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Gastro conditions Flashcards

1
Q

Achalasia

  1. Definition
  2. Aetiology/risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. normal musc activity of the oesophagus is disturbed due to failure or incomplete relaxation of the lower oesophageal sphincter; leads to delay in the passage of swallowed material into the stomach
  2. Caused by degeneration of the ganglion cells of the myenteric plexus in the oesophagus due to unknown cause; oesophageal infection with trypanosoma cruzi seen in central/south america, produces a similar disorder - chagas disease
  3. Any age, (25-60), both sexes equally affected, annual incidence 1/100,000
  4. Insidious onset: intermittent dysphagia, difficulty belching, regurg, heart burn, chest pain (atypical/cramping, retrosternal), weight loss
  5. Complication sx: aspiration pneumonia, malnutrition, weight loss
  6. CXR: widened mediastinum, double right heart border, air fluid level in upper chest, absence of normal gastric air bubble
    1. Barium swallow: dilated oesophagus, smooth taper down to the sphincter
    2. Endoscopy to exclude malignancy, mimic achalasia
    3. Manometry: to assess pressure at LOS = elevated resting LOS pressure, incomplete LOS relaxation, absence of peristalsis in SM portion of oesophagus
    4. Can do serology for Ab for chagas disease
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2
Q

Acute cholangitis

  1. Definition
  2. Aetiology/risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Infection of the bile duct
  2. Due to: obstruction of gallbladder/bile duct due to stones, ERCP, tumours, bile duct structure or stenosis, oarasitic infection
  3. 9% of pts admitted with gallstone disease will have acute cholangitis; M=F; median age - 50-60yrs
  4. Charcot’s triad: RUQ pain, jaundice, fever with rigors; with 2 others: mental confusion and septic shock Reynold’s pentad; may also have pruritus
  5. Fever, RUQ tenderness, mild hepatomegaly, jaundice, mental status changes, sepsis, hypotension, tachycardia, peritonitis
  6. Bloods: FBC high WCC, CRP/ESR ?raised, LFTs: obstructive jaundice so raised ALP and GGT; U+Es:sx of renal dysfunction; blood culture for sepsis; amylase raised if lower part of common bile duct involved
    1. Imaging: XR KUB for stones; Abdo USS for stones and dilation of common bile duct; contrast enhanced CT/MRI for dx; MRCP: necessary for non-calcified stones
  7. Resus if in septic shock
    1. Broad spec Abx: give after culture and those effective against anaerobes and GNB: cefuroximee and metronidazole
    2. Endoscopic biliary drainage usually required to treat underlying obstruciton
    3. Depends on severity:
      1. Stage 1: anti-microbial therapy, percutaneous, endoscopic, operative intervention for non-responders
      2. Stage 2: early percutaneous or endoscopic drainage (biliary is recommended)
      3. Stage 3: Severe includes shock, conscious disturbance, acute lung injury, AKI, hepatic injury or DIC; tx of organ failure with ventilatory support, VP; urgent percutaneous or endoscopic drainage
  8. Liver abscesses, liver failure, bacteraemia, GN sepsis, septic shock, AKI, organ dysfunction, percutaneous/endoscopic drainage can lead to intr-abdo/percutaneous bleeding, sepsis, fistulae, bile leakage
  9. Mortality between 17-40%
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3
Q

