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Gastroenterology Flashcards

1
Q

Define Achalasia.

A

Condition in which normal muscular activity of the oesophagus is disturbed (absent or un-cordinated) due to failure or incomplete relaxation of the lower oesophageal sphincter.

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2
Q

What are the presenting symptoms of achalasia?

A

o Insidious onset with gradual progression of:

  • intermittent dysphagia
  • difficulty breathing
  • regurgitation and heartburn - particularly at night
  • chest pain
  • weight loss - due to eating less
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3
Q

What are the signs of achalasia on examination?

A

Signs are signs of complications

  • Aspiration pneumonia
  • Malnutrition
  • Weight loss
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4
Q

What are the appropriate investigations for achalasia?

A

o CXR may show widened mediastinum, double right heart border (dilated oesophagus), air-fluid level in the upper chest, absence of the normal gastric air bubble

o Barium swallow may show dilated oesophagus which smoothly tapers down to the sphincter (beak-shaped)

o Endoscopy to exclude malignancy (which could mimic achalasia)

o Manometry (used to assess pressure at the LOS)

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5
Q

Define Acute Cholangitis.

A

Infection of the bile duct.

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6
Q

What are the causes of acute cholangitis?

A

Obstruction of the gallbladder or bile duct due to stones

ERCP

Tumours (e.g. pancreatic, cholangiocarcinoma)

Bile duct stricture or stenosis

Parasitic infection (e.g. ascariasis)

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7
Q

What are the presenting symptoms of acute cholangitis?

A
  • Charcot’s Triad = RUQ pain, jaundice and fever with rigors
  • Extended with 2 more symptoms to create Reynolds’ Pentad = mental confusion and septic shock
  • pruritus
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8
Q

What are the signs of acute cholangitis on examination?

A

Fever

RUQ tenderness

Mild hepatomegaly

Jaundice

Mental status changes

Sepsis

Hypotension

Tachycardia

Peritonitis (uncommon - check for alternative diagnosis)

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9
Q

What are the appropriate investigations for acute cholangitis?

A

o Bloods = high WCC, possibly raised CRP/ESR, raised ALP + GGT, U&Es may show signs of renal dysfunction, check for sepsis, raised amylase if the lower part of the common bile duct is involved

o Imaging

  • X-ray KUB: look for stones
  • Abdominal ultrasound: look for stones and dilation of the common bile duct
  • Contrast-enhanced CT/MRI: good for diagnosing cholangitis
  • MRCP: may be necessary to detect non-calcified stones
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10
Q

What is the management of acute cholangitis?

A
  • Broad-spectrum antibiotics once cultures have been taken
  • Endoscopic biliary drainage is usually required to clear the underlying blockage
  • Resuscitation?Ventilation if the patient becomes septic
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11
Q

What are the possible complications of acute cholangitis?

A

Liver abscesses

Liver failure

Bacteraemia

Gram-negative sepsis

Septic shock

AKI

Organ dysfunction

Percutaneous or endoscopic drainage can cause - intra-abdominal bleeding, sepsis, fistulae, bile leakage

Mortality = 17-40%

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12
Q

Define Alcoholic Hepatitis.

A

Inflammatory liver injury caused by chronic heavy intake of alcohol.

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13
Q

What are the presenting symptoms of alcoholic hepatitis?

A

May remain asymptomatic and undetected

May be mild illness with symptoms = nausea, malaise, epigastric pain, right hypochondrial pain, low-grade fever

More severe presenting symptoms = jaundice, abdominal discomfort or swelling, swollen ankles, GI bleeding

There may be events that trigger the disease (e.g. aspiration pneumonia, injury)

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14
Q

What are the signs of alcohol excess on examination?

A

Malnourished

Palmar erythema

Dupuytren’s contracture

Facial telangiectasia

Parotid enlargement

Spider naevi

Gynaecomastia

Testicular atrophy

Hepatomegaly

Easy bruising

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15
Q

What are the signs of severe alcoholic hepatitis on examination?

A

Febrile

Tachycardia

Jaundice

Bruising

Encephalopathy (e.g. liver flap, drowsiness, disorientation)

Ascites

Hepatomegaly

Splenomegaly

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16
Q

What are the appropriate investigations for alcoholic hepatitis?

A

o Bloods

  • FBC = Low Hb, High MCV, High WCC, Low platelets
  • LFTs = High AST + ALT, High bilirubin, High ALP + GGT, Low albumin
  • U&Es = Urea and K+ tend to be low
  • Clotting = prolonged PT is a sensitive marker for significant liver damage

o Ultrasound - check for other causes of liver impairment (e.g. malignancy)

o Upper GI Endoscopy - investigate varices

o Liver Biopsy - can help distinguish from other causes of hepatitis

o EEG - slow-wave activity indicates encephalopathy

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17
Q

What is the management of acute alcoholic hepatitis?

A

Thiamine, Vitamin C and other multivitamins (Pabrinex)

Monitor and correct K+, Mg2+ and glucose

Ensure adequate urine output

Treat encephalopathy with oral lactulose or phosphate enemas

Ascites - manage with diuretics (spironolactone with/without furosemide)

Therapeutic paracentesis

Glypressin and N-acetylcysteine for hepatorenal syndrome

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18
Q

What are the possible complication of alcoholic hepatitis?

A

Acute liver decompensation

Hepatorenal syndrome

Cirrhosis

  • 40% 1-year mortality and 10% 1-month mortality
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19
Q

Define Anal Fissure.

A

A painful tear in the squamous lining of the lower anal canal.

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20
Q

What are the causes of anal fissures?

A
  • Most are caused by hard faeces
  • Anal sphincter spasm can constrict the inferior rectal artery, causing ischaemia and impairing the healing process
  • Rare causes = syphilis, herpes, trauma, Crohn’s, anal cancer, psoriasis
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21
Q

What are the presenting symptoms of anal fissures?

A

Tearing pain when passing stools

There may be a little bit of blood in the faeces or on the paper

Anal itching (pruritus ani)

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22
Q

What are the signs of anal fissures on examination?

A

Tears in the squamous lining of the anus on examination.

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23
Q

What is the management of anal fissures?

A

o Conservative - high-fibre diet, softening the stools (laxatives), good hydration

o Medical - lidocaine ointment (LA), GTN ointment (relaxes the anal sphincter and promoted healing), diltiazem (relaxes the anal sphincter and promotes healing), botulinum toxin injection

o Surgical - lateral sphincterotomy

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24
Q

What are the possible complication of anal fissures?

A

Chronic anal fissures

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25
Q

Define appendicitis.

A

Inflammation of the appendix.

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26
Q

What are the presenting symptoms of appendicitis?

A

Periumbilical pain that moves to the right iliac fossa

Anorexia is an important feature

Vomiting (may occur after pain)

Constipation

Diarrhoea

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27
Q

What are the signs of appendicitis on examination?

A

o General Signs = tachycardia, fever, furred tongue, lying still, coughing hurts, foetor with/without flushing, shallow breaths

o RIF Signs = Guarding, Rebound and percussion tenderness, PR pain on the right side (sign of low-lying pelvic appendix)

o Special Signs

  • Rovsing’s Sign - palpation of the left iliac fossa causes more pain in the right iliac fossa than the left
  • Psoas Sign - pain on extending the hip (caused by retrocaecal appendix)
  • Cope Sign - pain on flexion and internal rotation of the hip (occurs if the appendix is in close proximity to the obturator internus)
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28
Q

What are the appropriate investigations for appendicitis?

A
  • Bloods = High WCC (mainly neutrophils) and High CRP
  • Ultrasound may help
  • CT - high diagnostic accuracy
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29
Q

What is the management of appendicitis?

A
  • Prompt appendicectomy
  • Antibiotics = broad-spectrum -> cefuroxime, metronidazole
  • Laparoscopy - diagnostic and therapeutic advantages
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30
Q

What are the possible complication of appendicitis?

A
  • Perforation
  • Appendix mass = occurs when the inflamed appendix becomes covered with omentum
  • Appendix abscess = may occur if appendix mass fails to resolve -> treatment involves drainage and antibiotics
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31
Q

Define autoimmune hepatitis.

A

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

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32
Q

What are the presenting symptoms of autoimmune hepatitis?

A

May be asymptomatic and discovered incidentally through abnormal LFT

Insidiously present with:

Malaise

Fatigue

Anorexia

Weight loss

Nausea

Jaundice

Amenorrhoea

Epistaxis

  • 25% with acute hepatits = fever, anorexia, juandice, nausea, vomiting, diarrhoea, RUQ pain, serum sickness
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33
Q

What are the signs of autoimmune hepatitis on examination?

A
  • Stigmata of chronic liver disease - spider naevi etc
  • Ascites, oedema and hepatic encephalopathy are late features
  • Cushingoid features
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34
Q

What are the appropriate investigations for autoimmune hepatitis?

A

o Bloods

  • LFTs = High: AST, ALT, GGT, ALP and bilirubin with Low: albumin
  • Clotting = High PT (in severe disease)
  • FBC = Low Hb, platelets and WCC (if hypersplenism from portal hypertension)
  • Hypergammaglobulinaemia = presence of ANA, ASMA and Anti-LKM antibodies

o Liver Biopsy = check whether hepatitis or cirrhosis

o US, CT or MRI of liver and abdomen

o ERCP - rule out primary sclerosing cholangitis

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35
Q

Define Barrett’s oseophagus.

A

Prolonged exposure of the normal squamous epithelium to refluxate of GORD leads to mucosal inflammation and erosion, leading to replacement of the mucosa with metaplastic columnar epithelium.

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36
Q

What are the presenting symptoms of Barrett’s oesophagus?

A

Patients are likely to experience symptoms of GORD = Heartburn, Nausea, Water-brash (sour taste in the mouth), Bloating, Belching, Burning pain when swallowing

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37
Q

What are the appropriate investigations for Barrett’s oesophagus?

A

OGD and biopsy

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38
Q

What are the possible complications of Barrett’s oesophagus?

A

Oesophageal adenocarcinoma = 5-10% over 10-20 years

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39
Q

Define cholecystitis.

A

Inflammation of the gallbladder.

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40
Q

What are the causes/risk factors of cholecystitis?

A

o Causes = Stones

o Riks factors = age, female, obese, DM, drugs (OCP, octreotide), family history, Caucasian, haemolytic disorder (or other irsk factor for pigment stone)

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41
Q

What are the presenting symptoms of cholecystitis?

A

o Systemically unwell

o Fever

o Prolonged abdominal pain

o Pain referred to the right shoulder

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42
Q

What are the clinical signs of cholecystitis on examination?

