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Year 3 SOFIA CONDITIONS > Gastrointestinal > Flashcards

Gastrointestinal Flashcards

1
Q

What is achalasia?

A

An oesophageal motility disorder, characterised by loss of peristalsis and failure of relaxation of the lower oesophageal sphincter (LOS)

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2
Q

What is the aetiology of achalasia?

A
  • Degeneration of ganglion cells of the meyenteric plexus in the oesophagus due to an unknown cause.
  • Oesophageal infection with Trypanosoma cruzi seen in Central and South America producers a similar disorder- Chaga’s disease
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3
Q

What is the epidemiology of achalasia?

A

Usual presentation age: 25-60 years

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4
Q

What are the presenting symptoms of achalasia?

A

Insidious onset and gradual progression of

  • Intermittent dysphagia involving solids and liquids
  • Difficulty belching
  • Regurgitation (particularly at night)
  • Heartburn
  • Chest pain (atypical/cramping, retrosternal)
  • Weight loss
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5
Q

What are the signs of achalasia on examination?

A

May reveal signs of complications

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6
Q

What are the investigations of achalasia?

A
  • CXR: may show widened mediastinum and double right border (dilated oesophagus), an air-fluid level in upper chest and absence of the normal gastric air bubble
  • Barium swallow: Dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)
  • Endoscopy: To exclude malignancy which can mimic achalasia
  • Manometry: Elevated resting LOS pressure (over 45mmHg), Incomplete LOS relaxation, Absence of peristalsis in the distal (smooth muscle portion) of the oesophagus
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7
Q

What is acute cholangitis?

A

Ascending cholangitis

  • Infection of the biliary tree, most commonly caused by obstruction.
  • In its less severe form, there is biliary obstruction with inflammation and bacterial seeding and growth int he biliary tree
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8
Q

What is the aetiology of acute cholangitis?

A
  • Most common aetiology is cholelithiasis leading to choledocholithiasis and biliary obstruction.
  • Iatrogenic biliary tract injury, most commonly caused via surgical injury cholecystectomy, can lead to benign strictures, which in turn can lead to obstructions
  • Acute prancreatitis
  • Malignant strictures
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9
Q

What is the epidemiology of acute cholangitis?

A
  • Relatively uncommon
  • Male to female ratio is equal
  • Median age of presentation is 50-60
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10
Q

What are the presenting symptoms of acute cholangitis?

A
  • Jaundice
  • Fever
  • Right upper quadrant pain
  • Right upper quadrant tenderness
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11
Q

What are the signs of acute cholangitis on examination?

A
  • Alcoholic stools
  • Pruritis
  • Hypotension
  • Mental status changes
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12
Q

What are the investigations for acute cholangitis?

A
  • FBC: Raised WBC, decreases platelets
  • Serum urea: Raised in severe cases
  • Serum creatinine: Raised in severe cases
  • ABG: Metabolic acidosis
  • LFT: Hyperbilinuraemia
  • CRP: Raised
  • Serum K & Mg: May be decreased
  • Blood cultures: Bacteria usually gram negative, but gram positive bacteria and anaerobes are also implicated in cholangitis
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13
Q

How is acute cholangitis managed?

A
  • IV antibiotics (Piperacillin/Tazobactam
  • Biliary decompression
  • Opioid analgesics
  • Lithotripsy
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14
Q

What are the possible complications of acute cholangitis?

A
  • Acute prancreatitis
  • Inadequate biliary drainage following performance of endoscopy, radiology or surgery
  • Hepatic abscess
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15
Q

What is the prognosis of acute cholangitis?

A
  • If adequate biliary drainage is quickly obtained, most patients experience rapid clinical improvement
  • Outcome worse for patient’s with underlying medical conditions
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16
Q

What is alcoholic hepatitis?

A

Inflammatory liver injury caused by chronic heavy intake of alcohol

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17
Q

What is the aetiology alcoholic hepatitis?

A

One of the three forms of liver disease caused by excessive intake of alcohol, a spectrum that ranges from alcoholic fatty liver (steatisus) to alcoholic hepatitis and chronic cirrhosis
- In alcoholic hepatitis, the liver histopathology shows centrilobar ballooning degeneration and necrosis of hepatocytes, steatosis, neutrophilic inflammation, cholestasis, Mallory hyaline inclusions and giant mitochondria

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18
Q

What is the epidemiology of alcoholic hepatitis?

A

10-35% of heavy drinkers develop this form of liver disease

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19
Q

What are the presenting symptoms of alcoholic liver disease?

A
  • May remain asymptomatic and undetected unless they present for other reasons
  • Mild illness with nausea, malaise, epigastric or right hypochondrial pain
  • Low grade fever
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20
Q

What are the signs of acute hepatitis on examination?

A
  • Signs of alcohol excess: Malnourishes, palmar erythema, Dupuytren’s contracture, facial telangiectasia, parotid enlargement, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising
  • Signs of severe alcoholic hepatitis: Febrile (50% pts), tachycardia, jaundice, bruising, encephalopathy, ascites, hepatomegaly, splenomegaly
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21
Q

What are the investigations for alcoholic hepatitis?

A
  • Blood: Decreased Hb, Increased MCV, Increased WCC, Decreased platelets. U&E: Urea and K low unless significant renal impairment. Clotting: Prolonged PT sensitive marker of sig. liver damage
  • Ultrasound: For other causes of liver impairment (e.g. malignancies
  • Upper GI endoscopy: Investigate for varices
  • Liver biopsy: Percutaneous or transjugular may be helpful to distinguish from other causes of hepatitis
  • Electroencephalogram: For slow wave activity indicative of encephalopathy
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22
Q

How is alcoholic hepatitis managed?

A
  • Acute: Thiamine, Vitamin C and other multivitamins. Monitor and correct K, MG and glucose abnormalities. Ensure adequate glucose output. Treat encephalopathy with oral lactose and phosphate enemas. Ascites manages by diuretics
  • Nutrition: Oral and or nasogastric feeding important with increased caloric intake. Protein restricted to be avoided unless patient is encephalopathic. Nutritional supplementation and vitamins started parenterally and continues orally after
  • Steroid therapy
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23
Q

What are the possible complications of alcoholic hepatitis?

A
  • Acute liver decompensation
  • Hepatorenal syndrome (renal failure secondary to advanced liver disease
  • Cirrhosis
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24
Q

What is the prognosis of alcoholic hepatitis?

A

Morality in first months is 10%; 40% in first year

  • If alcoholic intake continues, most progress to cirrhosis within 1-3 years
  • Maddrey’s discriminant function. If less than 32, indicates more than 50% 30-day mortality
  • Glasgow alcoholic score
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25
Q

What is an anal fissure?

A

Split in the skin of the distal anal canal characterised by pain on defecation and rectal bleeding

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26
Q

What is the aetiology of anal fissures?

A
  • Passage of hard stool bolus may precipitate an anal fissure
  • Fissure may begin during episode of loose stool, or often occurs spontaneously with no obvious precipitating factor
  • Opiate analgesia is associated with constipation and a subsequence increased incidence of anal fissure
  • Hard stool tears the anal skin at pectin (at dentate line)
  • Pregnancy is risk factor
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27
Q

What is the epidemiology of anal fissures?

A
  • Equally common in men and women
  • Often affects young adults ages 15-40, but may be seen in older adults
  • May be seen in younger adults due to poor toileting
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28
Q

What are the presenting symptoms of anal fissures?

A
  • Pain on defecation
  • Tearing sensation on passing stool
  • Fresh blood on stool or on paper
  • Anal spasm
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29
Q

What are the signs of anal fissures on examination?

A
  • Sentinel pile

- Fissure visible on retraction of buttock

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30
Q

What are the investigations for anal fissures?

A
  • Clinical diagnosis
  • Anal manometry: Low resting pressure
  • Anal ultrasound: Defects in external or internal anal sphincter
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31
Q

How are anal fissures managed?

A
  • Conservative treatment alone: high fibre diet, adequate fluid intake, sitz baths and topical analgesia
  • Topical glyceryl trinitrate
  • Topical diltiazem
    Resistant fissures:
  • Botulinium toxin injection
  • Surgical sphincterotomy
  • Anal advancement flap
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32
Q

What are the possible complications of anal fissures?

A
  • Chronic anal fissure
  • Incontinence after surgery
  • Recurrence
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33
Q

What is the prognosis of anal fissures?

A
  • 60% achieve healing of fissure after 6-8 weeks
  • Some patients relapse
  • Some require surgery
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34
Q

What is an appendicectomy?

A

Surgical removal of vermiform appendix

- Can be formed laparoscopically or as open operation

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35
Q

What are the indications of appendicectomy?

A
  • Appendicitis
  • Consider for patients with history of persistent abdominal pain, fever and clinical signs of localised or diffuse peritonitis especially if leucocytosis is present
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36
Q

What are the possible complications of appendectomy?

A
  • Bleeding
  • Wound infection
  • Infection, redness and swelling of belly can occur if appendix bursts during surgery (peritonitis)
  • Blocked bowels
  • Injury to nearby organs
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37
Q

What is appendicitis?

A
  • Acute inflammation of vermiform appendix, most likely due to obstruction of lumen of the appendix
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38
Q

What is the aetiology of appendicitis?

A
  • Obstruction is main cause

- Faecolith (hard mass of faecal matter), normal stool or lymphoid hyperplasia are main causes for osbtruction

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39
Q

What is the epidemiology of appendicitis?

A
  • One of the most acute abdominal surgical emergencies
  • Predominantly in 15-59 age group
  • Incidence lower in populations where high-fibre diet is consumed
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40
Q

What are the presenting symptoms of appendicitis?

A
  • Abdominal pain
  • Anorexia
  • Right lower quadrant tenderness
  • Nausea
  • Fever
  • Vomiting
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41
Q

What are the signs of appendicitis on examination?

A
  • Adolescence or early adulthood
  • Diminished bowel sounds
  • Rovsing’s sign (Pressing left side of abdominal cavity and eliciting pain in lower right quadrant)
  • Psoas sign (Extending right thigh on left lateral position elicits pain in right lower quadrant)
  • Obturator sign (Pain elicited in RLQ of abdomen by internal rotation of the flexed right thigh)
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42
Q

What are the investigations for appendicitis?

A
  • FBC: Mild leukocytosis
  • Abdominal and pelvic CT scan: Abnormal appendix, more than 6mm diameter
  • Urinary pregnancy test: Negative
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43
Q

How is appendicitis manage?

A
  • Appendectomy and supportive care

- Intravenous antibiotic therapy: cefoxitin

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44
Q

What are the possible complications of appendicitis?

A
  • Perforation
  • Generalised peritonitis
  • Appendicular mass
  • Appendicular abscess
  • Surgical wound infection
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45
Q

What is the prognosis of appendicitis?

A
  • Good if patients treated in timely fashion

- Laparoscopic appendectomy shown to reduce incidence of overall complications

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46
Q

What is autoimmune hepatitis?

A

Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of the circulating autoantibodies

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47
Q

What is the aetiology of autoimmune hepatitis?

A

In genetically predisposed individual, environmental agent may lead to hepatocyte expression of HLA antigens which then become focus of principally T-cell mediated autoimmune attack

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48
Q

What is the epidemiology of autoimmune hepatitis?

A

Type 1 occurs in all age groups (mainly in young women)

Type 2 generally a disease of girls and young women

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49
Q

What are the presenting symptoms of autoimmune hepatitis?

A

May be asymptomatic discovered incidentally by abnormal LFT
- Insidious onset: Malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis
- Acute hepatitis (25%): Fever, anorexia, jaundice, nausea, vomiting, diarrhoea, RUQ pain. May also present with serum sickness (e.g. arthalgia, polyarthritis, maculopapular rash
May be associated with keratoconjuctivitis sicca

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50
Q

What are the signs of autoimmune hepatitis on examination?

A
  • Stigmata of chronic liver disease e.g. spider naevi
  • Ascites, oedema and encephalopathy are late features
  • Cushingoid features e.g. rounded face, cutaneous striae, acne, hirsutism) may be present even before the administration of stoids
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51
Q

What are the investigations for autoimmune hepatitis?

A
  • Blood: Increased AST and ALT, Increased AlkPhos, Increase bilirubin, Decreased albumin, Increased PT, Decreased platelets and WCC from hypersplenism if portal hypertension present
  • Liver biopsy: Needed to establish the diagnosis, shows interface hepatitis or cirrhosis
  • Other: Rule out other causes of liver disease
  • Ultrasound, CT or MRI of liver and abdomen: Visualise structural lesions
  • ERCP: Rule out PSC
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52
Q

How is autoimmune hepatitis managed?

A

Indications- aminotransferases raised, the upper limit of normal and symptomatic

  • Immunosuppression: with steroids e.g. prednisolone, followed by maintenance treatment with gradual reduction in dose.
  • Monitor: Ultrasound ever 6-12 months to detect hepatocellular carcinoma
  • Hep A and B vaccinations
  • Liver transplant: for pts with refractory to or intolerant of immunosuppressive therapy and those with end-stage disease
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53
Q

What are the possible complications of autoimmune hepatitis?

A
  • Fulminant hepatic failure
  • Cirrhosis and complications or portal hypertension (e.g. varices, ascites)
  • Hepatocellular carcinoma
  • Side-effects of corticosteroid treatment
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54
Q

What is the prognosis of autoimmune hepatitis?

A
  • Older patients with type 1 autoimmune hepatitis are more likely to have cirrhosis at presentation but may be more likely to respond to treatment
  • 80% receive remission by 3 years
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55
Q

What is Barrett’s oesophagus?

A

Change in the normal squamous epithelium of the oesophagus to specialised intestinal metaplasia
- Associated with gastro-oesophageal reflux even if reflux is asymptomatic

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56
Q

What is the aetiology of Barrett’s oesophagus?