Alcoholic hepatitis

  1. Definition
  2. Aetiology/risk factors
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Inflammatory liver injury caused by chronic heavy intake of alcohol
  2. 3 types on the spectrum: alcoholic steatosis, hepatitis and chronic cirrhosis; histopath features of alcohol hepatitis:
    1. Centrilobular ballooning
    2. Degeneration and necrosis of hepatocytes
    3. Steatosis
    4. neutrophilic inflammation
    5. Cholestasis
    6. Mallory hyaline inclusions
    7. Giant mitochondria
  3. 10-35% of heavy drinkers
  4. May be asyx and undetected, or mild with: nausea, malaise, epigastric pain, right hypochondrial pain, low-grade fever; more severe:Jaundice, abdo discomfort or swelling, swollen ankles, GI bleeding ->15-20 yr hx of drinking
  5. Alcohol excess: malnourished, palmar erythema, dupuytren’s contracture, facial telngiectasia, parotid enlargment, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising
    1. Severe alcoholic hepatitis: febrile, tachycardia, jaundice, bruising, encephalopathy (liver flap, drowsiness, disorientation), ascites, hepato/splenomegaly
  6. 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: prolong PT
    1. US: other liver impairment causes
    2. Upper GI endoscopy: investigate varices
    3. Liver biopsy: distinguish from other causes of hepatitis
    4. EEG: slow wave activity = encephalopathy
  7. Mx:
    1. Acute: thiamine, vit C and multivits (pabrinex), monitor and correct K/Mg/glucose; adequate urine output; encephalopathy tx with oral lactulose or phosphate enemas; ascites with diuretics (spirono and frusemide); therapeutic paracentesis; glypressing and N-acetylcysteine for hepatorenal syndrome
    2. nutrition: via oral/NG feeding; protein restriction avoided unless ecephalopathic; nutritional supplementation and vit (B group, thiamine and folic acid) should be started parenterally initially and continued orally
    3. Steroid therapy: reduce short term mortality for severe alcoholic hepatitis
    4. NB:hepatorenal syndrome (dev of renal failure in pts with advanced chronic liver disease - RAS activated and vasoconstriction of vessels in kidney leads to kidney failure
  8. Acute liver decompensation, hepatorenal syndrome, cirrhosis
  9. Mortality: 1st month = 10%, first year = 40%, if alcohol intake continues, then progression into cirrhosis within 1-3yrs
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4
Q

Anal fissure

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigation
  7. Management
  8. Complication
  9. Prognosis
A
  1. A painful tear in the squamous lining of the lower anal canal - 90% of anal fissures are posterior (ant occur after childbirth
  2. Affects 1/10 people during their lifetime, both sexes are affected equally, can occur at any age; most cases occur in children and young adults - 10-30yrs
  3. Most caused by hard faeces; anal sphincter spasm can constrict the inferior rectal artery causing ischaemia impairing healing process;
    1. Rare causes: syphilis, herpes, trauma, crohn’s, anal cancer, psoriasis
  4. Tearing pain when passing stools; may be a little bit of blood in the faeces or on the paper; pruritus ani
  5. Tears in the squamous lining on the anus on examination
  6. Examine the anus
  7. Conservative: high fibre diet, softening the stools (laxative), good hydration
    1. Medical: lidocaine ointment, GTN ointment and diltiazem (relaxing anal sphincter and promoting healing), botulinum toxin injection
    2. Surgical: lateral sphincterotomy, relax anal sphincter and promotes healing but has complication, so reserved for non-tolerant pts to non-surgical tx
  8. Chronic anal fissure
  9. Most people it will heal within a week or so; tx revolves around easing pain by keeping the stools soft and relaxing the anal sphincter to promote healing
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5
Q

Appendicitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigation
  7. Management
  8. Complications
  9. Prognosis
A
  1. Inflammation of appendix
  2. Gut organisms invade appendix wall after lumen obstruction; leads to oedema, ischaemic necrosis and perforation
  3. Most common surgical emergency; can occur at any age; most commonly between 10-20
  4. Periumbilical pai that moves to right iliac fossa, anorexia, vomiting, constipation, diarrhoea
  5. General sx: tachycardia, fever, furred tongue, lying still, coughing hurts, foetor w/w/out flushing, shallow breaths
    1. RIF: guarding, rebound/percussion tenderness, PR pain on RHS (sx of low-lying pelvic appendix)
    2. Special sx:
      1. Rovsing’s sign: palpation of the left iliac fossa causes more pain in the right iliac fossa than the left
      2. Psoas sx: pain on extending hip
      3. Cope sx: pain on flexion and internal rotation of the hip
    3. Variations in clincal picture: inflammation of retrocaecal/retroperitoneal appendix may cause flank/RUQ pain; child would have vague abdo pain and won’t eat; shocked confused 80+ year old not in any pain
  6. Bloods: high WCC and CRP; US may help; CT for dx
  7. Prompt appendicectomy; ABx: cefuroxime, metronidazole; laparoscopy - dx and therapuetic advantages
  8. Perforation, appendix mass (occurs when inflamed appendix becomes covered with omentum); appendix abscess (may occur if appendix mass fails to resolve, tx involves drainage and Abx)
  9. Uncomplicated appendicitis - most people recover with no long term problems; ruptured appendix with greater risk of complications/death
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6
Q

