apthous)
                          (b) Neoplastic Lesion
                          (c) Candida (Oral lichen planus/thrush)
                          (d) Systemic Lupus Erythematosus (SLE)
                          (e) Leukoplakia


Xerostomia       Xerostomia is due to decreased salivation causing a dry mouth. Causes include:
                         (a) Sjörgen’s Syndrome
                         (b) Drugs (anti-Parkinson’s, antihistamine, lithium, antidepressants)
                         (c) Radiotherapy
                         (d) Psychogenic Causes
                         (e) Dehydration, Shock, Renal Failure


Oesophagitis     Oesophagitis is inflammation of the oesophagus. Causes include:
                        (a) Gastrooesophageal Reflux Disease (GORD)
                        (b) Infection
                        (c) Neoplastic Disease
                        (d) Swallowed Corrosives


Hiatus Hernia    There are two type of hiatus hernia

                 (a) Sliding (80%)                             (b) Rolling/Paraoesophageal (20%)

                                       Stomach slides                            Herniated sac trapped
                                       through diaphragm                          next to oesophagus


                   Diaphragm                                     Diaphragm




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 1 of 44
Nem’s Notes…                                                                     Phase 2 Year 2


GASTROENTEROLOGY 1 (page 2 of 4)
Oropharynx & Oesophagus

GORD           (a) Smoking                (f) Obesity
Risk Factors   (b) Alcohol                (g) Tight clothes
               (c) Dietary Fat            (h) Big Meals
               (d) Coffee                 (i) Surgery in Achalasia
               (e) Pregnancy              (j) Hiatus Hernia


Mechanisms     (a)      Low resting lower oesophageal sphincter (LOS) tone which does not
of GORD                 increase on lying flat (as is normal)
               (b)      LOS tone does not increase due to raised intraabdominal pressure (eg
                        pregnancy or tight clothing)
               (c)      Decreased peristalsis resulting in decreased acid clearance. Exacerbated by
                        hiatus hernia which traps acid in the hernial sac.
               (d)      Decreased oesophageal mucosal resistance to acid
               (e)      Hiatus hernia preventing the ‘pinchcock’ mechanism of diaphragm
               (f)      Delayed gastric emptying increasing chance of reflux


Treatment      (a) Drugs                  Magnesium Trisilicate
of GORD                                   Alginate containing antacids (Gaviscon)
                                          H2 receptor antagonists (Ranitidine/Cimetidine)
                                          Proton Pump inhibitors (Omeprazole)
                                          Prokinetic agents (Cisapride)
               (b) Helicobacter Pylori    Eradication (H. pylori can cause increased acid secretion
                                          in some patients)
               (c) Surgery                Hernia Repair (Laparoscopically)
                                          Anti-reflux Surgery (Fundoplication)


Effect of      (a) Heartburn due to stimulation of hypersensitive oesophageal mucosa by acid/heat
Oesophagitis   (b) Haematemesis, Iron deficiency anaemia from blood loss.
               (c) Regurgitation of food and acis into the mouth


Reflux &       There is a poor correlation between the degree of oesophagitis and heartburn due to
Oesophagitis   acid reflux, although oesophagitis is caused by irritation of the oesophagus.


Barrett’s      Barrett’s oesophagus is defined as oesophagus containing > 3cm of specialised
Oesophagus     columnar epitheilum extending up into the lower oesophageal mucosa. For this
               reason it is also known as columnar-lined oesophagus. It is usually due to long
               standing acid reflux, and is premalignant for adenocarcinoma ( Risk x40). Loss of the
               p53 tumour suppressor gene may be important.


Heartburn      Heartburn is a burning retrosternal pain anywhere between the epigastrium to the
               throat, characteristically worsening on stooping, lying, hot drinks and relieved by
               antacids. The differential diagnosis is MI or IHD.


Reflux         Reflux is a normal event occurring when gastric contents make contact with the lower
               oesophageal mucosa. It causes symptoms when the anti-reflux mechanisms fail to
               reduce acid contact time. This can cause heartburn, oesophagitis, barrett’s
               oesophagus, but may be asymptomatic until an episode of haematemesis or chronic
               anaemia.




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 2 of 44
Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 1 (page 3 of 4)
Oropharynx & Oesophagus

Dysphagia            Dysphagia is defined as difficulty swallowing. Causes include:
                            (a) Disease of Mouth & Tongue (eg tonsillitis)
                            (b) Neuromuscular Disorders (pharyngeal disorders, myasthenia gravis)
                            (c) Oesophageal Motility Disorders (achalasia, scleroderma, DM)
                            (d) Extrinsic Pressure (mediastinal glands, goitre, enlarged left atrium)
                            (e) Intrinsic Lesion (foreign body, stricture)
                            (f) Lower Oesophageal Rings


Management of (a) Drug treatment (see above)
Reflux Disease (b) Decrease intraabdominal pressure (lose weight, braces instead of belts)
               (c) Smaller low fat meals and no food <3hrs before bed
               (d) Regular endoscopic surveillance for Barrett’s
               (e) Multiple biopsies for detection of dysplasia
               (f) Oesophageal resection or Laser ablation if abnormalities found.


Oesophageal          (a) Benign        Leiomyoma
Tumours                                Squamous Papilloma
                     (b) Malignant     Squamous Carcinoma
                                       Adenocarcinoma


Epidemiology         High incidence in China, parts of Africa and Caspian regions of Iran.
Oesophageal Tumour   In UK oesophageal carcinoma has an incidence of 5-10 per 100,000 .
                     It represents 2.2% of all malignant disease in the UK.


Risk Factors         (a) Male
Oesophageal Tumour   (b) Heavy alcohol intake
                     (c) Heavy smoking
                     (d) Plummer-Vinson syndrome
                     (e) Achalasia
                     (f) Coeliac disease


Clinical             (a) Progressive and unrelenting dysphagia (first solids then liquids)
Appearance           (b) Weight loss secondary to dysphagia
Oesophageal Tumour   (c) Anorexia secondary to dysphagia
                     (d) Cough and aspiration of saliva into lungs (due to dysphagia)
                     (e) Lymphadenopathy in metastatic disease


Pathway of           (a) Ulcerative direct invasion of surrounding tissue
Spread               (b) Lymphatic spread
Oesophageal Tumour   NB Metastases rarely found on autopsy


Investigation        (a) Barium Swallow
Oesophageal Tumour   (b) Oesophagoscopy
                     (c) CT Scan of thorax and abdomen
                     (d) Endoscopic Ultrasound




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 3 of 44
Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 1 (page 4 of 4)
Oropharynx & Oesophagus

Management
Oesophageal Tumour
                      Treatment          Indication

                      Surgery            When tumour has not infiltrated beyond oesophageal wall


                      Radiotherapy       Squamous Carcinoma of upper two-thirds of the oesophagus


                      Chemotherapy       Often in combination with radiotherapy

                                         Stent dilatation of the oesophagus
                      Palliative
                                         Laser ablation
                      Therapy
                                         Alcohol injection

                     Overall 10% 5 yr survival; with treatment a 80% 5 yr survival is possible.


Achalasia            Achalasia is a motility disorder involving aperistalsis of the oesophagus and failure of
                     the LOS to relax, resulting in difficulty swallowing. Most cases are idiopathic. Often
                     degenerative lesions are found in the vagus. NO neurones are more affected than
                     cholinergic neurones causing lack of relaxation of the LOS. Two thirds of patients
                     have autoantibody against dopamine carrying protein.


Treatment            (a) Endoscopic dilatation of the LOS
Achalasia            (b) Endoscopic injection of botulinum toxin into the LOS
                     (c) Heller’s operation (laparoscopically) to divide muscle at lower end of oesophagus
                     (d) Nifedipine (20mg sublingually) in older patients


Motility             (a) Systemic Sclerosis (replacement of smooth muscle by fibrous tissue)
Disorders            (b) Diffuse Oesophageal Spasm

                     Symptoms:         (a) Atypical or non-cardiac chest pain due to lodged food.
                                       (b) Dysphagia is common
                                       (c) Regurgitation of food
                                       (d) Aspiration pneumonia secondary to (c)


Investigations of             (a) Barium swallow
the Oesophagus                (b) Chest X-Ray
                              (c) Ultrasonography
                              (d) CT Imaging of thorax/abdomen
                              (e) MRI Imaging
                              (f) Radionucleotide Imaging (detecting GORD)
                              (g) Endoscopy




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 4 of 44
Nem’s Notes…                                                                              Phase 2 Year 2


GASTROENTEROLOGY 2 (page 1 of 3)
Stomach & Duodenum

Acute Gastritis In acute gastritis there is an acute inflammatory infiltrate, predominantly of neutrophils,
                which invade the superficial gastric mucosa. There are various forms including:
                         (a) Acute erosive gastritis due to multiple small erosions
                         (b) Acute gastic ulceration due to multiple larger, less superficial erosions


Aetiology of    (a) Drugs NSAIDs esp aspirin
Acute Gastritis (b) Alcohol
                (c) Infection (CMV, HSV)
                (d) Stress
                (e) Secondary to burns (Curling ulcers)
                (f) Trauma, Shock, Renal failure


Complications       (a) Progression to chronic state
Acute Gastritis     (b) Ulceration
                    (c) Haemorrhage


Chronic             Chronic active gastritis consists of infiltration of the lamina propria with lymphocytes
Gastritis           plasma cells leading to atrophy of the mucosa and fibrosis.


Causes              (a) Helicobacter Pylori (main cause)
Chronic Gastritis   (b) Autoimmune (Pernicious anaemia – B12 malabsorption)
                    (c) Chronic Ingestion of NSAIDs/Aspirin
                    (d) Biliary Reflux


H. Pylori           Helicobacter Pylori initially causes acute gastritis leadin to chronic disease.
Infection           Infection causes: (a) Gastroduodenal Disease (duodenal ulcer)
                                      (b) Intestinal Metaplasia (gastric cancer)
                                      (c) Non-ulcer Dyspepsia


Complications       (a) H. Pylori infection     see above
                    (b) Autoimmune              pernicious anaemia
                    (c) Chronic NSAIDs          gastric erosion
                                                gastric ulcer


Peptic Ulcer        A break in the superficial epithelial cells penetrating down to the muscularis mucosa.
                    Ulcers can be either acute or chronic.

                    Acute caused by: (a) acute gastritis
                                     (b) complication of severe stress response
                                     (c) hyperacidity

                    Chronic causes: (a) H pylori infection
                                    (b) NSAIDs


Site of Ulcers      (a) Duodenum (mostly in duodenal cap)
                    (b) Stomach (mostly lesser curve)


Pathogenesis        (a) Gastric        (i) Destruction/loss of integrity of mucous barrier (reflux of bile)
Peptic Ulcer                           (ii) Increased acid secretion (not so important)
                    (b) Duodenal       (i) Increased acid production (due to H pylori)
                                       (ii) Infection causing metaplasia, inflammation and ulceration



more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 5 of 44
Nem’s Notes…                                                                             Phase 2 Year 2


GASTROENTEROLOGY 2 (page 2 of 3)
Stomach & Duodenum

Complications         (a) Perforation (spillage of gastric contents leading to peritonitis)
Peptic Ulcer          (b) Penetration (ulcer erodes into adjacent organ eg liver or pancreas)
                      (c) Haemorrhage (from eroded vessels)
                      (d) Pyloric Stenosis (obstruction due to oedema/scarring of ulcer)


Non-Ulcer             Non-ulcer dyspepsia is a common condition where the patient presents with
Dyspepsia             dyspepsia and other ulcer like symptoms but where investigation fails to find an ulcer.
                      Symptoms are mainly stress related and include:
                              (a) Indigestion
                              (b) Wind
                              (c) Nausea
                              (d) Early satiety
                              (e) Heartburn

                      Functional dyspepsia can be differentiated from peptic ulcer using the following table

                                          Functional Dyspepsia                Peptic Ulceration
                                          Diffuse all over                    Epigastric
                         Site of Pain
                                          Fits no recognisable pattern        Points with one finger
                          Frequency       Daily for long periods              Episodic
                                          Pain unaffected
                         Food/Meals                                           Exacerbates or helps pain
                                          Lasts all day
                           Antacids       No help                             Helps pain
                       Nocturnal Pain
                                          Rare                                Common
                       Waking Patient
                          Vomiting        No effect                           Relieves pain