A
  • Main aetiology is gastro-oesophageal reflux

- Evidence that combined bile and acid reflux are primary causative agents

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57
Q

What is the epidemiology of Barrett’s oesophagus?

A
  • More common in men and white people
  • Rare in children
  • More prevalent with age
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58
Q

What are the presenting symptoms of Barrett’s oesophagus?

A
  • Heart burn
  • Regurgitation
  • Dysphagia
  • Chest pain
  • Cough
  • SOB/wheezing
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59
Q

What are the signs of Barrett’s oesophagus on examination?

A
  • Laryngitis

- History of aspiration pneumonia

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60
Q

What are the investigations for Barrett’s oesophagus?

A
  • Upper GI contrast radiography: hiatal hernia and reflux

- Upper GI endoscopy with biopsy: Abnormal epithelium characteristic of Barrett’s oesophagus

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61
Q

How is Barrett’s oesophagus managed?

A
  • Proton pump inhibitor plus surveillance
  • Radiofrequency ablation
  • Anti-reflux surgery plus surveillance
  • Radiofrequency ablation
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62
Q

What are the possible complications of Barrett’s oesophagus?

A
  • Adenocarcinoma
  • Oesophageal stricture
  • Quality of life deficit
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63
Q

What is the prognosis for Barrett’s oesophagus?

A
  • Adenocarcinomas discovered while screening for Barrett’s oesophagus are early-stage lesions and have good prognosis
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64
Q

What is biliary colic?

A

When pain occurs due to a gallstone temporarily blocking the bile duct
Can last hours, associated with nausea and vomiting

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65
Q

What are the risk factors of biliary colic?

A
  • Previous episode of biliary pain (50% have another episode within a year)
  • Older age
  • Female sex
  • Obesity
  • Rapid weight loss
  • Drugs
  • Symptomatic stones, pregnancy, smoking
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66
Q

What is the epidemiology of biliary colic?

A
  • Sudden onset, severe RUQ pain
  • Constant in nature
  • Nausea and vomiting
  • May last hours
  • Radiates to back or right scapula and jaundice
  • Jaundice is common but can develop with choledocholelithiasis
  • Pain worse after fatty meal
    If fever present, suggests complication such as cholecystitis, cholangitis or pancreatitis
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67
Q

What are the signs of biliary colic on examination?

A
  • Right upper quadrant and epigastric tenderness
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68
Q

What are the investigations for biliary colic?

A
  • Abdominal ultrasound: For symptomatic patients
  • CT follow up if unremarkable
  • MRCP
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69
Q

How is biliary colic managed?

A
  • Analgesia
  • Rehydration
  • NBM
  • Elective laparoscopic cholestystectomy
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70
Q

What are the possible complications of biliary colic?

A
  • Cholangitis
  • Sepsis
  • Pancreatitis
  • Hepatitis
  • Choledocholithiasis
  • Gallbladder perforation
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71
Q

What is the prognosis for biliary colic?

A

Uncomplicated biliary colic has low mortality

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72
Q

What is cholecystectomy?

A
  • Surgical removal of gallbladder
  • Common treatment of symptomatic gallstones and other gallbladder conditions
  • Can be laparoscopic or open
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73
Q

What are the indications for a cholecystectomy?

A
  • Calcified gallbladder
  • Acute cholecystitis
  • Choledocholithiasis
  • Gallstone pancreatitis
  • Biliary pain
  • Biliary dyskinesia
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74
Q

What are the possible complications of cholecystectomy?

A
  • Bile leek
  • Bleeding
  • Blood clots
  • Infection
  • Pancreatitis
  • Pneumonia
  • Post-cholecystectomy syndrome
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75
Q

What is cholecystitis?

A

Acute gallbladder inflammation caused by an obstruction at the cystic duct

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76
Q

What are the causes of cholecystitis?

A

Acute: Stone or sludge impaction in the neck of the gallbladder
Chronic: Chronic inflammation and colic

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77
Q

What is the epidemiology of cholecystitis?

A

8% of >40yrs.

5 Fs: Fat, Forty, Female, Fertile, Fair

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78
Q

What are the presenting symptoms of cholecystitis?

A
  • Patient systemically unwell
  • Fever
  • Prolonged upper abdominal pain that may be referred to right shoulder (due to diaphragmatic irritation)
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79
Q

What are the signs of cholecystitis on examination?

A
  • Tachycardia
  • Pyrexia
  • Right upper quadrant or epigastric tenderness
  • They may be guarding. With or without rebound
  • Murphy’s signs is elicited by placing a hand at the costal margin in the RUQ and asking patient to breathe deeply
  • Patient stops breathing as the inflamed gallbladder descends and contacts the palpating fingers
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80
Q

What are the investigations for cholecystitis?

A
  • Ultrasound: image stones and assess CBD diameter

- MRCP: to find CBD stones

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81
Q

How is cholecystitis managed?

A
  • Cholecystectomy

- If US shows dilated GB with stones → ERCP and sphincterotomy before surgery

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82
Q

What are the possible complications of cholecystitis?

A
  • Perforation
  • Suppurative cholecystitis
  • Gangrenous cholecystitis
  • Bile duct injury due to surgery
  • Gallstone ileus
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83
Q

What is the prognosis for cholecystitis?

A

Removing the gallbladder and the contained gallstones when biliary pain starts will prevent further biliary attacks and reduce the risk of developing cholecystitis. If the gallbladder perforates, mortality is 30%.

Untreated acute acalculous cholecystitis is life-threatening and is associated with up to 50% mortality.

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84
Q

What is cirrhosis?

A

End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.
Decompensated when there are complications such as ascites, jaundice, encephalopathy or GI bleeding

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85
Q

What is the aetiology of cirrhosis?

A
  • Chronic alcohol misuse
  • Chronic viral hepatitis
  • Autoimmune hepatitis
  • Drugs: e.g. methotrexate, hepatotoxic drugs
  • Inherited: haemochromatosis, Wilson’s disease, galactosaemia, cystic fibrosis, a1-Antitrypsin deficiency
  • Vascular: Budd-Chiari syndrome or hepatic venous congestion
  • Chronic biliary diseases: Primary biliary cirrhosis (PBC), primary sclerosing cholangitis, biliary atresia
  • Cryptogenic
  • Non-alcoholic steatohepatitis (NASH)
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86
Q

What is the epidemiology of cirrhosis?

A

Among the top 10 leading cause of deaths worldwide

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87
Q

What are the presenting symptoms of cirrhosis?

A

Early non-specific symptoms: Anorexia, nausea, fatigue, weakness, weight loss

  • Symptoms caused by decreased liver synthetic function: Easy bruising, abdominal swelling, ankle oedema
  • Reduced detoxification function: Jaundice, personality change, altered sleep pattern, amenorrhoea
  • Portal hypertension: Abdominal swelling, haematemesis, PR bleeding or melaena
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88
Q

What are the signs of cirrhosis on examination?

A

Stigmata of chronic liver disease: ABCDE

  • Asterixis (liver flap)
  • Bruises
  • Clubbing
  • Dupuytren’s contracture
  • Erythema (palmar)
  • Jaundice, gynaecomastia, leukonychia, parotid enlargement, spider naevi, stretch marks, ascites (shifting dullness and fluid thrill), enlarged liver, testicular atrophy, caput medusae, splenomegaly
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89
Q

What are the investigations for cirrhosis?

A
  • Blood: Decreased Hb and platelets. LFTs may be normal. Prolonged PT. Serum AFP Increased in chronic liver disease
  • Other: to determine cause
  • Ascitic tap: microscopy
  • Liver biopsy: Percutaneous or transjugular if clotting deranged or ascites present
  • Imaging: US, CT or MRI
  • Endoscopy: Examine for varices,
  • Child-Pugh grading
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90
Q

How is cirrhosis managed?

A

Treat cause if possible, avoid alcohol, sedative, opiates, NSAIDs and drugs that affect the liver. Nutrition important if intake poor
Treat complications
Encephalopathy- Treat infections
Ascites: Diuretics

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91
Q

What are the possible complications of cirrhosis?

A
  • Portal hypertension with ascites
  • Encephalopathy or variceal haemorrhage
  • SBP
  • Hepatocellular carcinoma
  • Renal failure (hepatorenal syndrome)
  • Pulmonary hypertension (hepatopulmonary syndrome)
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92
Q

What is the prognosis of cirrhosis?

A
  • Depends on the aetiology and complications
  • Generally poor: Overall 5 year survival is 50%
  • In presence of ascites, 2 year survival of 50%
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93
Q

What is coeliac disease?

A

Inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption

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94
Q

What is the aetiology of coeliac disease?

A
  • Sensitivity to gliadin component of the cereal protein, triggers an immunological reaction int he small intestine, leading to mucosal damage and loss of villi
  • 10% risk of first-degree relatives being affected and there is clear genetic susceptibility associated with HLA-B8, DR3 and DQW2 haplotypes
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95
Q

What is the epidemiology of coeliac disease?

A

UK Prevalence is 1 in 2000

- Rare in East Asia

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96
Q

What are the presenting symptoms of coeliac disease?

A
  • May be asymptomatic
  • Abdominal discomfort: pain and distension
  • Steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away) diarrhoea
  • Tiredness, malaise, weight loss (despite normal diet
  • Failure to thrive in children, amenorrhoea in young adults
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97
Q

What are the signs of coeliac disease on examination?

A
  • Signs of anaemia: pallor
  • Signs of malnutrition: Short stature, abdominal distension and wasted buttocks in children. Triceps skinfold thickness gives an indication of fat stores
  • Signs of vitamin or mineral deficiencies (e.g. osteomalacia, easy bruising)
  • Intense, itchy blisters on elbows, knees or buttock (dermatitis herpetiforms)
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98
Q

What are the investigations for coeliac disease?

A
  • Blood: Decreased Hb, iron and folate, albumin, phosphate
  • Serology: Testing for IgG anti-gliadin, IgA, and IgG anti-endomysial translutaminase antibodies can be diagnostic. IgA deficiency is common
  • Stool: Culture to exclude in infection
  • D-xylose test: Reduced urinary excretion after an oral xylose load indicates small bowel malabsorption
  • Endoscopy: Direct visualisation shows villous atrophy in small intestine, giving mucosa a flat smooth appearance. Biopsy shows villous atrophy with crypt hyperplasia of the duodenum. Epithelium adopts a cuboidal appearance, there is inflammatory infiltrate of lymphocytes and plasma cells in lamina propria
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99
Q

How is coeliac disease managed?

A
  • Advice: Withdrawal of gluten from the diet, with avoidance of all wheat, rye and barley products. Education and expert dietary advice is essential. The Coeliac Society offer patient support and advice
  • Medical: Vitamin and mineral supplements. Oral corticosteroids may be used if the disease does not subside with gluten withdrawal
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100
Q

What are the possible complications of coeliac disease?

A
  • Iron, folate and Vitamin B12 deficiency
  • Osteomalacia
  • Ulcerative jejunoiletis
  • Gastrointestinal lymphoma (particular T cell)
  • Bacterial overgrowth
  • Rarely can cause cerebellar ataxia
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101
Q

What is the prognosis for coeliac disease?

A
  • Strict adherence to gluten-free diet, most patients make a full recovery
  • Symptoms usually resolve within weeks
  • Histological changes may take longer to resolve
  • A gluten-free diet needs to followed for life
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102
Q

What is a colonoscopy?

A

An endoscopic examination of the large bowel and the distal part of the small bowel with a CCD camera or a fiber optic camera on a flexible tube passed through the anus
- Can provide visual diagnosis (polyps, ulceration) and grants opportunity for biopsy or removal of suspected colorectal cancer lesions

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103
Q

What are the indications for a colonoscopy?

A
  • Gastrointestinal haemorrhage
  • Unexplained changes in bowel habit
  • Suspicion of malignancies
  • Diagnose colon cancer and IBD
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104
Q

What are the possible complications of a colonoscopy?

A
  • Gastrointestinal perforation
  • Bleeding: by cauterisation via the instrument. Delayed bleeding at site of polyp removal up to weak after procedure
  • Splenic rupture
  • Dehydration caused by laxatives usually administered during bowel preparation
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105
Q

What is Crohn’s disease?

A

Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract.
Grouped with ulcerative colitis and together they are known as inflammatory bowel disease

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106
Q

What is the aetiology of Crohn’s disease?

A

Cause has not yet been elucidated, but thought to involve an interplay between genetic and environmental factors
- Inflammation can occur anywhere along GI tract (40% involving the terminal ileum) and ‘skip’ lesions with inflamed segments of bowel interspersed with normal segments is not unusual

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107
Q

What is the epidemiology of Crohn’s disease?

A
  • Prevalence is 50-80 in 100,000

- Affects any age but peak incidence is in teen or twenties

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108
Q

What are the presenting symptoms of Crohn’s disease?

A
  • Crampy abdominal pain (caused by inflammation, fibrosis or bowel obstruction)
  • Diarrhoea (may be blood or steatorrhoea)
  • Fever, malaise, weight loss
  • Symptoms of complications
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109
Q

What are the signs of Crohn’s disease on examination?

A

Weight loss, clubbing, signs of anaemia

  • Aphthous ulceration of the mouth
  • Perianal skin tags, fistulae and abscesses
  • Signs of complications (eye disease, joint disease, skin disease)
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110
Q

What are the investigations for Crohn’s disease?

A
  • Blood: FBC (Decreased Hb, Raised platelets * WCC), U&E, LFT (low albumin), increased ESR, haematinics to look for deficiency states, ferritin, Vit B12 and red cell folate
  • Stool microscopy and culture: to exclude infective colitis
  • AXR: evidence of toxin megacolon
  • Erect CXR: If risk of perforation
  • Small bowel barium follow through: May reveal fibrosis/ strictures (string sign of Kantor), deep ulceration (rose thorn), cobblestone mucosa
  • Endoscopy and biopsy: May help differentiate between ulcerative colitis and Crohn’s.
  • Radionuclide-labelled neutrophil scan
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111
Q

How is acute exacerbation of Crohn’s disease managed?