Autoimmune hepatits

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
A
  1. Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoAb
  2. Genetically predisposed individual and env agent may lead to hepatocyte expression of HLA ag, which then become the focus of a principally T-cell-mediated autoimmune attack; Raised titre of ANA and anti-SM Ab, anti-liver/kidney microsomes are NOT thought to directly injure the liver; 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 cirrhosis
    1. Type 1: ANA, ASMA, anti-actin Ab, anti-soluble liver Ag
    2. Type 2: ab to liver/kidney microsomes, antibodies to liver cytosol Ag
  3. Type 1: occurs in ALL age groups, mainly young women; type 2: generally occurs in girls and young women
  4. Asyx and discovered incidentally through abnormal LFT; insidiously present with: malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis
    1. Acute hepatitis (25%): fever, anorexia, jaundice, N/V/D, RUQ pain, some present with serum sickness = arthralgia, polyarthritis, maculopapular rash
    2. Check for FHx of other AI diseases; full Hx important to rule out other causes of hepatitis
  5. Stigmata of chronic liver disease, ascites, oedema, hepatic encephalopathy are late features; cushingoid features may be present even before the admin of steroids
  6. Bloods: LFTs: high: AST/ALT/GGT/ALP/bilirubin, low: albumin (severe); Clotting: high PT; FBC: low Hb, platetes and WCC; hypergammaglobulinaemia: presence of ANA, ASMA ad anti-LKM Ab
    1. Liver biopsy: needed to establish dx and check hepatitis vs cirrhosis
    2. Rule out other causes of liver disease: viral serology, urinary copper/caeruloplasmin, ferritin and transferrin saturation, alpha-1 antitrypsin, anti-mitochondrial antibodies
    3. US/CT/MRI of liver and abdo: visualise structural lesions
    4. ERCP: rule out PSC
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7
Q

Barrett’s oesophagus

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx and sx
  5. Investigations
  6. Management
  7. Complication
  8. Prognosis
A
  1. 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; metaplastic change from squamous -> columnar; main problem: barrett’s could progress to oesophageal adenocarcinoma
  2. Reflux will occur if the cardiac sphincter is not working properly; hiatus hernia makes GORD more likely
  3. 1/10 adults have heart burn every day; 3-5% of people with GORD will develop Barrett’s oesophagus
  4. Heartburn, nausea, waterbrash, bloating, belching, burning pain when swallowing
  5. OGD and biopsy: show replacement of squamous epithelium with columnar epithelium
  6. Premalignant/high grade dysplasia: oesophageal resection, eradicative mucosectomy
    1. Other techniques: endoscopic targeted mucosectomy, mucosal ablation by epithelial laser, radiofrequency or photodynamic ablation
    2. Low-grade dysplasia: annual endoscopic surveillance is recommend
    3. No pre-malingant changes found: surveillance endoscopy and biopsy performed every 1-3yrs, anti-reflux measures
  7. Main complication: development of oesophageal adenocarcinoma; risk of dysplasia
  8. Barrett’s oesophagus carries a 30-60x higher risk of oeophageal adenocarcinoma than the general popn; 5-10% of those with barrett’s oesophagus will develop adenocarcinoma over 10-20yrs
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8
Q

