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Gastroenterology Review

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1 Gastroenterology Review

2 Gastroenterology History
Dyspepsia & Heartburn Dysphagia & Odynophagia Nausea and vomiting Abdoinal pain Abdominal swelling Appetite/weight gain Diarrhoea Constipation Bleeding Jaundice Pruritus

3 Dyspepsia & Peptic Ulcer Disease


5 Dyspepsia Common problem in the community - affects up to 40% of individuals in 1 year Up to 60% of patients do not have an identifiable organic cause - “functional” Nevertheless can be the presenting symptom of a number of serious conditions May be the only symptom of malignancy Has Eesophageal, Stomach and Duodenal pathologies May indicate underlying gallstone disease Warrants OGD in patients over 55 or with alarming symptoms & signs

6 Etiology of DYSPEPSIA 1-NON-ULCER (Functional) DYSPEPSIA (50 % ).
{Dyspepsia of at least 3 Months duration for which no biochemical or structural abnormality is found to explain the patients symptoms }. 2- PEPTIC ULCER DISEASE (20 % ). 3-REFLUX ESOPHAGITIS (15 – 20 % ). 4-N.E.R.D,Motility disorders 5 -Pancreatico-Biliary Disorders. 6- Medications :NSAIDs ,Antibiotics ,Theophyllins , Irons. 7-Dietary factors :Caffeine , Alcohol. 8- Metabolic & Endocrine : D.M , Hyperthyroidism , 9-H .pylori. 10 –GASTRIC MALIGNANCY Is found in 1 – 2 % of patients with dyspepsia, Age > 55 years + Alarm symptoms.

Ulcer-type symptoms Epigastric pain Relief with food or Antacid Pain worse at night Reflux symptoms Acid regurgitation Heartburn U.G.I. Flatulence Retrosternal pain Dysmotility symptoms Anorexia /Early satiety Postprandial bloating Nausea & or Vomiting

8 Dyspepsia Functional Dyspepsia Non-GI Causes Structural Dyspepsia
(cardiac disease, muscular pain, etc.) Structural Dyspepsia (GERD, PUD, Pancreatic disease, Gallstones, etc.)

9 (Alarm Symptoms & Signs) Indicators for investigation
Vomiting (persistent) Bleeding/anaemia Abdominal mass/unexplained weight loss Dysphagia (progressive) (Age > 55)

10 Hiatal Hernia and Gastroesophageal Reflux GERD

11 Gastroesophageal reflux (GERD)
GER is the reflux of chyme from the stomach to the esophagus If GER causes inflammation of the esophagus, it is called reflux esophagitis A normal functioning lower esophageal sphincter maintains a zone of high pressure to prevent chyme reflux Conditions that increase abdominal pressure can contribute to GER More common in people with hiatus hernia Manifestations Heartburn, regurgitation of chyme, and upper abdominal pain within 1 hour of eating

12 Characteristics of Heartburn
Figure Characteristics of heartburn. Heartburn is a symptom complex characterized by substernal (burning) pain radiating toward the mouth, which is worsened by meals and recumbency and ameliorated by antacid ingestion. When typical, recurrent heartburn is adequate for the diagnosis of gastroesophageal reflux disease (GERD). Acid regurgitation, the spontaneous eructation of bitter material in the esophagus and mouth, and water brash, the spontaneous appearance of a bland or salty fluid in the mouth, are also common symptoms of GERD. Odynophagia, however, is very uncommon in those with GERD and usually reflects mucosal destruction from pills (doxycycline or tetracycline, nonsteroidal antiinflammatory agents, vitamin C, quinine) or infectious agents (Herpes simplex virus, cytomegalovirus, Candida albicans, HIV).