A
  • Fluid resuscitation
  • IV or oral corticosteroids
  • 5-ASA analogues (e.g. mesalazine, sulfasalazine) may induce a remission in colonic Crohn’s disease
  • Analgesia
  • Elemental diet may induce remission (more often used in children)
  • Parenteral nutrition may be necessary
  • Monitor markers of activity (fluid balance, ESR, CRP, platelets, stool frequency, Hb and albumin)
  • Assess for complications
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112
Q

How is Crohn’s disease managed in the long term?

A
  • Steroids: For treating acute exacerbations
  • 5-ASA analogues (e.g. sulfasalazine, mesalazine) decreased relapses: useful for mild-moderate disease
  • Immunosuppression: Using steroid-sparing ages (e.g. azathioprine, 6-mercaptopurine, methotrexate) to reduce relapses
  • Anti-TNF agents (e.g. infliximab, adalimumab): Very effective agents in achieving and maintaining remission. Usually reserved for refractory cases
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113
Q

What advice is given to patient’s with Crohn’s disease?

A
  • Stop smoking
  • Dietician referral
  • Education and advice (e.g. from inflammatory bowel disease nurse specialists
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114
Q

When is surgery for Crohn’s disease indicated?

A
  • When medical treatment fails
  • Failure to thrive in children or the presence of complications
  • Involves resection of affected bowel and stoma formation, although there is a risk of disease recurrence
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115
Q

What are the possible GI complications of Crohn’s disease?

A
  • Haemorrhage
  • Bowel strictures
  • Perforation
  • Fistulae (between bowel, bladder, vagina)
  • Perianal fistulae and abscess
  • GI carcinoma (5% risk in 10 years)
  • Malabsorption
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116
Q

What are the extraintestinal features of complications of Crohn’s disease?

A
  • Uveitis
  • Episcleritis
  • Gallstones
  • Kidney stones
  • Arthropathy
  • Sacroilitis
  • Ankylosing spondylitis
  • Erythema nodosum and pyoderma gangrenosum
  • Amyloidosis
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117
Q

What is the prognosis of Crohn’s disease?

A
  • Chronic relapsing condition

- 2/3 will require will surgery at some stage and 2/3 of these have more than 1 surgical procedure

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118
Q

What is diverticulosis?

A

Presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel

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119
Q

What is diverticular disease?

A

Diverticulosis associated with complications e.g. haemorrhage, infection, fistulae

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120
Q

What is diverticulitis?

A

Acute inflammation and infection of colonic diverticulae

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121
Q

What is the aetiology of diverticular disease?

A
  • Low fibre diet leads to loss of stool bulk
  • Consequently, high colonic intraluminal pressures must be generated to propel the stool, leading to herniation of the mucosa and submucosa through the muscularis
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122
Q

What is the epidemiology of diverticular disease?

A

Common

  • 60% of people living in industrialised countries will develop colonic diverticula
  • Rare, under 40 years
  • Right sided diverticula are more common in Asia
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123
Q

What are the presenting symptoms of diverticular disease?

A
  • Often asymptomatic (80-90%)
  • PR bleeding
  • Diverticulitis: left iliac fossa or lower abdominal pain, fever
  • Diverticular fistulation into bladder: pneumaturia, faecaluria and recurrent UTI
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124
Q

What are the signs of diverticular disease on examination?

A

Diverticulitis:

  • Tender abdomen
  • Signs of local or generalised peritonitis if perforation has occurred
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125
Q

What are the investigations for diverticular disease?

A
  • Blood: FBC, Raised WCC and CRP in diverticulitis, check clotting and cross match if bleeding
  • Barium enema: Demonstrates presence of diverticulae with a saw-toothed appearance of lumen, reflecting pseudohypertrophy of circular muscle
  • Flexible sigmoidoscopy and colonscopy: Diverticulae can be seen and other pathology can be excluded
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126
Q

How is diverticular disease managed?

A
  • Asymptomatic: Soluble high fibre diet. Probiotics and anti-inflammatories (mesalazine)
  • GI Bleed: PR bleeding managed with IV rehydration, antibiotics, blood transfusion if necessary. Angiography and surgery if severe
  • Diverticulitis: IV antibiotics and IV fluid rehydration and bowel rest.
  • Surgery: May be necessary with recurrent attacks or when complications develop e.g. perforation and peritonitis. Can be open (Hartmann’s, one-stage resection) or laparoscopic
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127
Q

What are the possible complications of diverticular disease?

A
  • Diverticulitis
  • Pericolic abscess
  • Perforation
  • Faecal peritonitis
  • Colonic obstruction
  • Fistula formation (bladder, small intestine, vagina)
  • Haemorrhage
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128
Q

What is the prognosis for diverticular disease?

A
  • 10-25% of patients will have one or more episodes of diverticulitis
  • Of these 30% will have a second episode
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129
Q

Endoscopic retrograde cholangiopancreatography?

A

A technique that combines the use of endoscopy and fluoroscopy to diagnose and treat certain problems of the biliary or pancreatic ductal systems
- Through the endoscopy, the physical can see the inside of the stomach and duodenum , and inject a contrast medium into the ducts in the biliary tree and pancreas so they can be seen on radiographs

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130
Q

What are the indications for Endoscopic retrograde cholangiopancreatography?

A
  • Obstructive jaundice
  • Gallstones with dilated bile ducts
  • Indeterminate biliary strictures and suspected bile duct tumours
  • Suspected injury to bile ducts either as a result of trauma or iatrogenic
  • Sphincter of Oddi dysfunction
  • Chronic pancreatitis
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131
Q

What are the possible complications of Endoscopic retrograde cholangiopancreatography?

A
  • Pancreatitis
  • Intestinal perforation
  • Risks associated with the contrast dye in patients who are allergic to compounds containing iodine
  • Oversedation can results in low BP, respiratory depression, nausea and vomiting
  • Cholangitis
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132
Q

What is an endoscopy?

A

Refers to looking inside the body for medical reasons using an endoscope, an instrument used to examine the interior of a hollow organ or cavity of the body. Unlike most other medical imaging techniques, endoscopes are inserted directly into the organ.

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133
Q

What are the indications for an endoscopy?

A
  • Investigation of symptoms, such as symptoms in the digestive system including nausea, vomiting, abdominal pain, difficulty swallowing and gastrointestinal bleeding
  • Confirmation of diagnosis, most commonly by performing a biopsy to check for conditions such as anaemia, bleeding, inflammation and cancers of the digestive system
  • Giving treatment, such as cauterisation of a bleeding vessel, widening a narrow oesophagus
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134
Q

What are the possible complications of an endoscopy?

A
  • Infection
  • Over-sedation
  • Perforation
  • Tear of the stomach or oesophagus lining
  • Bleeding
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135
Q

What is gastro-oesophageal reflux disease?

A

Inflammation of the oesophagus caused by reflux of gastric acid and/or bile

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136
Q

What is the aetiology of gastro-oesophageal reflux disease?

A
  • Disruption of mechanisms that prevent reflux (physiological LOS, mucosal rosette, acute angle of junction, intra-abdominal portion of oesophagus)
  • Prolonged oesophageal clearance contributes to 50% of cases
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137
Q

What is the epidemiology of gastro-oesophageal reflux disease?

A

Common

Prevalence 5-10% adults

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138
Q

What are the presenting symptoms of gastro-oesophageal reflux disease?

A
  • Substernal burning discomfort or ‘heartburn’ aggravated by lying supine, blending or large meals and drinking alcohol
  • Pain relieved by antacids
  • Waterbrash
  • Regurgitation of gastric contents
  • Aspiration may results in voice hoarseness, laryngitis, nocturnal cough and wheeze & pneumonia
  • Dysphagia (caused by formation of peptic stricture after long-standing reflux)
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139
Q

What are the signs of gastro-oesophageal reflux disease on examination?

A
  • Usually normal

- Occasionally, epigastric tenderness, wheeze on chest, auscultation, dysphonia

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140
Q

What are the investigations for gastro-oesophageal reflux disease?

A
  • Upper GI endoscopy: Biopsy and cytological bushings: To confirm the presence of oesophagitis, exclude the possibility of malignancy (all patients over 45 years)
  • Barium swallow: To detect hiatus hernia, peptic stricture, extrinsic compression of oesophagus can be visualised
  • CXR: Not specifically for GORD. Incidental finding of hiatus hernia (gastric bubble behind cardiac shadow)
  • Twenty-four hour oesophageal pH monitoring: pH probe placed in lower oesophagus determined the temporal relationship between symptoms and oesophageal pH
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141
Q

How is gastro-oesophageal reflux disease managed?

A
  • Advice: Lifestyle changes, weight loss, elevating head of bed, avoid provoking factors, stopping smoking, lower fat meals, avoiding large meals late in the evening
  • Medical: Antacids and alginates, H2 antagonists (e.g. ranitidine) or proton pump inhibitors (e.g. Iansoprazole) are sufficient for most patients
  • Endoscopy: Annual endoscopic surveillance for Barrett’s oesophagus, may be necessary for stricture dilation or stenting
  • Surgery: Antireflux surgery for those with symptoms despite optimal medical management or those intolerance of medication
  • Nissen fundoplication: (fundus of the stomach is wrapped around the lower oesophagus and held with sermuscular sutures) helps reduce any hiatus hernia and reduce hiatus
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142
Q

What are the possible complications of gastro-oesophageal reflux disease?

A
  • Oesophageal ulceration
  • Peptic stricture
  • Anaemia
  • Barrett’s oesophagus
  • Oesophageal adenocarcinoma
  • Associated with asthma and chronic laryngitis
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143
Q

What is the prognosis of gastro-oesophageal reflux disease?

A
  • 50% respond to lifestyle measures alone
  • In patients who require drug therapy withdrawal is often associated with relapse
  • 20% of patients undergoing endoscopy for GORD have Barrett’s oesophagus
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144
Q

What is gastroenteritis?

A

Acute inflammation of the lining of the GI tract, manifested by nausea, vomiting, diarrhoea and abdominal discomfort

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145
Q

What is the aetiology of gastroenteritis?

A

Can be caused by viruses, protozoa or toxins contained in contained in contaminated food or water

  • Viral: Rotavirus, adenovirus, astrovirus, calcivirus, Norwalk virus, small round structured viruses
  • Bacterial: Campylobacter jejuni, E coli, Salmonella, Shigella, V cholerae, Listeria,
  • Protozoal: E hystolycia, C parvum
  • Toxins: From S aureus, C bolutinum, C perfingens, mushrooms, heavy metals, seafood
  • Non inflammatory mechanisms: V cholerae
  • Inflammatory mechanisms: Shigella, E coli release cytotoxins and invade and damage the epithelium
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146
Q

What is the epidemiology of gastroenteritis?

A
  • Common
  • Often under-reported
  • Serious case of morbidity and mortality in the developing world
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147
Q

What are the presenting symptoms of gastroenteritis?

A
  • Sudden onset nausea
  • Vomiting
  • Anorexia
  • Diarrhoea (bloody or watery)
  • Abdominal pain or discomfort
  • Fever and malaise
  • Enquire about recent travel
  • Antibiotic use and recent food intake (how cooked, source and whether anyone ill)
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148
Q

What are the signs of gastroenteritis on examination?

A
  • Diffuse abdominal tenderness
  • Abdominal distension and bowel sounds are often increased-
  • If severe, pyrexia, dehydration, hypotension, peripheral shutdown
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149
Q

What are the investigations for gastroenteritis?

A
  • Blood: FBC, Blood culture (helps identification if bacteraemia present), U&E’s (dehydration)
  • Stool: Faecal microscopy for polymorphs, parasites, oocytes, culture, electron microscopy (used to diagnose viral infections). Analysis for toxins, particularly for pseudomembranous colitis (C diff toxin)
  • AXR or ultrasound: To exclude other causes of abdominal pain
  • Sigmoidoscopy: Often unnecessary unless inflammatory bowel disease needs to be excluded
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150
Q

How is gastroenteritis managed?

A
  • Bed rest
  • Fluid and electrolyte replacement with oral rehydration solution (containing glucose and salt)
  • IV rehydration may be necessary in those with severe vomiting
  • Most infections are self limiting. Antibiotic treatment is only warranted if severe or the infective agent has been identified (e.g. ciprafloxacin against Salmonella, Shigella, Campylobacter
  • Botulism: Botulinum antitoxin IM and manage in ITU
  • Public health: Often a notifiable disease. Educate on basic hygiene and cooking.
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151
Q

What are the possible complications of gastroenteritis?

A
  • Dehydration
  • Electrolyte imbalance
  • Prerenal failure
  • Secondary lactose intolerance (particularly in infants)
  • Sepsis and shock (particularly Salmonella and Shigella)
  • Haemolytic uraemia syndrome is associated with toxins from E coli
  • Guillian-Barre syndrome may occur weeks after recovery from Campylobacter gastroenteritis
  • Botulism: Respiratory muscle weakness or paralysis
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152
Q

What is the prognosis of gastroenteritis?

A

Generally good, as the majority of cases are self-limiting

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153
Q

What is gastrointestinal perforation?

A

Hole in the wall of part of the gastrointestinal tract

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154
Q

What is the aetiology of gastrointestinal perforation?

A

Underlying causes include:

  • Gastric ulcers
  • Duodenal ulcers
  • Appendicitis
  • Gastrointestinal cancer
  • Diverticulitis
  • Inflammatory bowel disease
  • Superior mesenteric artery syndrome
  • Trauma
  • NSAIDs
  • Typhoid
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155
Q

What is the epidemiology of gastrointestinal perforation?