A

o Tachycardia

o Pyrexia

o RUQ/epigastrium pain/tenderness

o Guarding or rebound tenderness

o Positive Murphys sign = when hands place under costal margin and patient inspires they will stop and wince

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43
Q

What are the appropriate investigations for cholecystitis?

A

o Bloods = FBC (high WBCC), LFT (high ALP and GGT in ascending cholangitis), blood cultures, amylase (exclude pancreatitis

o Imaging = USS, AXR

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44
Q

What is the management plan for cholecystitis?

A

o Conservative (only mild biliary colic) = follow a low-fat diet

o Medical = NBM, IV fluids, Analgesia, Anti-emetics, Antibiotics (if infection is present) - If there is an obstruction, urgent biliary drainage by ERCP or via a percutaneous route is necessary

o Surgical = Laparoscopic Cholecystectomy

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45
Q

What are the possible complications of cholecystitis?

A

o Stones within the gallbladder = Biliary colic, Cholecystitis, Gallbladder empyema, Gallbladder cancer (RARE)

o Stones outside the gallbladder = Obstructive jaundice, Pancreatitis, Ascending cholangitis, Cholecystoduodenal fistula, Gallstone ileus, Bouveret syndrome (gallstones cause gastric outlet obstruction), Mirizzi syndrome

o Complications of cholecystectomy = Bleeding, Infection, Bile leak, Post-cholecystectomy syndrome, Port-site hernia

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46
Q

Define cirrhosis.

A

End-stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes.

o Cirrhosis is considered DECOMPENSATED if it becomes complicated by any of:

  • Ascites
  • Jaundice
  • Encephalopathy
  • GI bleed
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47
Q

What are the risk factors for cirrhosis?

A

o Chronic alcohol misuse (most common in the UK)

o Chronic viral hepatitis (hep B/C - most common worldwide)

o Autoimmune hepatitis

o Drugs (e.g. methotrexate, hepatotoxic drugs)

o Inherited = Alpha1-antitrypsin deficiency, Haemochromatosis, Wilson’s disease, Galactosaemia, Cystic Fibrosis

o Vascular = Budd-Chiari Syndrome, Hepatic Venous Congestion

Chronic Biliary Diseases

o Non-Alcoholic Steatohepatitis (NASH)

o Associated with obesity, diabetes, total parenteral nutrition, short bowel syndromes, hyperlipidaemia and drugs (e.g. amiodarone, tamoxifen)

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48
Q

What are the presenting symptoms of cirrhosis?

A

o Non-specific early symptoms = Anorexia, Nausea, Fatigue, Weakness, Weight loss

o Decreased liver function = Bruising, Abnormal swelling, Ankle oedema

o Reduced detoxicification function = Jaundice, Personality change, Altered sleep, Amenorrhoea, Galactorrhoea

o Portal Hypertension = Abdominal swelling/Ascites, Haematemesis, PR bleeding/malaena

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49
Q

What are the clinical signs of cirrhosis on examination?

A

Asterixis

Bruises

Clubbing

Dupuytren’s contracture

Palmar erythema

Jaundice

Gynaecomastia

Leukonychia

Parotid enlargement

Spider naevi

Scratch mark (from cholestatic pruritis)

Ascites

Enlarged liver (may be shrunken in the later stages)

Testicular atrophy

Caput medusae

Splenomegaly

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50
Q

What are the appropriate investigations for cirrhosis?

A

Bloods = FBC (low platelets + Hb - due to hypersplenism because of portal hypertension), LFTs (normal sometimes but often = High AST, ALT, ALP, GGT and bilirubin and Low albumin), Clotting ( prolonged PT) Serum alpha-fetoprotein (Tumour marker for liver cancer and Raised in chronic liver disease)

o Investigations to determine CAUSE = Viral serology, alpha1-antitrypsin, Caeruloplasmin (copper-carrying complex that is LOW in Wilson’s disease), Iron studies, Anti-mitochondrial antibody, ANA, ASMA (autoimmune hepatitis)

o Ascitic Tap = MC&S (ascitic tap with neutrophils > 250/mm3 = spontaneous bacterial peritonitis (SBP)), Biochemistry, Cytology

o Liver Biopsy = Grading (Child-Pugh) and Staging

o Imaging = USS, CT or MRI - to detect complications such as: acites, HCC, hepatic or portal vein thrombosis, exclude biliary obstruction, MRCP

o Endoscopy = examine varices

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51
Q

What is the management plan for cirrhosis?

A

o Treat the CAUSE if possible

o Avoid alcohol, sedatives, opiates, NSAIDs and drugs that affect the liver

o Nutrition is important - enteral supplements should be given -> NG feeding may be indicated

o Treating Complications

  • Encephalopathy = Treat infections, Exclude GI bleed, Use lactulose and phosphate enemas, Avoid sedation
  • Ascites = Diuretics (spironolactone with/without furosemide), Sodium restriction, Therapeutic paracentesis, Monitor weight, Fluid restrict if plasma sodium < 120 mmol/L, Avoid alcohol and NSAIDs

o Spontaneous Bacterial Peritonitis = Antibiotics, Prophylaxis against recurrent SBP with ciprofloxacin

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52
Q

What are the possible complications of cirrhosis?

A

Portal hypertension with ascites

Hepatic encephalopathy

Variceal haemorrhage

SBP

HCC

Renal failure (hepatorenal syndrome)

Pulmonary hypertension (hepatopulmonary syndrome)

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53
Q

What are the indications for an appendectomy?

A

o Appendicitis

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54
Q

What are the possible complications of an appendectomy?

A

Bleeding

Wound infection

Infection and redness and swelling (inflammation) of the belly that can occur if the appendix bursts during surgery (peritonitis)

Blocked bowels

Injury to nearby organs

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55
Q

What are the indications for a cholecystectomy?

A

o Acute cholecystitis

O gallstone complications - pancreatitis, jaundice

o Gallbladder trauma

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56
Q

What are the possible complications of a cholecystectomy?

A

Bile leak

Bleeding

Infection

Injury to nearby structures, such as the bile duct, liver and small intestine

Risks of general anesthesia

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57
Q

Define coeliac disease.

A

An inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption.

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58
Q

What are the risk factors for coeliac disease?

A

o Sensitivity to gliadin (compenent of gluten)

o Genetics = HLA-B8, HLA-DR3 and HLA-DQW2 haplotypes

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59
Q

What are the presenting symptoms of coeliac disease?

A

May be asymptomatic

Abdominal discomfort, pain and distention

Steatorrhoea

Diarrhoea

Tiredness, malaise, weight loss (despite normal diet)

Failure to ‘thrive’ in children

Amenorrhoea in young adults

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60
Q

What are the clinical signs of coeliac disease on examination?

A

o Signs of anaemia = pallor

o Signs of malnutrition = Short stature, Abdominal distension, Wasted buttocks in children (Triceps skinfold thickness gives indication of fat stores)

o Signs of vitamin/mineral deficiencies = Osteomalacia, Easy bruising

o Dermatitis herpetiformis = Intense, Itchy blisters on elbows, Knees or Buttocks

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61
Q

What are the appropriate investigations for coeliac disease?

A

o Blood = FBC (low Hb, iron and folate), U&E, Albumin, Calcium, Phosphate

o Serology = IgG anti-gliadin antibodies, IgA and IgG anti-endomysial tranglutaminase antibodies can be diagnostic

o Stool = Culture to exclude infection, Faecal fat tests for steatorrhoea

o D-xylose test = Reduced urinary excretion after oral xylose indicates small bowel malabsorption

o Endoscopy = Allows direct visualisation of villous atrophy in the small intestine (mucosa appears flat and smooth)

o Biopsy will show villous atrophy and crypt hyperplasia in the duodenum

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62
Q

What is the management plan for coeliac disease?

A

o Advice = Avoid gluten (wheat, rye and barley products)

o Medical = Vitamin and mineral supplements, Oral corticosteroids if disease does not subside with avoidance of gluten

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63
Q

What are the possible complications of coeliac disease?

A

Iron, folate and B12 deficiency

Osteomalacia

Ulcerative jejunoileitis

GI lymphoma (particularly T cell)

Bacterial overgrowth

Cerebellar ataxia (rarely)

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64
Q

What are the indications for a colonoscopy?

A

o Lower GI bleeding

o Suspicion of cancer

History of colonic polyps

o Suspicion of inflammation - IBD (Crohn,s UC), diverticulitis

o Therapeutic indications

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65
Q

What are the possible complications of a colonoscopy?

A

o PR bleeding

o Infection

o Bloating, nausea, pain and cramping

o Anaesthetic risks

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66
Q

Define Crohn’s disease.

A

Chronic granulomatous inflammatory disease that can affect any part of the gastrointestinal tract.

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67
Q

What are the presenting symptoms of Crohn’s disease?

A

Crampy abdominal pain (due to inflammation, fibrosis or bowel obstruction)

Diarrhoea (may be bloody or steatorrhoea)

Fever, malaise, weight loss

Symptoms of complications

Sometimes right iliac fossa pain due to inflammation of terminal ileum

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68
Q

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

A

Weight loss

Clubbing

Signs of anaemia

Aphthous ulcers in mouth

Perianal skin tags, fistulae and abscesses

Uveitis, erythema nodosum, pyoderma gangrenosum

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69
Q

What are the appropriate investigations for Crohn’s disease?

A

o Blood = FBC (low Hb, high platelets, high WCC), U&Es, LFTs (low albumin) High ESR, Normal or raised CRP

o Stool microscopy and culture = Exclude infective colitis

o AXR = Could show evidence of toxic megacolon

o Erect CXR = If there is a risk of perforation

o Small bowel barium follow-through could show = Fibrosis/strictures, Deep ulceration (rose thorn ulcers), Cobblestone mucosa

o Endoscopy (OGD, colonoscopy) and Biopsy = Differentiate UC and CD, Useful for monitoring malignancy and disease progression, Can show mucosal oedema and ulceration with ‘rose thorn fissures’, Fistulae and abscesses, Transmural chronic inflammation with infiltration of macrophages, lymphocytes and plasma cells, Granulomas with epithelioid giant cells may be seen in blood vessels and lymphatics

o Radionucide-labelled neutrophil scan = Localise the inflammation

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70
Q

What is the management plan for Crohn’s disease?

A

o Acute Exacerbation = Fluid resuscitation, IV/oral corticosteroids, 5-ASA analogues, Analgesia, Parenteral nutrition if necessary, Monitor markers of disease activity e.g. fluid balance, ESR, CRP, platelets, Hb

o Long-Term = 5-ASA analogues (more commonly used in UC), Immunosuppression (using steroid-sparing agents), Anti-TNF agents

o General Advice = Stop smoking, Dietician referral (low fibre diet necessary if there are stricture present)

o Surgery indicated if = Medical treatment fails, Failure to thrive in children in the presence of complications

  • Involves resection of affected bowel and stoma formation
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71
Q

What are the possible complications of Crohn’s disease?