13 Epidemiology ~25% of the adult population experience symptoms at least monthly 5% experience daily symptoms. Incidence increases with age

14 “Alarm Symptoms” Urgent referral for endoscopy for patients of any age with dyspepsia when presenting with any of: Chronic gastrointestinal bleeding Progressive unintentional weight loss Progressive difficulty swallowing Persistent vomiting Iron deficiency anaemia Epigastric mass Choking (acid causing coughing, shortness of breath , or hoarsness) Chest pain Longstanding symptoms requiring continuous treatment

15 Diagnosis Therapeutic trial (3 months) Endoscopy Motilitiy studies
Alarm sx To note mucosal changes Esophageal biopsies Motilitiy studies Low LES pressures are associated with reflux pH monitoring ( GOLD STANDARD ) The most precise measure for the presence of acid in the esophageal lumen (24 hour monitoring)

16 GERD Complications Benign stricture Perforation Haematemesis
Barrett’s oesophagus >3cm columnar epithelium in lower 1/3 of oesophagus Must be confirmed by biopsy Risk of adenocarcinoma (20% for low grade dysplasia, 50% for high grade displasia Monitor with OGD, PPI, ? Oesophagectomy for high grade dysplasia in young fit adults

17 GERD Management Advice – weight loss, stop smoking, stop alcohol, avoid stooping Medical – exclude CA if >55, control acid secretion (PPI/H2antagonist), protect oesophagus (alginates), prokinetics (metoclopramide) Surgical – Nissen fundoplication Failed medical management Complications Long term dependance on medical therapy

18 Peptic Ulcer Disease A break in the epithelium of the oesophagus, stomach or duodenum 5 – 10% of the general population will have PUD in their lifetime, 50% will recur Due to Imbalance between protective and aggressive factors Investigations – FBC, FOB, OGD, Urease breath test 0001% mortality rate

19 Gastric Mucosa & Secretions
The Defensive Forces Bicarbonate Mucus layer Mucosal blood flow Prostaglandins Growth factors The Aggressive Forces Helicobacter pylori HCl acid Pepsins NSAIDs Bile acids Ischemia and hypoxia. Smoking and alcohol

20 Peptic Ulcer

21 Etiology H.Pylori Drugs Hyperacidity Cigarette smoking
Almost all patients with H. pylori have antral gastritis Eradication of H. pylori eliminates gastritis Nearly all patients with DU have H. pylori gastritis 80% of patients with GU have H. pylori gastritis Drugs NSAIDS Corticosteroids Hyperacidity Zollinger – Ellison Syndrome Cigarette smoking Rapid gastric emptying No effect of spicy foods

22 Helicobacter pylori 80% 95%

23 H pylori and disease Half of worlds population infected
100 % damage to gastric structure Many infected indiviudals no (silent) disease 17 % Peptic Ulcer (90 – 95 % duodenal ulcer patients has Hp) (70 – 85 % gastric ulcer patients has Hp) 2 % Gastric carcinoma (85 % of patients has Hp) X % Nonulcer dyspepsia (50 % non ulcer dyspepsia patients) MALT lymphoma Coronary Artery Disease

24 Mean Range NSAIDs: Prevalence of Endoscopic NSAID-Induced Ulceration
Gastric Ulcer % to 30% Duodenal Ulcer % to 10 % Clinically Significant Ulcers 2% to 4%

25 Risk Factor Analysis Family History: Smoking:
For both DU and GU, FH pattern appears distinct: 1st-degree relatives of DU patients have a 3x increase in DU; in contrast, relatives of patients with GU have a 3x increase in the GU. Smoking: Evidence supports an association between smoking and PUD in H. pylori infected subjects, but it does not increase the recurrence of peptic ulcers after successful eradication of H. pylori. Dietary fat: No association Coffee: No association High stress / Type A: In a case-control study: quantifying the # of stressful life events and distress scores did not differentiate patients with DU from age-matched controls.