A

Children: blunt trauma
Adults:
Duodenal perforation more than gastric perforation

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156
Q

What are the presenting symptoms of gastrointestinal perforation?

A
  • History of penetrating issue
  • NSAID or aspirin use
  • Abdominal pain
  • Vomiting
  • Hiccuping
  • History of travel
  • Sharp severe sudden onset (perf peptic ulcer)
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157
Q

What are the signs of gastrointestinal perforation on examination?

A
  • External injury, abrasion, ecchymyosis

- Breathing pattern, distension, discolouration of abdomen

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158
Q

What are the investigations for gastrointestinal perforation?

A
  • Bloods: WCC, CRP, Cultures, Group & Save, Cross Match, Amylase to rule out pancreatitis, ABG, LFT
  • Urinalysis
  • USS: Localised gas collection, thickens bowel loop
  • CT: If no delay
  • Plain AXR: Rigler’s sign, Visible falciform ligament RUQ -> umbilicus
  • CXR if peritonitic or over 50: gas under diaphragm
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159
Q

How is gastrointestinal perforation managed?

A

Laparoscopy

Laparotomy

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160
Q

What are the possible complications of gastrointestinal perforation?

A
  • Bleeding
  • Sepsis
  • Bowel infarction
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161
Q

What is the prognosis of gastrointestinal perforation?

A

Chances of recovery improve with early diagnosis and treatment

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162
Q

What is a haemorrhoidectomy?

A

Surgical excision of the hemorrhoid used primarily only in severe cases.

  • Associated with significant post-operative pain
  • Excisional haemorrhoidectomy (Milligan Morgan) - scalpel, laser, electrocautery
  • Stapled haemorrhoidopexy (if prolapsed) - ?less pain, shorter stay
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163
Q

What are the possible complications of a haemorrhoidectomy?

A
  • Anal fistula or fissure
  • Constipation
  • Excessive bleeding
  • Excessive discharge
  • Inability to urinate or have bowel movement
  • Excessive discharge of fluid from the rectum
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164
Q

What are the indications for a haemorrhoidectomy?

A
  • Prolapse

- Haemorrhoids

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165
Q

What are haemorrhoids?

A
  • Haemorrhoidal cushions are normal anatomical structures located within the anal canal, usually occupying the left lateral and right anterior and posterior positions
  • As they enlarge, they can protrude outside the anal canal and cause symptoms
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166
Q

What is the aetiology of haemorrhoids?

A
  • Excessive straining due to either chronic constipation or diarrhoea
  • Repetitive or prolonged straining causes downward stress on the vascular haemorrhoidal cushions, leading to the disruption of the supporting tissue elements with subsequent elongation, dilation, and engorgement of the haemorrhoidal tissues.
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167
Q

What is the epidemiology of haemorrhoids?

A
  • More common in white patients than black patients

- Presentation peaking between ages 45-65

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168
Q

What are the presenting symptoms of haemorrhoids?

A
  • Perianal pain/discomfort
  • Constipation
  • Rectal bleeding
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169
Q

What are the signs of haemorrhoids on examination?

A
  • Anal pruritus
  • Tender palpable anal lesion
  • Anal mass
  • Ascites
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170
Q

What are the investigations for haemorrhoids?

A
  • Anoscopic examination: haemorrhoids
  • Colonoscopy: Usually normal, may reveal other pathologies
  • FBC: May demonstrate microcytic/hypochromic anaemia
  • Stool for occult haem: Positive
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171
Q

How are haemorrhoids managed?

A
  • Dietary & lifestyle modifications
  • Topical corticosteroids
  • rubber band ligation or sclerotherapy or infrared photocoagulation or haemorrhoid arterial ligation or stapled haemorrhoidopexy
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172
Q

What are the possible complications of haemorrhoids?

A
  • Anaemia from continuous/ excessive bleeding
  • Thrombosis
  • Incarceration
  • Faecal incontinence
  • Pelvic sepsis
  • Anal stenosis
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173
Q

What is the prognosis of haemorrhoids?

A
  • Prognosis following treatment is good
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174
Q

What are inguinal hernias?

A
  • Protrusion of a viscus through an abnormal opening
  • Above and medial to pubic tubercle
    Indirect: Protrusion through internal inguinal ring passes along inguinal canal through abdominal wall, Failure of inguinal canal to close properly after passage of the testes in utero or during neonatal period
    Direct: Protrudes directly through a weakness in the posterior wall of the inguinal canal, Occurs in Hesselbach’s triangle
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175
Q

What are the risk factors of inguinal hernias?

A
  • Infants, prematurity, male
  • Adults: male, obesity, constipation, heavy lifting, chronic cough, ascites, urinary obstruction, past abdominal surgery
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176
Q

What is the epidemiology of inguinal hernias?

A
  • More common in men
  • Direct: elderly
  • Indirect: common in children
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177
Q

What are the presenting symptoms of inguinal hernias?

A
  • Swelling in the groin (may appear with lifting and associated with sudden pain)
  • Indirect hernias are more prone to cause pain (dragging sensation)
  • Congenital hernias occur at birth
  • In older children and adults they develop gradually and can occur with episode of heavy lifting causing rupture
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178
Q

What are the signs of inguinal hernias on examination?

A
  • Appears above and medial to pubic tubercle
  • Ask to cough, increase in swelling, palpable
  • Reduces on lying
  • Reduce hernia and occlude internal ring. IF restrained= indirect
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179
Q

What are femoral hernias?

A
  • Bowel enters the femoral canal, below the inguinal canal
  • Point down the leg (not towards groin like inguinal)
  • Inferior and lateral to pubic tubercle
180
Q

What are the risk factors of femoral hernias?

A
  • Women

- Middle aged and elderly

181
Q

What are the presenting symptoms of femoral hernias?

A
  • Lump in groin, inferior and lateral to pubic tubercle
182
Q

What are the signs of femoral hernias on examination?

A
  • Appears or swells on coughing
  • Reduces when lying
  • Cough impulse
  • Lower abdominal pain if incarceration occurs
  • May be possible to reduce
183
Q

What is an amyand hernia?

A

Inguinal hernia which occurs when the appendix is included in the hernial sac and becomes incarcerated

184
Q

What is a pantaloon hernia?

A

Direct inguinal hernia

Sac straddles the inferior epigastric vessels

185
Q

What is a paraumbilical hernia?

A
  • Herniation through linea alba
  • Occurs just below or above the umbilicus
  • Risk factors= obesity and diabetes
  • Omentum or bowel herniates through defect
186
Q

What is an umbilical hernia ?

A

Congenital: Opening in muscle that allows umbilical cord to pass fails to close
Acquired: Increased intra-abdominal pressure- pregnancy, obesity, heavy lifting

187
Q

What is an epigastric hernia?

A

Through linea alba above umbilicus

188
Q

What is an incisional hernia?

A
  • Caused by incompletely healed surgical wound

- Open repair not easy if obese

189
Q

What is a spigelian hernia?

A

Occurs through linea semilunaris at the lateral edge of the rectus sheath below and lateral to the umbilicus

190
Q

What is an Obturator hernia?

A
  • Through obturator canal
  • Pain on medial side of thigh in thin women
  • Howship Romberg sign: pain along medial sign on abduction, extension, internal rotation
191
Q

What is a gluteal hernia?

A

Through gluteal foramen or greater sciatic foramen

192
Q

What is a lumbar hernia?

A

Through inferior or superior lumbar triangles in the posterior abdominal wall

1) Petit hernia: Inferior lumbar hernia
2) Grynfeltt hernia: Superior lumbar hernia

193
Q

What is Richter’s hernia?

A
  • Involve the bowel wall only, not the whole lumen

- Features of strangulation without obstruction

194
Q

What is Littre’s hernia?

A

Hernial sacs containing a strangulated Meckel’s diverticulum

195
Q

What is Maydl’s hernia?

A

Involving a herniating double loop of bowel

- Strangulated portion may reside as a single loop inside abdominal cavity

196
Q

What is a sciatic hernia?

A
  • Passes through lesser sciatic foramen

- GI obstruction and gluteal mass

197
Q

What is a sliding hernia?

A
  • Contains a partially extraperitoneal structure (caecum on right, signmoid colon on left)
  • Sac does not completely surround the contents
198
Q

What is a gastroschisis hernia?

A

Herniation through abdominal wall with no sac

199
Q

What is a omphalocele hernia?

A

Herniation through abdominal wall with sac

200
Q

What are the investigations for inguinal hernias?

A
  • Clinical diagnosis
  • Groin ultrasound scan
  • CT of groin
  • Herniography
  • MRI of groin
201
Q

How are inguinal hernias managed?

A
  • Open repair
  • Open mesh repair
  • Laparoscopic inguinal herniorrhaphy or open preperitoneal repair with mesh placement
202
Q

What are the possible complications of inguinal hernias?

A
  • Urinary retention post-operative
  • Scrotal haematoma
  • Wound infection
  • Seroma
  • Paraesthesias
  • Numbness in groin
203
Q

What is the prognosis for inguinal hernias?

A
  • Excellent prognosis after repair
204
Q

What is a hiatus hernia?

A

Protrusion of intra-abdominal contents through an enlarged oesophageal hiatus of the diaphragm

  • Commonly contains variable portion of the stomach
  • Herniated contents usually contained within sac of peritoneum
205
Q

What are the risk factors of hiatus hernias?

A
  • Obesity
  • Previous gastro-oesophageal procedure
  • Male
  • Elevated intra-abdominal pressure
  • Advanced age
206
Q

What is the epidemiology of hiatus hernias?

A
  • 50% in western populations

- Lower prevalence in eastern populations

207
Q

What are the presenting symptoms of hiatus hernias?

A
  • Heartburn
  • Regurgitation
  • Chest pain
  • Dysphagia
  • Shortness of breath
  • Cough
208
Q

What are the signs of hiatus hernias on examination?

A

May be asymptomatic

  • Bowel sounds in chest
  • Weight loss
209
Q

What are the investigations for hiatus hernias?

A
  • Barium swallow
  • CXR: Air fluid level above the left hemi-diaphragm
  • Upper GI endoscopy visualises the mucosa
  • OGD
210
Q

How are hiatus hernias managed?

A
  • Lose weight
  • Treat reflex
  • Surgery:
211
Q

What are the possible complications of hiatus hernias?

A
  • Bloating following surgery
  • Gastric volvulus
  • Obstruction
  • Dysphagia following surgery
  • GI bleeding
212
Q

What is the prognosis of hiatus hernias?

A

Most patients with an uncomplicated sliding hiatal hernia will have adequate relief of symptoms (but not cure) with medical therapy.

213
Q

What is infectious colitis?

A

Large bowel inflammation with mucosal destruction and inflammatory exudates forming pseudomembranes on the bowel wall (raised yellow and white plaques) associated with toxin releasing C.difficile

214
Q

What is the aetiology of infectious colitis?

A
  • C d.ifficile, a gram positive anaerobic bacillus.
    Colonic overgrowth of toxin forming bacteria associated with disturbance of gut microflora brought about by Abx use. In rare cases, occurs without prior Abx use
215
Q

What is the epidemiology of infectious colitis?

A
  • Commonly carried asymptomatically in 2%

- Common in hospitals where there is both increased carriage and antibiotics use

216
Q

How does infectious colitis present?

A

1) Asymptomatic carrier state
2) Mild self limited diarrhoea
3) Pseudomembranous colitis
4) Fulminant colitis

217
Q

What are the presenting symptoms of infectious colitis?

A
  • Water diarrhoea, may become bloody (loose stools to severe diarrhoea)
  • Absence of diarrhoea = paralytic ileus, toxic megacolon
  • Abdominal cramps
  • Fever
  • Rigors, septicaemia
218
Q

What are the signs of infectious colitis on examination?

A
  • High temperature
  • Abdominal tenderness
  • In severe cases, toxic megacolon or perforation
  • Colitis: yellow adherant plaques on inflamed non-ulcerated mucosa
219
Q

What are the investigations of infectious colitis on examination?

A

Blood: FBC (high WCC, high CRP, U+E’s, lactate, blood culture (excludes other organisms

  • Cytotoxic tissue culture assay (diagnostic standard)
  • Stool (Demonstration of C diff toxin by ELISA
  • Sigmoidoscopy/colonoscopy
220
Q

What is intestinal ischaemia?

A

Inflammation of the colon due to decreased colonic blood supply
- Ischaemia leads to mucosal inflammation, oedema, necrosis and inflammation

221
Q

What is the aetiology of intestinal ischaemia?

A
  • Thrombosis/embolism: occlusion of large vessels
  • Iatrogenic litigation: AAA surgery
  • Hypovolaemia
  • Younger patients: small vessel vasculitis, vasospasm (cocaine), hypercoagulable states
  • No specific cause
222
Q

What are the presenting symptoms of intestinal ischaemia?

A

May be acute or chronic

  • Crampy abdominal pain
  • Post-prandial (gut claudication) giving food fear
  • Fever
  • Nausea
  • Bloody diarrhoea ‘current jelly stool’
223
Q

What are the the signs of intestinal ischaemia on examination?

A
  • Abdominal distension and tenderness
  • Local peritonism (worse on left)
  • Fever
  • Tachycardia (depends on severity)
  • Proctoscopy shows normal rectal mucosa with blood from higher source
224
Q

What is the epidemiology of intestinal ischaemia?

A
  • Elderly (60-80 years)

- Equal gender distribution

225
Q

What are the investigations for intestinal ichaemia?

A 
FBC
chemistry panel
arterial blood gas/lactate level
ECG
erect CXR
abdominal x-rays
sigmoidoscopy or colonoscopy
226
Q

What is intestinal obstruction?