A

o GI = Haemorrhage, Strictures, Perforation, Fistulae, Perianal fistulae and Abscesses, GI cancer, Malabsorption

o Extraintestinal Features = Uveitis, Episcleritis, Gallstones, Kidney stones, Arthropathy, Sacroiliitis, Ankylosing spondylitis, Erythema nodosum, Pyoderma gangrenosum, Amyloidosis

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72
Q

Define diverticulosis disease.

A

The presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of the large bowel.

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73
Q

Define diverticular disease.

A

Diverticulosis associated with complications.

  • e.g. haemorrhage, infection, fistulae
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74
Q

Define diverticulitis.

A

Acute inflammation and infection of colonic diverticulae.

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75
Q

What are the risk factors for diverticular disease?

A

o low-fibre diet -> loss of stool bulk -> high colonic intrluminal pressure in order to propel stool out -> herniation of the mucosa and submucosa through muscularis

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76
Q

What are the presenting symptoms of diverticular disease?

A

o Often ASYMPTOMATIC (80-90%)

o Complications can lead to symptoms such as:

  • PR bleeding
  • Diverticulitis (causing LIF and lower abdominal pain and fever)
  • Diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
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77
Q

What are the clinical signs of diverticular disease on examination?

A

o Diverticulitis - tender abdomen and signs of local or generalised peritonitis if a diverticulum has perforated

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78
Q

What are the appropriate investigations for diverticular disease?

A

o Bloods = FBC (increased WCC, increased CRP), Clotting and cross-match if bleeding

o Barium Enema (with or without air contrast) = Saw-tooth appearance of lumen

o Flexible Sigmoidoscopy and Colonoscopy = Diverticulae can be visualised and other pathology (e.g. polyps and tumours) can be excluded

  • Barium enema and colonoscopy shouldn’t be performed in the acute setting because there is a high risk of perforation -> in acute setting = CT scan
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79
Q

What is the appropriate management for diverticular disease?

A

o Asymptomatic = soluble high-fibre diet (20-30 g/day)

o GI Bleed = IV rehydration, antibiotics and blood transfusion if necessary, angiography and embolisation or surgery if severe

o Diverticulitis = IV antibiotics, IV fluid rehydration, Bowel rest, Abscesses may be drained by radiologically sited drains

o Surgery = Patients with recurrent attacks or complications (e.g. perforation and peritonitis), Open surgery (Hartmann’s procedure (proctosigmoidectomy leaving a stoma), One-stage resection and anastomosis (with or without defunctioning stoma)), Laparoscopic drainage, peritoneal lavage and drain placement can be effective

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80
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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81
Q

Define gastroenteritis.

A

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

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82
Q

What are the cuases of gastroenteritis?

A

o Viral = Rotavirus, Adenovirus, Astrovirus, Calcivirus, Norwalk virus, Small round structures viruses

o Bacterial = Campylobacter jejuni, , E coli (particularly O157), Salmonella, Shigella, Vibrio cholerae, Listeria, Yersinia enterocolitica

o Protozoal = Entamoeba histolytica, Cryptosporidium parvum, Giardia lamblia

o Toxins (from) = Staphylococcus aureus, Clostridium botulinum, Clostridium perfringens, Bacillus cereus, Mushrooms, Heavy metals, Seafood

o Commonly contaminated foods = Improperly cooked meat, Old rice, Eggs and poultry, Milk and cheeses, Canned food

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83
Q

What are the presenting symptoms of gastroenteritis?

A

o Sudden onset nausea, vomiting, anorexia, diarrhoea (bloody or watery)

o Abdominal pain or discomfort

o Fever and malaise

o Recent travel, antibiotic use and recent food intake, anyone else is ill?

o Time of Onset: Toxins = early (1-24 hours), Bacterial/viral/protozoal = 12+ hours

  • Botulinum causes paralysis and Mushrooms can cause fits, renal or liver failure
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84
Q

What are the clinical signs of gastroenteritis on examination?

A

o Diffuse abdominal tenderness

o Abdominal distension

o Bowel sounds are often INCREASED

o In SEVERE gastroenteritis = pyrexia, dehydration (due to diarrhoea), hypotension and peripheral shutdown

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85
Q

What are the appropriate investigations for gastroenteritis?

A

o Bloods = FBC, blood culture (identify bacteraemia), U&Es (dehydration)

o Stool = Faecal microscopy and analysis for toxins (particularly for the toxin causing pseudomembranous colitis (C. difficile toxin)

o AXR or ultrasound = exclude other causes of abdominal pain (e.g. bowel perforation)

- Sigmoidoscopy: usually unnecessary unless inflammatory bowel disease needs to be excluded

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86
Q

What is the appropriate management of gastroenteritis?

A

o Bed rest

o Fluid and electrolyte replacement with oral rehydration solution

o IV rehydration may be necessary in those with severe vomiting

o Antibiotic treatment is only used if severe or if infective agent has been identified

  • If botulism is present treat with botulinum antitoxin (IM) and manage in ITU (often a notifiable disease and is an important public health issue)
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87
Q

What are the indications for ERCP?

A

Suspected:

o Obstructive jaundice

o Pancreatitis

o Cholangitis

o Recurrent biliary colic

o Post-liver injury bile lead

o Post-laproscopic cholecystectomy with bile leak

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88
Q

What are the possible complications of ERCP?

A

o Prancreatitis

o Vein irritation leading to a tender lump for a couple of days

o Cholangitis

o Infection

o Perforation

o Sedation risks

o Pneumonia is very frail patients

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89
Q

What are the indications for endoscopy?

A

o Dyspepsia/indigestion

o Haematemesis/malaena

o Vomiting

o Anaemia

o History of peptic ulcers

o Dysphagia

o Epigastric mass

o Weight loss

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90
Q

What are the possible complications of endoscopy

A

o Infection

o Perforation

o Sedation risks

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91
Q

Define biliary colic.

A

Very severe, RUQ pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone - can be poorly localised due to its visceral nature.

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92
Q

What are the risk facts for biliary colic?

A

o Caucasian

o Fat

o Fertile

o Forty

o Female

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93
Q

What are the presenting symptoms of biliary colic?

A

o Severe, crampy RUQ pain - can also be poorly localised due to its visceral nature -> doesn’t fluctuate and has a tendency to persist

  • Pain may radiate to the right scapula

o Nausea and vomiting

o Individuals may present with pain following ingestion of a fatty meal

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94
Q

What are the clinical signs of biliary colic on examination?

A

o RUQ/epigastric pain/tenderness

o Jaundice

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95
Q

What are the approrpiate investigations for biliary colic?

A

o Urinalysis, CXR and ECG to exclude other causes (e.g. basal pneumonia, inferior MI)

o Ultrasound - dilatation of the CBD, gallbladder wall may be thickened

o LFT

o ERCP - useful diagnostically and therapeutically

o CT - may be useful if other forms of imaging have been insufficient

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96
Q

What are the possible complications biliary colic?

A

o Complications of surgery

  • Injury to the bile duct
  • Fat intolerance - due to inability to secrete a large amount of bile into the intestine because the patient no longer has a gallbladder
  • Post-cholecystectomy syndrome - presence of abdominal symptoms (e.g. dyspepsia, nausea/vomiting, RUQ pain) after the removal of the gallbladder
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97
Q

What is the management plan for biliary colic?

A

o Analgesia

o IV fluids

o NBM

o Laparoscopic cholecystectomy - ERCP can also be used to help remove stones or stent a blocked bile duct

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98
Q

Define IBS.

A

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

o Altered stool passage

o Abdominal bloating

o Symptoms made worse by eating

o Passage of mucous

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99
Q

What are the risk factors for IBS?

A

o Visceral sensory abnormalities

o Gut motility abnormalities

o Psychosocial factors (e.g. stress)

o Food intolerance (e.g. lactose)

o Many more…..

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100
Q

What are the presenting symptoms of IBS?

A

o 6+ months history of abdominal pain - pain is often colicky, in the lower abdomen

o Pain relieved by defecation or passing of flatus

o Altered bowel frequency (> 3 motions per day or < 3 motions per week)

o Abdominal bloating

o Change in stool consistency

o Passage with urgency or straining

o Tenesmus

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101
Q

What are the clinical signs of IBS on examination?

A

o Normal

  • May show a slightly distended abdomen which is mildly tender on palpation of the iliac fossae
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102
Q

What are the appropriate investigations for IBS?

A

o Diagnosis is mainly from the history but organic pathology must be excluded

  • Blood = FBC (anaemia), LFT, ESR, CRP, TFT, anti-endomysial/anti-tranglutaminase antibodies (coeliac disease)
  • Stool examination = microscopy and culture for infective cause
  • Ultrasound = exclude gallstone disease
  • Urease breath test = exclude dyspepsia due to Helicobacter pylori
  • Endoscopy = if other pathologies suspected
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103
Q

What is the management plan for IBS?

A

o Advice = Dietary modification

o Medical = Depends on the main symptoms affecting the patient

  • Antispasmodics (e.g. buscopan)
  • Prokinetic agents (e.g. domperidone, metaclopramide)
  • Anti-diarrhoeals (e.g. loperamide)
  • Laxatives (e.g. senna, movicol, lactulose)
  • Low-dose tricyclic antidepressants (may reduce visceral awareness)
  • Psychological therapy (CBT, relaxation and psychotherapy)
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104
Q

What are the possible complications of IBS?

A

Physical and psychological morbidity

Increased incidence of colonic diverticulosis

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105
Q

Define gastrointestinal perforation.

A

Perforation of the wall of the GI tract with spillage of bowel contents.

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106
Q

What are the risk factors for GI perforation?

A

o Large Bowel = Diverticulitis, Colorectal cancer, Appendicitis, Volvulus, UC (toxic megacolon)

o Gastroduodenal = Perforated duodenal or gastric ulcer, Gastric cancer

o Small Bowel (RARE) = Trauma, Infection (e.g. TB), Crohn’s disease

o Oesophagus = Boerhaave’s perforation - rupture of the oesophagus following forceful vomiting

o Risk factors of cause (e.g. gastroduodenal - NSAIDs, steroids, bisphosphonates)

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107
Q

What are the presenting symptoms of large bowel perforation?

A

o Peritonitic abdominal pain

  • Make sure you rule out ruptured AAA
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108
Q

What are the presenting symptoms of gastroduodenal perforation?