26 Clinical Presentation
Recurrent Epigastric Pain (The most common symptom) Burning Hunger Pain ( Occurs 1-3 hours after meals ) Relieved by food  DU Precipitated by food  GU Relieved by antacids Radiate to back (consider penetration) Pain may be absent or less characteristic in one-third of patients especially in elderly patients on NSAIDs

27 Duodenal Ulcer and Type II Gastric Ulcer (Prepyloric and Antral)
Male Hunger pain, relieved by food, periodicity Back pain if ulcer is penetrating Posterior erosion – haematemesis Anterior erosion – peritonitis Pyloric stenosis – gastric outflow obstruction Position of gastroduodenal ulcer

28 Type I Gastric Ulcer (Proximal)
Less male predominance (still more common in males) Older age group (>50) Epigastric pain worse on eating Weight loss Nausea and vomiting Gastritis and chronic anaemia

29 Peptic Ulcer Disease Duodenal Ulcers Gastric Ulcers > 50 years old
20 to 50 years old High stress occupations Genetic predisposition Pain when stomach is empty Pain at night Frequency = 4 times more common than gastric ulcers Usually associated with hyperacidity Gastric Ulcers > 50 years old Work at jobs requiring physical activity Pain after eating or when stomach is full Usually no pain at night

30 H. Pylori Diagnosis Serology– 90% sensitive, 95% specific – not good for following treatment Biopsy– 98% sensitive – 98% specific Urea breath test– 95% specific, 98% specific – can be used to document eradication Stool antigen test – 90% sensitive, 95% specific – can be used to confirm eradication

31 Natural History 20 – 50% heal untreated
80% heal in 4 weeks of treatment 75% recur in 6 – 12 months More recur in patients with H. pylori, smokers, NSAID users Milk and tobacco slow healing

32 Management of Peptic Ulceration
Medical : Eradication therapy for H pylori ( Tripple Therapy ) Surgical – Elective treatment for ulcers no longer performed, therapeutic OGD/laparotomy for acute complications

33 Strategies in Ulcer therapy
Pre-Hp Reduce acid Take antacids Surgery Post-Hp Find cause Eliminate cause Control symptoms in the meantime Long-term therapy!!


35 H. Pylori Treatment

36 Recurrence Rate/year in Healed PUD
H.P(without Eradication) Anti-Ulcer Therapy H.P Eradication G.U % % % D.U % % %


38 Dysphagia Difficulty Swallowing Types Common causes Investigations
Mechanical obstructions ( Tumours / Stricture ) Neuromuscular ( Stroke , Myasthenia Gravis ) Motility & Functional obstructions ( Achalasis & DES ) Common causes Young adults –Reflux strictures, Achalasia Older adults –Malignancy, Reflux strictures Investigations CBC Gastroduedenoscopy vs. Barium Swallow CXR

39 Carcinoma of the Oesophagus
Common (90% are malignant ) Presents with dysphagia, weight loss, anaemia, anorexia Associated with male sex, alcohol, esophagitis, achalasia, smoking 8% of Barrett’s develop into adenocarcinomas 90% are squamous , 10% adenocarcinoma Diagnosed on Ba swallow/OGD 5 year survival rate : 5 15 %

40 Esophageal carcinoma Squamous cell carcinoma Adenocarcinoma
More prevalent worldwide Risk factors: long-standing esophagitis, achalasia, smoking, alcohol, diet (low vitamins and zinc), genetics 50% in middle 1/3 Adenocarcinoma More common in USA Occurs on top of Barrett esophagus More in distal 1/3

41 Achalasia: Clinical Pearls
Majority present between 20 to 40 years Solid and liquid dysphagia common >90% Regurgitation, weight loss, chest pain 40-60% Barium Study: Accuracy ~95% Endoscopy Decreased Sensitivity (retained food) Necessary to r/o pseudoachalasia More rapid onset of symptoms Late onset (age >60) Difficult to pass scope through EGJ Manometry Gold Standard ↑LES tone, ↓LES relaxation, aperistalsis distal 2/3 esophagus

42 Achalasia: Clinical Pearls, cont.
Treatment Medical (don’t usually work) Nitrates CCB Botulinum toxin Pneumatic Dilation Surgical Myotomy Heller's Myotomy. Open or laparoscopic