A

Obstruction to free passage of contents of the gut
Ileus: Reduced bowel motility causes functional obstruction (no pain and bowel sounds present)
- Simple obstructed bowel: One obstructing point, no vascular compromise
- Closed loop obstructed bowel: Obstruction at 2 points forming a loop of grossly distended bowel at risk of perforation
- Strangulated obstructed bowel

227
Q

What is the aetiology of intestinal obstruction?

A 
Small bowel:
- Hernias and adhesions 
- Malignancy 
- Volvulus 
Large bowel:
- Colon cancer 
- Constipation 
- Diverticular stricture 
- Volvulus 
Rare:
- Crohn's stricture 
- Gallstone ileus
228
Q

What is the epidemiology of intestinal obstruction?

A
  • Most are small bowel obstruction

- Many colorectal malignancies will present with obstruction

229
Q

What are the presenting symptoms of intestinal obstruction?

A
  • Vomiting, nausea and anorexia
  • Colicky pain
  • Constipation: absolute if no flatus passed
  • Distension
230
Q

What are the signs of intestinal obstruction on examination?

A
  • Severe tenderness suggesting ischaemia or perforation
  • Dehydration, poor peripheral perfusion, tachycardia, hypotension
  • Tinkling bowel sounds, absent bowel sounds in ileus
  • Distension
  • Visible peristalsis
  • Hernias may be present
  • Fever
231
Q

What are the investigations for intestinal obstruction?

A
  • Erect CXR: for intestinal perforation
  • AXR Small bowel: central gas shadows, no gas in large bowel
  • AXR Large bowel: Gas shadows proximal to obstruction, not in rectum, large bowel haustra
232
Q

How is intestinal obstruction managed?

A
  • Drip & Suck: NG tube and IV fluids

- Analgesia

233
Q

What are the possible complications of intestinal obstruction?

A
  • Tissue death

- Infection

234
Q

What is the prognosis of intestinal obstruction?

A
  • Proper diagnosis and early treatment, good outcome

- 15% of partial small bowel obstructions need surgery

235
Q

What is irritable bowel syndrome (IBS)?

A

A functional bowel disorder defined as recurrent episodes (in the absence of detectable, organic pathology) of abdominal pain/discomfort for more than 6 months of the previous year, associated with two of the following

  • Altered stool passage
  • Abdominal bloating
  • Symptoms made worse by eating
  • Passage of mucous
236
Q

What is the aetiology of IBS?

A

Unknown
- Visual sensory abnormalities, gut motility abnormalities, psychosocial factors (particularly stress) food intolerance (e.g. lactose) are all implicated

237
Q

What is the epidemiology of IBS?

A
  • Common
  • Prevalence 10-20% of adults
  • More common in females (2:1 ratio to males)
238
Q

What are the presenting symptoms of IBS?

A
  • More than six months of abdominal pain (often colicky, in the lower abdomen and relieved by defecation or flatus
  • Altered bowel frequency with more than 3 bowel motions daily or less than 2 weekly
  • Abdominal bloating
  • Change in stool consistency
  • Passage with urgency or straining. Tenesmus
  • Screen for ‘red flag’ alarm symptoms ( Weight loss, anaemia, PR bleeding, late onset 60 years)
239
Q

What are the signs of IBS on examination?

A
  • Normally nothing on examination

- In some cases the abdomen ma appear distended and be mildly tender to palpation in one or both iliac fossa

240
Q

What are the investigations for IBS?

A

Diagnosis mainly from history but may be vital to exclude organic pathology

  • Blood: FBC (for anaemia), LFT, ESR, CRP, TFT
  • Stool examination: microscopy and culture for parasites
  • Ultrasound: To exclude gallstone disease
  • Hydrogen breath test: To exclude dyspepsia associated with Helicobacter pylori
  • Endoscopy: Upper GI endoscopy, sigmoidoscopy
241
Q

How is IBS managed?

A
  • Advice: Explanation & support with establishment of a positive doctor-patients relationship. Dietary modification (e.g. reducing dietary insoluble fibre) may help with constipation, other approaches include exclusion diets and use of probiotics
  • Medical: According to predominant symptoms (Antispasmodics, Prokinetic agents, Antidiarrhoeals, Laxatives)
  • Psychosocial therapies
242
Q

What are the possible complications of IBS?

A
  • Physical and psychological morbidity

- Increased incidence of colonic diverticulosis

243
Q

What is the prognosis of IBS?

A

A chronic relapsing and remitting course, often exacerbated by psychosocial stresses

244
Q

What is laparoscopic abdominal surgery?

A

Surgical technique in which operations are performed far from their location through small incisions (usually 0.5-1.5cm) elsewhere in the body
- Used to see and biopsy

245
Q

What are the indications of abdominal laparoscopic surgery?

A
  • Varices
  • Malignancy
  • Ulcers
  • Dyspepsia
  • Appendicits
  • Ruptured AAA
  • Ruptured spleen
  • Bowel obstruction
246
Q

What are the possible complications of abdominal laparoscopic surgery?

A
  • Trocar injuries
  • Abdominal wall hematoma
  • Umbilical hernia
  • Umbilical wound infection
  • Penetration of blood vessels or small or large bowel
247
Q

What are liver abscesses and cysts?

A

Liver infection resulting in a walled off collection of pus or cyst fluid

248
Q

What is the aetiology of liver abscesses and cysts?

A
  • Pyogenic: E. coli, Klebsiella, enterococcus, bacteroides, streptococci, staphylococci
  • Amoebic: Entamoeba hystolytica
  • Hydatid cyst: Tapeworm Echnicoccus granulosis
  • Other: Tuberculosis
249
Q

What is the epidemiology of liver abscesses and cysts?

A
  • Pyogenic: Incidence 0.8 in 100,000, mean age 60, most common liver abscess in industrialised world
  • Amoebic: Most common type worldwide
  • Hydatid disease: Common in sheep-rearing countries
250
Q

What are the presenting symptoms of liver abscesses and cysts?

A
  • Fever, malaise, nausea, anorexia, night sweats, weight loss
  • RUQ pain or epigastric pain, which may be referred to shoulder (diaphragmatic irritation)
  • Jaundice, diarrhoea, pyrexia of unknown origin
  • Ask about foreign travel
251
Q

What are the signs of liver abscesses and cysts on examination?

A
  • Fever (continuous or spiking), jaundice
  • Tender hepatomegaly, right lobe affected more commonly than left
  • Dullness to percussion and reduced breath sounds at right base of lung, caused by reactive pleural effusion
252
Q

What are the investigations for liver abscesses and cysts?

A
  • Blood: FBC (mild anaemia, leukocytosis, raised eosinophils in hydatid disease, LFTs, raised ESR, raised CRP
  • Stool microscopy, cultures: For E. histolytica or tapeworm eggs
  • Liver ultrasound or CT/MRI: Localises structure or mass
  • CXR: Right pleural effusion or atelactasis, raises hemidiaphragm
  • Aspiration and culture of the abscess material
253
Q

What is liver failure?

A

Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy

  • Hyperacute liver failure: Jaundice with encephalopathy occurring in less than 7 days
  • Acute: Jaundice with encephalopathy occurring from 1 to 4 weeks of onset
  • Subacute: Jaundice with encephalopathy occurring within 4-12 weeks of onset
  • Acute-on-chronic: Acute deterioration (decompensation) in patients with chronic liver disease
254
Q

What is the aetiology of liver failure?

A
  • Viral: Hepatitis A, B, D, E, ‘non-A-E hepatitis’
  • Drugs: Paracetamol overdose, idiosyncratic drug reactions
  • Less common: Autoimmune hepatitis, Budd-Chiari syndrome, pregnancy-related, malignancy (e.g. lymphoma), hemochromatosis, mushroom poisoning, Wilson’s disease
255
Q

What is the pathogenesis of the manifestations of liver failure?

A
  • Jaundice: Reduced secretion of conjugated bilirubin
  • Encephalopathy: Increased delivery of gut-derived products into the systemic circulation and brain from reduced extraction of nitrogenous products by liver and portal systemic shunting. Ammonia may play a part
  • Coagulopathy: Reduced synthesis of clotting factors, reduced platelets (hypersplenism if chronic portal hypertension) or platelet functional abnormalities associated with jaundice or renal failure
256
Q

What is the epidemiology of liver failure?

A

Paracetamol overdose accounts for 50% of acute liver failure in the UK

257
Q

What are the presenting symptoms of liver failure?

A
  • May be asymptomatic

- Fever, nausea and possibly jaundice

258
Q

What are the signs of liver failure on examination?

A
  • Jaundice, encephalopathy, liver asterixis, fetor hepaticus
  • Ascites and splenomegaly
  • Bruising or bleeding from puncture sites or GI tracts
  • Look for secondary causes (e.g. bronze skin colour, Kayser-Fleischer rings)
  • Pyrexia may reflect infection or liver necrosis
259
Q

What are the investigations for liver failure?

A
  • Identify the cause: Viral serology, paracetamol levels, autoantibodies (e.g. ASM, LKM antibody, immunoglobulins) ferritin, caeruloplasmin and urinary copper
  • Blood (in addition to above): FBC: Reduced Hb in GI bleed, Raised WCC if infection. U&E: renal failure. Glucose, LFT, group and save
  • Ultrasound liver, CT scan: image liver
  • Ascitic fluid: Tap ascites and send for microscopy, culture, biochemistry
  • Doppler screening of hepatic or portal veins: To exclude Budd-Chiari syndrome
  • Electroencephalogram: To monitor encephalopathy
260
Q

How is liver failure managed?

A
  • Resuscitation: (According to airway, breathing, circulation): ITU care and specialist unit support essential
  • Treat the cause if possible: N-acetylcysteine for paracetamol overdose
  • Treatment/prevention of complications: Monitor, Manage encephalopathy, Antibiotic and antifungal prophylaxis, Hypoglycaemia treatment, Coagulopathy treatment, Gastric mucosa protection, Avoid sedatives or drugs metabolised by liver
261
Q

What are the possible complications of liver failure?

A
  • Infection
  • Coagulopathy
  • Hypoglycaemia
  • Disturbances of electrolyte acid-base and cardiovascular system, hepatorenal syndrome, cerebral oedema, raised intracranial pressure, respiratory failure
262
Q

What is the prognosis of liver failure?

A

Depends on severity and aetiology of liver failure

- Traditional prognostic score for surgical mortality is the Child-Pugh score

263
Q

What is a Mallory-Weiss tear?

A

Characterised by a tear or laceration at or near the gastro-oesophageal junction
Patients present with non-variceal upper-GI bleeding

264
Q

What is the aetiology of a Mallory-Weiss tear?

A
  • Coughing, retching, vomiting, straining, hiccups, close-chested pressure or cardiopulmonary resuscitation, acute abdominal blunt trauma, primal scream therapy, alcohol, medications (aspirin, NSAIDs), chemotherapeutic agents and oesophageal instrumentation associated with MWT
  • Hiatus hernia present in 40-100% of MWT cases
265
Q

What is the epidemiology of Mallory-Weiss tears?

A
  • MWT represents 3-15% of cases of upper GI bleeding
  • More common in me than in women, ratio of 3:1
  • No racial predilection
  • Most common in people ages 30-50
266
Q

What are the presenting symptoms of a Mallory-Weiss tear?

A
  • Haematemesis
  • Light-headedness/dizziness
  • Postural/orthostatic hypotension
  • Dysphagia
267
Q

What are the signs of a Mallory-Weiss tear on examination?

A

Notice blood in vomit

268
Q

What are the investigations for a Mallory-Weiss tear?

A
  • FBC
  • Urea: high in patients with ongoing bleeding
  • Flexible OGD
269
Q

How is a Mallory-Weiss tear managed?

A
  • Urgent evaluation plus monitoring
  • Endoscopy with or without intervention
  • Supportive treatment, angio and embolise if unstable
270
Q

What are the possible complications of a Mallory-Weiss tear?

A
  • Vasopressin infusion-related abdominal pain
  • Re-bleeding
  • MI
271
Q

What is the prognosis for a Mallory-Weiss tear?

A
  • Most cases bleeding is self-limiting, bleeding would have stopped in most patients at the time of endoscopy
  • Prognosis excellent in pts without associated disease or complications
272
Q

What is nasogastric tube insertion?

A
  • Gastric intubation via the nasal passage

- Provides access to the stomach for diagnostic and therapeutic purposes

273
Q

What are the indications for nasogastric tube insertion?

A
  • Evaluation of upper gastrointestinal GI bleeding
  • Aspiration of gastric fluid content
  • Identification of the oesophagus and stomach on a chest radiograph
  • Administration of radiographic contrast to the GI tract
  • Feeding
  • Bowel irrigation
  • Gastric decompression
274
Q

What are the possible complications of nasogastric tube insertion?

A
  • Pneumothorax caused by tube entering lungs
  • Oesophagus perforation
  • Tube entering brain
  • Tracheobronchial trauma
275
Q

What is non-alcoholic steatohepatitis (NASH)?

A

Clinico-histopathological entity that includes that includes a spectrum of conditions characterised histologically by macrovesicular hepatic steatosis in those who do not consume alcohol in amounts generally considered harmful to the liver
- With NASH, there is inflammation and liver cell damage along with fat in liver

276
Q

What is the aetiology of non-alcoholic steatohepatitis?

A
  • Medications
  • Surgical procedures
  • Total parenteral nutrition
  • Obesity
277
Q

What is the epidemiology of non-alcoholic steatohepatitis?

A
  • 20-40% in Western world
  • Asian and Pacific regions less affected
  • 40-60 years majority
278
Q

What are the presenting symptoms of non-alcoholic steatohepatitis?

A
  • Fatigue and malaise
  • Hepatosplenomegaly
  • Truncal obesity
  • Absence of significant alcohol use
279
Q

What are the signs of non-alcoholic steatohepatitis on examination?

A
  • RUQ abdominal discomfort
  • Pruritis
  • Jaundice
  • Nail changes
  • Palmar erythema
280
Q

What are the investigations of non-alcoholic steatohepatitis?