Biliary colic

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complication
  9. Prognosis
A
  1. Pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone; pain which is very severe, is usually felt in upper abdo but can also be poorly localised due to its visceral nature
  2. Occurs due to contractions of the biliary tree in an attempt to relieve an obstruction; risk factors of gallstones:
    1. Fair, fat, fertile, 40, female
  3. 10-15% of people in the adult western world will develop gallstones; biliary colic is most common presentation of gallstone disease
  4. Crampy RUQ pain, N/V, pain may radiate to right scapula; pain doesn’t fluctuate and has tendency to persist; individuals may present with pain following ingestion of fatty meal
  5. RUQ pain and epigastric tenderness
  6. Urinalysis, CXR, ECG to exclude other causes; US: look for dilatation of CBD, gallbladder wall may be thickened; LFT; ERCP dx and therapeutically; CT: may be useful if other forms of imaging have been insufficient
  7. Analgesia, IV fluids, NBM; surgical: laproscopic cholecystectomy; ERCP can also be used to help remove stones or stent a blocked bile duct
  8. Complication of surgery - injury to bile duct; fat intolerance due to inability to secrete large amount of bile into intestine because the pt no longer has a gallbladder; post-cholecystectomy syndrome: presence of abdo syx (dyspepsia, N/V, RUQ pain) after the removal of the gallbladder
  9. Good prognosis with appropriate tx
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9
Q

Cholecystitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Inflammation of the gallbladder
  2. Types of stones: Mixed stones (80%) - contains cholesterol, Ca bilirubinate, PO4 and protein; form due to imbalance between bile salts, PL, cholesterol, nucleation factors and gallbladder motility
    1. Pure cholesterol stones
    2. Pigment stones - black stones made of calcium bilirubinate, form due to increased bilirubin
    3. RF: age, female, fat, DM, drugs (OCP, octreotide), Fhx, ethnicity, pigment stone risk factors: haemolytic disorders
  3. Very common, UK prevalence of gallstone disease = 10%, 3x more common in females, more common with increasing age
  4. systemically unwell, fever, prolonged abdo pain, pain may be referred to right shoulder due to diaphragmatic irritation
  5. Tachycardia, pyrexia, RUQ pain or epigastric tenderness, murphy’s sign positive
  6. Bloods: FBC - high WCC in cholecystites and cholangitis; LFT high ALP/GGT; blood cultures; amylase
    1. US: show gallstones, increased thickness of gallbladder wall, dilatation of biliary tree
    2. AXR: but only 10% of gallstones are radioopaque
    3. Other imaging - to exclude differentials
  7. Conservative - mild biliary colic, follow low-fat diet
    1. Medical: NBM, IV fluids, analgesia, anti-emetics, Abx; if obstruction: urgent biliary drainage by ERCP or via percutaenous route is necessary
    2. Surgical: laproscopic cholecytectomy
  8. Stones within the gallbladder: biliary colic, cholecystitis, gallbladder empyema, gallbladder cancer (rare)
    1. Stones outside the gallbladder: obstructive jaundice, pancreatitis, asc cholangitis, cholecystoduodenal fistula, gallstone ileus, bouveret syndrome (gallstones cause gastric outlet obstruction), mirizzi syndrome
    2. Complications of cholecystectomy: bleeding, infection, bile leak, post-cholecystectomy syndrome; port-site hernia
  9. Gallstones don’t cause syx most of the time; surgery offers excellent cure if syx
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10
Q