Investigations        (a) Endoscopy
Non-Ulcer Dyspepsia   (b) Ultrasound (to detect gallstones)
                      (c) Detailed History (to detect psychogenic causes)


Management            (a) Explanation & Reassurance
Non-Ulcer Dyspepsia   (b) Encourage patient to stop smoking and drinking alcohol
                      (c) Drugs (antacids/prokinetics)
                      (d) Counselling for stress (eg marriage/divorce, financial/employment difficulties)
                      (e) Formal psychotherapy for major chronic psychological disorders


Gastric               Tumours of the stomach include:
Carcinoma                    (a) Benign leiomyoma
                             (b) Benign gastric polyps
                             (c) Malignant carcinoma
                             (d) Malignant lymphoma
                             (e) Malignant stromal tumour


Epidemiology          In the UK gastric carcinoma causes 12/13 deaths per 100,000
Gastric Carcinoma     More common in China, Japan, S America
                      Uncommon in USA even in Japanese migrants
                      More common in men
                      Incidence rises after 50 yrs of age




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 6 of 44
Nem’s Notes…                                                                           Phase 2 Year 2


GASTROENTEROLOGY 2 (page 3 of 3)
Stomach & Duodenum

Risk Factors        (a) Smoking
Gastric Carcinoma   (b) Alcohol
                    (c) H pylori
                    (d) Dietary factors (high salted, pickled, smoked food, low vitamin A and C)
                    (e) Autoimmune gastritis (pernicious anaemia)
                    (f) Adenomatous gastric polyps


Early Gastric       Most gastric cancers are quite advanced at time of initial diagnosis and only 45% of
Cancer              cases can be operated on. This accounts for the poor prognosis of gastric cancers.
                    Thus early diagnosis of symptoms is extremely important.

                    Gastric cancers can be classed as either:
                    (a) Early confined to mucosa or submucosa (90% 5yr survival)
                    (b) Late extending into muscle coats of stomach (10-15% 5yr survival)
                    Classification is independent of lymph node involvement.


Appearance          Endoscopically visible as slightly elevated plaque or shallow depression.
Gastric Carcinoma          (a) Intestinal Carcinoma glandular formation of mucous secreting
                                                          cells with well demarcated ‘pushing’ border
                           (b) Diffuse Carcinoma          chains of single cells with less well demarcated
                                                          border


Spread              (a) Direct (pancreas, transverse colon, liver, spleen)
Gastric Carcinoma   (b) Lymphatic (nodes of the left and right gastric arteries)
                    (c) Blood (via portal vein metastasising to the liver)




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 7 of 44
Nem’s Notes…                                                                           Phase 2 Year 2


GASTROENTEROLOGY 3 (page 1 of 4)
The Small Intestine

Coeliac Disease (also called Gluten-sensitive Enteropathy).


Epidemiology        (a) Common in Europe        1 in 1500 (UK)    1 in 300 (Ireland)
(Coeliac Disease)   (b) Rare in Black Africans
                    (c) Increased incidence (10-15%) in first-degree relatives
                    (d) Increased incidence (30%) in monozygotic twins
                    (e) Linked to specific HLA types (90% have HLA DQ2)

                    Therefore a mixture of genetic and environmental factors


Pathogenesis        Uncertain pathogenesis and may be due to a variety of possible factors such as:
(Coeliac Disease)           (a) Toxicity of α-Gliadin (a peptide product of gluten)
                            (b) Immunogenetic factors (due to high incidence with specific HLA types)
                            (c) Environmental factors (possibly a viral infection)


Pathology           Affects the mucosa of the proximal small bowel, but decreasing in severity from
(Coeliac Disease)   jejunum to ileum (since the gluten is broken down to smaller non-toxic fragments).
                              (a) Absence of villi at the mucosal surface
                              (b) Elongated crypts
                              (c) Chronic inflammatory cells found in lamina propria


Causes of       Subtotal (Flat)                (a) Coeliac Disease
Villous Atrophy                                (b) Dermatitis Herpetiformis
                                               (c) Zollinger-Ellison Syndrome (rare)
                                               (d) Hypogammaglobulinaemia (rare)
                    Partial (Convoluted)       (a) Tropical Sprue
                                               (b) Giardiasis


Clinical            Coeliac disease can present at any age. Symptoms are very variable & non-specific:
Features                     (a) Tiredness and malaise
(Coeliac Disease)            (b) Diarrhoea or Steatorrhoea
                             (c) Abdominal discomfort or pain
                             (d) Weight Loss
                             (e) Intermittent Mouth Ulcers
                             (f) Intermittent Stomatitis

                    Rare complications might include tetany, osteomalacia, gross malnutrition with
                    peripheral oedema.

                    Increased incidence of atopy and autoimmune disease such as thyroid disease and
                    IDDM. Other associated diseases are inflammatory bowel disease, chronic liver
                    disease.

                    There are usually few physical signs and are related to anaemia and malnutrition.


Investigation       (a) Endomysial antibodies (IgA)      Antibodies very specific and sensitive to coeliac
(Coeliac Disease)                                        disease and is carried out using
                                                         immunoflouresence on monkey oesophagus for
                                                         transglutamase antigen.
                    (b) Jejunal biopsy                   The mucosal appearance of the biopsy
                                                         is diagnostic for Coeliac Disease.
                    (c) Anti-reticulin antibodies        Antibodies also very sensitive but also present in
                                                         other GI diseases such as Crohn’s.
                    (d) Haematology                      Mild/moderate microcytic or macrocytic anaemia
                                                         in 50% of cases


more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 8 of 44
Nem’s Notes…                                                                           Phase 2 Year 2


GASTROENTEROLOGY 3 (page 2 of 4)
The Small Intestine

Treatment           The removal of gluten from diet results in rapid clinical and morphological
(Coeliac Disease)   improvement in patients with Coeliac Disease.


Complications       (a) Intestinal lymphoma
(Coeliac Disease)   (b) Ulcerative jejunitis
                    (c) Carcinoma



Malabsorption       Malabsorption is the reduced absorption of food due to either:
                    (a) intraluminal maldigestion (deficiency of enzymes)
                    (b) mucosal malabsorption (due to decreased surface area)
                    (c) postmucosal lymphatic obstruction (prevents uptake due to lymphatic blockage)

                    SEE Gastroenterology 6 (page 2 of 5)



Protein Losing Excessive loss of protein into the gut lumen sufficient to cause hypoproteinaemia
Enteropathy
               Causes: (a) With mucosal erosions/ulcerations
                                 (i) Crohn’s Disease
                                 (ii) Ulcerative Colitis
                                 (iii) Oesophageal, Gastric, Colonic Ulcer
                                 (iv) Lymphoma
                                 (v) Radiation Damage

                             (b) Without mucosal erosions/ulcerations
                                      (i) Ménétrier’s Disease
                                      (ii) Bacterial Overgrowth
                                      (iii) Coeliac Disease
                                      (iv) Tropical Sprue
                                      (v) Eosinophilic gastroenteritis
                                      (vi) SLE

                             (c) With lymphatic obstruction
                                       (i) Intestinal lymphangiectasia
                                       (ii) Constrictive pericarditis
                                       (iii) Lymphoma
                                       (iv) Whipple’s Disease



Bacterial           SEE Gastroenterology 6 (page 2 of 5)
Overgrowth
                     Causes of Bacterial Overgrowth
                     Hypo/Achlorhydria                   Pernicious anaemia
                                                         Partial gastrectomy
                     Decreased Motility                  Scleroderma
                                                         Diabetic autonomic neuropathy
                     Structural Abnormality              Gastric surgery (blind loops)
                                                         Jejunal diverticulosis
                                                         Enterocolic fistulae
                                                         Strictures
                     Impaired Immunity                   Hypogammaglobulinaemia




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 9 of 44
Nem’s Notes…                                                                     Phase 2 Year 2


GASTROENTEROLOGY 3 (page 3 of 4)
The Small Intestine

Intestinal     Effects:          (a) 30-50% resection can be tolerated
Resection                        (b) Gastric hypersecretion
                                 (c) Gallstones
                                 (d) Decreased fat absorption
                                 (e) Hyperplasia/hypertrophy of bowel (adaptation)
                                 (f) Increased bile salt synthesis (due to decreased absorption)
                                 (g) Pernicious anaemia (decreased B12 absorption)
                                 (h) Short gut syndrome

               Investigation:    (a) SBFT
                                 (b) B12 measurement
                                 (c) Bile salt measurement
                                 (d) Fat absorption tests

               Treatment:        (a) B12 replacement
                                 (b) Low fat diet for steatorrhoea
                                 (c) Cholestyramine or aluminium hydroxide for diarrhoea
                                 (d) Parenteral nutrition in short gut syndrome


Whipple’s      This is a rare disease usually affecting males who present with steatorrhoea, weight
Disease        loss, abdominal pain and fever.
               Villi are stunted and contain periodic acid-Schiff (PAS) positive macrophages
               (diagnostic). On electron microscopy bacilli can be seen within the macrophages.
               Treatment is with penicillin, tetracycline and sulphonamides.


Radiation      Radiation over 50 Gy will damage the intestine (usually the ileum and rectum due to
Enteritis      pelvic irradiation). Symptoms of diarrhoea and abdominal pain usually improve within
               6 weeks. Chronic radiation enteritis is diagnosed if symptoms persist for longer than 3
               months.

               There is muscle atrophy, ischaemic ulceration & obstruction due to fibrosed strictures.
               Malabsorption and bacterial overgrowth can occur. Treatment is symptomatic.


Meckel’s       Most common abnormality of the GI tract affecting 2-3% of the population where a
Diverticulum   diverticulum projects from the wall of the ileum. It is usually asymptomatic but 50%
               contain mucosa which secrete hydrochloric acid. Peptic ulceration and bleeding can
               occur. Acute inflammation may also occur which is indistinguishable from appendicitis.
               Treatment is surgical removal.


Amyloid        Systemic amyloidosis may cause amyloid deposits in the GI tract. Deposits in the
               small intestine result in diarrhoea.


Connective     Disorders of the connective tissue can affect the GI tract. Systemic sclerosis most
Tissue         commonly affects the oesophagus although occasionally the small bowel and colon. It
               is frequently asymptomatic but diarrhoea and steatorrhoea may occur due to bacterial
               overgrowth secondary to decreased motility, dilatation and presence of diverticulae.
               Rheumatoid arthritis and SLE may also cause GI problems.


Tumours
                Benign                           Malignant
                Adenomas                         Adenocarcinomas
                Leiomyomas                       Carcinoid Tumours
                Lipomas                          Leiomyosarcoma
                Hamartomas                       Lymphoma




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 10 of 44
Nem’s Notes…                                                                 Phase 2 Year 2


GASTROENTEROLOGY 3 (page 4 of 4)
The Small Intestine

Lymphoma      Predisposing Factors:    (a) Coeliac Disease
                                       (b) Crohn’s Disease
                                       (c) Immunoproliferative Small Intestine Disease

              Pathological Features:   (a) Most frequently found in ileum
                                       (b) Most common is B-cell derived lymphoma (from MALT)
                                       (c) Annular or polypoid masses
                                       (d) T-cell lymphomas are ulcerated plaques or proximal
                                       bowel strictures

              Clinical Features:       (a) Abdominal pain
                                       (b) Diarrhoea
                                       (c) Anorexia
                                       (d) Weight loss
                                       (e) Anaemia
                                       (f) May have a palpable mass

              Investigation:           (a) SBFT
                                       (b) USS
                                       (c) CT

              Treatment:               (a) Surgery
                                       (b) Radiotherapy
                                       (c) Chemotherapy


Carcinoid     Pathological Features:   (a) Originate from enterochromaffin cells of intestine
Tumour                                 (b) Common sites are appendix, terminal ileum and rectum

              Clinical Features:       (a) Small bowel obstruction
                                       (b) Intestinal ischaemia
                                       (c) Hepatic metastases (pain, hepatomegaly, jaundice)
                                       (d) Flushing/wheezing
                                       (e) Diarrhoea
                                       (f) Cardiac involvement
                                       (g) Facial telangiectasia

              Investigation:           (a) USS

              Treatment:               (a) Octreotide relieves flushing and diarrhoea
                                       (b) Surgical resection




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 11 of 44
Nem’s Notes…                                                                               Phase 2 Year 2


GASTROENTEROLOGY 4 (page 1 of 5)
Colon, Rectum & Anus

Diverticular             Diverticulosis              Presence of diverticula
Disease                  Diverticulitis              Inflammation of the diverticula
                         Diverticular disease        General term for disease involving diverticula
                         Diverticula                 Protrusions of gut mucosa covered by peritoneum and
                                                     present in 50% of patients over 50


Epidemiology             Found more commonly in populations with low intake of dietary fibre. This may be due
(Diverticular Disease)   to small volume stools which require higher intraabdominal pressure for propulsion
                         and may lead to herniation of mucosa. Female preponderance.