A
  • Serum AST and ALT: Elevated
  • Total bilirubin: elevated
  • Alkaline phosphatase: elevated
  • FBC: Anaemia or thromocytopenia
  • Serum albumin: Decreased
281
Q

How is non-alcoholic steatohepatitis managed?

A
  • Diet and exercise
  • Weight loss pharmacotherapy
  • With diabetes: insulin sensitiser
  • With dyslipidaemia: lipid lowering therapy
282
Q

What are the possible complications of non-alcoholic steatohepatitis?

A
  • Ascites
  • Variceal haemorrhage
  • Portosysemic encephalopathy
  • Hepatorenal syndrome
283
Q

What is the prognosis for non-alcoholic steatohepatitis?

A
  • NASH associated with increased overall mortality, result of CVD and lesser extent liver-related causes
  • Progress to cirrhosis 9-20 % of time
284
Q

What is acute pancreatitis?

A

Acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems

285
Q

What is the aetiology of acute pancreatitis?

A

Insult results in activation of pancreatic proenzymes within the duct/acini resulting in tissue damage and inflammation
Most common: Gallstones, alcohol (80% of cases)

286
Q

What is the epidemiology of acute pancreatitis?

A
  • Common
  • Peak age is 60 yrs
  • Alcohol induced in more common in males while in females, principle cause is gallstones
287
Q

What are the presenting symptoms of acute pancreatitis?

A
  • Severe epigastric or abdominal pain (radiating to back, relieved by sitting forward, aggravated by movement)
  • Associated with anorexia, nausea and vomiting
  • May be history of gallstones or alcohol intake
288
Q

What are the signs of acute pancreatitis on examination?

A
  • Epigastric tenderness, fever
  • Shock, tachycardia, tachypnoea
  • Reduced bowel sounds (due to ileus)
  • If severe and haemorrhagic, Turner’s sign (flank bruising) or Cullen’s sign (periumbilical bruising)
289
Q

What are the investigations for acute pancreatitis?

A
  • Blood: Increased Amylase, FBC (Increased WCC), U&E’s, Raised glucose, CRP, Decreased Ca
  • USS: for gallstones or biliary dilatation
  • Erect CXR: May be pleural effusion, mainly for excluding other causes
  • AXR: To exclude other causes of acute abdomen. Psoas shadow may be lost
  • CT
290
Q

How is acute pancreatitis managed?

A
  • Medical: Fluid and electrolyte resuscitation, urinary catheter and NG tube if vomiting. Analgesia and blood sugar control
  • ERCP and sphincterotomy
  • Surgiccal: patient with necrotizing pancreatitis should be managed in a specialist unit
291
Q

What are the possible complications of acute pancreatitis?

A
  • Local: pancreatic necrosis, pseudocyst, abscess, ascites, pseudoaneurysm or venous thrombosis
  • Systemic: Multiorgan dysfunction, sepsis, renal failure, ARDS< DIC, hypocalcemia, diabetes
  • Long term: Chronic pancreatitis
292
Q

What is the prognosis of acute pancreatitis?

A
  • 20% follow severe fulminating course with high mortality (infected pancreatic necrosis associated with 70% mortality)
293
Q

What is chronic pancreatitis?

A

Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endocrine and exocrine function and recurrent abdominal pain

294
Q

What is the aetiology of chronic pancreatitis?

A

Alcohol (70%), Idiopathic in 20%
Rare: Recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism, hypertiglycidaemia

295
Q

What is the epidemiology of chronic pancreatitis?

A

Mean age- 40-50 years in alcohol-associated disease

1/100000, Annual UK incidence

296
Q

What are the presenting symptoms of chronic pancreatitis?

A
  • Recurrent severe epigastric pain, radiating to back, relieved by sitting forward, can be exacerbated by eating or drinking alcohol
  • Over many years, weight loss, bloating and pale offensive stools (steatorrhoea)
297
Q

What are the signs of chronic pancreatitis on examination?

A
  • Epigastric tenderness

- Signs of complications e.g. weight loss, malnutrition

298
Q

What is the pathogenesis of chronic pancreatitis?

A
  • Disruption of normal pancreatic glandular architecture due to chronic inflammation and fibrosis, calcification, parenchymal atropy, ductal dilatation, cyst and stone formation
  • Pancreatic stellate cells are thought to play a role, converting from quiescent fat storing cells to myofibroblast-like cells forming extracellular matric, cytokines and growth factors in response to injury
  • Pain is associated with raised intraductal pressures and inflammation
299
Q

What are the investigations for chronic pancreatitis?

A
  • Blood: Glucose (increase indicates endocrine dysfunction, glucose tolerance test. Raised immunoglobulins, especially IgG4 in autoimmune pancreatitis
  • USS: percutaneous or endoscopic, can show hyperechoic foci with post-acoustic shadowing
  • ERCP or MRCP: Early changes include main duct dilatation and stumping of branches. Late manifestations are duct strictures with alternating dilatation
  • AXR: Pancreatic calcification may be visible
  • CT: Pancreatic cysts, calcification
  • Tests of pancreatic exocrine function: Faecal elastase
300
Q

How is chronic pancreatitis managed?

A
  • General: Mainly symptomatic and supportive tx, e.g. dietary, abstinence from alcohol and smoking, treatment of diabetes, oral pancreatic enzyme replacements
  • Endoscopic therapy: Sphincterotomy, stone extraction, dilatation or stenting of strictures
  • Surgical: May be indicated if medical management has failed. Later pancreaticojejunal drainage, resection or limited resection of the pancreatic head
301
Q

What are the possible complications of chronic pancreatitis?

A
  • Psuedocytsts
  • Biliary duct stricture
  • Duodenal obstruction
  • Pancreatic ascites
  • Pancreatic carcinoma
302
Q

What is peptic ulcer disease?

A

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin
- Most commonly gastric and duodenal (can also occur in oesophagus and Meckel’s diverticulum)

303
Q

What is the aetiology of peptic ulcer disease?

A

Cause is an imbalance between damaging action of acid an pepsin and mucosal protective mechanisms. Strong correlation with Helicobacter pylori infection, but it is unclear how to organism causes formation of ulcers
Rare: Zollinger-Ellison syndrome

304
Q

What is the epidemiology of peptic ulcer disease?

A
  • Common
  • More common in males
  • Duodenal ulcers have mean age in thirties, gastric ulcers mean age in fifties
305
Q

What are the presenting symptoms of peptic ulcer disease?

A
  • Epigastric abdominal pain, relieved by antacids
  • Symptoms have a variable relationship to food
  • If worse soon after eating, most likely to be gastric ulcer
  • If worse several hours later, more likely to be duodenal
  • May present with complications (e.g. haematemesis, melaena)
306
Q

What are the signs of peptic ulcer disease on examination?

A
  • May be no physical findings
  • Epigastric tenderness
  • Signs of complications (e.g. anaemia, succession splash in pyloric stenosis)
307
Q

What are the investigations for peptic ulcer disease?

A
  • Blood: FBC (for anaemia, amylase (to exclude pancreatitis). U&E’s, clotting screen , LF T
  • Endoscopy: Four quadrant gastric ulcer biopsies to rule out malignancy
  • Rockall scoring: for severity after a GI bleed, less than 3 carries good prognosis
  • Testing for H pylori
  • Histology of biopsies
308
Q

What is peptic ulcer disease managed?

A
  • Acute: Resuscitation if perforated or bleeding, close monitoring of vital signs and proceeding endoscopic or surgical treatment
  • Endoscopy: Haemostasis by injection sclerotherapy, laser or electrocoagulation
  • Surgery: If perforated or ulcer-related bleeding cannot be controlled
309
Q

What are the possible complications of peptic ulcer disease?

A
  • Rate of major complication is 1% per year including haemorrhage (haematemesis, melaena, iron deficiency anaemia), perforation, obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)
310
Q

What is the prognosis of peptic ulcer disease?

A
  • Overall lifetime risk

- Generally good as peptic ulcers associated with H pylori can be cured by eradication

311
Q

What is gastritis?

A

Histological presence of gastric mucosal inflammation

- Broader term gastropathy encompasses lesions characterised by minimal or no inflammation

312
Q

What is the aetiology of gastritis?

A
  • Acute non-erosive gastritis commonly due to H pylori infection
313
Q

What is the epidemiology of gastritis?

A

Prevalence of H pylori infection higher in developing countries and is impacted by multitude of factors, including geography, age, strain, virulence, environmental factors and socio-economic status

314
Q

What are the presenting symptoms of gastritis?

A
  • Dyspepsia/epigastric discomfort
  • No suspicious features of malignancy
  • Nausea, vomiting and loss of appetite
315
Q

What are the signs of gastritis on examination?

A
  • Acute abdominal pain
  • Glossitis
  • Cognitive impairment
316
Q

What are the investigations for gastritis?

A
  • H pylori urea breath teat
  • H pylori faecal antigen test
  • FBC: May be reduced Hb and Hct and increased MCV in autoimmune gastritis. Leukocytosis with left shift in phlegmonous gastritis
317
Q

How is gastritis managed?

A
  • H pylori eradication therapy

- Cyanocobalamin (autoimmune)

318
Q

What are the possible complications of gastritis?

A
  • Achlorhydria
  • Vit B12 deficiency
  • Peptic ulcer disease
  • Gastric carcinoma
319
Q

What is the prognosis of gastritis?

A

Dependent on underlying aetiology and type

- With H pylori, good prognosis

320
Q

What is a perineal fistula?

A

A type of anorectal malformation that involves a misplaces anal passage that is often narrowed

321
Q

What is a perineal abscess?

A

Collection of pus outside the anus

322
Q

What is the aetiology of aperineal abscess?

A

Bacteria enters through a tear in the lining of anus or rectum
Most often occurs between internal and external sphincters

323
Q

What is the epidemiology of perineal abscesses?

A

Common

Mean age is 40 years

324
Q

What are the signs of perineal abscesses on examination?

A
  • Rectal exam may confirm presence of an anorectal exam
325
Q

What are the investigations for a perineal abscess?

A

Proctosigmoidoscopy

326
Q

How are perineal abscesses managed?

A
  • Prompt incision and drainage of abscess
  • Deeper abscesses may require surgery
  • Antibiotics
327
Q

What are the possible complications of perineal abscesses?

A
  • Systemic infection
  • Anal fistula formation
  • Recurrence
  • Scarring
328
Q

What is the prognosis for perineal abscesses?

A

Good following prompt treatment

329
Q

What is peritonitis?

A

Inflammation of the peritoneum

330
Q

What is the aetiology of peritonitis?

A
  • Perforation of part of the gastrointestinal tract (perforation of distal oesophagus, stomach etc)
  • Disruption of peritoneum
  • Spontaneous bacterial peritonitis
  • Pelvic inflammatory disease
  • Leakage of sterile body fluids into peritoneum such as blood
  • Sterile abdominal surgery
  • History of alcoholism
  • Liver disease
331
Q

What are the presenting symptoms of peritonitis?

A
  • Abdominal pain
  • Abdominal tenderness
  • Fever
  • Nausea
  • Vomiting
  • Bloating
332
Q

What are the signs of peritonitis on examination?

A
  • Blumberg sign (rebound tenderness)

- Abdominal guarding

333
Q

What are the investigations for peritonitis?

A
  • FBC: Leukocytosis, hypokalaemia, hypernatraemia, acidosis
  • Abdominal X-ray: dilated, edematous intestines
  • CT: differentiate causes of abdominal pain
334
Q

How is peritonitis managed?

A
  • Supportive: IV rehydration
  • IV antibiotics
  • Laparotomy
335
Q

What are the possible complications of peritonitis?

A

If untreated, almost always fatal

336
Q

What is the prognosis of peritonitis?

A

Mortality rises to 40% in elderly people

337
Q

What is a pilonidal sinus?

A
  • Caused by forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area
  • Promotes chronic inflammatory reaction, causing an epithealised sinus
338
Q

What is the aetiology of a pilonidal sinus?

A
  • Hair in the natal cleft and is more common in hirsute people
  • Risk may depend on hair type, the force of insertion created within the natal cleft, and the vulnerability of the tissues of the natal cleft to hair insertion
339
Q

What is the epidemiology of pilonidal sinus?

A
  • Common
  • Affects men more than women
  • Mean age of presentation of 20 years
340
Q

What are the presenting symptoms of pilonidal sinus?

A
  • Sacrococcygeal discharge
  • Sacrococcygeal pain and swelling
  • Fever
341
Q

What are the signs of pilonidal sinus on examination?

A
  • Sacrococcygeal sinus tracts
  • Skin maceration
  • Hx of prior rupture of fluid into natal cleft
342
Q

What are the investigations for pilonidal sinus?

A

Clinical diagnosis: Pilonidal sinus or abscess

343
Q

How are pilonidal sinuses managed?

A
  • Local hair removal
  • Antibiotic treatment
  • Pain relief
344
Q

What are the possible complications of a pilonidal sinus?

A
  • Necrotising fasciitis

- Suppurative, post-operative collection deep to sutures

345
Q

What is the prognosis of a pilonidal sinus?

A

Depending on the surgical technique chosen, recurrence rates are variable and average 6.9%.

346
Q

What is portal hypertension?

A

Increase in blood pressure in the portal venous system

347
Q

What is the aetiology of portal hypertension?

A
  • Cirrhosis of the liver
  • Blood clots in the portal vein
  • Schistosomiasis
  • Focal nodular hyperplasia
348
Q

What is the epidemiology of portal hypertension?

A

It is thought to account for 5 to 10 percent of patients with portal hypertension in developed countries and up to a third of patients in developing countries (because of an increased frequency of infectious complications that predispose to PVT)

349
Q

What are the presenting symptoms of portal hypertension?

A
  • Ascites
350
Q

What are the signs of portal hypertension on examination?