A

o Sudden onset sever epigastric pain - worse on movement -> pain then become generalised

o Gastric cancer red flags as clue for cause - weight loss, vomiting/nausea

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109
Q

What are the presenting symptoms of oesophageal perforation?

A

Severe pain following an episode of violent vomiting

Neck/chest pain and dysphagia develop soon afterwards

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110
Q

WHat are the signs of GI perforation on examination?

A

o Very UNWELL

o Signs of shock

o Pyrexia

o Pallor

o Dehydration

o Signs of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds)

o Loss of liver dullness (due to overlying gas)

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111
Q

What are the appropriate investigations for GI perforation?

A

o Bloods = FBC, U&E, LFTs, Amylase (slightly aised with perforation)

o Erect CXR = Air under the diaphragm

o AXR = Abnormal gas shadowing

o Gastrograffin Swallow = For suspected oesophageal perforations

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112
Q

What is the management plan for GI perforation?

A

o Resuscitation = Correct fluid and electrolytes, IV antibiotics

o Large Bowel = Peritoneal lavage, Resection of perforated section (usually as part of a Hartmann’s procedure)

o Gastroduodenal = Laparotomy, Peritoneal lavage, Perforation is closed with an omental patch, Gastric ulcers are biopsied for H. pylori

o Oesophageal = Pleural lavage, Repair of ruptured oesophagus

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113
Q

What are the possible complications of GI perforation?

A

o Large and Small Bowel = Peritonitis -> sepsis and multiorgan failure

o Oesophagus =Mediastinitis, Shock, Sepsis, Death

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114
Q

Define GORD.

A

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

115
Q

What are the risk factors for GORD?

A

o Disruption of mechanisms that prevent reflux

  • Mechanisms that prevent reflux:
  • Lower oesophageal sphincter
  • Acute angle of junction
  • Mucosal rosette
  • Intra-abdominal portion of oesophagus (diaphragm acts as a sphincter)
  • o Prolonged oesophageal acid clearance contributes to 50% of cases*
116
Q

What are the presenting symptoms of GORD?

A

o Epigastric/substernal burning discomfort or ‘heartburn’ - aggravated by Lying supine, Bending, Large meals, Drinking alcohol and relieved by Antacids

o Waterbrash (regurgitation of an excessive accumulation of saliva from the lower part of the oesophagus often with some acid material from the stomach)

o Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze

o Dysphagia - caused by formation of peptic stricture after long-standing reflux

117
Q

What are the clinical signs of GORD on examination?

A

o Usually NORMAL

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

118
Q

What are the appropriate investigations for GORD?

A

o Often a CLINICAL diagnosis

o Upper GI endoscopy, biopsy and cytological brushings - Confirms presence of oesophagitis and can exclude malignancy

o Barium Swallow can detect = Hiatus hernia, Peptic stricture, Extrinsic compression of the oesophagus

o CXR = CXR can lead to the incidental finding of a hiatus hernia

o 24 hr oesophageal pH monitoring

119
Q

What is the managment plan for GORD?

A

o Advice = Weight loss, Elevating head of bed, Avoid provoking factors, Stop smoking, Lower fat meals, Avoid large meals late in the evening

o Medical = Antacids, Alginates, H2 antagonists (ranitidine) Proton pump inhibitors (lansoprazole, omeprazole)

o Endoscopy =Annual endoscopic surveillance - looking for Barrett’s Oesophagus

o Surgery = Antireflux surgery - Nissen Fundoplication (fundus of the stomach is wrapped around the lower oesophagus - helps reduce the risk of hiatus hernia and reduce reflux)

120
Q

What are the possible complications of GORD?

A

o Oesophageal ulceration

o Peptic stricture

o Anaemia

o Barrett’s oesophagus

o Oesophageal adenocarcinoma

o Associated with asthma and chronic laryngitis

121
Q

Define haemorrhoids.

A

Anal vascular cushions become enlarged and engorged with a tendency to protrude, bleed or prolapse in the anal canal.

122
Q

What are the risk factors for haemorrhoids?

A

Constipation

Prolonged straining

Derangement of the internal anal sphincter

Pregnancy

Portal hypertension

123
Q

What are the presenting symptoms of haemorrhoids?

A

o Usually asymptomatic

o Bleeding - bright red blood that is on the toilet paper and drips into the pan after passage of stool

o Absence of red flag symptoms (weight loss, anaemia, change in bowel habit, passage of clotted or dark blood, mucus mixed with the stool)

o Itching

o Anal lumps

o Prolapsing tissue

124
Q

What are the clinical signs of haemorrhoids on examination?

A

1st or 2nd degree haemorrhoids are NOT usually visible on external inspection

Internal haemorrhoids are NOT normally palpable on DRE unless they are thrombosed

Haemorrhoids are usually visible on proctoscopy

125
Q

What are the appropriate investigations for haemorrhoids?

A

o DRE

o Proctoscopy

o Rigid or flexible sigmoidoscopy - exclude a rectal or sigmoid source of bleeding

  • Haemorrhoids are common so the presence of haemorrhoids doesn’t mean that you shouldn’t consider any other source of bleeding
126
Q

What is the management plan for haemorrhoids?

A

o Conservative = High-fibre diet, Increase fluid intake, Bulk laxatives, Topical creams (e.g. local anaesthetics)

o Injection Sclerotherapy to induce fibrosis of the dilated veins

o Banding = Barron’s bands are applied proximal to the haemorrhoids

o Surgery (reserved for symptomatic 3rd and 4th degree haemorrhoids) = Milligan-Morgan haemorrhoidectomy, Stapled haemorrhoidectomy

127
Q

What are the possible complications of haemorrhoids?

A

o Bleeding

o Prolapse

o Thrombosis

o Gangrene

o Injection Sclerotherapy = Prostatitis, Perineal sepsis, Impotence, Retroperitoneal sepsis, Hepatic abscess

o Haemorrhoidectomy = Pain, Bleeding, Incontinence, Anal stricture

128
Q

Define inguinal hernia.

A

The abnormal protrusion of a peritoneal sac through a weakness of the abdominal wall in the inguinal region.

  • Direct = Protrusion of the hernial sac directly through a weakness in the transversalis fascia and posterior wall of the inguinal canal
  • Indirect = Protrusion of the hernial sac through the deep inguinal ring, following the path of the inguinal canal
129
Q

What are the risk factors for inguinal hernias?

A

o Male

o Prematurity

o Age

o Obesity

o Raised intra-abdominal pressure (e.g. chronic cough)

o Constipation

o Bladder outflow obstruction

o Intraperitoneal fluid (e.g. ascites)

130
Q

What are the presenting symptoms of inguinal hernias?

A

o Asymptomatic

o Patient notices a ‘lump in the groin’

o May cause discomfort and pain

o May be irreducible

o May present because it has increased in size

o May present because of complications (e.g. bowel obstruction)

131
Q

What are the clinical signs of inguinal hernias?

A

o Groin lump that extends to the scrotum (males) or labia (women)

o Distinguishing inguinal and femoral hernias

  • Inguinal = superior and medial to the pubic tubercle
  • Femoral = inferior and lateral to the pubic tubercle

o Check for cough impulse

o Indirect hernias can be reduced and controlled by applying pressure over the deep inguinal ring

o Auscultation - there may be bowel sounds over the hernia

o Tenderness if strangulated

o Check for signs of complications -> e.g. Bowel obstruction and systemic upset (pyrexia, tachycardia etc.)

132
Q

What are the appropriate investigations for an inguinal hernia?

A

o Bloods = FBC, U&Es, CRP, Clotting, Group and save (if operation is likely), ABGs (may show lactic acidosis from bowel ischaemia)

o Imaging = Erect CXR (check for perforation), USS (exclude other causes of groin lump), AXR (check for obstruction)

133
Q

What is the management plan for inguinal hernias?

A

o Surgical - usually elective repair of uncomplicated hernias

  • Mesh Repair = hernia is surgically reduced and a mesh is inserted to reinforce the defect in the transversalis fascia -> can be done laparoscopically

o Emergency (obstructed or strangulated) = laparotomy with bowel resection may be indicated if the bowel is gangrenous

134
Q

What are the possible complications of inguinal hernias?

A

o Incarceration

o Strangulation

o Bowel obstruction

o Maydl’s hernia (strangulated W-shaped loop of small bowel)

o Richter’s hernia (strangulation of only part of the bowel circumference)

o Surgery Complications = Pain, Wound infection, Haematoma, Penile/scrotal oedema, Mesh infection, Testicular ischaemia

135
Q

Define hiatus hernia

A

Prolapse of the upper stomach through the diaphragmatic oesophageal hiatus.

136
Q

What are the risk factors for a hiatus hernia?

A

o Obesity

o Low-fibre diet

o Chronic oesophagitis

o Ascites

o Pregnancy

137
Q

What are the presenting symptoms of hiatus hernias?

A

o Most are asymptomatic - Sliding hernias are more likely to cause symptoms

o Patients may present with symptoms of GORD

o Heartburn

o Waterbrash

- No correlation between the size of the hernia and severity of the symptoms

138
Q

What are the clinical signs of hiatus hernia on examination?

A

o None

139
Q

What are the appropriate investigations for a hiatus hernia?

A

o Bloods = FBC (check for iron deficiency anaemia)

o Radiology = CXR (gastric air bubble may be seen above the diaphragm), Barium swallow

o Endoscopy

140
Q

What is the management plan for a hiatus hernia?

A

o Medical = Modify lifestyle factors (e.g. lose weight), Inhibit acid production (e.g. PPIs), Enhance upper GI motility

o Surgical - unnecessary in a MAJORITY of patients -> usually performed in patients with complications of reflux disease despite aggressive medical treatment or pulmonary complications (e.g. aspiration pneumonia)

  • Nissen Fundoplication = stomach is pulled down through the oesophageal hiatus and part of the stomach is wrapped (360 degrees) around the oesophagus to make a new sphincter
  • Belsey Mark IV Fundoplication = 270 degree wrap
  • Hill Repair = gastric cardia is anchored to the posterior abdominal wall
141
Q

What are the possible complications of hiatus hernias?

A

o Oesophageal

  • Intermittent bleeding
  • Oesophagitis
  • Erosions
  • Barrett’s oesophagus
  • Oesophageal strictures

o Non-Oesophageal

  • Incarceration of hiatus hernia -> can lead to strangulation and perforation
142
Q

Define infectious colitis.

A

Inflammation of the colon due to bacteria, parasites or viruses.

143
Q

What are the risk factors for infectious colitis?

A

o Lack of sanitation

o Drinking contaminated water

o Antibiotic use

144
Q

What are the presenting symptoms of infectious colitis?