Pathology                (a) Protrusions of mucosa covered by peritoneum
(Diverticular Disease)   (b) Hypertrophy of circular muscle
                         (c) Inflammation can result from impaction of faecaliths
                         (d) Repeated inflammation leads to narrowing or obstruction of the lumen


Clinical                 (a) Usually asymptomatic (90% cases)
Features                 (b) May be associated with constipation or spasm
(Diverticular Disease)   (c) Colicky pain in left iliac fossa
                         (d) Can produce rectal bleeding
                         (e) Acute cases present with severe pain and fever


Complications            (a) Perforation leading to generalised peritonitis
(Diverticular Disease)   (b) Fistula formation into bladder or vagina
                         (c) Intestinal obstruction


Investigation            (a) Blood test may show PMN leucocytosis
(Diverticular Disease)   (b) Spiral CT
                         (c) Ultrasound
                         (d) Flexible sigmoidoscopy


Treatment                (a) Asymptomatic cases require no treatment
(Diverticular Disease)   (b) Acute cases treated with cephalosporin & metronidazole as outpatient
                         (c) Emergent cases may require surgery and bowel resection




Colonic Polyps Colonic polyps are protrusions above the colon epithelium and may be epithelial or
               mesenchymal.


Histology                Harmartomatous Polyps       Large, stalked.
(Colonic Polyps)         Inflammatory Polyps         Involve granulation due to excess regeneration during
                                                     inflammatory bowel disease.
                         Neoplastic Polyps           Can be either tubular or villous. Tubular polyps are small
                                                     (<10mm diameter), have numerous crypts, mucous-
                                                     secreting epithelium and are stalked. Villous polyps have
                                                     elongated villi with columnar epithelium.
                         Hyperplastic Polyps         Elongated crypts without dysplasia and a ‘serrated’ upper
                                                     surface to the crypts.
                         Lymphoid Polyps             ?




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 12 of 44
Nem’s Notes…                                                                               Phase 2 Year 2


GASTROENTEROLOGY 4 (page 2 of 5)
Colon, Rectum & Anus

Clinical Features                 Most polyps are asymptomatic and found when patients are investigated for
(Colonic Polyps)                  other GI tract disorders, such as pain, altered bowel habit, bleeding
                                  haemorrhoids etc.


Extraintestinal                   (a) Subcutaneous epidermoid cysts
Features                          (b) Lipomas
(Colonic Polyps)                  (c) Benign osteomas (esp skull and angle of mandible)
                                  (d) Desmoid tumours
                                  (e) Dental abnormalities
                                  (f) Congenital hypertrophy of retinal pigment epithelium (CHRPE)


Risk Factors                      (a) Large size (>2cm)
for Malignancy                    (b) Multiple polyps
(Colonic Polyps)                  (c) Villous architecture
                                  (d) Dysphasia


Adenoma-Carcinoma                 (a) Activation of Oncogenes
Sequence                          (b) Loss or mutation of tumour suppressor genes
                                  (c) Defective genes of the DNA repair pathway
                                  (d) Genomic instability



Colorectal Carcinoma

Epidemiology             (a) Rare in the underdeveloped world
(Colorectal Carcinoma)   (b) Common in Western populations (60 per 100,000 UK)
                         (c) Increasing incidence with increasing age (esp >50)


Risk Factors             Non-Dietary Factors                           Dietary Factors
(Colorectal Carcinoma)   (a) Colorectal adenomas                       (a) High red meat & saturated fat
                         (b) Chronic extensive ulcerative colitis      (b) Low fibre intake
                         (c) Acromegaly                                (c) Low fruit/veg intake
                         (d) Pelvic radiotherapy                       (d) Low calcium/folic acid intake
                         (e) Obesity and sedentary lifestyle
                         (f) Alcohol and tobacco use


Pathology                (a) Arise from an adenomatous polyp
(Colorectal Carcinoma)   (b) >50% in rectosigmoid region
                         (c) Lymphatic invasion common at presentation
                         (d) Metatases to liver through systemic/portal circulation


Duke’s Staging
(Colorectal Carcinoma)
                                                                                         % of     5 yr Survival
                          Stage                        Description
                                                                                        Cases         Rate
                            A      Tumour confined to bowel wall                         10%         90-100%

                            B      Beyond bowel wall but no metatases                    35%         65-75%

                            C      Involving lymph nodes                                 30%         30-40%
                                   Distant metatases or residual disease following
                            D                                                            25%          <5%
                                   surgery



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Nem’s Notes…                                                                                  Phase 2 Year 2


GASTROENTEROLOGY 4 (page 3 of 5)
Colon, Rectum & Anus

Clinical                 (a) Altered bowel habit
Features                 (b) Rectal bleeding
(Colorectal Carcinoma)   (c) Iron deficiency anaemia
                         (d) Bowel obstruction
                         (e) Weight loss


Management               (a) Surgical removal of tumour by resection
(Colorectal Carcinoma)   (b) Adjuvant chemotherapy for stage C colon cancer patients
                         (c) Combination radiotherapy for stage C rectal cancer patients


Prevention &             (a) Healthcare agencies advocate low-fat, high-fibre diet
Screening                (b) Endoscopic screening with polyp removal for families with FAP (Familial
(Colorectal Carcinoma)   Adenomous Polyposis) and HNPCC (Hereditary Non Polyposis Colon Cancer)
                         (c) Possible flexible sigmoidoscopy at age 55



Ischaemic                Caused by insufficient or blocked blood supply to the mesenteric arteries or veins
Colitis


Pathology                (a) Anoxic or hypoxic injury depending on adequacy of collateral supply
(Ischaemic Colitis)      (b) Cell death due to calcium ion movement through damaged membranes
                         (c) Free radical damage on reperfusion with oxygen (in non-occlusive cases)


Causes                   (a) Occlusive                 (i) Superior mesenteric embolus/thrombosis
(Ischaemic Colitis)                                    (ii) Mesenteric vein thrombosis
                         (b) Non-occlusive             (i) Systemic hypotension
                                                       (ii) Vasoconstriction
                                                       (iii) Viscosity disturbances
                                                       (iv) Arterial narrowing
                                                       (v) Pharmacological effects (eg digitalis, cocaine)


Clinical                 (a) Sudden Abdominal pain
Features                 (b) Passage of bright red blood with or without diarrhoea
(Ischaemic Colitis)      (c) Distended abdomen
                         (d) Signs of shock
                         (e) Signs of cardiovascular disease


Investigation            (a) Sigmoidoscopy to rule out bleeding from diverticular disease or ulcerative colitis
(Ischaemic Colitis)      (b) Barium enema to see characteristic ‘thumb-printing’ on colon wall


Complications            (a) May develop strictures
(Ischaemic Colitis)      (b) May develop gangrene


Treatment                (a) Treatment of cardiovascular problems
(Ischaemic Colitis)      (b) Surgery if required to resect bowel




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 14 of 44
Nem’s Notes…                                                                          Phase 2 Year 2


GASTROENTEROLOGY 4 (page 4 of 5)
Colon, Rectum & Anus

Megacolon &    Megacolon refers to a number of different congenital and acquired conditions where
Hirschsprung’s the colon is dilated.
Disease        Presents in first years of life when an aganglionic segment of the rectum gives rise to
               constipation and subacute obstruction.
               Anticholinesterase is increased. Failure of relaxation of the internal sphincter can be
               treated successfully with surgery.
               Treatment of megacolon is similar to constipation, but saline wash-outs and manual
               removal of faeces is sometimes required.


Solitary Rectal   Features             (a) Bowel Irregularity
Ulcer                                  (b) Rectal bleeding with the passage of mucous
                                       (c) Mainly due to excess straining at stool

                  Management           (a) Rectal exam
                                       (b) Sigmoidoscopy reveals redness/ulcer 10com from rectal margin
                                       (c) Histology is diagnostic – non-specific inflammatory changes
                                       (d) Treatment is unsatisfactory. Local steroids may help


Melanosis Coli &Pigmentation of mucosa (melanosis coli) caused by surreptitious laxative ingestion
Laxative Abuse Commonly seen in young females with anorexia or bulemia.

                  (a) Diarrhoea of high volumes (1 litre per day)
                  (b) Pigmented mucosa
                  (c) Histological rectal biopsy shows pigment-laden macrophages
                  (d) Phenolphthalein laxatives detected by NaOH poured onto stools


Faecal Impaction               Requires manual removal of faeces and care to prevent recurrence


Pruritis Ani      Causes               (a) Soiling of perianal skin
                                       (b) Local anal lesions eg infection of haemorrhoids
                                       (c) Hydrocortisone creams
                  Management           (a) Hygiene – weak local steroids mixed with antiseptic eg timodine


Haemorrhoids      Haemorrhoids are varicosities resulting from the dilatation of internal haemorrhoidal
                  venous plexus and require no treatment if minor. Otherwise treated with topical
                  emollients and high fibre diet.

                    Classification                                 Symptom
                         st
                     1 degree                                    Bleeding only
                         nd
                     2        degree     Prolapse at defaecation, but spontaneous return to anal canal
                         rd
                     3 degree                     Prolapse and requires manual replacement
                         th
                     4 degree                                  Can’t be replaced



Anal Fissures     Anal fissures result in painful defaecation and minor rectal bleeding. They can be
                  treated using local anaesthetic gels.




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 15 of 44
Nem’s Notes…                                                                      Phase 2 Year 2


GASTROENTEROLOGY 4 (page 5 of 5)
Colon, Rectum & Anus


Anal Abscess   Perianal abscesses develop between internal and external sphincters. They usually
& Fistulae     result from infection. Crohn’s is sometimes responsible. Symptoms include:
                         (a) Extreme perianal pain
                         (b) Fever
                         (c) Discharge of pus
               Spontaneous rupture may lead to fistulae. Abscesses are treated by surgical drainage
               and fistulae are laid open with car to avoid damage to the anal sphincters.



Faecal         Causes           (a) Faecal impaction with overflow diarrhoea
Incontinence                    (b) Anorectal       (i) rectal prolapse
                                                    (ii) anal stricture
                                                    (iii) haemorroidectomy
                                                    (iv) anal dilatation
                                                    (v) rectal carcinoma
                                (c) Post childbirth damage to pelvic floor innervation
                                (d) Neurological disorders (i) spinal trauma to S2-4
                                                               (ii) spina bifida
                                                               (iii) multiple sclerosis
                                (e) Senile dementia
                                (f) Congenital abnormalities of anus/rectum
                                (g) Impalement injuries
                                (h) Diabetes mellitus with autonomic involvement

               Management       Treatment for underlying causes is often unsatisfactory




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 16 of 44
Nem’s Notes…                                                                          Phase 2 Year 2


GASTROENTEROLOGY 5 (page 1 of 2)
Inflammatory Bowel Disease

Inflammatory  There are two major forms of non-specific inflammatory bowel disease. These are:
Bowel Disease         (a) Crohn’s Disease
                      (b) Ulcerative Colitis
              However, since their aetiology is unknown, they may in fact be manifestations of the
              same disease.