Cirrhosis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigation
  7. Management
  8. Complications
  9. Prognosis
A
  1. End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes; cirrhosis is considered decompensated if complicated by: ascites, jaundice, encehalopathy, GI bleed; can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis
  2. Chronic alcohol misuse, chronic viral hepatitis, autoimmune hepatitis, drugs, inherited (alpha1 antitrypsin def, haemochromatosis, wilson’s disease, galactosaemia, cystic fibrosis), vascular (budd-chiari syndrome, hepatic venous congestion), chronic biliary diseases (PBC, PSC, biliary atresia), unknown, non-alocholic steatohepatitis (obesity, DM, total parenteral nutrition, short bowel syndromes, hyperlipidaemia, drugs
  3. One of the top 10 causes of death worldwide
  4. Early non specific syx: anorexia, nausea, fatigue, weakness, weight loss
    1. Syx due to decreased liver synthetic function: easy bruising, abnormal swelling, ankle oedema
    2. Syx due to reduced detoxification function: jaundice, personality change, altered sleep pattern, amenorrhoea, galactorrhoea
    3. Syx due to portal HTN: abdo swelling, haematemesis, PR bleeding or maelena
  5. Asterixis, bruises, clubbing, dupuytren’s contracture, palmar erythema, jaundice, gynaecomastia, leukonychia, parotid enlargement, spider naevi, scratch mark, ascites, enlarged liver, testicular atrophy, caput medusae, splenomegaly
  6. Bloods: FBC: low pts+Hb, LFTs: normal but often high AST/ALT/ALP/GGT/bilirubin, low albumin; clotting: prolonged PT; serum AFP: raised chronic liver disease, high levels suggest hepatocellular carcinoma
    1. To determine cause: viral serology, A1anti-trypsin, caeruloplasmin, iron studies for haemochromatosis, anti-mitochondrial Ab, ANA/ASMA
    2. Ascitic tap: MC+S, biochem, cytology, ascitic tap w/neutrophils >250/mm3 = spontaneous bacterial peritonitis
    3. Liver biopsy: performed percutaneously, transjugular; histopathological features of cirrhosis: periportal fibrosis, loss of normal liver architecture, nodular appearance; Grade: indicates degree of inflammation; Stage: degree of architectural distortion
    4. Imaging: US, CT, MRI for ascites, HCC, hepatic/portal vein thrombosis, exclude biliary obstruction; MRCP
    5. Endoscopy - varices
    6. Child pugh grading: score for estimating prognosis in chronic liver disease/cirrhosis: albumin, bilirubin, PT, ascites encephalopathy; cirrhosis divided into classes using: Class A: 5-6, Class B: 7-9, Class C: 10-15
  7. Tx the cause; avoid alcohol, sedative, opiates, NSAIDs and drugs that affect the liver, nutrition is important, enteral supplements should be given, NG feeding may be indicated; Tx complications:
    1. Encephalopathy: tx infections, exclude GI bleed, use lactulose and phosphate enemas, avoid sedation
    2. Ascites: Diuretics, dietary Na restriction, therapeutic paracentesis, monitor weight, fluid restrict if plasma Na <120 mmol/L, avoid alcohol and NSAIDs
    3. Spontaneous bacterial peritonitis: Abx, prophylaxis against recurrent SBP with ciprofloxacin
    4. Surgical: consider Transjugular intrahepatic portosystemic shunt, helps reduce portal HTN; liver transplant is only curable method
  8. Portal HTN with ascites, hepatic encephalopathy, variceal haemorrhage, SBP, HCC, Renal failure, pulm HTN
  9. Depends on aetiology and complications; poor prognosis: overall 5yr survival = 50%, if ascites = 2 year survival = 50%
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11
Q

Coeliac Disease

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. An inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption -> subtotal villous atrophy and crypt hyperplasia
  2. Due to sensitivity to gliadin component of gluten, which triggers an immuno reaction in the small intestine leading to mucosal damage and loss of villi; 10% risk of 1st degree relatives affected; clear genetic susceptibility associated with HLA-B8/DR3/DQW2 haplotypes
  3. UK: 1/2000, west ireland: 1/300; rare in East Asia
  4. May be asyx; abdo discomfort, pain and distention;steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away), diarrhoea, tiredness, malaise, weight loss, failure to thrive in children, amenorrhoea in young adults
  5. Sx of anaemia: pallor;
    1. sx of malnutrition: short stature, abdo distention, wasted buttocks in children, triceps skinfold thickness indicates fat stores)
    2. sx of vit/mineral deficiencies: OM, easy bruising
    3. Intense, itchy blisters on elbow, knees and buttocks
  6. Blood: FBC (low Hb, iron, folate), U+Es, albumin, calcium, Phosphate
    1. Serology: IgG anti-gladin Ab, IgA and IgG anti-endomysial tranglutaminase Ab can be dx; IgA def quite common
    2. Stool: culture to exclude infection, faecal fat tests for steatorrhoea
    3. D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption
    4. Endoscopy: direct visualisation of vilous atrophy in the small intestine, villous atrophy and crypt hyperplasia in duodenum
  7. Advice: avoid gluten
    1. Medical: vit and mineral supplements, oral corticosteroids if disease doesn’t subside with avoidance of gluten
  8. Iron, folate and B12 def; OM, ulcerative jejunoileitis; GI lymphoma, Bacterial overgrowth, cerebellar ataxia
  9. Full recovery in most pts who strictly adhere to gluten free diet; syx usually resolve within weeks though histological changes may take longer; gluten free diet must be followed for life
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12
Q