A

o Diarrhoea

o Blood and mucus in the stools

o Lower abdominal pain

o Malaise

o Low-grade fever

145
Q

What are the appropriate investigations for infectious colitits?

A

o Diagnosis is largely clinical

o Stool culture may be used to identify the causative organism

146
Q

Define intestinal ischaemia.

A

Obstruction of a mesenteric vessel leading to bowel ischaemia and necrosis.

  • ‘Watershed zone’ (area between the supply of the superior and inferior mesenteric arteries - near the splenic flexure) is most vulnerable to intestinal ischaemia
147
Q

What are the causes of intestinal ischaemia?

A

o Embolus (60%) and Thrombosis (40%)

  • Can be a consequence of: Volvulus, Intussusception, Bowel strangulation, Failed surgical resection
148
Q

What are the risk factors for intestinal ischaemia?

A

o AF

o Endocarditis (can throw emboli)

o Arterial Thrombosis: hypercholesterolaemia, hypertension, diabetes mellitus, smoking

o Venous Thrombosis: portal hypertension, splenectomy, septic thrombophlebitis, OCP, thrombophilia

149
Q

What are the presenting symptoms of intestinal ischaemia?

A

o Severe acute colicky abdominal pain

o Vomiting

o Rectal bleeding

o History of chronic mesenteric artery insufficiency = Gross weight loss, Post-prandial abdominal pain

o History of heart or liver disease

150
Q

What are the clinical signs of intestinal ischaemia on examination?

A

o Diffuse abdominal tenderness

o Abdominal distension

o Tender palpable mass (ischaemic bowel)

o Bowel sounds may be absent

o Disproportionate degree of cardiovascular collapse

151
Q

What are the appropriate investigations for intestinal ischaemia?

A

o Diagnosis based on clinical suspicion or after laparotomy

o Imaging = AXR (thickening of small bowel folds and signs of obstruction), Mesenteric Angiography

o Bloods = ABG (lactic acidosis), FBC, U&Es, LFTs, Clotting, Cross-match

152
Q

Define intestinal obstruction.

A

Obstruction of the normal movement of bowel contents.

o Classifications:

  • Small or Large bowel
  • Partial or Complete obstruction
  • Simple or Strangulated
153
Q

What are the risk factors for intestinal obstruction?

A

o Extramural = Hernia, Adhesions, Bands, Volvulus

o Intramural = Tumours, Inflammatory strictures (e.g. Crohn’s strictures, diverticulitis)

o Intraluminal = Pedunculated tumours, Foreign body

154
Q

What are the presenting symptoms of intestinal obstruction?

A

o Severe gripping colicky pain with periods of ease

o Abdominal distension

o Frequent vomiting (it may be bile-stained or faeculent)

o Absolute constipation

155
Q

What are the clinical signs of intestinal obstruction on examination?

A

o Abdominal distension with generalised tenderness

o May see visible peristalsis

o Tinkling bowel sounds

o Peritonitis - absent bowel sounds, guarding and rebound tenderness

o Look for abdominal scars - previous abdominal surgery increases the risk of adhesions

o Inspect for abdominal mass (e.g. hernias, intussusception, carcinoma)

156
Q

What are the appropriate investigations for intestinal obstruction?

A

o AXR = check for valvulae conniventes (small bowel) or haustra (large bowel)

o Water-Soluble Contrast Enema

o Barium follow through

157
Q

What is the management plan for intestinal obstruction?

A

o Medical = Drip and Suck

  • Gastric aspiration via NG tube if the patient is vomiting
  • IV fluids
  • Electrolyte replacement
  • Monitor vital signs, fluid balance and urine output

o Surgical = Emergency laparotomy in acute obstruction

158
Q

What are the possible complications of intestinal obstruction?

A

o Dehydration

o Bowel perforation

o Peritonitis

o Sepsis/Toxaemia

o Gangrene of ischaemic bowel wall

159
Q

Define liver abscess.

A

Liver infection resulting in a walled off collection of pus.

160
Q

Define liver cyst.

A

Liver infection resulting in a walled off collection of cyst fluid.

161
Q

What are the causes of liver abscesses/cysts?

A

o Pyogenic (producing pus) = E coli, Klebsiella, Enterococcus, Bacteriodes, Streptococci, Staphylococci, 60% are caused by biliary tract disease (e.g. gallstones, strictures, congenital cysts)

o Amoebic abscess = Entamoeba histolytica

o Hydatid cyst = Tapeworm - Echinococcus granulosis

o Other causes = TB

162
Q

What are the presenting symptoms of liver abscesses/cysts?

A

o Fever

o Malaise

o Nausea

o Anorexia

o Night sweats

o Weight loss

o RUQ/epigastric pain that may be referred to the shoulder

o Jaundice

o Diarrhoea

o Pyrexia of unknown origin

o Recent foreign travel

163
Q

What are the clinical signs of liver abscesses/cysts on examination?

A

o Fever - continuous or spiking

o Jaundice

o Tender hepatomegaly (right lobe affected more than left)

o Right lung base = Dullness to percussion and reduced breath sounds - Due to reactive pleural effusion

164
Q

What are the appropriate investigations for liver abscesses/cysts?

A

o Bloods = FBC (mild anaemia, leukocytosis, high eosinophils (if hydatid disease)), LFTs (high ALP, high bilirubin), ESR and CRP

o Blood cultures = Amoebic and hydatid serology

o Stool MC&S = E. histolytica

o Liver US or CT/MRI - localises structure of mass

o CXR - check for right pleural effusion or atelectasis, raised hemidiaphragm

165
Q

Define liver failure.

A

Severe liver dysfunction leading to jaundice, encephalopthy and coagulopathy.

  • Can be hyperacute, acute or chronic
  • Acute-on-Chronic Liver Failure = acute deterioration (decompensation) in patients with chronic liver disease
166
Q

What are the causes of liver failure?

A

o Viral = Hepatitis A, B, C, D and E

o Drugs = Paracetamol overdose, Idiosyncratic drug reactions

- Less common causes = Autoimmune hepatitis, Budd-Chiari syndrome, Pregnancy-related, Malignancy (e.g. lymphoma), Haemochromatosis, Mushroom poisoning (Amanita phalloides), Wilson’s disease

167
Q

What are the presenting symptoms of liver failure?

A

o Many are asymptomatic

o Fever

o Nausea

o Jaundice

o Symptoms of the cause

168
Q

What are the clinical signs of liver failure on examination?

A

o Jaundice

o Encephalopathy

o Asterixis

o Fetor hepaticus (bad breath due to thiols shunting into the lung because of portal hypertension)

o Ascites and splenomegaly (less common if acute or hyperacute)

o Bruising or bleeding

o Signs of secondary causes (e.g. bronze skin colour, Kayser-Fleisher rings)

o Pyrexia - may indicate infection or liver necrosis

169
Q

What are the appropriate investigations for liver failure?

A

o Identify the cause = Viral serology, Paracetamol levels/tox-screen, Autoantibodies (e.g. ASM, Anti-LKM), Ferritin (haemochromatosis), Caeruloplasmin and urinary copper (Wilson’s disease)

o Bloods = FBC (low Hb (if GI bleed), high WCC (if infection)), U&Es (may show renal failure (hepatorenal syndrome)), Glucose, LFTs (high bilirubin, high AST, ALT, ALP, GGT, low albumin), ESR/CRP, Coagulation screen, ABG, Group and save

o Liver USS/CT

o Ascitic Tap - send for MC&S -> if neutrophils > 250/mm3 = spontaneous bacterial peritonitis

o Doppler scan of hepatic or portal veins = check for Budd-Chiari syndrome

o EEG - monitor encephalopathy

170
Q

What is the management plan for liver failure?

A

o Resuscitation - ABC

o Treat the cause if possible

o Treatment/prevention of complications - invasive ventilation and cardiovascular support is often required

  • Manage encephalopathy = lactulose and phosphate enemas
  • Antibiotic and antifungal prophylaxis
  • Hypoglycaemia treatment
  • Coagulopathy treatment = IV vitamin K, FFP, platelet infusions
  • Gastric mucosa protection = PPIs or sucralfate
  • Avoid drugs metabolised by the liver
  • Cerebral oedema = decrease ICP with mannitol
  • Renal Failure = haemodialysis and nutritional support

o Surgical = Liver transplant

171
Q

What are the possible complications of liver failure?

A

o Infection

o Coagulopathy

o Hypoglycaemia

o Disturbance of electrolyte balance and acid-base balance

o Disturbance of cardiovascular system

o Hepatorenal syndrome

o Cerebral oedema (causing raised ICP)

o Respiratory failure

172
Q

Define Mallory-Weiss tear.

A

Tearing of the lining of the oesophagus around the junction with the stomach as a result of violent vomiting or straining to vomit.

173
Q

What are the risk factors for Mallory-Weiss tear?

A

o Chronic alcohol abuse

o Bulimia

o Other causes: trauma, intense coughing, gastritis

174
Q

What are the presenting symptoms of Mallory-Weiss tear?

A

o Most cases do not cause any symptoms

o Abdominal pain

o Severe vomiting

o Haematemesis

o Involuntary retching

o Malaena

o Symptoms of hypovolaemia if SEVERE blood loss (e.g. light-headedness)

175
Q

What are the appropriate investigations for Mallory-Weiss tear?

A

o Bloods = FBC (anaemia)
o OGD

176
Q

What is the management plan for Mallory-Weiss tears?

A

o 80-90% of the time, the bleeding from a Mallory-Weiss tear will stop on its own - surgery may be necessary if the bleeding doesn’t stop

  • Injection sclerotherapy
  • Coagulation therapy
  • Arteriography

o Transfusions may be required if blood loss has been severe

o Anti-reflux medications may also be prescribed

177
Q

What are the possible complications of Mallory-Weiss tear?

A

o Boerhaave’s perforation

178
Q

What are the indiciations for a NG tube?

A

o Stomach decompressions

o Reduce incidence and risk of vomiting

o Monitor/evaluate GI bleeding

o Prolonged ileus

o Administration of medications or oral contrast in a patient who is unable to swallow

o Detection of transdiaphragmatic stomach herniation

179
Q

What are the complications of a NG tube?

A

o Bleeding

o IC placement

o Pulmonary placement

o Pneumothorax

o Vomiting/retching

o Perforation

o Sinusitis

o Aspiration

180
Q

Define non-alcoholic steatohepatitis (NASH).

A

A term used to describe a range of conditions caused by the build-up of fat in the liver due to causes other than excessive alcohol use.

- Increases the risk of DM, MI, stroke

181
Q

What are the presenting symptoms of NASH?