43 Diffuse Esophageal Spasm (DES)
Related Disorders of Esophageal Hypermotility Barium Study Corkscrew pattern Manometry >20% simultaneous nonperistaltic contractions (>30mmHg) Potential Therapeutic options (most ineffective) Medical (TCAs, Nitrates, CCBs) Dilation Botox Injection

1- Drug Induced Esophagitis: 2-Infectious Esophagitis : Candidia /HSV /CMV. 3- Corrosive Esophagitis . 4- Severe Reflux Esophagitis

45 Drugs-Induced Esophagitis
Drug-Induced Esophagitis ASA/NSAIDS Doxycycline FeSO4 Alendronate potassium

46 Gastrointestinal Dysfunction
Nausea A subjective experience that is associated with a number of conditions The common symptoms of vomiting are hypersalivation and tachycardia Anorexia A lack of a desire to eat despite physiologic stimuli that would normally produce hunger Retching Nonproductive vomiting Vomiting ( Neuromuscular reflex ) The forceful emptying of the stomach and intestinal contents through the mouth Several types of stimuli initiate the vomiting reflex Projectile vomiting Projectile vomiting is spontaneous vomiting that does not follow nausea or retching

47 Causes of Nausea and Vomiting
Peptic ulcer disease Gastric outlet obstruction Intestinal obstruction Acute gastritis Acute cholecystitis Acute pancreatitis Acute hepatitis

*Gastric Distention. *Sudden temperature changes. *C.N.S . Pathology. *Metabolic : Uraemia /D.M / Hypocapnia /Electolytes imbalance /Toxic drugs &Alcohol. *Vagus &Phrenic nerve irritation. *Surgical :Anaesthesia &postoperative. *Psychogenic &Emotional stress.

49 Constipation Constipation is defined as infrequent or difficult defecation Pathophysiology Neurogenic disorders, functional or mechanical conditions, low-residue diet, sedentary lifestyle, excessive use of antacids, changes in bowel habits *Medications opioids calcium-channel blockers anticholinergic *Decreased motility Ileus *Mechanical obstruction *Metabolic abnormalities Spinal cord compression *Dehydration *Autonomic dysfunction *Malignanc

50 DIARRHEA It is a Symptom or a Sign NOT a Disease AS A SYMPTOM
Frequency of bowel action Looseness of stools Increase in stool volume AS A SIGN Stools weight more than 240 gm/24 hours A Combination of these

51 Abdominal Pain Is a symptom of a number of gastrointestinal disorders

52 Gastrointestinal bleeding
Upper gastrointestinal bleeding Esophagus, stomach, or duodenum Lower gastrointestinal bleeding Below the ligament of Treitz, or bleeding from the jejunum, ileum, colon, or rectum Hematemesis Hematochezia Melena Occult bleeding ? Malignancy

53 Upper Gastrointestinal Bleeding
Acute (> 90% of cases) NSAIDs Peptic ulcer disease Erosive gastritis Ruptured esophagogastric varices Mallory-Weiss tear Erosive esophagitis

54 Upper GI Bleeds Young – PUD, congenital lesions, varices
Old – Tumours, PUD, angiodysplasia Investigations –CBC, Fluid balance, LFTs, clotting, OGD, angiography, cross match Minor bleeds – observe, monitor, arrange OGD Major bleeds – resuscitate, urgent OGD (PPI given afterwards only), treat the cause

55 Oesophageal Bleeds Reflux – small volumes, bright red, Hx
CA – scanty debris, rusty, other symptoms Varices – sudden onset, painless, large volumes, darker, portal HT *treat with pressors* Mallory-Weiss – bright red, history of vomiting

56 Stomach Bleeds Gastritis – small volumes, bright, follows NSAIDS/alcohol/stress Ulcer – larger size, painless, herald smaller bleeds, ? coffee grounds CA – rare, small bleeds, suggestive history Congenital lesions – spontaneous in young, otherwise well, moderate bleeds