Crohn’s disease

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Chronic granulomatous inflammatory disease that can affect any part of the GIT; grouped with UC and known, together, as IBD
  2. Cause unknown but thought to be due to interplay between genetic and env factors; though inflammation can occur anywhere from mouth to anus; 40% involves the terminal ileum
  3. UK annual incidence: 5-8/100,000; UK prevalence: 50-80/100,000; any age but peaks in teens, 20s and 40s
  4. Crampy abdo pain, diarrhoea, fever, malaise, weight loss, syx of complications, sometimes RIF pain due to inflammation of terminal ileum
  5. Weight loss, clubbing, sx of anaemia, aphthous ulcers in mouth, perianal skin tags, fistulae and abscesses, uveitis, erythema nodosum, pyoderma gangrenosum
  6. Blood: FBC - low Hb, high platelets, high WCC; U+Es, LFTs - low albumin; high ESR, CRP may be high or normal
    1. Stool microscopy and culture: exclude infective colitis
    2. AXR to show toxic megacolon; erect CXR if there is a risk of perf
    3. Small bowel barium follow through - fibrosis/strictures, deep ulceration, cobblestone mucosa
    4. Endoscopy and biopsy: for UC vs CD; useful for monitoring malignancy and disease progression; show mucosal oedema and ulceration with rose thorn fissures; fistulae and abscesses; transmural chronic inflammation of macrophages, lymphocytes and plasma cells; granulomas with epitheliod giant cells may be seen in blood vessels and lymphatics
    5. Radionuclide labelled neutrophil scan: can localise the inflammation
  7. Acute exacerbation: fluid restriction, IV/oral corticosteroids, 5-ASA analogues, analgesia, parenteral nutrition may be necessary, monitor markers of disease activity
    1. Long term:
      1. Steroids for acute exacerbation
      2. 5-ASA analogues - decreases freq of relapses
      3. Immunosuppression: using steroid sparing agents reduces freq of relapses
      4. Anti-TNF agents: very effective at inducing/maintaining remission
    2. General advice: stop smoking, dietician referral
    3. Surgery indicated if: medical tx fails, failure to thrive in children with complications; involves resection of affected bowel and stoma formation
  8. GI: haemorrhage, stricture, perf, fistulae (bowel, bladder, vagina), perianal fistulae and abscesses, GI cancer, malabsorption
    1. Extraintestinal features: uveitis, episcleritis, gallstones, kidney stones, arthropathy, sacroiliitis, ankspond, erythema nodosum, pyoderma gangrenosum, amyloidosis
  9. Chronic relapsing condition
    1. 2/3 of pts will require surgery at some stage and require more than 1 op
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13
Q

Diverticular disease

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complication
  9. Prognosis
A
  1. Duverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of large bowel
    1. Diverticular disease: diverticulosis with complications
    2. Diverticulitis: acute inflammation and infection of colonic diverticulae
    3. Hinchey classificaion of acute diverticulitis: Ia phlegmon, Ib and II: localised abscesses, III: perf and purulent peritonitis, Iv: faecal peritonitis
  2. Aetiology: low fibre diet = loss of stool bulk leads to high colonic intraluminal pressures to propel stool out, leading to herniation of the mucosa and submucosa through the muscularis
    1. Pathogenesis: Found in sigmoid and descending colon, might be right sided; found at sites of nutrient artery penetration; diverticular obstruction by thickened faeces can lead to bacterial ovegrowth, toxin production and mucosal injury -> leading to:
      1. diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
  3. Diverticular disease is common; 60% develop it; rare <40
  4. Often Asyx (80-90%); complications lead to syx like: PR bleed, diverticulitis causing LIF and lower abdo pain and fever; diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
  5. diverticulitis: tender abdomen and sx of local or generalised peritonitis if diverticulum has perf
  6. Bloods: FBC increased WCC and CRP, check clotting and cross-match if bleeding
    1. Barium enema: shows presence of diverticulae (saw tooth appearance of lumen); reflects psuedohypertrophy of circular muscle
    2. Flexible sigmoidoscopy and colonoscopy: diverticulae can be visualised and other pathology can be excluded
    3. ACUTE: CT scan for evidence of disease and complications may be performed
  7. Asyx: soluble high fibre diet, some drugs for preventing recurrent flares of diverticulitis
    1. GI bleed: PR bleeeding usually managed conservatively with IV rehydration, Abx, blood transfusion if necessary; angiography and embolism or surgery if severe
    2. Diverticulitis: IV Abx, fluid rehydration, bowel rest , abscesses may be drained by radiologically sited drains
    3. Surgery: pt with recurrent attacks or complications; open: hartmann’s procedure leaving stoma, one-stage resection and anastamosis; laproscopic drainage, peritoneal lavage and drain placement can be effective
  8. Diverticulitis, pericolic abscess, perforation, faecal peritonitis, colonic obstruction, fistula formation, haemorrhage
  9. 10-25% have one or more episodes of diverticulitis
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14
Q