A

o Usually no symptoms in the early stages - usually found as an incidental finding

o Dull or aching RUQ pain

o Fatigue

o Unexplained weight loss

o Weakness

o Symptoms of cirrhosis will be experienced in the most advanced stages of NASH

182
Q

What are the risk factors for NASH?

A

o Obesity

o Type 2 diabetes mellitus

o Hypertension

o Hypercholesterolaemia

o Age > 50 yrs

o Smoking

183
Q

What are the clinical signs of NASH on examination?

A

o RUQ pain/tenderness

o Signs of cirrhosis (e.g. jaundice, ascites, pruritus - in advanced stages of NASH)

184
Q

What are the appropriate investigations for NASH?

A

o Bloods = LFTs (elevated AST and ALT)

o Liver Ultrasound = may show steatosis

o Liver Biopsy

185
Q

What is the management plan for NASH?

A

o Conservative - controlling risk factors:

  • Blood pressure
  • Diabetes
  • Cholesterol
  • Lose weight
  • Stop smoking
  • Exercise regularly
  • Reduce alcohol consumption - although it is not caused by excessive alcohol, drinking can make it worse
186
Q

What are the possible complications of NASH?

A

o Cirrhosis

  • Ascites
  • Oesophageal varices
  • Hepatic encephalopathy
  • Hepatocellular carcinoma
  • End-stage liver failure
187
Q

Define acute pancreatitis.

A

An acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems.

188
Q

What are the causes of acute pancreatitis?

A

o GET SMASHED

  • Gallstones
  • Ethanol
  • Trauma
  • Steroids
  • Mumps/HIV/Coxsackie
  • Autoimmune
  • Scorpion Venom
  • Hypercalcaemia/hypercalcaemia/hypothermia
  • ERCP
  • Drugs (e.g. sodium valproate, steroids, thiazides and azathioprine)
189
Q

What are the presenting symptoms of acute pancreatitis?

A

o Severe epigastric pain

o Radiating to the back

o Aggravated by movement but relieved by sitting forward

o Associated with anorexia, nausea and vomiting

o Check whether the patient has a history of high alcohol intake or gallstones

190
Q

What are the clinical signs of acute pancreatitis on examination?

A

o Epigastric tenderness

o Fever

o Shock

o Decreased bowel sounds (due to ileus)

o In severe pancreatitis = Cullen’s sign (periumbilical bruising), Grey-Turner sign (flank bruising)

191
Q

What are the appropriate investigations for acute pancreatitis?

A

o Bloods = Very high serum amylase (doesn’t correlate with severity), High WCC, U&Es (to check for dehydration), High glucose, High CRP, Low Calcium (saponification - calcium binds to digested lipids from the pancreas to form soap), LFTs (may be deranged if gallstone pancreatitis or alcohol), ABG

o Imaging

  • USS = check for evidence of gallstones in biliary tree
  • Erect CXR = check for pleural effusion or bowel perforation
  • AXR = exclude other causes
  • CT Scan = if diagnosis is uncertain or if persisting organ failure
192
Q

What is the management plan for acute pancreatitis?

A

o Assessment of severity has TWO main scales = Modified Glasgow Score (combined with CRP (> 210 mg/L) and APACHE-II Score

o Medical Management:

  • Fluid and electrolyte resuscitation
  • Urinary catheter and NG tube if vomiting
  • Analgesia
  • Blood sugar control
  • HDU and ITU care
  • Prophylactic antibiotics may be useful in reducing mortality

o ERCP and Sphincterotomy = used for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct

o Surgical (necrotising pancreatitis should be managed by specialists) = Necresectomy (drainage and debridement of necrotic tissue) may be necessary

193
Q

What are the possible complications of acute pancreatitis?

A

o Local = Pancreatic necrosis, Pseudocyst, Abscess, Ascites, Pseudoaneurysm, Venous thrombosis

o Systemic = Multiorgan dysfunction, Sepsis, Renal failure, ARDS, DIC, Hypocalcaemia, Diabetes

o Long-Term = Chronic pancreatitis

194
Q

Define 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.

195
Q

What are the causes of chronic pancreatitis?

A

o Alcohol - 70%

o Idiopathic - 20%

o Rare = recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism

196
Q

What are the presenting symptoms of chronic pancreatitis?

A

o Recurrent severe epigastric pain

o Pain radiates to the back

o Pain relieved by sitting forward

o Pain can be aggravated by eating or drinking alcohol

o Over many years -> weight loss, bloating and steatorrhoea

197
Q

What are the clinical signs of chronic pancreatitis on examination?

A

o Epigastric tenderness

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

198
Q

What are the appropriate investigations for chronic pancreatitis?

A

o Bloods = High glucose (endocrine dysfunction), Amylase and lipase usually normal, High Ig (especially IgG4 in autoimmune pancreatitis)

o Ultrasound

o ERCP or MRCP = early changes that can be seen include main duct dilatation and stumping of branches with late manifestations including duct strictures with alternating dilatation

o Abdominal X-Ray = pancreatic calcification

o CT Scan = pancreatic calcification and pancreatic cysts

Tests of pancreatic exocrine function:

o Faecal elastase (reflects pancreatic exocrine function)

199
Q

What is the management plan for chronic pancreatitis?

A

o General = symptomatic and supportive (e.g. dietary advice, stop smoking/drinking, treat diabetes, oral pancreatic enzyme replacement, analgesia)

o Endoscopy Therapy = Sphincterotomy, Stone extraction, Dilatation and stenting of strictures, Extracorporial shock-wave lithotripsy (ESWL) is sometimes used to fragment larger pancreatic stones before removal

o Surgical:

  • Lateral pancreaticojejunal drainage (modified Puestow procedure)
  • Pancreatic resection (pancreaticoduodenectomy or Whipple’s procedure)
  • Limited resection of pancreatic head (Beger procedure)
  • Combining opening of the pancreatic duct and excavation of the pancreatic head (Frey procedure)
200
Q

What are the possible complications of chronic pancreatitis?

A

o Local = Pseudocysts, Biliary duct stricture, Duodenal obstruction, Pancreatic ascites, Pancreatic carcinoma

o Systemic = Diabetes, Steatorrhoea, Chronic pain syndromes, Dependence on strong analgesics

201
Q

Define peptic ulcer disease and gastritis.

A

Ulceration of areas of the GI tract caused by exposure to gastric acid and pepsin.

- Peptic ulcers are most commonly gastric and duodenal (but they can also occur in the oesophagus and Meckel’s diverticulum).

202
Q

What are the common causes of peptic ulcer disease and gastritis?

A

o Helicobacter pylori

o NSAIDs

o RARE = Zollinger-Ellison syndrome - condition in which a gastrin-secreting tumour or hyperplasia of the islet cells in the pancreas cause overproduction of gastric acid, resulting in recurrent peptic ulcers

203
Q

What are the presenting symptoms of peptic ulcer disease and gastritis?

A

o Epigastric pain

o Relieved by antacids

o Symptoms have a variable relationship to food intake:

  • Gastric = pain is worse soon after eating (50 year olds)
  • Duodenal = pain is worse several hours after eating (30 year olds)

o Patients may present with complications e.g. haematemesis, melaena

204
Q

What are the clinical signs of peptic ulcer disease and gastritis?

A

o Commonly there are no physical findings

o Epigastric tenderness

o Signs of complications e.g. anaemia

205
Q

What are the appropriate investigations for peptic ulcer disease and gastritis?

A

o Bloods = FBC (for anaemia), Serum amylase (to exclude pancreatitis), U&Es, Clotting screen, LFT, Cross-match if active bleeding, Secretin test (if Zollinger-Ellison syndrome suspected (tumour causes too much gastric acid production)) - IV secretin causes a rise in serum gastrin in ZE patients but not in normal patients)

o Endoscopy = Visualization and biopsies of gastric ulcers can be taken to rule out malignancy

o Rockall Scoring = Scores the severity after a GI bleed (< 3 carries good prognosis but > 8 carries high risk of mortality)

o Testing for H. pylori

  • C13-urea breath test = radio-labelled urea is given by mouth -> C13 is detected in the expelled air
  • Serology = IgG antibody against H. pylori confirms exposure to H. pylori but NOT eradication
  • Campylobacter-like organism (CLO) test = gastric biopsy is placed with a substrate of urea and a pH indicator -> if H. pylori is present, ammonia is produced from the urea and there is a colour change from yellow to red
206
Q

What is the management plan for peptic ulcer disease and gastritis?

A

o Acute

  • Fluid resuscitation needed if the ulcer is perforated or bleeding, Close monitoring of vital signs
  • Endoscopy -> injection sclerotherapy, laser coagulation, electrocoagulation
  • Surgical treatment

o Surgery = Indicated if ulcer has perforated or if the bleeding ulcer can’t be controlled

o Helicobacter pylori eradication = Triple therapy for 1-2 weeks

o I fpeptic ulcer isn’t H. pylori based = Treat with PPIs or H2 antagonists, Stop NSAID use or use misoprostol if NSAID use is necessary

207
Q

What are the possible complications of peptic ulcer disease and gastritis?

A

o Rate of major complication = 1 % per year

o Major complications = haemorrhage (haematemesis, melaena, iron-deficiency anaemia), perforation, obstruction/pyloric stenosis (due to scarring, penetration, pancreatitis)

208
Q

Define perineal abscess.

A

A pus collection in the perineal region.

209
Q

Define perineal fistula.

A

An abnormal chronically infected tract communicating between the perineal skin and either the anal canal or the rectum.

210
Q

What are the risk factors for perineal abscesses and fistula?

A

o IBD

o Diabetes mellitus

o Malignancy

211
Q

What are presenting symptoms of (peri)anal abscesses and fistula?

A

o Constant throbbing pain in the perineum

o Intermittent discharge (mucus or faecal staining) near the anal region

o Personal or family history of IBD

212
Q

What are the clinical signs of (peri)anal abscesses and fistula?

A

o Localised tender perineal mass (may be fluctuant)

o Small skin lesion near the anus (opening of the fistula)

o DRE = thickened area over the abscess/fistula may be felt but DREs are not always possible due to pain and anal sphincter spasm

o Goodsall’s Law = a rule that allows you to correlate the location of the internal fistula opening based on the location of the external fistula opening

  • if the external fistula opening is anterior to the anal canal, the fistula runs radially and directly into the anal canal
  • a fistula that is 3 cm away and any fistula that has an external fistula opening lying posterior to the transverse anal line will follow a curved path and open internally in the posterior midline
213
Q

What are the appropriate investigations for (peri)anal abscesses and fistula?