A
  • Splenomegaly
  • Oesophageal varices
  • Caput medusae
  • Haemorrhoids
  • Encephalopathy
351
Q

What are the investigations for portal hypertension?

A
  • Hepatic venous pressure gradient= less than equal than 5mmHg
  • Liver biopsy for suspected cirrhosis
352
Q

How is portal hypertension managed?

A
  • Postsystemic shunts
  • Non specific B blockers
  • Diuretics
  • Antibiotics
353
Q

What are the possible complications of portal hypertension?

A
  • Intestinal ischaemia
  • Septic portal vein thrombosis
  • Portal cholangiopathy
354
Q

What is the prognosis for portal hypertension?

A

ival rates according to Child-Pugh class are: one-year survival in class A is 100%; class B 81%; class C 45%.

355
Q

What is primary biliary cirrhosis?

A

Chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts, leading to cholestasis and ultimately, cirrhosis

356
Q

What is the aetiology of primary biliary cirrhosis?

A
  • Unknown
  • Autoimmune aetiology is likely
  • Genetic and environmental factors have also been proposed
  • An environmental trigger (possibly infection, chemical or toxi) may cause bile epithelial injury
  • In susceptible individuals, leads to a T-cell mediated autoimmune response directed against bile duct epithelial cells
357
Q

What is the epidemiology of primary biliary cirrhosis?

A
  • Prevalence in 10-20 in 100,000 in UK

- Usually affects middle-aged women. Ratio if 9:1, women:men

358
Q

What are the presenting symptoms of primary biliary cirrhosis?

A
  • May be an incidental finding on blood tests (e.g. raised AlkPhos, raised cholesterol)
  • Insidious onset. Fatigue, weight loss and pruritis
  • Discomfort in the RUQ of the abdomen (rarely)
  • May present with a complication of liver decompensation (e.g. jaundice, ascites, variceal haemorrhage)
  • Symptoms of associated conditions, e.g. Sjogren’s syndrome (dry eyes and mouth), arthritis, Raynaud phenomenon
359
Q

What are the signs of primary biliary cirrhosis?

A
  • Early: May be no signs
  • Late: Jaundice, skin pigmentation, scratch marks, xanthomas (secondary to hypercholesterolaemia), hepatomegaly, ascietes and other signs of liver disease may be present
    Signs of chronic liver disease, e.g. palmar erythema, clubber and spider naevi
360
Q

What are the investigations for primary biliary cirrhosis?

A
  • Blood: LFT (raised AlkPhos, GGT, bilirubin may be normal or raised in later stages. Transaminases initially normally, raised with disease progression and cirrhosis. Raised IgM and cholesterol are typical.
  • Ultrasound: To exclude extrahepatic biliary obstruction (e.g. by gallstones or strictures)
  • Liver biopsy: Chronci inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes. Repeat liver biopsies whilst on treatment
361
Q

What is primary sclerosing cholangitis?

A

Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts

362
Q

What is the aetiology of primary sclerosing cholangitis?

A
  • Unknwon
  • Postulated immune and genetic predisposition and toxic or infective triggers
  • Close association with IBD, especially UC
  • About 5% of those with UC will develop PSC
363
Q

What is the epidemiology primary sclerosing cholangitis?

A

Usually presents between 25 and 40 years

364
Q

What are the presenting symptoms of primary sclerosing cholangitis?

A
  • May be asymptomatic and diagnosed after persisently increased AlkPhos
  • May present with intermittent jaundice, pruritis, RUQ pain, weight loss and fatigue
  • Episodes of fever and rigors caused by acute cholangitis are less common
  • History of UC
  • Symptoms of complications
365
Q

What are the signs of primary sclerosing cholangitis on examination?

A

May have no signs of evidence of jaundice, hepatosplenomegaly, spider naevi, palmar erythema or ascites

366
Q

What is the pathogenesis of primary sclerosing cholangitis?

A

Periductal inflammation with periductal concentric fibrosis, portal oedema, bile duct proliferation and expansion of portal tracts, progressive fibrosis and development of biliary cirrhosis

367
Q

What are the investigations for primary sclerosing cholangitis?

A
  • Blood: LFT (raised AlkPhos, GGT, transaminases). In later stages, reduced albumin and raised bilirubin
  • Serology: Immunoglobulin levels (raised IgG in children, IgM in adults
  • ERCP: Stricturing and interspersed dilation of intrahepatic and occasionally extrahepatic bile ducts, small diverticular on the common bile duct may be seen
  • MRCP: Enables non-invasive imagining of the biliary tree
  • Liver biopsy: Confirms diagnosis and allows staging of disease
368
Q

What is rectal prolapse?

A
  • Rectal walls have prolapsed to a degree where they protrude out the anus and are visible outside the body
369
Q

What is the aetiology of rectal prolapse?

A
  • Chronic constipation or chronic diarrhoea
  • Long term history of straining during bowel movements
  • Older age
  • Weakening of the anal sphincter
  • Prior injury to the anal or pelvic areas
  • Damage to nerves
370
Q

What is the aetiology of rectal prolapse?

A
  • More common in elderly women
371
Q

What are the presenting symptoms of rectal prolapse?

A
  • Pain
  • Constipation
  • Faecal incontinence
  • Mucous discharge
  • Rectal bleeding
372
Q

What are the the signs of rectal prolapse on examination?

A
  • Concentric rings of mucosa= differentiation of haemorrhoids
  • Rectal ulcer
  • Decreased anal sphincter tone
373
Q

What are the investigations for rectal prolapse?

A
  • Sigmoidoscopy/colonoscopy
  • Videodefecography
  • Colonic transit studies
  • Anorectal manometry
374
Q

What is ulcerative colitis?

A

Chronic relapsing and remitting inflammatory disease affecting the large bowel

375
Q

What is the aetiology of ulcerative colitis?

A
  • Unknown
  • Suggested hypotheses include genetic susceptibility, immune response to bacterial or self-antigens , environmental factors, altered neutrophil function
376
Q

What is the epidemiology of ulcerative colitis?

A
  • Higher prevalence in Ashkenazi Jews, Caucasians
  • Uncommon before age of 10 yrs, peak onset age 20-40 yrs
  • Equal sex ratio up to age of 40, then higher in males
377
Q

What are the presenting symptoms of ulcerative colitis?

A
  • Bloody or mucous diarrhoea (stool frequency related to severity of disease)
  • Tenesmus and urgency
  • Crampy abdominal pain before passing stool, weight loss, fever
  • Symptoms of extra-Gi manifestations
378
Q

What are the signs of ulcerative colitis on examination?

A
  • Signs of iron-deficiency anaemia, dehydration
  • Clubbing
  • Abdominal tenderness, tachycardia
  • Blood, mucous and tenderness on PR examination
  • Signs of extra GI manifestation
379
Q

What are the investigations for ulcerative colitis?

A
  • Blood: (decreased Hb, Raised WCC, ESR, CRP, decreased albumin
  • Stool: Culture as infectious colitis is a differential diagnosis. Faecal calprotectin-marker for disease severity
  • AXR: To rule out toxic megacolon
  • Flexible sigmoidoscopy: Determines severity, histological confirmation, detection of dysplasia
  • Barium enema: Mucosal ulceration with granular appearance and filling defects. Colonoscopy and barium enema may be dangerous in acute exacerbations (risk of perforation)
380
Q

How is ulcerative colitis managed?

A
  • Markers of activity
  • Acute exacerbation: IV rehydration, IV corticosteroids, antibiotics, bowel rest, parenteral feeding may be necessary and DVT prophylaxis. Monitor fluid balance and vital signs
  • Mild disease: oral or rectal 5-aminoslicyclic acid derivatives e.g. sulphasalazine and/or rectal steroids
  • Moderate to sever: oral steroids and oral 5-ASA
  • Advice
  • Surgical
381
Q

What are the possible complications of ulcerative colitis?

A
  • Gastrointestinal: haemorrhage, toxic megacolon, perforation, colonic carcinoma, gallstones and PSC
  • Extra-gastrointestinal manifestations: Uveitis, renal calculi, arthropathy, sacroliitis, ankylosing spondulitis, erythema nodosum, pyoderma gangrenosum, osteoporosis, amyloidosis
382
Q

What it the prognosis of ulcerative colitis?

A

Relapsing and remitting condition, with normal life expectancy
- Poor prognostic factors (ABCDEF): Albumin, blood PR, CRP raised, dilated loops of bowel, eight of more bowel movements per day, fever

383
Q

What is viral hepatitis?

A

Liver inflammation due to viral infection, may present in acute or chronic forms

384
Q

What is the aetiology of viral hepatitis?

A

The most common causes of viral hepatitis are the five unrelated hepatotropic viruses Hepatitis A, Hepatitis B, Hepatitis C, Hepatitis D, and Hepatitis E. In addition to the nominal hepatitis viruses, other viruses that can also cause liver inflammation include Cytomegalovirus, Epstein–Barr virus, and Yellow fever. Up to 1997 there has been also 52 cases of Viral hepatitis caused by Herpes simplex virus

385
Q

What is the epidemiology of viral hepatitis?

A

There is the opportunity to prevent or treat the most common types. Hepatitis A and hepatitis B can be prevented by vaccination. Effective treatments for hepatitis C are available but expensive.

In 2013 about 1.5 million people died from viral hepatitis. Most deaths are due to hepatitis B and hepatitis C.East Asia is the region of the world most affected.

386
Q

What are the presenting symptoms of viral hepatitis?

A
  • Jaundice
  • Low grade fever
  • Headache
  • Muscle aches
  • Fatigue
  • Loss of appetite
  • Nausea
  • Vomiting
387
Q

What are the signs of viral hepatitis on examination?

A
  • Hepatomegaly
  • Splenomegaly
  • Palmar erythema
  • Spider naevi
  • Spider angioma
388
Q

What are the investigations for viral hepatitis?

A
  • Liver function tests (AST and ALT elevated out of proportion to alkaline phosphatase, usually with hyperbilirubinemia)
  • Viral serologic testing
  • PT/INR measurement
  • Seriology
  • Biopsy
389
Q

How is viral hepatitis managed?

A

Supportive care

No treatments attenuate acute viral hepatitis. Alcohol should be avoided because it can increase liver damage. Restrictions on diet or activity, including commonly prescribed bed rest, have no scientific basis.

Most patients may safely return to work after jaundice resolves, even if AST or ALT levels are slightly elevated.

For cholestatic hepatitis, cholestyramine 8 g po once/day or bid can relieve itching.

Viral hepatitis should be reported to the local or state health department.

390
Q

What are the possible complications of viral hepatitis?

A
  • Acute or subacute hepatic necrosis.
  • Chronic active hepatitis.
  • Chronic hepatitis.
  • Cirrhosis.
  • Hepatic failure.
  • Hepatocellular carcinoma (HCC) in patients with HBV or HCV infection.
391
Q

What is the prognosis of viral hepatitis?

A

Virtually all patients with acute infection with hepatitis A and most adults (greater than 95%) with acute hepatitis B recover completely

392
Q

What is volvulus?

A

Loop of intestine twists around itself and the mesentery that supports it

393
Q

What is the aetiology of volvulus?

A
  • Midgut volvulus occurs in people who are predisposed because of intestinal malrotation
  • Segmental volvulus occurs because of abnormal intestinal contents or adhesions
  • Volvulus of the cecum, transverse colon, or sigmoid colon occurs, usually in adults, with only minor predisposing factors such as redundant (excess, inadequately supported) intestinal tissue and constipation
394
Q

What is the epidemiology of volvulus?

A

Sigmoid volvulus is a leading cause of acute colonic obstruction in South America, Africa, Eastern Europe and Asia but is rare in developed countries such as the USA, UK, Japan and Australia. Sigmoid volvulus is the third leading cause of colon obstruction in adults but is rare in infants and children.

395
Q

What are the presenting symptoms of volvulus?

A
  • Nausea or vomiting
  • Abdominal tenderness
  • Bloody or dark red stool
  • Constipation
  • Distended abdomen
396
Q

What are the signs of volvulus on examination?

A
  • Abdominal examination reveals a tympanitic, distended (but usually non-tender) abdomen and a palpable mass may be present.
  • Empty rectal ampulla on rectal examination
397
Q

What are the investigations for volvulus?

A
  • Plain abdominal X-ray: single grossly dilated sigmoid loop commonly reaching the xiphisternum.
  • May need limited barium enema without bowel preparation (can result in decompression itself).
  • CT scanning is the least invasive imaging technique that allows assessment of bowel wall ischaemia
398
Q

What is Wilson’s disease?

A

An autosomal recessive disorder characterised by reduced biliary excretion of copper and accumulation in the liver and brain, especially in the basal ganglia. Also known as hepatolenticular degeneration

399
Q

What is the aetiology of Wilson’s disease?

A
  • Gene responsible is on chromosome 13, and codes for a copper transporting ATPase in hepatocytes
  • Mutations interfere with transport of copper into the intracellular compartments for incorporation into caeruloplasmin (and secreition into plasma) or excretion in the bile. Excess copper damages hepatocyte mitochondria, causing cell death and release of free copper into plasma, which is subsequently deposited in other tissues
400
Q

What is the epidemiology of Wilson’s disease?

A

Liver disease may be present in children over 5

- Neurological disease usually presents in young adults

401
Q

What are the presenting symptoms of Wilson’s disease?

A
  • Liver: May present with hepatitis, liver failure or cirrhosis. Jaundice, easy bruising, variceal bleeding, encephalopathy
  • Neurological: Dyskinesia, rigidity, tremor, dystonia, dysarthia, dysphagia, drooling, dementia, ataxia
  • Psychiatric: Conduct disorder, personality change, psychosis
402
Q

What are the signs of Wilson’s disease on examination?