57 Duodenal Bleeds Ulcer – history, usually melaena present, risk factors, coffee grounds Aorto-enteric fistula – rare (except in post-op AAA patients), fatal

58 Rectal bleeding - Questions
Duration of symptoms – yrs, months Previous episodes or treatment Is the blood: mixed in with stool separate – found on toilet paper/splashes in toilet bowl Fresh or altered blood - ? Lower vs upper GI bleed Main differentials : Haemorrhoids (piles) Colonic carcinoma Diverticular disease / bleeding ulcer Anal fissure Anal carcinoma (rare)

59 Lower Gastrointestinal Bleeding
Acute (> 90% of cases) Diverticulosis Ischemic colitis Angiodysplasia Colonic polyps Carcinoma Hemorrhoids Radiation colitis

60 Gastrointestinal Bleeding

61 Gastric Carcinoma Clinical features of all upper GI presentations with post-prandial fullness Male/Female 2:1, Predisposing factors – diet (fish, pickled vegetables), atrophic gastritis, pernicious anaemia, previous gastric surgery, polyps, blood group A Investigations –CBC, LFT, OGD, Ba Meal, CT scan 5 year survival rate : 5% Common sites of metastasis include peritoneum, spleen, pancreas, transverse colon

62 Treatment of Gastric CA
Most are not resectable Poor response to combination chemotherapy Palliative surgery – gastrectomy, gastrojejunostomy If resectable usually total gastrectomy and oesophagojejunostomy with node clearance Gastrectomy for bleeding Gastroenterostomy for pyloric obstruction

63 Esophagoscopy

64 Indications and Contraindications
Indications include: Dysphagia Reflux Hematemesis Atypical chest pain Many other conditions Contraindications: To assess reflux symptoms that respond to medical management A uncomplicated sliding hiatal hernia

65 Complications The minor ones: Major complication
Lacerations of the lips or tongue Dislodgment or fracture of teeth and possible aspiration Major complication Esophageal perforation Cervical esophagus (40%) Mid esophagus (25%) Distal esophagus (35%) Morbidity and mortality from perforation is directly related to the time interval between the occurrence of injury, diagnosis and repair

66 Malabsorption Mostly medical causes Giardiasis ( Watery Diarrhoea )
Coeliac disease – clasically diarrhoea, steatorrhoea and weight loss, although often vague symptoms Whipples disease – fat malabsorption secondary to infection, presents with steatorrhoea, arthralgia and malaise Radiation and ischaemic enteropathy Tropheryma whippelii

67 Surgical Causes Crohn’s disease
Short bowel syndrome - <50cm functioning terminal ileum, global malabsorption B12 deficiency after terminal ileum resection Iron deficiency after gastrectomy Blind loop bacterial overgrowth – exclusion of a loop of ileum (Crohn’s, post surgery, fistula) with bacterial growth digesting nutrients

68 Diagnosis of Infectious Diarrhea
History Work Travel Eating Ill contacts Recent antibiotics HIV or immunocompromised Stool C&S, O&P (x1), fecal blood and leukocytes if no improvement in 48 hours or severe disease with bloody stools, fever, dehydration : Consider sigmoidoscopy

69 Liver Diseases & Dentistry

70 Liver : Normal physiology
Secretion of bile for fat absorption Short term sugar storage (glycogen) Aged RBC breakdown and excretion of bilirubin Synthesis of coagulation factors Synthesis of albumin Drug metabolism

71 ESLD: (Regardless of Cause)
Loss of Synthetic function: Vit K dependant coagulation factors (II, VII, IX, X) Hypoalbuminemia (edema) Portal hypertension Esophageal, umbilical, hemorroidal varices Ascites (abdominal fluid build-up) Splenomegaly (thrombocytopenia) Loss of de-toxification function: ammonia Encephalopathy