Epidemiology      (a) Crohn’s Disease         Incidence:         5-8 per 100,000 (and rising)
                                              Prevalence:        50-60 per 100,000

                  (b) Ulcerative Colitis      Incidence:         6-15 per 100,000 (relatively stable)
                                              Prevalence:        80-120 per 100,000

                  Both conditions are more common in the West, although have a worldwide distribution
                  suggesting combined environmental and genetic aspects to the conditions.



Pathogenesis      (a) Familial – Both conditions are more common in relatives of patients, than in the
                  general population. Crohn’s also has a high monozygotic twin concordance.
                  (b) Genetic – There are no HLA markers but HLA-B27 is increased in patients with
                  inflammatory bowel disease.
                  (c) Diet – There is little evidence of a dietary factor, although Crohn’s has been linked
                  to patients with high dietary sugar intake.
                  (d) Smoking – Patients with Crohn’s are more likely to be smokers whilst those with
                  Ulcerative Colitis are more likely to be non-smokers or ex-smokers.
                  (e) Infection – Possible infective agent theory behind Crohn’s, but no bacterium, virus
                  or parasite has been identified as being definitely linked. However two agents have
                  been investigated: (i) Measle’s virus; (ii) Mycobacterium.
                  (f) Multifocal gastrointestinal infarction due to granulomatous angiitis has been
                  suggested as a primary event in Crohn’s.
                  (g) Inducible nitric oxide synthase (iNOS) is expressed after activation by
                  mediators. It produces NO in acute colitis and could damage host cells.



Pathology         Crohn’s Disease may affect the whole bowel, but more commonly the small bowel.
Crohn’s Disease   Macroscopic:    (a) Affected parts of small bowel have thick wall and narrow lumen
                                  (b) Deep ulcers and fissures found in the mucosa
                                  (c) Fistulae and abscesses may be found in the colon
                                  (d) ‘Cobblestone’ appearance due to mucosal damage
                  Microscopic:    (a) Transmural inflammation (through all layers of mucosa)
                                  (b) Increased chronic inflammatory cells
                                  (c) Lymphoid hyperplasia
                                  (d) Granulomas in 50% of patients



Clinical          (a) Terminal ileum, colon, perianal region (but may affect any part of GI tract)
Features          (b) Abdominal pain
Crohn’s Disease   (c) Weight loss
                  (d) Diarrhoea



Intestinal        (a) Malabsorption
Complications     (b) Nutritional defects
Crohn’s Disease   (c) Bowel stenosis
                  (d) Fistulae




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Nem’s Notes…                                                                          Phase 2 Year 2


GASTROENTEROLOGY 5 (page 2 of 2)
Inflammatory Bowel Disease

Pathology            Ulcerative Colitis affects only the colon and rectum.
Ulcerative Colitis   Macroscopic:       (a) Superficial inflammation
                                        (b) Reddened, inflamed, easily bleeding mucosa
                                        (c) Ulceration and inflammatory polyps in severe cases
                     Microscopic:       (a) Chronic inflammatory cells in lamina propria
                                        (b) Crypt abscesses
                                        (c) Goblet cell depletion


Clinical             (a) Rectum and descending colon
Features             (b) Diarrhoea
Ulcerative Colitis   (c) Urgency
                     (d) Rectal bleeding


Intestinal           (a) Toxic megacolon
Complications        (b) Colorectal carcinoma
Crohn’s Disease




Natural History Inflammatory Bowel Disease is a relapsing disease. Without treatment patients will
                experience at least one exacerbation episode a year. 10-15% of those with ulcerative
                colitis, and 50% of those with Crohn’s, will require surgical resection.


Systemic             (a) Eyes            Conjunctivitis
Complications                            Scleritis
                                         Uvetis
                     (b) Joints          Monoarticular arthritis
                                         Ankylosing spondylitis
                     (c) Skin            Erythema nodosum
                                         Pyoderma gangrenosum
                     (d) Biliary tree    Sclerosing cholangitis


Differentials        (a) Infection (bacterial, viral, protozoal)
                     (b) Vascular disease
                     (c) Drugs
                     (d) Idiopathic


Investigations       (a) Sigmoidoscopy (typical eryhtema and ulcerated surface)
                     (b) Colonoscopy
                     (c) Biopsy for histology
                     (d) MRI or US
                     (e) Barium studies


Management           (a) Prednisolone for acute episodes
                     (b) 5-amino salicyclates for mild relapses and prevention
                     (c) Topical treatment
                     (d) Surgery (can cure ulcerative colitis)

                     There is no cure for Crohn’s Disease




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Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 6 (page 1 of 5)
Diarrhoea & GI Tract Infections

True Diarrhoea Increase in stool weight > 300g/24hrs usually accompanied by increased frequency
               Patients and doctors often define diarrhoea in different ways. Other frequent uses of
               the word are for loose stools or increased frequency.


Pathophysiology             (a) Osmotic Diarrhoea
                            The gut mucosa acts as a semipermeable membrane allowing fluid to enter
                            the gut if there are large quantities of hypertonic substances in the lumen
                            The diarrhoea usually stops after stopping eating.
                                       (i) Ingestion of unabsorbable purgative or substance
                                       (ii) Malabsorption
                                       (iii) Specific absorptive defect

                            (b) Secretory Diarrhoea
                            This mechanism is due to seretion of electrolytes and fluid into the gut as
                            well as decreased absorption. The diarrhoea does not stop when the patient
                            stops eating.
                                     (i) Enterotoxin (cholera, E. coli)
                                     (ii) Hormones (vasoactive intestinal peptide)
                                     (iii) Bile acids/fatty acids in colon after ileal resection
                                     (iv) Some laxatives

                            (c) Inflammatory Diarrhoea (Mucosal Destruction)
                            Damage to intestinal mucosal cells leads to loss of fluid and blood into the
                            lumen. In addition there is defective absorption of fluid and electrolytes.
                                      (i) Infection (dysentery due to shigella)
                                      (ii) Inflammatory bowel disease (ulcerative colitis)

                            (d) Abnormal Motility
                            Not a true diarrhoea since it is usually due to increased frequency rather than
                            volume or weight. It is due to abnormal upper gut motility.
                                     (i) Diabetes
                                     (ii) Post-vagotomy
                                     (iii) Hyperthyroid


Causes
                   Chronic                                      Acute
                   (a) Inflammatory Bowel Disease
                   (b) Parasitic/fungal infection
                   (c) Malabsorption                            (a) Dietary Indiscretion
                   (d) Gut resection                            (b) Infective
                                                                Food poisoning
                   (e) Drugs                                    Viral gastroenteritis
                   (f) Colonic neoplasia                        (c) Traveller’s Diarrhoea
                   (g) Endocrine                                E. coli
                   Panreatic tumour                             Giardia
                   Medullary carcinoma                          Shigella
                   Thyrotoxicosis                               Entamoeba histolytica
                   Diabetic neuropathy
                   (h) Faecal impaction in elderly


Investigations   Investigation is only required if the diarrhoea has lasted for more than 1 week. In
                 chronic diarrhoea investigation is always required. The basic repertoire of tests
                 include: (a) Stool culture and exam (cysts, parasites)
                          (b) Sigmoidoscopy
                          (c) Rectal biopsy
                          (d) Small bowel follow through (SBFT)
                          (e) VIP
                          (f) ERCP




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Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 6 (page 2 of 5)
Diarrhoea & GI Tract Infections

Malabsorption   Malabsorption is the decreased absorption of food from the gut leading to clinical
                symptoms and can be caused by the following mechanisms:
                        (a) Intraluminal maldigestion due to deficiency of bile or pancreatic
                        enzymes leading to inadequate solubilisation and hydrolysis.
                        (b) Mucosal malabsorption due to small bowel resection or small intestine
                        epithelial damage causing decreased surface area for absorption.
                        (c) Postmucosal Lymphatic Obstruction which prevents uptake and
                        transport of absorbed lipids into the lymphatic vessels. The increased
                        pressure causes leakage back into the intestinal lumen.


Effects of      (a) General      Lethargy
Malabsorption                    Depression
                                 Anaemia (Fe, folate, B12 deficiency)
                                 Poor wound healing (vitamin C, protein, zinc deficiency)
                                 Purpura/Bruising (vitamin C, K deficiency)

                (b) Mouth        Angular stomatitis (Fe, folate, B12 deficiency)

                (c) Limbs        Peripheral neuropathy (B12 deficiency)
                                 Peripheral oedema (hypoalbuminaemia)
                                 Paraesthesia, tetany (Ca, Mg deficiency)

                (d) Bone         Osteomalacia, rickets (vitamin D, Ca deficiency)

                (e) Muscle       Wasting (protein deficiency)
                                 Proximal myopathy (vitamin D)


Investigation   (a) Haematology Microcytic anaemia (Iron deficiency)
                                   Macrocytic anaemia (Folate, B12 deficiency)
                                   Increased Prothrombin Time (vitamin K deficiency)
                (b) Biochemistry Hypoalbuminaemia
                                   Hypocalcaemia, vitamin D deficiency
                                   Hypomagnesaemia
                                   Phosphate, zinc deficiency
                (c) 14C-trolein breath test (increased fat)
                (d) Duodenal biopsy, aspirate
                (e) Barium studies
                (f) Pancreatic function tests
                (g) Imaging (CT/MRI)


                                                                   3
Small Bowel     Normal upper intestine organisms never exceed 10 /ml. In bacterial overgrowth the
Bacterial       normal mechanisms controlling organisms in the mouth fail and there may be
                   8   10
Overgrowth      10 -10 /ml. Caused by: (a) decreased acid
                                          (b) decreased motility
                                          (c) structural abnormalities
                                          (d) decreased immunity
                Symptoms include:         (a) Watery diarrhoea +/- steatorrhoea
                                          (b) B12 deficiency anaemia
                                          (c) Symptoms of underlying GI problems
                Investigations include:   (a) FBC
                                          (b) Barium follow through
                                          (c) Endoscopic duodenal biopsy
                Management                (a) Treat underlying cause
                                          (b) Tetracycline/Metronizadole/Ciprofloxacin
                                          (c) B12 supplements IM in chronic cases




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Nem’s Notes…                                                                    Phase 2 Year 2


GASTROENTEROLOGY 6 (page 3 of 5)
Diarrhoea & GI Tract Infections

Escherichia     E. Coli is one of the organisms which can cause Traveller’s Diarrhoea. Clinical
Coli            features include: (a) Diarrhoea
                                    (b) Vomiting
                                    (c) Abdominal cramps/pain
                                    (d) Fever
                Enterotoxigenic E. Coli (ETEC) produces toxins and acts on cAMP to secrete water
                and electrolytes into the lumen.
                Management:         (a) Oral fluids and electrolytes
                                    (b) Ciprofloxacin in severe cases
                Prophylaxis to ETEC is with trimethoprim and doxycycline alongside good hygiene
                and well cooked food.


Salmonella      Salmonella can cause:
                         (a) Gastroenteritis (S. enteritidis, S. typhimurium)
                                  Diarrhoea
                                  Malaise
                                  Nausea
                                  Headache
                         (b) Typhoid fever (S. typhi)
                                  Insiduous onset of headache
                                  Increasing fever
                                  Cough, sore throat
                                  Initial constipation leading to diarrhoea
                Investigations:   (a) FBC/Blood culture (leucopenia, positive culture)
                                  (b) Widal test (serum agglutins to O and H antigens)
                Management:       (a) Ciprofloxacin/Chloramphenocol/Cotrimoxazole/Amoxycillin
                Prophylaxis:      (a) Good food hygiene
                                  (b) Annual vaccination


Shigella        Gram negative bacteria usually causing disease in children under 5 yrs.
                Symptoms:       (a) Acute fever
                                (b) Malaise                  symptoms increasing in severity
                                (c) Abdominal pain
                                (d) Watery diarrhoea
                Investigation:  (a) Sigmoidoscopy (inflamed mucosa and ulcers)
                                (b) Stool culture is diagnostic
                Treatment:      (a) Symptomatic treatment
                                (b) Antibiotics in severe cases


Campylobacter Gram negative bacteria causing the following symptoms:
                              (a) Acute diarrhoea +/- blood
                              (b) Asymptomatic carriers in children
                              (c) Fever
                              (d) Headache
                              (e) Severe cramping abdominal pain
              Investigation:  (a) Sigmoidoscopy (shows acute colitis)
                              (b) Stool microscopy is diagnostic
                              (c) Blood/stool culture
              Management:     (a) Usually self-limiting in 5-7 days
                              (b) Antibiotics if severe




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Nem’s Notes…                                                                      Phase 2 Year 2


GASTROENTEROLOGY 6 (page 4 of 5)
Diarrhoea & GI Tract Infections

Yersinia         Causes enterocolitis which presents with the following symptoms:
Enterocolitica                       (a) Fever
                                     (b) Diarrhoea
                                     (c) Severe abdominal pain
                                     (d) Arthritis
                 Usually self-limiting and no treatment is needed unless severe.