A
  • Liver: Hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia
  • Neurological
  • Eyes: Green or brown Kayser-Fleischer ring at the corneal limbus, sunflower cataract (copper accumulation in the lens, seen with slit lamp)
403
Q

What are the investigations for Wilson’s disease?

A
  • Blood: LFT (Raised AST, ALT and AlkPhos), serum caerulolasmin and copper (may be low but may provide false negatives as caeruloplasmin is an acute phase protein)
  • 24h urinary copper levels: Increased
  • Liver biopsy: Increased copper content
  • Genetic analysis: Wide variety of mutations in the gene cause the disease, so there is no simple genetic test and sequencing requires specialist genetic advice
404
Q

What is autoimmune hepatitis?

A

Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating antibodies

405
Q

What is the aetiology of autoimmune hepatitis?

A
  • In a genetically predisposed individual, an environmental agent (e.g. viruses or drugs) may lead to hepatocyte expression of HLA antigens which then become the focus of principally T-cell-mediate autoimmune attack
  • The chronic inflammatory changes are similar to those seen in chronic viral hepatitis with lymphoid infiltration of the portal tracts and hepatocyte necrosis, leading to fibrosis and, eventually, cirrhosis
406
Q

What are the types of autoimmune hepatitis?

A
  • Type 1 (classic): ANA, anti-smooth muscle antibodies (ASMA), anti-actin antibodies (AAA), anti-soluble liver antigen (anti-SLA)
  • Type 2: Antibodies to liver/kidney microsomes, antibodies to liver cytosol antigen
407
Q

What is the epidemiology of autoimmune hepatitis?

A
  • Type 1 hepatitis occurs in all age groups (although mainly in young women)
  • Type 2 is generally a disease of girls and young women
408
Q

What are the presenting symptoms of autoimmune hepatitis?

A
  • May be asymptomatic and discovered incidentally with abnormal LFT
  • Insidious onset: Malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis
  • Acute: Fever, anorexia, jaundice, nausea, vomiting, diarrhoea, RUQ pain. Some present with serum sickness (e.g. arthralgia, polyarthritis, maculopapular, rash)
  • May be associated with keratoconjunctivitis sicca
  • Personal or Fhx of autoimmune disease e.g. T1DM and vitiligo. Important to take full history to rule out potential causes of liver disease (e.g. alcohol, drugs)
409
Q

What are the signs of autoimmune hepatitis on examination?

A
  • Stigmata of chronic liver disease e.g. spider naevi
  • Ascites, oedema and encephalopathy are late features
  • Cushinhoid features (e.g. rounded face, cutaneous striae, acne, hirsuitism) may be present even before the administration of steroids
410
Q

What are the investigations for autoimmune hepatitis?

A
  • Blood: LFT (raised AST, ALT, GGT, Alkphos, bilirubin. Low albumin if severe) Clotting (Raised PT if severe). FBC Mild reduced Hb and platelets).
  • Hypergammaglobulinaemia is typical with presence of ANA ASMA or anti-LKM autoantibodies
  • Liver biopsy: Needed to establish the diagnosis. Shows interface hepatitis or cirrhosis
  • Other investigations: Rule out other cases of liver disease
  • US, CT, MRI of liver & abdo: visualise structural lesions
  • ERCP: Rule out PSC
411
Q

How is autoimmune hepatitis managed?

A
  • Indicated if aminotransferases more than 10x upper limit of normal
  • Immunosuppression: with steroids e.g. prednisolone. Azathioprine or 6-mercaptopurine can be used in maintenance phase as steroid-sparing agent with frequent monitoring of LFT & FBC
  • Monitor: US and a-fetoprotein level every 6-12 months in pts with cirrhosis
  • Hep A & B vaccinations
  • Liver transplant: For pts who are refractory to or intolerant of immunosuppressive therapy and those with end-stage disease
412
Q

What are the possibly complications of autoimmune hepatitis?

A
  • Fulminant hepatic failure
  • Cirrhosis and complications of portal hypertension (e.g. varices, ascites)
  • Hepatocellular carcinoma
  • Side effects of corticosteroid treatment
413
Q

What is the prognosis for autoimmune hepatitis?

A
  • Older pts with type 1 are more likely to have cirrhosis at presentation but may be more likely to respond to treatment
  • Approx 80% achieve remission y 3 years
  • 50% require lifelong maintenance
414
Q

What is viral hepatitis A & E?

A

Hepatitis caused by infection with the RNA viruses, hep A (HAV) or hep E virus (HEV), that follow an acute course without progression to chronic carriage

415
Q

What is the aetiology of viral hepatitis A & E?

A
  • HAV is picornavirus and HEV is a calcivirus: Both are small-non enveloped single stranded linear RNA viruses with transmission by the faecal-oral route
  • The viruses replicate in hepatocytes and are secreted into bile
  • Liver inflammation and hepatocyte necrosis is caused by the immune response with targeting of infected cells by CD8+ T cells and NK cells
416
Q

What is the epidemiology of viral hepatitis A&E?

A
  • HAV is an endemic in the developing world, infection often occurs subclinically
  • HEV endemic in Asia, Africa and Central America
417
Q

What are the presenting symptoms of viral hepatitis A & E?

A

Incubation period for HAV and HEV is 3-6 weeks

  • Prodromal period: Malaise, anorexia (distaste for cigarettes in smokers), fever, nausea and vomiting
  • Hepatitis: Prodrome followed by dark urine, pale stools and jaundice lasting approx. 3 weeks. Occasionally, itching and jaundice last several weeks in HAV infection
418
Q

What are the signs of viral hepatitis A & E on examination?

A
  • Pyrexia, jaundice, tender hepatomegaly, spleen may be palpable (20%)
  • Absence of stigmata of chronic liver disease, although a few spider naevi may appear, transiently
419
Q

What are the investigations for viral hepatitis A & E?

A
  • Blood: LFT (raised AST, ALT, bilirubin, Alkphos) Raised ESR, if severe, low albumin and raised platelets
  • Viral seriology
    1) Hep A: Anti HAV IgM, anti HAV IgG
    2) Hep E: Anti HEV IgM, anti HEV IgG. Hep B an C serology to rule out these
  • Urinalysis: Positive for bilirubin, raised urobilinogen
420
Q

How is viral hepatitis A & E managed?

A
  • No specific management. Bed rest and symptomatic treatment (e.g. antipyretics, antiemetics) Colestyramine for servere pruritis
  • Prevention and control
    1) Public health: safe water, sanitation, food hygiene standards
    2) Immunisation: Passive immunisation with IM human immunoglobulin only effect for short period
421
Q

What are the possible complications of viral hepatitis A & E?

A
  • Fulminant hepatic failure develop in some cases, but increased in pregnant women
  • Cholestatic hepatitis with prolonged jaundice and pruritis may develop after HAV infection
  • Post-hepatitis syndrome: Continued malaise for weeks to months
422
Q

What is the prognosis for hepatitis A & E?

A
  • Recovery usually within 3-6 weeks
  • Occasionally, a relapse during recover
  • No chronic sequelae
  • Fulminant hepatic failure has 80% mortality
423
Q

What is viral hepatitis B & D?

A
  • Hepatitis caused by infection with HBV which may follow an acute or chronic (viraemia and hepatic inflammation continuing more than 6mths) course
  • HDV, a defective virus, may only co-infect HBV or superinfect persons who are already carriers of HBV
424
Q

What is the aetiology of hepatitis B & D?

A
  • HBV is an enveloped partially double stranded DNA virus. Transmission is by sexual contact, blood and vertical transmission. Various viral proteins are produced,
  • HDV is single stranded RNA virus
  • Antibody and cell mediated immune responses to viral replication lead to liver inflammation and hepatocyte necrosis
425
Q

What are the risk factors for Hep B?

A
  • IB drug abuse, unscreened blood and blood products, infants of HbeAg pos mothers and sexual contact with HBV carriers
  • Risk of persistent HV varies with age, with younger individuals, especially babies, more likely to develop chronic carriage
426
Q

What is the epidemiology of Hep B & D?

A
  • Common
  • Common in Southeast Asia, Africa and Mediterranean countries
  • HDV found worldwide
  • Uncommon in UK
427
Q

What are the presenting symptoms of Hep B & D?

A

Incubation period 3-6 months

  • 1-2 weeks prodrome of malaise, headache, anorexia, nausea, vomiting, diarrhoea and RUQ pain
  • May experience serum-sickness type illness (e.g. fever, arthralgia, polyarthritis, urticaria, maculopapular rash
  • Jaundice develops with dark urine and pale stools
  • Recovery is usual within 4-8 weeks.
  • Chronic carriage may be diagnosed after routing LFT
428
Q

What are the signs of Hep B & D on examination?

A
  • Acute: Jaundice, pyrexia, tender hepatomegaly, splenomegaly and cervical lymphadenopathy in 10-20%. Occasionally urticarial/maculopapular rash
  • Chronic: May have no findings, signs of chronic liver disease or decompensation
429
Q

What are the investigations for Hep B & D?

A
  • Viral serology: Acute HBV (HbsAg positive, IgM anti- HbcAg) Chronic HBV (HbsAG positive, IgG anti-HBcAg, HbeAG positive or negative). HDv : detected by IgM or IgG against HDV
  • PCR: for detection of HBV DNA
  • LFT: Raised AST & ALT, bilirubin, alkphos
  • Clotting: raised PT in severe disease
  • Liver biopsy: Percutaneous or tranjugular if clotting is deranged or ascites is present
430
Q

How is Hep B & D managed?

A
  • Prevention: Blood screen, instrument sterilisation, safe sex practices
  • Passive immunisation: Hep B immunoglobulin following acute exposure to neonates born to HbeAg-pos mothers
  • Active immunisation: Recombinant HbsAg vaccine for individuals at risk and neonates born to HBV-positive mothers. Immunisation against HBV protects against HDV
431
Q

How is Acute HBV hepatitis managed?

A
  • Symptomatic treatment with bed rest, antiemetics, antipyretics and cholestyramine for pruritis
  • Notification to consultant in communicable disease control
432
Q

How is chronic HBV managed?

A
  • Indications for tx with antivirals: HbeAg-pos or Hbe-AG neg chronic hepatitis, compensated cirrhosis and high HBV DNA, decompensated cirrhosis and detectable HBV DNA by PCR
  • Pts may be treated with interferon alpha or nucleos/tide analogues
  • Interferon alpha is cytokine which augments natural antiviral mechanisms. Side-effects include flu-like symptoms, fever, chills, myalgia, headaches, bone marrow suppression and depression, necessitating discontinuation in 5-10% pts
433
Q

What are the possibly complications of hep B & D?

A
  • Fulminant hepatic failure
  • Chronic HBV infection
  • Cirrhosis and hepatocellular carcinoma
  • Extrahepatic immune complex disorders including glomerulonephritis, polyarteritis nodosa
  • Superinfection with HDV may lead to acute liver failure or rapidly progressive disease
434
Q

What is the prognosis of hep B & D?

A
  • In adults, 10% infections become chronic and of these 20-30% develop cirrhosis
435
Q

What is viral hepatitis C?

A

Hepatitis caused by infection with HCV, often following a chronic course

436
Q

What is the aetiology of viral hepatitis C?

A
  • Small enveloped single-stranded RNA virus of the flavivirus family.
  • Transmission occurs via parenteral route, and at-risk groups include recipients of blood and blood products prior to screening, IV drug users, non-sterile acupuncture and tattooing, those on haemodialysis and health care workers.
437
Q

What is the epidemiology of viral hepatitis C?

A
  • Common

- 0.5-2% prevalence in developed countries, higher rates in areas because of poor sterilisation practices

438
Q

What are the presenting symptoms of viral hepatitis C?

A
  • 90% of acute infections are asymptomatic with less than 10% becoming jaundiced with mild flu-like illness
  • May be diagnosed after incidental abnormal LFT or in older individuals with complications of cirrhosis
439
Q

What are the signs of viral hepatitis C on examination?

A
  • May be no signs or may be signs of chronic liver disease in long-standing infection
  • Less common extra-hepatic manifestations include:
  • Skin rash, caused by mixed cryoglobulinaemia causing a small-vessel vasculitis and
  • Renal dysfunction, caused by glomerulonephritis
440
Q

What are the investigations for viral hepatitis C?

A
  • Blood: HCV serology (Anti-HCV antibodies, wither IgM (acute) or IgG (past exposure or chronic)). Reverse-transcriptase PCR: Detection and genotyping of HCV DNA. LFT: Acute infection causes raised AST and ALT, mild raised bilirubin. Chronic infection causes 2-8x raised levels
  • Liver biopsy: Assess degree of inflammation and liver damage
441
Q

How is viral hepatitis C prevented?

A
  • Screening of blood, blood products and organ donors
  • Needle exchange schemed for IV drug abusers
  • Instrument sterilisation
  • No vaccine currently available
442
Q

How is viral hepatitis C managed medically?

A
  • No specific management and mainly supportive (e.g. antipyretics, antiemetics, cholestyramine)
  • Specific antiviral treatment can be delayed for 3-6 months
443
Q

How is chronic hepatitis C managed?

A

Combined treatment with pegylated-interferon-alpha (augments natural antiviral mechanisms) and ribavirin

  • Monitoring of HVC viral load is recommended after 12 weeks of treatment to determine efficacy of tx
  • Regular US of liver may be necessary if pt has cirrhosis
444
Q

What are the possible complications of hepatitis C?

A
  • Fulminant hepatic failure in acute phase
  • Chronic HCV carriage
  • Cirrhosis and hepatocellular carcinoma
  • Less common are porphyria cutanea tarda, cryoglobulinaemia and glomerulonephritis
445
Q

What is the prognosis for hepatitis C?

A
  • Approx 8% of exposed progress to HCV infection

- Of these 20-30% develop cirrhosis over 10-20 years

Year 3 SOFIA CONDITIONS (16 decks)

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