72 ESLD: (Regardless of Cause)
Bone marrow toxicity: anemia, leukopenia and thrombocytopenia Endocrine disturbances: testicular atrophy and gynecomastia Esophagitis / gastritis Elevated Liver enzymes: AST / ALT

73 ESLD: (Regardless of Cause)
Elevated bilirubin: causing Jaundice Elevated INR: causing bleeding Decreased albumin: causing edema and ascites Altered drug metabolism: unpredictable Drug effect can be Up or Down


75 Etiology of Chronic Liver Diseases & Cirrhosis
Alcoholic liver disease Viral hepatitis Parasites (schistosomiasis) Autoimmune Liver Diseases( Biliary disease ) Primary hemochromatosis Cryptogenic cirrhosis Wilson’s, 1AT def Hepatic-Venous outflow obstruction Toxicant and drugs Metabolic abnormality NASH Malnutrition

76 Clinical Manifestation
Onset: Slowly Progressive Majority: 3~5 years or 10 years Minority: 3~6 months Stages: Compensated Decompensated

77 Compensated Stage Fatigue Loss of appetite Anorexia Abdominal discomfort Abdominal pain Hepatomegaly (slightly or moderately) Splenomegaly

78 Deterioration of Liver Function Feature of Portal Hypertention
Decompensated Stage Deterioration of Liver Function Feature of Portal Hypertention

79 Complications of Cirrhosis
Portal Hypertension Synthetic Dysfunction Coagulopathy Encephalopathy Immunodeficiency Malnutrition HCC 79

80 Xanthelasma Scleral icterus Jaundice Fetor hepaticus Parotid hypertrophy Spider angioma Gynecomastia Ms wasting Bleeding tendency (bruising) Anemia Palmar erythema Dupuytern’s cont Astrexis Ankle edema

81 Jaundice

82 Jaundice Jaundice is a yellowish discoloration of the sclera, skin, mucus membranes, and body fluids caused by the deposition of bile pigments It is usually caused by either an increased production or decreased excretion of bilirubin from the body Jaundice can be classified into: Prehepatic jaundice (increased production) Hepatic jaundice (decreased excretion) Post-hepatic jaundice (decreased excretion)

83 Pre-Hepatic Haemolytic anaemia – hereditary spherocytosis, sickle cell, thalassaemia, Gilbert’s syndrome High levels of unconjugated bilirubin, normal LFTs, raised reticulocytes Investigate further with blood film and autoantibody screen

84 Hepatic Hepatic injury – viral hepatitis, sclerosis, cirrhosis, poisons, drugs Bilirubin tends to be conjugated, (jaundice occurs out of failure to excrete, not conjugate) Abnormal LFTs (raised ALT/AST) Investigate further with viral titres, USS, liver biopsy

85 Post-Hepatic Wall Lumen Outside Lumen
Raised conjugated bilirubin (absorbed from biliary tree) Decreased urinary urobilinogen (bilirubin does not make it to the small bowel) Obstructed LFTs (raised ALP and GGT) Further investigation with USS, and then ERCP/CT as appropriate

86 Jaundice ALP ↑Production: Haemolysis ↓Uptake
Pre-Hepatic/ Unconjugated hyperbilirubinaemia ↑Production: Haemolysis ↓Uptake ↓Conjugation – Gilbert’s, Crigler-Najjar Hepatic /Mixed ALT/AST Hepatocellular damage +/- cholestasis: Viruses: Hep A,B,C…CMV, EBV Alcoholic Hepatitis, Cirrhosis, metastases Drugs – Paracetamol od, TB, Valproate, MAOI Obstruction of CBD: Gallstones, Ca Head Panc, LN Drugs: Abx Biliary cirrhosis, atresia, cholangitis Mirrizi’s Syndrome ALP Post Hepatic/ Conjugated hyperbilirubinaemia

87 Jaundice

PRE-HEPATIC heamolysis INTRA-HEPATIC hepatitis, cirrhosis, congenital hyperbiliruniaemia POST-HEPATIC gallstones, tumours, strictures, biliary atresia Unconjugated bilirubin Conjugated bilirubin (water soluble)