Clostridium      Gram positive bacteria which causes pseudomembranous colitis. It is usually hospital-
Difficile        acquired and becomes established when colonic bacterial flora are disrupted by
                 antibiotic treatment. It produces endotoxins and causes mucosal inflammation and
                 ulceration and, if severe, an adherent ‘pseudomembrane’ (fibrin, debris, polymorphs).
                 Symptoms:           (a) Insidious onset of lower abdominal pain
                                     (b) Profuse watery diarrhoea
                 Management:         (a) Stop antibiotics
                                     (b) Vancomycin/Metronizadole


Clostridium      Causes food poisoning due to spores in food which survive boiling.
Perfringens      Symptoms:       (a) Watery diarrhoea
                                 (b) Cramping abdominal pain
                 Investigation:  Stool/food culture is diagnostic


Mycobacterium Droplet infection of M. tuberculosis causes TB and tuberculous peritonitis. Symptoms
Tuberculosis  include:           (a) Insidious onset of fever
                                 (b) Anorexia
                                 (c) Weight loss
                                 (d) Abdominal pain
                                 (e) Ascites
              Investigation:     (a) Peritoneal fluid exam/culture
                                 (b) Tubercle biopsy (laparoscopically)
              Management:        (a) Chemotherapy for 18 months – 2 years


Giardiasis       Usually ingested in contaminated water in tropical regions. Incubation of 1-3 weeks.
                 Symptoms:         (a) Diarrhoea/Steathorrhoea
                                   (b) Abdominal pain
                                   (c) Weakness
                                   (d) Anorexia
                                   (e) Nausea/Vomiting
                 Investigation:    (a) Malabsorption of xylose, B12
                                   (b) Lactose intolerance
                                   (c) Sigmoidoscopy (partial villous atrophy)
                                   (d) Stool exam for cysts
                 Management:       (a) Tinidazole/Metronizadole


Amoebiasis       Commonly caused by entamoeba histolytica which is ingested in food contaminated
                 with human faeces. The organism causes amoebic ulceration. Symptoms are chronic
                 including:      (a) Abdominal pain
                                 (b) Alternating diarrhoea/constipation
                                 (c) Mucous in stool
                 Investigation:  (a) Naked eye stool exam for organisms
                                 (b) Sigmoidoscopy shows ulcers and scraping examined
                 Management:     (a) Metronizadole/Tinidazole




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Nem’s Notes…                                                                    Phase 2 Year 2


GASTROENTEROLOGY 6 (page 5 of 5)
Diarrhoea & GI Tract Infections

Cryptosporidiosis       Usually caused by cryptosporidium parvum, a protozoan with a 7-10 day
                        incubation causing:       (a) Watery diarrhoea
                                                  (b) Abdominal cramp
                        Investigation:   (a) Faecal microscopy for cysts
                        Management:      (a) Not necessary unless immuno-compromised


Strongyloides   This is a nematode parasite found in the tropics, sub-tropics and Far East. The worm
                burrows into the skin causing initial dermatalogical symptoms and then into the gut
                mucosa inducing inflammation and malabsorption.
                Symptoms:         (a) Abdominal pain
                                  (b) Diarrhoea
                                  (c) Steatorrhoea
                                  (d) Weight loss
                Investigation:    (a) Faecal microscopy will show motile larvae
                Management:       (a) Ivermectin/Albendazole


AIDS & GIT      Weight loss and diarrhoea are extremely common in HIV infection. Wasting is usually
Problems        due to systemic effects causing anorexia. ‘HIV enteropathy’ is a syndrome of
                diarrhoea, malabsorption and weight loss where there is no other pathology. This is
                probably due to infection of white cells in the gut mucosa by the HIV virus.




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Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 7 (page 1 of 4)
Pancreas

Investigation        (a) Serum amylase           (raised in acute disease)
Exocrine Function    (b) Serum lipase            (raised in acute disease)
                     (c) Duodenal enzymes        (chronic disease)
                     (d) PABA test               (pancreatic insufficiency)
                                                             14
                     (e) Fat absorption tests    (faecal fat, C-triolein breath test)



Imaging              (a) Conventional USS     (gallstones, fluid collection)
                     (b) Endoscopic USS       (small pancreatic tumours, small bile duct stones)
                     (c) Laparascopic USS
                     (d) Helical CT
                     (e) MRI
                     (f) MRCP (magnetic resonance cholangio-pancreatography)
                     (g) ERCP
                     (h) Arteriography



Pancreatitis         Pancreatitis can be classified as either:
                     (a) Acute         In acute pancreatitis there may be isolated or recurrent attacks with
                                       the pancreas returning to normal after the attack.
                     (b) Chronic       In chronic pancreatitis there will be continuing inflammation,
                                       irreversible structural changes and eventual loss of endocrine and
                                       exocrine function.



Causes                        Common (90%)                          Rare
Acute Pancreatitis            Gallstones                            Post-ERCP
                              Alcohol                               Post-surgery
                              Idiopathic                            Trauma
                                                                    Drugs
                                                                    Metabolic
                                                                    Infection



Mechanism            Mechanism is unclear but activation of zymogen granules has been implicated, which
Acute Pancreatitis   release proteases into the pancreas causing autodigestion.



           Defective intracellular transport &                     Reflux of infected bile or duodenal
           secretion of pancreatic zymogens                          contents into pancreatic duct



                                                 PROENZYMES



               Pancreatic duct obstruction                            Hyperstimulation of pancreas
                 eg gallstones, tumours                                      eg alcohol, fat


                                          ACTIVATED PROTEOLYTIC
                                                 ENZYMES




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Nem’s Notes…                                                                             Phase 2 Year 2


GASTROENTEROLOGY 7 (page 2 of 4)
Pancreas

Pathology            (a) Acute oedematous pancreatitis Interstitial inflammation and oedema with peri-
Acute Pancreatitis                                      pancreatic fat necrosis but sparing acinar cells
                     (b) Necrotising pancreatitis       As above but with destruction of acinar cells
                     (c) Acute haemorhagic pancreatitis Bleeding into the pancreas and retroperitoneum



Complications
Acute Pancreatitis
                      Systemic                       Pancreatic                   Gastrointestinal
                      Shock/Renal Failure            Abscess                      Upper GI bleed
                      Hypoxia                        Pseudocyst                   Variceal haemorrhage
                      Hyperglycaemia                 Pancreatic ascites           Duodenal obstruction
                      Hypocalcaemia                  Pleural effusion             Obstructive jaundice
                      Low serum albumin




Clinical             (a) Severe upper abdo pain radiating to back building over 15-60 mins
Features             (b) Nausea/vomiting
Acute Pancreatitis   (c) Marked epigastric tenderness (initially without guarding or rebound tenderness)
                     (d) Severe cases may cause hypovolaemic shock and hypoxia



Differentials        (a) Perforated viscus
Acute Pancreatitis   (b) Acute cholecystitis
                     (c) Myocardial Infarction



Prognosis            Overall mortality is 10% in acute pancreatitis. Mortality is at least 50% in necrotising
Acute Pancreatitis   pancreatitis or pancreatic abscess. Mortality is nearer 100% when there are multiple
                     complications. The following are bad prognostic indicators in the first 48hrs.
                                                                                                         -1
                      Age                    >55                     urea                 >16 mmol l
                                                     9                                            -1
                      WBC                    >15 x 10 /l             albumin              <30 g l
                                                         -1                                         -1
                      Blood Glucose          >10 mmol l              aminotransferases    >200 Ul
                                                                                                        -1
                      Pa02                   <8.0 kPa                calcium              <2 mmol l
                                                                                                     -1
                                                                     LDH                  >600 U l

                     The right hand column are serological tests. LDH is lactate dehydrogenase.



Investigation        (a) Serum amylase (x5 normal suggests pancreatitis)
Acute Pancreatitis   (b) USS
                     (c) Contrast enhanced dynamic CT
                     (d) MRI
                     (e) Peritoneal aspiration & lavage



Management           (a) Analgesia (usually pethidine)
Acute Pancreatitis   (b) Fluids/electrolytes to correct hypovolaemia
                     (c) Intensive care if in shock/respiratory failure
                     (d) Parenteral IV nutrition
                     (e) ERCP for gallstones
                     (f) Surgery in complicated cases



more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 25 of 44
Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 7 (page 3 of 4)
Pancreas

Cystic Fibrosis Cystic fibrosis is an inherited autosomal recessive disorder due to a defective
                epithelial membrane chloride channel gene (CFTR). This causes cystic dilatation of
                ducts and fibrosis.



Complications          (a) Pancreatic insufficiency leading to steatorrhoea
Cystic Fibrosis        (b) Meconium ileus (mucous obstruction of intestine)
                       (c) Peptic ulcer
                       (d) Hepatobiliary disease (usually cholesterol stones)
                       (e) Malnutrition due to anorexia and malabsorption secondary to (a)



                                                 2+                          -1
Diagnosis              (a) Sweat testing (high Na concentration > 60 mmol l )
Cystic Fibrosis        (b) Immunoreactive trypsin assay
                       (c) Genetic studies
                       (d) Pancreatic function tests



Treatment              (a) Pancreatic supplements (high dose pancreatin)
Cystic Fibrosis        (b) Increased calorie intake (150% recommended daily intake with vit supplements)
                       (c) Treatment of respiratory problems (antibiotics, transplantation)



Carcinoma of           Carcinoma of the pancreas has an prevalence of around 10-15 per 100,000 in the
Pancreas               West. The prevalence is greatest in those over 70 (100 per 100,000). Men are twice
                       as likely to be affected as women. There is a link to smoking and high cholesterol.



Pathology              90% are adenocarcinomas arising from the pancreatic ducts. They metastasise to the
Pancreatic Carcinoma   lymph nodes early. 70% of tumours are in the head of the pancreas and spread to
                       local organs such as the duodenum, liver and spleen.



Clinical               Head or Ampulla of Vater (a) Painless obstructive jaundice
Features                                        (b) Abdominal pain
Pancreatic Carcinoma                            (c) Anorexia and weight loss
                       Body or Tail of Pancreas (a) Abdominal pain (dull, boring, radiating to back)
                                                (b) Anorexia and weight loss

                       There is a palpable mass in 20% of cases and all will eventually have hepatomegaly



Differentials          (a) All causes of painless jaundice
Pancreatic Carcinoma   (b) All causes of upper abdominal pain



Investigation          (a) USS
Pancreatic Carcinoma   (b) CT
                       (c) Fine Needle Aspirate (FNA) or biopsy
                       (d) ERCP for tumours at the head of the pancreas




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 26 of 44
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 7 (page 4 of 4)
Pancreas



Neuroendocrine These arise from neuroendocrine tissue in the pancreas. The majority are non-
Tumours        secretory, metastasise late and grow slowly. Other tumours secrete hormones which
               affects the clinical presentation. The tumour can be single but are usually multifocal.