A

o Bloods = FBC, CRP, ESR, Blood culture

o Imaging = MRI, Endoanal Ultrasound (less useful than MRI)

214
Q

What is the management plan for (peri)anal abscesses and fistula?

A

o Requires Surgical treatment

  • Open Drainage of Abscess
  • Laying Open of Fistula

o Antibiotics

215
Q

What are the possible complications of (peri)anal abscesses and fistulae?

A

o Recurrence

o Damage to internal anal sphincter

o Incontinence

o Persisting pain

216
Q

Define peritonitis.

A

Inflammation of the peritoneal lining of the abdominal cavity. It can be localised to one part of the peritoneum or generalised.

217
Q

What are the risk factors for peritonitis?

A

o Localised Peritonitis = Appendicitis, Cholecystitis, Diverticulitis, Salpingitis

o Primary Generalised Peritonitis (bacterial infection) = Ascites, Nephrotic syndrome

o Secondary Generalised Peritonitis (bacterial translocation or spillage of bowel contents = Peptic ulcers, recent surgery

218
Q

What are the presenting symptoms of peritonitis?

A

o Inflammation of the parietal peritoneum is usually continuous, sharp, localised, exacerbated by movement and coughing

o Symptoms may be vague in those with liver disease and ascites (due to confusion caused by encephalopathy)

219
Q

What are the clinical signs of peritonitis on examination?

A

o Check vital signs and look for signs of dehydration or compromised perfusion

o Localised Peritonitis = Tenderness on examination, Guarding, Rebound tenderness

o Generalised Peritonitis = Very unwell, Systemic signs of toxaemia or sepsis, Patient will lie still, Shallow breathing, Rigid abdomen, Generalised abdominal tenderness, Reduced bowel sounds, DRE may show anterior tenderness (suggests pelvic peritonitis)

220
Q

What are the appropriate investigations for peritonitis?

A

o Bloods = FBC, U&Es, LFTs, Amylase, CRP, Clotting, Group & Save, Blood cultures, Pregnancy test, ABG

o Imaging = Erect CXR (check for air under the diaphragm), AXR (check for bowel obstruction), USS or CT abdomen, Laparoscopy

o If Ascites = Tap and cell count, SBP = > 250 neutrophils/mm3, Gram stain and culture

221
Q

What is the management plan for peritonitis?

A

o Localised Peritonitis = depends on cause -> some require surgery (e.g. appendicitis) but some can be treated with antibiotics (e.g. salpingitis)

o Generalised Peritonitis = Patient may be at risk of DEATH from sepsis or shock

  • IV fluids, IV antibiotics, Urinary catheter, NG tube, Central venous line, Laparotomy, Antibiotics
222
Q

What are the possible complications of peritonitis?

A

o Early = Septic shock, Respiratory failure, Multiorgan failure, Paralytic ileus, Wound infection, Abscesses

o Late = Incisional hernia, Adhesions

223
Q

Define pilonidal sinus.

A

An abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in the natal cleft.

224
Q

What are the risk factors for pilonidal sinus.

A

o Hirsutism

o Spending a long time sitting down

o Occupational (e.g. hairdressers may develop interdigital pilonidal sinus)

225
Q

What are the presenting symptoms of pilonidal sinus?

A

o Painful natal cleft

o Discharging swelling

o Often recurrent

226
Q

What are the clinical signs of pilonidal sinus on examination?

A

o Midline openings or pits between the buttocks

o Hairs may protrude from the swelling

o If infection or abscess, the swelling will become tender

o It may be fluctuant and discharge pus or blood-stained fluid on compression

227
Q

What are the appropriate investigations for pilonidal sinus?

A

o None needed

o Bloods = WCC (check for infection) and fasting glucose (diabetics are at risk)

228
Q

What is the management plan for pilonidal?

A

o Acute Pilonidal Abscess = Incision and drainage

o Chronic Pilonidal Sinus = Excision under general anaesthesia with exploration

o Prevention = Good hygiene, Shaving

229
Q

What are the possible complications of pilonidal sinus?

A

o Pain

o Infection

o Abscess

o Recurrence

230
Q

Define portal hypertension.

A

Abnormally high pressure within the hepatic portal vein.

-clinically significant portal hypertension is defined as a hepatic venous pressure gradient > 10 mm Hg

231
Q

What are the risk factors for portal hypertension?

A

o Pre-Hepatic = Congenital stenosis, Portal vein thrombosis, Splenic vein thrombosis, Extrinsic compression

o Hepatic = CIRRHOSIS, Chronic hepatitis, Schistosomiasis, Myeloproliferative disease

o Post-Hepatic = Budd-Chiari syndrome (hepatic vein obstruction), Constrictive pericarditis, Right heart failure

232
Q

What are the presenting symptoms of portal hypertension?

A

o Features of Liver Disease = Jaundice, History of alcohol abuse, Risk factors for viral hepatitis, Family history (e.g. haemochromatosis)

o Complications of Portal Hypertension = Haematemesis or melaena, Lethargy, irritability, changes in sleep (hepatic encephalopathy), Ascites, Abdominal pain and fever (spontaneous bacterial peritonitis), Pulmonary involvement

233
Q

What are the clinical signs of portal hypertension?

A

o Signs of Portal Hypertension = Caput medusae, Splenomegaly, Ascites

o Signs of Liver Failure = Jaundice, Spider naevi, Palmar erythema, Confusion, Asterixis, Fetor hepaticus, Enlarged or small liver, Gynaecomastia, Testicular atrophy

234
Q

What are the appropriate investigations for portal hypertension?

A

o Bloods = LFTs, U&Es, Blood glucose, FBC, Clotting screen (prolongation of PT is one of the earliest signs of liver failure), Ferritin (haemochromatosis), 1-antitrypsin levels, Caeruloplasmin (Wilson’s disease)

o Hepatitis serology

o Autoantibodies (e.g. anti-smooth muscle antibodies in autoimmune hepatitis)

o Imaging = Abdominal USS, Doppler USS, CT/MRI, Endoscopy (check for oesophageal varices)

o Measure hepatic venous pressure gradient (HVPG)

o Liver Biopsy - if indicated

235
Q

What is the management plan for portal hypertension?

A

o Treatment is mainly focused on treating the underlying cause where possible

o Conservative = Salt restriction, Diuretics

o Liver transplant

236
Q

What are the possible complications of portal hypertension?

A

o Bleeding from oesophageal varices

o Ascites

o Pulmonary complications

o Liver failure

o Hepatic encephalopathy

o Cirrhotic cardiomyopathy

237
Q

Define primary biliary cirrhosis.

A

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

238
Q

What are the presenting symptoms of primary biliary colic?

A

o Asymptomatic with incidental finding on blood tests

o Insidious onset with vague symptoms such as = Fatigue, Weight loss, Pruritis

o Discomfort in the RUQ (rare)

o Complication of liver decompensation = e.g. jaundice, ascites, variceal haemorrhage

o Symptoms of associated conditions = e.g. Sjogren’s syndrome, arthritis, Raynaud’s phenomenon

239
Q

What are the clinical signs of primary biliary cirrhosis on examination?

A

o Early = No signs

o Late = Jaundice, Skin pigmentation, Scratch marks, Xanthomas (secondary to hypercholesterolaemia), Hepatomegaly, Ascites, Signs of chronic liver disease

240
Q

What are the appropriate investigations for primary biliary cirrhosis?

A

o Bloods = LFTs (High ALP + GGT, bilirubin may be high or normal, ALT and AST are normal initially but will increase as the disease progresses and cirrhosis develops), Clotting (prolongation of PT), High Cholesterol, TFTs (associated with thyroid disease)

o Antibodies = Antimitochondrial antibodies (typical feature of PBC), High IgM

o Ultrasound = exclude extrahepatic biliary obstruction (e.g. gallstones)

o Liver Biopsy = chronic inflammatory cells and granulomas around the intrahepatic bile ducts, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes

241
Q

Define primary sclerosing cholangitis.

A

A chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts.

242
Q

What are the presenting symptoms of primary sclerosing cholangitis?

A

o May be asymptomatic and diagnosed after persistently raised ALP

o May present with:

  • Intermittent jaundice with pruritis
  • RUQ pain
  • Weight loss
  • Fatigue
  • Episodes of fever and rigors caused by acute cholangitis
  • Must check for a history of ulcerative colitis
243
Q

What are the clinical signs of primary sclerosing cholangitis?

A

o May have no signs

o Jaundice

o Hepatosplenomegaly

o Spider naevi

o Palmar erythema

o Ascites

244
Q

What are the appropriate investigations for primary sclerosing cholangitis?

A

o Bloods = LFTs (high ALP + GGT, mildly elevated ALT + AST, low albumin with high bilirubin in later stages)

o Serology = IgG high in children, IgM high in adults, ASMA and ANA present in 30%, perinuclear anti-neutrophil cytoplasmic antibodies (pANCA) present in 70%

o ERCP = stricturing and interspersed dilation of intrahepatic and extraheptic bile ducts, small diverticuli on the common bile duct may be seen

o MRCP = enables non-invasive imaging of the biliary tree

o Liver Biopsy = Confirm diagnosis and allows staging

245
Q

Define rectal prolapse.

A

The abnormal protrusion of the full thickness (or only the mucosal layer) of rectum through the anus.

246
Q

What are the risk factors for rectal prolapse?

A

o Constipation

o Causes of increased straining

o Cystic fibrosis (in children)

o Previous trauma to the anus/perineum

o Neurological conditions (e.g. cauda equina syndrome, MS)

247
Q

What are the presenting symptoms of rectal prolapse?

A

o Protruding anal mass

o Initially associated with defecation

o May require digital replacement

o Constipation

o Faecal incontinence

o PR mucus or bleeding

- May be an emergency if irreducible or strangulated prolapse

248
Q

What are the clinical signs of rectal prolapse on examination?

A

o Prolapse may be seen on straining

o May be ulcerated or necrotic if the vascular supply is compromised

o Reduced anal sphincter tone

249
Q

What are the appropriate investigations for rectal prolapse?

A

o Imaging = Proctosigmoidoscopy, Defecating proctogram or barium enema

o Anal sphincter manometry

o Pudendal nerve studies

o Sweat Chloride Test = Performed in children to test for cystic fibrosis

250
Q

Define UC.

A

Chronic relapsing and remitting inflammatory disease affecting the large bowel.

251
Q

What are the risk factors for UC?

A

o Ashkenazi jews and Caucasians

o Peak onset = 20-40 yrs

252
Q

What are the presenting symptoms of UC?

A

o Bloody or mucous diarrhoea (stool frequency depends on severity of disease)

  • < 4 = mild, 4-6 = moderate, 6+ = severe

o Tenesmus and urgency

o Crampy abdominal pain before passing stool

o Weight loss

o Fever

o Extra-GI manifestations = e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum

253
Q

What are the clinical signs of UC on examination?