89 Causes of Hepatomegaly
Regular generalized enlargement without jaundice Regular generalized enlargement with jaundice Irregular generalized enlargement without jaundice Irregular generalized enlargement with jaundice Localized swellings

90 Manifestation of ESLD

91 Manifestation of ESLD Spider telangiectasias Palmar erythema
Nail changes Dupuytren's contracture Gynecomastia Testicular atrophy Hepatomegaly Splenomegaly Ascites Caput medusae Fetor hepaticus Jaundice Asterixis

92 Symptoms of Advanced Cirrhosis
Fatique, weakness Nausea, vomiting and loss of appetite Weight loss, muscle wasting Jaundice, dark urine Unusual bruising Spider naevi, caput Medusae Bloody, black stools or unusually light-colored stools Vomiting of blood Abdominal swelling Swollen feet or legs Red palms Gynecomastia Loss of sex drive Menstrual changes in women Generalized itching Sleep disturbances, confusion,desorientation, tremor, ataxia, asterixis

93 Visible signs of advanced liver cirrhosis
Gynecomastia Ascites Caput Medusae Umbilical hernia

94 Complications of ESLD Malnutrition Encephalopathy Coagulopathy Portal Hypertension Variceal Hemorrhage Pulmonary Hypertension {Hepatopulmonary syndrome} Hepatorenal Syndrome {HRS} Spontaneous Bacterial Peritonitis {SBP} Hyponatremia

95 Signs of ESLD

96 Caput Medusae

97 Spider Angiomas Spider angiomas



100 Esophageal Varices


102 Laboratory Findings Aminotransferases -AST & ALT Alkaline phosphatase
Gamma-glutamyl transpeptidase (GGT) Bilirubin Albumin Globulins Serum sodium Hematologic abnormalities - Anemia -Thrombocytopenia -Leukopenia -Neutropenia -Coagulation defects (PT & INR)

103 Pancreatitis Caused by gallstones and/or alcohol
Enzymatic spillage, inflammation, oedema and necrosis of the pancreas Presents with moderate upper abdominal pain radiating to back, nausea, vomiting, pyrexia, tachycardia, paralytic ileus and occasionally retroperitoneal bleeding (Grey Turner’s and Cullen’s signs) Confirm diagnosis with amylase >1000 (lab dependent) ABG, CXR, ECG – these patients are often very sick

104 Complications Acutely – abscess, sepsis, necrosis, ATN, haemorrhage, pseudocyst formation Chronic pancreatitis - CBD obstruction, diabetes, fibrosis, inflammation, steatorrhoea - Surgical management (drainage of dilated ducts) appropriate in a small minority

105 Treatment of Pancreatitis
IV fluids, analgesia, anti-emetic Monitor observations, renal and respiratory function Analgesia Evidence for ERCP if proven CBD stone Highly conservative

106 Pancreatic Neoplasms Adenocarcinoma affecting any part of the pancreas
Endocrine tumours cause a variety of syndromes from secreted peptides M>F, more common after age 50 Predisposed to by smoking, diabetes, chronic pancreatitis Symptoms and presentation dependent on site - Tail (15%) malignant ascites, anaemia, metastases (peritoneal, liver) - Body (25%) back pain, anorexia, weight loss, steatorrhoea, diabetes - Head (55%) painless progressive jaundice - Periampullary (5%) as above, occasionally with duodenal obstruction causing vomiting

107 Investigations and Prognosis
USS – biliary tree, occasionally visible mass CT scan +/- biopsy or ERCP +/- biopsy 90% of patients are dead within 12 months of diagnosis Tissue type important (better prognosis for non-pancreatic peri-ampullary tumour)

108 Management Palliation Curative Coeliac nerve ablation (body tumours)
Enzyme supplements, insulin Relieve jaundice by ERCP Surgery Curative Rarely appropriate Requires early presentation Whipple’s pancreatico-duodenectomy

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