                   Tumour               Hormone             Effect
                   Gastrinoma           Gastrin             Peptic ulcer, steatorrhoea
                   Insulinoma           Insulin             Recurrent hypoglycaemia
                   VIPoma               VIP                 Watery diarrhoea, hypokalaemia
                   Glucagonoma          Glucagon            DM, necrolytic migratory erythema
                   Somatostatinoma      Somatostatin        DM, steatorrhoea




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 27 of 44
Nem’s Notes…                                                                          Phase 2 Year 2


GASTROENTEROLOGY 8 (page 1 of 5)
Liver 1

Functions
                 Nutrient Metabolism                                      Protein Synthesis
                 Carbohydrates                                            Albumin
                 Proteins                                                 Coagulation Factors
                 Lipids                                                   Complement Factors
                                                                          Haptoglobin
                                                                          Caeruloplasmin
                                            Liver                         Transferrin
                                                                          Protease Inhibitors




                                                                Excretion
                 Storage                  Gallbladder           Bile Salts
                 Iron                                           Bilirubin
                 Copper
                 Vitamins A, D, B12



Functional       The functional unit of the liver is the hepatic acinus. Blood arrives in the acinus via the
Anatomy          portal triad (portal vein, hepatic artery, bile duct). The zone closest to the vein and
                 artery is zone 1 and is well oxygenated. The zone furthest away is zone 3 and
                 relatively hypoxic. This allows the liver to perform different functions in different
                 physiological zones. Blood is then drained into the hepatic veins. Bile flows in the
                 opposite direction to the blood draining from the liver into the bile duct and to the
                 gallbladder.


Liver Function   (a) FBC
Tests            (b) Coagulation Tests
                 (c) Biochemistry Bilirubin
                                  Aminotransferases
                                  Alkaline Phosphatase (ALP)
                                  γ-glutamyl transferase
                                  Proteins/albumin


Imaging          (a) USS
                 (b) CT
                 (c) MRI
                 (d) MRCP
                 (e) Abdominal X-Ray
                 (f) Endoscopy
                 (g) Endoscopic US
                 (h) ERCP


Liver Biopsy     Liver biopsy is indicated for the following:
                          (a) Unexplained hepatomegaly
                          (b) Some cases of jaundice
                          (c) Persistent abnormal liver biochemistry
                          (d) Acute/chronic hepatitis
                          (e) Cirrhosis
                          (f) Infiltration
                          (g) Tumour
                          (h) Screening relatives




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 28 of 44
Nem’s Notes…                                                                               Phase 2 Year 2


GASTROENTEROLOGY 8 (page 2 of 5)
Liver 1

Portal                    Portal hypertension occurs when there is a prolonged elevation of portal venous
Hypertension              pressure (normally 2-5 mmHg). Clinical features are usually due to pressure greater
                          than 12 mmHg.

                          Normal blood flows into the         (a) Portal vein into the liver
                                  branching into the          (b) Portal venules (pre-sinusoidal)
                                  branching into the          (c) Hepatic capillaries (sinusoidal)
                                  draining into the           (d) Hepatic venules (post-sinusoidal)
                                  draining into the           (e) Hepatic vein
                                  draining into the           (f) Inferior Vena Cava



Causes
Portal Hypertension
                           Prehepatic                   Intrahepatic                Posthepatic
                                                        Cirrhosis
                                                        Alcoholic hepatitis         Budd-Chiari syndrome
                           Portal Vein Thrombosis
                                                        Idiopathic                  Veno-occlusive disease
                                                        Schistosomiasis




Consequences The increased resistance in the portal vein leads to the development of collateral
Portal Hypertension vessels allowing the direct return of blood to the systemic circulation. This occurs
                    particularly in the oesophagus, stomach and rectum.



Complications             (a) Variceal bleeding
Portal Hypertension       (b) Congestive gastropathy
                          (c) Hypersplenism
                          (d) Ascites
                          (e) Renal failure
                          (f) Hepatic encephalopathy



Investigation             (a) X-Ray (to detect varices)
Portal Hypertension       (b) Endoscopy (to detect varices)
                          (c) USS (to detect splenomegaly or collateral vessels)
                          (d) Portal venography



Management                (a) Blood & Plasma (to restore circulation)
Acute Variceal Bleeding   (b) Endoscopy (to confirm diagnosis)
                          (c) Injection sclerotherapy
                          (d) Variceal banding
                          (e) Balloon tamponade
                          (f) Vasoconstriction (Octreotide/Vasopressin)
                          (g) Transjugular intrahepatic shunt (TIPS)
                          (h) Emergency surgery (transection & ligation of oesophagus)



Prevention of             (a) Long term sclerotherapy
Recurrence                (b) Long term variceal banding
Acute Variceal Bleeding   (c) β-adrenoreceptor blockade (decreasing heart rate with propranolol)
                          (d) Surgery (TIPS, transection/ligation)


more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 29 of 44
Nem’s Notes…                                                                         Phase 2 Year 2


GASTROENTEROLOGY 8 (page 3 of 5)
Liver 1

Ascites          Ascites is the presence of fluid within the peritoneal cavity. Several factors are
                 involved including:
                 (a) Sodium and water retention
                 (b) Portal hypertension leading to increased lymph production
                 (c) Low serum albumin due to decreased hepatic function leading to decreased
                 plasma oncotic pressure preventing vascular leakage



Causes           Common            (a) Malignant Disease
Ascites                            (b) Cardiac Failure
                                   (c) Hepatic Cirrhosis
                 Other             (d) Hypoproteinaemia
                                   (e) Hepato-venous occlusion
                                   (f) Infection
                                   (g) Pancreatitis
                                   (h) Lymphatic obstruction



Clinical         (a) Abdominal distension
Features         (b) Shifting dullness on percussion
Ascites          (c) Fluid thrill
                 (d) Peripheral oedema
                 (e) Pleural effusion at right base



Investigation    A diagnostic aspiration of 10-20 ml of fluid should be obtained and the following tests
Ascites          performed:        (a) Cell count (neutrophils > 250 cells suggests bacterial peritonitis)
                                   (b) Gram stain/culture
                                                      -1
                                   (c) Protein (<11 gl suggests transudate, otherwise exudate)
                                   (d) Cytology for malignancy
                                   (e) Amylase to exclude pancreatic ascites



Management       The main aim is to reduce sodium intake and increase sodium excretion to allow
Ascites          reabsorption and mobilisation of ascitic fluid.
                         (a) Sodium restriction (40 mmol/day)
                         (b) Water restriction (0.5-1.0 l/day)
                         (c) Diuretic drugs (spironolactone/frusemide)
                         (d) Paracentesis (3-5 l/day)
                         (e) Shunts (LeVeen into veins of neck/TIPS)



Hepatic        This is a neuropsychiatric syndrome secondary to liver disease. It is generally
Encephalopathy considered to be due to abnormal brain biochemistry. There are a number of
               precipitating factors including:
                         (a) Uraemia
                         (b) Drugs
                         (c) GI bleeding
                         (d) Excess dietary protein
                         (e) Constipation
                         (f) Paracentesis (of volumes > 3-5 l/day)
                         (g) Hypokalaemia
                         (h) Infection
                         (i) Trauma/surgery
                         (j) Portasystemic shunts




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 30 of 44
Nem’s Notes…                                                                                Phase 2 Year 2


GASTROENTEROLOGY 8 (page 4 of 5)
Liver 1

Clinical               (a) Change of intellect/emotion/personality/consciousness
Features               (b) Later apathy, poor concentration, confusion, disorientation, slurred speech, coma
Hepatic Encephalopathy (c) Convulsion
                       (d) Asterixis
                       (e) Fetor hepaticus (sweet, musty odour to breath)


Differentials            (a) Subdural Haematoma
Hepatic Encephalopathy   (b) Drug/alcohol intoxication
                         (c) Delirium tremens
                         (d) Wernicke’s Encephalopathy
                         (e) Primary psychiatric disorders
                         (f) Hypoglycaemia
                         (g) Neurological Wilson’s Disease


Clinical Grading
Hepatic Encephalopathy
                              Grade        Features
                                           Poor concentration, slurred speech, slow
                                 I
                                           mentation
                                           Drowsy but easily roused, occasionally
                                 II
                                           aggressive, lethargic
                                           Marked confusion, drosy, sleepy but responding
                                III
                                           to pain and voice, gross disorientation
                                           Unconscious, unresponsive to voice, may or
                                IV
                                           may not respond to painful stimuli



Investigation            (a) Usually diagnosed clinically
Hepatic Encephalopathy   (b) EEG – diffuse slowing of α waves



Acute Liver              Acute liver failure can be caused by a number of things including:
Failure                           (a) Virus (Hep A, B, D)
                                  (b) Drugs (paracetamol, halothane, aspirin, antituberculous drugs)
                                  (c) Poisons (amanite phalloides, carbon tetrachloride)
                                  (d) Miscellaneous (Wilson’s disease, shock, cardiac failure)
                                  (e) Leptospirae



Clinical                 (a) Hepatic Encephalopathy
Features                 (b) Weakness
Acute Liver Failure      (c) Nausea, vomiting
                         (d) Jaundice



Complications            (a) Encephalopathy
Acute Liver Failure      (b) Cerebral oedema
                         (c) Respiratory failure
                         (d) Hypotension
                         (e) Hypothermia
                         (f) Infection
                         (g) Bleeding
                         (h) Pancreatitis
                         (i) Renal failure
                         (j) Metabolic effects


more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 31 of 44
Nem’s Notes…                                                                             Phase 2 Year 2


GASTROENTEROLOGY 8 (page 5 of 5)
Liver 1

Investigation         (a) Toxicology screen of blood/urine
Acute Liver Failure   (b) IgM anti-Hbs
                      (c) IgM anti-HAV
                      (d) Anti-HEV, CMV, HSV, EBV
                      (e) Caeruloplasmin, serum copper, urinary copper
                      (f) Autoantibodies
                      (g) Doppler US of liver and heaptic veins
                      (h) CXR


Chronic Liver         Chronic liver failure develops when liver function can no longer maintain normal
Failure               physiological conditions. The term ‘hepatic decompensation’ is used when chronic
                      liver failure occurs and may be precipitated by a number of events including infection
                      or variceal haemorrhage.

                      It is a syndrome characterised by clinical and laboratory features including:
                                 (a) Hepatic encephalopathy
                                 (b) Jaundice
                                 (c) Hypoalbuminaemia
                                 (d) Coagulation abnormalities




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 32 of 44
Nem’s Notes…                                                                            Phase 2 Year 2


GASTROENTEROLOGY 9 (page 1 of 2)
Functional Bowel Disorders



Functional     This is a general term covering two main syndromes:
Bowel Disorder           (a) Non-ulcer dyspepsia
                         (b) Irritable bowel syndrome
               These syndromes are extremely common and frequently overlap in pathology. They
               make up 60-80% of the patients presenting in GI clinic. There is a very strong
               psychological link to functional bowel disorders.




Non-Ulcer             Symptoms are mainly stress related and include:
Dyspepsia                      (a) Indigestion
                               (b) Wind
                               (c) Nausea
                               (d) Early satiety
                               (e) Heartburn
                      No ulcer can be found.

                      Functional dyspepsia can be differentiated from peptic ulcer using the following table

                                           Functional Dyspepsia              Peptic Ulceration
                                           Diffuse all over                  Epigastric
                         Site of Pain
                                           Fits no recognisable pattern      Points with one finger
                         Frequency         Daily for long periods            Episodic
                                           Pain unaffected
                         Food/Meals                                          Exacerbates or helps pain
                                           Lasts all day
                          Antacids         No help                           Helps pain
                       Nocturnal Pain
                                           Rare                              Common
                       Waking Patient
                          Vomiting         No effect                         Relieves pain




Investigation         (a) Endoscopy
Non-Ulcer Dyspepsia   (b) Barium studies




Management            (a) Reassurance
Non-Ulcer Dyspepsia   (b) Antacids and H2-receptor antagonists probably have a placebo effect
                      (c) Cisapride or Metoclopramide may help




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 33 of 44
Nem’s Notes…                                                                              Phase 2 Year 2


GASTROENTEROLOGY 9 (page 2 of 2)
Functional Bowel Disorders



Irritable Bowel   The clinical features of irritable bowel syndrome include:
Syndrome                    (a) Pain in left iliac fossa relieved by defecation or wind
                            (b) Constipation or diarrhoea
                            (c) Frequent small volume stools
                            (d) Abdominal distension and bloating
                            (e) Recurrent episodes with long symptom free periods
                            (f) Patient generally looks well




Mechanism         The pathophysiology is extremely variable from patient to patient. Motility
Irritable Bowel   abnormalities are sometimes found but psychological factors are extremely important.
                  Stress often exacerbates symptoms and depression may be present




Investigation     (a) May not be necessary – avoid over investigation
Irritable Bowel   (b) Rectal exam
                  (c) Sigmoidoscopy
                  (d) Barium studies




Management        (a) Discuss lifestyle and reassure
Irritable Bowel   (b) Reassurance of benign nature of disease
                  (c) High fibre diet
                  (d) Antispasmodics
                  (e) Antidepressants therapy
                  (f) Other therapy




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 34 of 44
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 10 (page 1 of 4)
Liver 2

Tumours         Tumours of the liver can either be: (a) primary arising in the liver
                                                    (b) secondary metastasising from elsewhere

                Secondary tumours are abut 50 times commoner than primary tumours.