A

o Signs of iron deficiency anaemia

o Dehydration

o Clubbing

o Abdominal tenderness

o Tachycardia

o Blood, mucus and tenderness on PR examination

o Extra-GI manifestations = e.g. uveitis, scleritis, erythema nodosum, pyoderma gangrenosum

254
Q

What are the appropriate investigations for UC?

A

o Bloods = FBC (low Hb, high WCC, high ESR or CRP, low albumin)

o Stool = Faecal calprotectin allows differentiation of IBS from IBD -> it is raised in inflammatory processes (i.e. IBD)

o AXR = Rule out toxic megacolon

o Flexible Sigmoidoscopy or Colonoscopy (and biopsy) = Determines severity, Histological confirmation, Detection of dysplasia

o Barium Enema = Show mucosal ulceration with granular appearance and filling defects (due to pseudopolyps), Narrowed colon, Loss of haustral pattern/ leadpipe appearance

- Colonoscopy and barium enema may be dangerous during an acute exacerbation -> risk of perforation

255
Q

What is the management plan for UC?

A

o Mild Disease = Oral or rectal 5-ASA derivatices (e.g. mesalazine, olsalazine, sulphasalazine) and/or rectal steroids

o Moderate to Severe Disease = Oral steroids, Oral 5-ASA, Immunosuppression (with azathioprine, cyclosporine, 6-mercaptopurine or infliximab

o Advice = Patient education and support

o Regular colonoscopic surveillance

o Surgical = If medical treatment fails, presence of complications or to prevent colonic carcinoma = Proctocolectomy with ileostomy or Ileo-anal pouch formation

256
Q

What is the management plan for an acute exacerbation of UC?

A

o IV rehydration

o IV corticosteroids

o Antibiotics

o Bowel rest

o Parenteral feeding may be necessary

o DVT prophylaxis

o If toxic megacolon = patient is likely to need a proctocolectomy because toxic megacolon has a high mortality

257
Q

What are the possible complications of UC?

A

o GI = Haemorrhage, Toxic megacolon, Perforation, Colonic carcinoma, Gallstones, Primary sclerosing cholangitis

o Extra-gastrointestinal = Uveitis, Renal calculi, Arthropathy, Sacroiliitis, Ankylosing spondylitis, Erythema nodosum, Pyoderma gangrenosum, Osteoporosis (from chronic steroid use), Amyloidosis

258
Q

Define viral hepatitis (A and E).

A

Hepatitis caused by infection with the RNA viruses, hepatitis A or hepatitis E virus, that follow an acute course without progression to chronic carriage.

259
Q

What are the presenting symptoms of viral hepatitis?

A

o Incubation period of HAV and HEV: 3-6 weeks

o Prodromal period symptoms = Malaise, Anorexia, Fever, Heachache, Nausea and vomiting

o Hepatitis symptoms = Dark urine, Pale stools, Jaundice lasting around 3 weeks, Itching and Jaundice may last several weeks in HAV infection

o Asymptomatic in 90% of HCV

260
Q

What are the clinical signs of viral hepatitis on examination?

A

o Pyrexia

o Jaundice

o Tender hepatomegaly

o Spleen may be palpable

o Absence of stigmata of chronic liver disease - some spider naevi may appear transiently

o Often No signs with HCV

261
Q

Define viral hepatitis B.

A

Hepatitis caused by infection with hepatitis B virus (HBV), which may follow an acute or chronic course.

262
Q

What is the mode of transmission of HAV and HEV?

A

o Faecal-Oral

263
Q

What is the mode of transmission of HBV, HCV and HDV?

A

o Sexual contact

o Blood

o Vertical tranmission - mother to baby

264
Q

What is the management plan for viral hepatitis (A and E)?

A

o There is no specific management other than bed rest and symptomatic treatment (e.g. antipyretics, antiemetics or cholestyramine (for severe pruritus))

o Prevention and Control = Public Health -> safe water, sanitation and food hygiene

o Immunisation is available for HAV

- Is a notifiable diseases

265
Q

What are the possible complications of viral hepatitis?

A

o Fulminant hepatic failure (more common with HBV) - has 80% mortality

o Chronic infection

o Cirrhosis

o Cholestatic hepatitis with prolonged jaundice and pruritus can develop after HAV infection

o Extra-hepatic immune complex disorders (e.g. glomerulonephritis, polyarteritis nodosa)

o Post-hepatitis syndrome = continued malaise for weeks to months

266
Q

What are the risk factors for viral hepatitis?

A

o IV drug use

o Unscreened blood and blood products

o Infants of HBeAg-positive mothers

o Sexual contact with HBV carriers

o Younger individuals (particularly babies) are more likely to become chronic carriers

o Genetic factors are associated with varying rates of viral clearance

o Tattooing

267
Q

Define viral hepatitis D.

A

Hepatitis D virus is a defective virus, that may only co-infect with HBV or superinfect people who are already carriers of HBV.

268
Q

Define viral hepatitis C.

A

Hepatitis caused by infection with hepatitis C virus (HCV), often following a chronic course (in 80% of cases).

269
Q

What is the management plan for viral hepatitis (B and D)?

A

o Prevention = blood screening, safe sex, instrument sterilisation

o Passive immunisation

o Active immunisation

o Acute HBV Hepatitis = Symptomatic treatment (antipyretics, antiemetics and cholestyramine) and bed rest

o Chronic HBV = Nucleoside/nucleotide analogues (adefovir, entecavir, telbivudine, tenofovir) and Interferon alpha -> SE = flu-like symptoms such as fever, chills, myalgia, headaches, bone marrow suppression and depression

- Notifiable disease

270
Q

What is the management plan for viral hepatitis C?

A

o Prevention = screen blood, blood products and organ donors

o NO VACCINE AVAILABLE

o Medical

  • Acute = Supportive (antipyretics, antiemetics, cholestyramine)
  • Chronic = Pegylated interferon, Ribavirin (guanosine nucleotide analogue)

o Regular USS of the liver may be needed if the patient has cirrhosis

271
Q

Define volvulus.

A

Rotation of a loop of small bowel around the axis of its mesentery that results in bowel obstruction and potential ischaemia.

o The areas usually affected = Sigmoid colon (65%), Caecum (30%)

- Volvulus Neonatorum - occurs in neonates and typically affects the midgut

272
Q

What are the risk factors for volvulus.

A

o Adults = Long sigmoid colon, Long mesentery, Mobile caecum, Chronic constipation, Adhesions, Chagas disease, Parasitic infections

o Neonatal = Malrotation

273
Q

What are the presenting symptoms of volvulus?

A

o Severe colicky abdominal pain and swelling

o Absolute constipation

o Vomiting

o History of transient attacks in which spontaneous reduction of the volvulus has occurred

o Neonatal volvulus presents around 3 months

274
Q

What are the clinical signs of volvulus on examination?

A

o Signs of bowel obstruction with abdominal distension and tenderness

o Absent or tinkling bowel sounds

o Fever

o Tachycardia

o Signs of dehydration

275
Q

What are the appropriate investigations for volvulus?

A

o AXR

o Erect CXR = if perforation is suspected

o Water-soluble contrast enema = Shows site of obstruction

o CT Scan

276
Q

Define Wilson’s disease.

A

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

277
Q

What are the presenting symptoms of Wilson’s disease?

A

o Liver = May present with hepatitis, liver failure, cirrhosis - Jaundice, Easy bruising, Variceal bleeding, Encephalopathy

o Neurological = Dyskinesia, Rigidity, Tremor, Dystonia, Dysarthria, Dysphagia, Drooling, Dementia, Ataxia

o Psychiatric = Conduct disorder, Personality change, Psychosis

278
Q

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

A

o Liver = Hepatosplenomegaly, Jaundice, Ascites/oedema, Gynaecomastia

o Eyes = Kayser-Fleischer Rings, Sunflower cataract (copper accumulation in the lens, seen with a slit lamp)

279
Q

What are the appropriate investigations for Wilson’s disease?

A

o Bloods = LFTs (high AST, ALT, ALP), Low serum caeruloplasmin (caeruloplasmin is an acute phase protein so may give false-negatives if there is an underlying infectious/inflammatory process), Raised serum copper

o 24 hour urinary copper levels = increased in Wilson’s disease

o Liver biopsy = increased copper content

o Genetic analysis - Wilson’s is caused by a wide variety of gene mutations so there isn’t a simple genetic test that can be done

280
Q

Define haemochromatosis.

A

An autosomal recessive disease in which increased intestinal absorption of iron causes accumulation of iron in tissues, which may lead to organ damage.

281
Q

What are the presenting symptoms and signs of haemochromatosis?

A

o Often asymptomatic until the late stages of the disease - symptoms usually start between 40-60 yrs

o Early symptoms are vague = Fatigue, Weakness, Arthropathy, Erectile dysfunction, Heart problems

o Late symptoms = Diabetes mellitus, Bronzed skin, Hepatomegaly, Impotence, Amenorrhoea, Hypogonadism, Cirrhosis, Cardiac, Neurological and Psychiatric problems

282
Q

What are the appropriate investigations for haemochromatosis?

A

o Bloods = Serum ferritin (high), Transferrin (low), Transferrin saturation (high), TIBC (low), LFT

o Tests to exclude other causes of high ferritin = CRP (inflammation), Chronic alcohol consumption, ALT (liver necrosis)

o LFTs

o Other investigations for abnormal liver function (e.g. hepatitis serology)

o Genetic testing

o Liver biopsy (rarely required)

283
Q

What are the appropriate investigatiosn for viral hepatitis?

A

o Bloods = LFTs (high AST, ALT, ALP and bilirubin), High ESR, Low albumin, FBC (high platelets (if severe)), Clotting (prolonged PT (severe))

o Vital Serology

  • HAV = Anti-HAV IgM (during acute illness, disappears after 3-5 months) then Anti- HAV IgG (recovery phase and lifelong persistence)
  • HBV = HBsAg positive, IgM anti-HBcAg (acute phase) then HBsAg positive, IgG anti-HBcAg, HBeAg positive or negative (chronic) - Anti-HBsAg antibody positive or IgG anti-HBcAg shows a cleared HBV or vaccinated
  • HCV = Anti-HCV antibodies -> IgM (acute) or IgG (chronic)
  • HDV = IgM or IgG against HDV or PCR
  • HEV = Anti-HEV IgM (raised 1-4 weeks after onset) then Anti-HEV IgG

o Urinalysis = Positive for bilirubin and Raised urobilinogen

o Liver biopsy

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