                  Primary Tumours
                  Malignant                                  Benign
                  Hepatocellular Carcinoma (HCC)
                                                             Hepatic Adenoma
                  Cholangiocarcinoma
                                                             Haemangioma
                  Angiosarcoma
                                                             Focal Nodular Hyperplasia
                  Hepatoblastoma
                                                             Fibroma
                  Fibrosarcoma




Carcinoma       HCC is rare in the west (1-2 per 100,000 per year). Common in Africa and SE Asia.
                Cholangiocarcinoma is rare comprising about 10% of hepatic malignancy. it is most
                common between the ages of 50 and 70 yrs.



Risk Factors    (a) Carriers of HBV/HCV
Carcinoma       (b) Cirrhosis
                (c) Male sex
                (d) Aflatoxin (fungus found in groundnut)
                (e) OC Pill

                Prevention is by widspread HBV vaccination



Pathology       The tumour is either single or occurs in multiple nodules. Histologically the tumour
Carcinoma       contains cells resembling heaptocytes. The tumour may metastasise via the hepatic
                portal vein to lymph node, bones and lungs.



Clinical        Usually presents below the age of 50 with rapid onset in cirrhotic patients
Features                 (a) Weight loss
Carcinoma                (b) Anorexia
                         (c) Fever
                         (d) Aching right hypochondrium
                         (e) Ascites
                         (f) Hepatomegaly
                In cholangiocarcinoma a jaundice is also seen.

                Prognosis: survival is not usually more than 6 months



Investigation   (a) USS shows large filling defects
Carcinoma       (b) Serum α-fetoprotein (raised)
                (c) Ultrasound guided liver biopsy is diagnostic



Treatment       (a) Surgical resection sometimes possible
Carcinoma       (b) Transplantation
                (c) Chemotherapy/Radiotherapy usually unhelpful



more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 35 of 44
Nem’s Notes…                                                                          Phase 2 Year 2


GASTROENTEROLOGY 10 (page 2 of 4)
Liver 2

Wilson’s           Wilson’s Disease is due to accumulation of copper in the body, particularly the liver.
Disease            Dietary copper is usually absorbed from the stomach and upper small intestine and
                   transported in the liver loosely bound to albumin. It is incorporated into caeruloplasmin
                   which is a glycoprotein synthesized in the liver and secreted in the blood. Copper is
                   normally excreted in the bile. Dysfunction of the enzymes involved in transport of
                   copper causes Wilson’s Disease.



Genetics           Wilson’s is an autosomal recessive disorder within a copper transporting ATPase. The
Wilson’s Disease   problem is due to failure of biliary excretion of copper and the consequential
                   accumulation in the body.



Clinical           Hepatic                              Non-Hepatic
Features           Acute hepatitis                      Kayser-Fleischer rings in cornea
Wilson’s Disease   Fulminant hepatic failure            Tremor
                   Chronic hepatitis                    Dysarthria
                   Cirrhosis                            Involuntary movement
                                                        Dementia



Pathology          (a) Hepatic damage varies from chronic hepatitis to macronodular cirrhosis
Wilson’s Disease   (b) Periportal distribution of copper stain
                   (c) Basal ganglia show damage & cavitation
                   (d) Kidneys show tubular degradation
                   (e) Bones show erosions



Investigations     (a) Serum copper and caeruloplasmin decreased (but can be normal)
Wilson’s Disease   (b) Urinary copper increased
                   (c) Liver biopsy
                   (d) Haemolysis and anaemia



Treatment          Lifetime treatment with penicillamine to chelate copper. Dose dependent on urinary
Wilson’s Disease   copper monitoring. Siblings and children should be screened and treatment given for
                   copper accumulation even if asymptomatic.



Haemo-             Haemochromatosis is the primary accumulation of iron in the body due to a genetic
chromatosis        defect causing excess iron absorption leading to fibrosis of various organs, including
                   the liver, and eventual organ failure.
                   Haemosiderosis is a secondary overload of iron and can be distinguished from
                   haemochromatosis by MRI which shows pancreatic destruction in haemochromatosis,
                   but is spared in haemosiderosis.

                   (Normal iron metabolism discussed in Blood & Lymph 2)



Genetics           Haemochromatosis is an autosomal recessive disorder with a prevalence in
Haemochromatosis   caucasians of 1/400 affected homozygotes and 1/10 heterozygous carriers. There is
                   an association with HLA-A3.




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 36 of 44
Nem’s Notes…                                                                                     Phase 2 Year 2


GASTROENTEROLOGY 10 (page 3 of 4)
Liver 2

Clinical                    Less clinical manifestation in women due to physiological blood loss and lower iron.
                                                           th
Features                    Most cases present in the 5 decade.
Haemochromatosis                      (a) Bronze skin pigmentation
                                      (b) Hepatomegaly
                                      (c) Diabetes Mellitus
                                      (d) Hypogonadism (secondary to pituitary dysfunction)
                                      (e) Heart failure and arrythmias
                                      (f) Liver iron deposition and fibrosis
                                      (g) Liver cirrhosis (late feature)


Pathology                   Total body iron of 20-40g (normal is 2-4g). Liver and pancreas show 50-100 times
Haemochromatosis            normal iron level. Iron is initially deposited in the periportal hepatocytes and then later
                            distributed to the rest of the liver.


Investigation               (a) Raised serum iron
Haemochromatosis            (b) Raised serum ferritin
                            (c) Liver biochemistry normal
                            (d) Liver biopsy
                            (e) MRI


Treatment                   (a) Venesection
Haemochromatosis            (b) Chelation therapy (desferrioxamine)
                            (c) Screening of family members


α1-Antitrypsin              α1-AT is aglycoprotein which inhibits the proteolytic enzyme neutrophil elastase.
Deficiency                  1/10 North Europeans carry a deficiency gene. The abnormal protein is produced and
                            not secreted causing liver accumulation. This results in low plasma levels of
                            α1-antitrypsin.


Clinical                  (a) Cirrhosis in 10-15% (usually > 50 yrs)
Features                  (b) Respiratory Problems in 75% (eg emphysema)
α1-Antitrypsin Deficiency (c) Chronic hepatitis
                          (d) Cholestatic jaundice in neonates
                          (e) Hepatocellular Carcinoma (HCC) (late feature)


Investigation               Serum α1-antitrypsin decreased (10% of normal in homozygotes)
α1-Antitrypsin Deficiency




Treatment                   No treatment other than for the complications of liver disease. Transplantation is a
α1-Antitrypsin Deficiency   possibility. Patients should be encouraged to stop smoking to prevent emphysema.


Liver Infection             Infection of the liver can cause:
                                      (a) Pyogenic abscess (E. coli, streptococcus faecalis, vulgaris, aureus)
                                      (b) Amoebic abscess (entamoeba histolytica)
                                      (c) Schistosomiasis (schistosoma mansoni, schistosoma japonicum)
                                      (d) Hydatid Disease (echinococcus granulosus)


Routes of                   (a) Intra-abdominal sepsis (eg appendicitis)
Infection                   (b) Portal venous system
                            (c) Trauma/surgery




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 37 of 44
Nem’s Notes…                                                                        Phase 2 Year 2


GASTROENTEROLOGY 10 (page 4 of 4)
Liver 2

Liver Abscess    Liver abscess can be either:          (a) Bacterial
                                                       (b) Amoebic
                 The clinical presentation is variable and can include the following features:
                                                       (a) Fever
                                                       (b) Rigors
                                                       (c) Weight loss
                                                       (d) Vomiting
                                                       (e) Abdominal pain
                                                       (f) Jaundice


Treatment        (a) Aspiration of abscess under ultrasound
Liver Abscess    (b) Broad-spectrum antibiotics


Liver Disease    (a) Viral hepatitis (B, C, D)
in AIDS          (b) Neoplasia (Kaposi’s sarcoma, non-Hodgkin’s lymphoma)
                 (c) Opportunistic infection (mycobacterium tuberculosis, cryptococcus, candida)
                 (d) Drug hypertoxicity
                 (e) Sclerosing cholangitis


Schistosomiasis The bacterial ova reach the liver via the venous system obstructing the portal
                branches. The pathology involves granuloma, fibrosis and inflammation (but no
                cirrhosis). Clinically there is hepatosplenomegaly and presinusoidal portal
                hypertension. Investigation shows increased alkaline phosphatase and ova in the
                stool. Treatment is with praziquantel.


Veno-occlusive This involves widespread occlusion of the central hepatic veins often due to toxins in
Disease        certain teas, but also chemotherapy or body irradiation before bone marrow
               transplantation. Clinical features include:  (a) Acute abdominal pain
                                                            (b) Nausea and vomiting
                                                            (c) Tender hepatomegaly
                                                            (d) Ascites


Budd-Chiari      This syndrome is due to obstruction of venous outflow of the liver due to occlusion of
Syndrome         the hepatic vein.
                 Causes: (a) Idiopathic (~50%)
                           (b) Hypercoaguability (eg polycythaemia vera)
                           (c) OC Pill
                           (d) Leukaemia
                           (e) Tumours
                           (f) Radiotherapy
                           (g) Trauma
                 The clinical features are similar to those of veno-occlusive disease.


Venous Outflow Hepatic venous outflow obstruction can occur in:
Obstruction             (a) Small hepatic veins
                        (b) Large hepatic veins
                        (c) Inferior vena cava
                        (d) Heart


Cardiac          Hepatic damage due to congestion is present in cardiac failure from any cause but
Disease          particularly:   (a) Acute hepatitis following MI or decompensation
                                 (b) Ascites due to cardiac failure




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Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 1 of 4)
Liver 3

Acute             Acute hepatitis can be caused by a number of things including:
Hepatitis                 (a) Viral (Hep A, B, C, E, (D), EBV, CMV, Yellow Fever)
                          (b) Non-viral (toxoplasma gondii, leptospira icterohaemorrhagiae)
                          (c) Drugs (paracetamol, halothane)
                          (d) Alcohol
                          (e) Poison (mushroom, aflatoxin, carbon tetrachloride)
                          (f) Other (pregnancy, circulatory insufficiency)


Viral Hepatitis

                             HAV              HBV             HCV              HDV             HEV
              Group       Enterovirus       Hepadna         Flavivirus     Incomplete       Calcivirus
  Virus     Genetics         RNA              DNA             RNA              RNA             RNA
               Size         27nm              42nm          30-38nm           35nm            27nm
             Faecal                                                                         
              Blood       Uncommon                                                           
 Spread       Saliva                                                         ?               ?
             Sexual       Uncommon                        Uncommon                            ?
            Vertical                                     Uncommon                            
      Incubation          2-4 weeks        4-20 weeks      2-26 weeks       6-9 weeks       3-8 weeks
  Chronic Infection           No             5-10%             50%                             



Hepatitis A       Most common viral hepatitis worldwide. Poor sanitation and hygiene cause epidemics.

                  Clinical Features: (a) Fever
                                     (b) Lethargy
                                     (c) Jaundice

                  Diagnosis:         (a) IgM anti-HAV
                                     (b) Alkaline phosphatase increased
                                     (c) Alanine transferase increased
                                     (d) Bilirubin increased

                  Prevention:        (a) Immunisation by inactivated vaccine

                  Treatment:         (a) No specific treatment


Hepatitis B       2000 million people affected with 300 million carriers worldwide. UK and USA have
                  lower prevalence of carriers than Africa, Far and Middle East. Risk factors include
                  multiple sexual partners and IV drug use.

                  Clinical Features: (a) Same as HAV
                                     (b) Chronic (asymptomatic) hepatitis
                                     (c) Cirrhosis (also ascites, variceal haemorrhage, encephalopathy)

                  Natural History:   (a) 30% die of cirrhosis
                                     (b) Hepatocellular carcinoma
                                     (c) HBe antigen negative virus may emerge

                  Diagnosis:         (a) Markers for HBV
                                     (b) ALT increased

                  Prevention:        (a) Passive and active immunisation

                  Treatment:         (a) No specific treatment




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 39 of 44
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 2 of 4)
Liver 3

Hepatitis C   Rates of infection in healthy blood donors is 0.02% in Europe, 6% in Africa, 19% in
              Egypt. Transfusion before the screening of donor’s blood is a major risk factor.

              Clinical Features: (a) Mild flu-like symptoms
                                 (b) Jaundice
                                 (c) May present with chronic liver disease years after infection
                                 (d) Extrahepatic manifestations (arthritis, aplastic anaemia)

              Natural History:   (a) Progresses over 15-50 years to cirrhosis in 20-30% of cases
                                 (b) 2-3% die of hepatocellular carcinoma per year

              Diagnosis:         (a) Anti-HCV
                                 (b) HCV-RNA positive

              Prevention:        None

              Treatment:         (a) Interferon-α plus ribavarin for 6-12 months



Hepatitis D   Can only be acquired by patients with pre-existing HBV infection

              Clinical Features: (a) Severe hepatitis if HBV and HDV infect together
                                 (b) Progressive disease if HDV superimposed on HBV

              Diagnosis:         (a) IgM anti-HDV
                                 (b) IgM anti-HBc antigen

              Prevention:        (a) None

              Treatment:         (a) None



Hepatitis E   Epidemics seen in developing countries

              Clinical Features: (a) Mild hepatitis (more severe in pregnancy)
                                 (b) Frequently cholestatic
                                 (c) Mortality from fulminant hepatic failure

              Diagnosis:         (a) ELISA for IgG and IgM anti-HEV (unreliable)

              Prevention:        (a) Good sanitation and hygiene

              Treatment:         (a) Conservative



Hepatitis G   Hepatitis G is a parenterally transmitted flavivirus (also GBV-C). It replicates to a
              minor degree in the liver, but the main site is unknown. It rarely causes mild hepatitis
              but usually causes chronic disease. No treatment is needed.




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 40 of 44
Nem’s Notes…                                                                       Phase 2 Year 2


GASTROENTEROLOGY 11 (page 3 of 4)
Liver 3

Alcoholic Liver Epidemiology     (a) Causes 12% of male and 3% of female deaths.
Disease                          (b) Causes 27% of medical and 20% of psychiatric admissions.
                                 (c) There is strong evidence for a genetic component to the disease
                                 and its aetiology.

               Pathology         (a) Fatty change in liver cells (especially zone 3).
                                 (b) Acute hepatitis (with Mallory’s hyalin)
                                 (c) Architectural damage (eg portal fibrosis, cirrhosis)

               Clinical Features (a) Can have few or mild symptoms (diagnosed histologically)
                                 (b) Jaundice
                                 (c) Ascites
                                 (d) Abdominal Pain
                                 (e) Fever
                                 (f) Hepatomegaly

               Diagnosis         (a) Elevated MCV
                                 (b) High serum gamma-glutamyl transferase
                                 (c) Fat in liver histology
                                 (d) High serum bilirubin
                                 (e) High serum AST and ALT
                                 (f) High ALP
                                 (g) Increased PT

               Treatment         (a) Encourage patient to stop drinking
                                 (b) Diazepam or chlormethiazole for delirium tremens
                                 (c) Bed rest
                                 (d) Protein and vitamin supplements



Cirrhosis      Liver cirrhosis is a condition in which the liver responds to injury or death of some of
               its cells by producing interlacing strands of fibrous tissue between which are nodules
               of regenerating cells.

               Causes            (a) Hepatitis B, C or D
                                 (b) Alcohol
                                 (c) Biliary cirrhosis
                                 (d) Primary sclerosing cholangitis
                                 (e) Haemochromatosis
                                 (f) Wilson’s Disease
                                 (g) α-antitrypsin deficiency

               Complications     (a) Portal hypertension
                                 (b) GI haemorrhage
                                 (c) Ascites
                                 (d) Encephalopathy
                                 (e) Renal failure
                                 (f) Hepatocellular carcinoma

               Investigation     (a) Liver function tests
                                 (b) Liver biochemistry
                                 (c) Serum electrolytes
                                 (d) Imaging
                                 (e) Liver biopsy (if PT is not too long)

               Management        (a) US scan and α-fetoprotein every 6 months to check for HCC




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 41 of 44
Nem’s Notes…                                                                    Phase 2 Year 2


GASTROENTEROLOGY 11 (page 4 of 4)
Liver 3

Chronic Biliary Causes Common (a) Gallstones
Disease                       (b) Infections
                              (c) Strictures (benign or malignant)
                       Rare   (a) Primary biliary cirrhosis
                              (b) Sclerosing cholangitis
                              (c) Drugs
                              (d) Congenital (biliary atresia, fibropolycystic disease)

                 Clincal Features (a) Abdominal Pain
                                  (b) Jaundice
                                  (c) Dark urine, pale stools
                                  (d) Itching
                                  (e) Nausea and vomiting
                                  (f) Fevers and rigors
                                  (g) Hepatomegaly
                                  (h) Weight loss
                                  (i) Skin pigmentation
                                  (j) Xanthomas, xanthalasmas

                 Biochemistry      (a) Increased bilirubin
                                   (b) Increased alk phosp
                                   (c) Increased transaminases
                                   (d) Increased cholesterol
                                   (e) Increased prothrombin time
                                   (f) Normal albumin

                 Imaging           (a) Abdo X-Ray
                                   (b) USS
                                   (c) CT
                                   (d) MRI
                                   (e) ERCP
                                   (f) Percutaneous transhepatic cholangiography (PTC)




more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 42 of 44
Nem’s Notes…                                                                                 Phase 2 Year 2


GASTROENTEROLOGY 12 (page 1 of 2)
Gall Bladder & Biliary Tract

Gallstones               Gallstones occur in the gallbladder or biliary tract and can be composed of either:
                                  (a) Cholesterol (more common in industrialised countries)
                                  (b) Bile Pigment (more common in developing countries)


Epidemiology             In the UK gallstones occur in 7% of males and 15% of females between 18 and 65.
Gallstones               There is an overall prevalence of 11%
                         Common in N America, Europe, Australia
                         Less common in India, Far East, Africa


Pathogenesis             (a) Cholesterol    Cholesterol is held in solution in bile by bile acids and phospholipid
Gallstones                                  which form micelles and vesicles. Due to either excess cholesterol
                                            or deficiency of bile salts, bile becomes supersaturated or
                                            lithogenic. Cholesterol becomes crystallized out of the lithogenic
                                            bile by other factors which are poorly defined.

                         (b) Bile Pigment Brown pigment stones contain cholesterol, calcium salts of fatty
                                          acids and calcium bilirubinate. They form due to stasis or infection
                                          of the common bile duct and are due to precipitation of
                                          deconjugated bilirubin with calcium. They mainly form in the
                                          common bile duct. Commonly associated with parasitic infection of
                                          the biliary tract.

                                            Black pigment stones contain calcium salts of bilirubin which can be
                                            caused by haemolysis in chronic haemolytic disease. Other
                                            pathogenic mechanisms are unclear. They mainly form in the
                                            gallbladder.


Risk Factors             (a) Increasing age          (e) High saturated fat diet
Cholesterol Gallstones   (b) Female > Male           (f) OC Pill & other drugs
                         (c) Obesity                 (g) Diabetes
                         (d) Rapid weight loss       (h) Liver cirrhosis


Complications            (a) Acute cholecystitis due to prolonged occlusion of the cystic duct
Gallstones               (b) Chronic cholecystitis
                         (c) Biliary colic due to migration of gallstones to the common bile duct
                         (d) Pancreatitis
                         (e) Gallstone ileus due to the fistula allowing migration of stone to gut
                         (f) Carcinoma of the gallbladder


Management               (a) No treatment if asymptomatic
Gallstones               (b) Cholesystectomy (open/laparascopic)
                         (c) Bile acids (chenodeoxycholic/urodeoxycholic acid) (non-calcified stones only; 10%)
                         (d) Lithotripsy (shock-wave treatment)


Acute                    Gallstones occur in 90% of cases of acute cholecystitis. Obstruction of the neck of the
Cholecystitis            gallbladder or cystic duct occurs due to an impacted stone. This causes inflammation
                         which can be mild (causing slight abdominal pain and a palpable gallbladder) or
                         severe (causing localised peritonitis and acute pain).


Clinical                 (a) Severe, continuous, increasing, epigastric or right hypochondrial pain
Features                 (b) Mild jaundice in 20%
Acute Cholecystitis      (c) Fever
                         (d) Murphy’s sign (pain worse on inspiration causing shallow breathing)
                         (e) Guarding & rebound tenderness


more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 43 of 44
Nem’s Notes…                                                                               Phase 2 Year 2


GASTROENTEROLOGY 12 (page 2 of 2)
Gall Bladder & Biliary Tract
Investigations        (a) FBC/Blood Film moderate leucocytosis
Acute Cholecystitis   (b) Biochem slightly raised bilirubin, alkaline phosphatase, aminotranserases
                      (c) USS sonographic Murphy’s sign, gallbladder wall thickening, distension, sludge
                      (d) Iodida Scintiscan blockage of cystic duct
                      (e) X-Ray gallstones in 10%; excludes lower lobe pneumonia


Differentials         (a) Perforated peptic ulcer
Acute Cholecystitis   (b) Retrocaecal appendicitis
                      (c) Acute pancreatitis
                      (d) Right basal pneumonia
                      (e) Myocardial Infarction


Management            (a) Bed rest, opiate analgesia, antibiotics (amoxycillin/cephalosporin)
Acute Cholecystitis   (b) Cholecystectomy


Chronic               This is due to chronic inflammation of the gallbladder as a consequence of gallstones.
Cholecystitis         Pathology          Inflammation of gallbladder
                                         Shrunken gallbladder on USS/radiology
                      Clinical Features Vague symtpoms including recurrent indigestion, right abdominal
                                         pain/distension often at night and following a heavy meal
                      Investigation      Same as for acute cholecystitis
                      Differential       Functional bowel disease
                      Management         Same as for acute cholecystitis


Common Bile           10-15% of gallstones occur in the common bile duct due to migration from the
Duct Stones &         gallbladder. Primary bile duct stones may develop within the bile duct due to an
Cholangitis           accumulation of biliary sludge. Cholangitis is a bacterial infection of the bile duct
                      secondary to bile duct abnormality.


Clinical              (a) May be asymptomatic
Features              (b) Abdominal pain (epigastric, right hypochondrium)
                      (c) Fever
                      (d) Jaundice
                      (e) Rigor (in cholangitis)


Investigation         (a) LFTs (cholestatic pattern/bilirubinaemia)
                      (b) FBC/Blood film (leucocytosis)
                      (c) USS (dilated intra/extra-hepatic ducts, gallstones)
                      (d) ERCP


Differentials         (a) Gallstones
                      (b) Tumours of gallbladder/bile duct
                      (c) Biliary motor disorders
                      (d) Cholesterolosis
                      (e) Adenomyomatosis of gallbladder


Management            (a) Analgesia
                      (b) IV fluids
                      (c) Broad-spectrum antibiotics
                      (d) Surgical/endoscopic stone removal

Haemobilia            This can occur as a result of hepatic trauma (occasionally tumour). Blood enters the
                      biliary tree and produces a cholestatic jaundice or GI bleeding



more online at http://homepage.virgin.net/nemonique.sam/noteindx.htm page 44 of 44

								
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