Gastroenteritis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigation
  7. Management
  8. Complications
  9. Prognosis
A
  1. Acute inflammation of the lining of the GIT, manifested by N/V/diarrhoea/abdo discomfort
  2. Viral: rotavirus, adenovirus, astrovirus, calcivirus, norwalk virus;
    1. Bacterial: campylobacter jejuni, e. coli, salmonella, shigella, vibrio cholerae, listeria, yersinia enterocolitica
    2. Protozoal: entamoeba histolytica, cryptosporidium parvum, giardia lamblia
    3. Toxins from: staph aureus, clostridium botulinum/perfringens, bacillus cereus, mushrooms, heavy metals, seafood
    4. Commonly contaminated foods: improperly cooked meat, old rice, eggs and poultry, milk and cheeses, canned food
  3. Common, serious cause of morbiditu and mortality in the developing world
  4. Sudden onset N/V/anorexia, diarrhoea (bloody/watery), abdopain or discomfory, fever and malaise, (ASK recent travel, Abx use and recent food intake)
    1. Time of onset: toxins = early 1-24hrs, bacterialviral/protozoal = 12+hrs
    2. Pay attention to the other effects of toxins: botulinum causes paralysis, mushrooms cause fits, renal or liver failure
  5. Diffuse abdo tenderness, abdo distention; bowel sounds often increased; severe gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown; DEHYDRATION
  6. Bloods: FBc, blood culture, U+Es
    1. Stool: faecal microscopy, analysis for toxins, pseudomembranous colitis
    2. AXR/US: exclude other causes of abdo pain
    3. Sigmoidoscopy: usually unnecessary unless IBD excluded
  7. Bed rest, fluid and electrolyte replacement with oral rehydration solution; IV rehydration may be necessary with severe vomiting; most are self-limiting; Abx tx only if severe or if infective agent identified
  8. Dehydration, electrolyte imbalance, prerenal failure, 2ry lactose intolerance; sepsis shock; HUS; Guillan Barre S may occur weeks after recovery from campylobacter gastroenteritis
  9. Good prognosis as most are self limiting
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15
Q

Gastrointestinal perforation

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Perforation of the wall of GIT with spillage of bowel contents
  2. Large bowel: Common: diverticulitis, colorectal cancer, appendicitis; others: volvulus, UC (toxic megacolon)
    1. gastroduodenal: common: perf duodenal or gastric ulcer; or gastric cancer
    2. Small bowel (rare): trauma, infection, crohn’s
    3. Oesophagus: boerhaave’s perf
    4. RF of cause: NSAIDs, steroids, bisphosphonates
  3. Incidence depends on cause
  4. Large bowel: peritonitic abdo pain; rule out AAA rupture
    1. Gastroduodenal: sudden-onset severe epigastric pain, worse on movement, pain becomes generalised gastric malignancy with wt loss and N/V
    2. Oesophageal: severe pain following episode of violent vomiting; neck/chest pain and dysphagia develop soon afterwards
  5. Very unwell, sx of shock, pyrexia, pallor, dehydration, sx of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds, loss of liver dullness due to overlying gas
  6. Bloods: FBC, U+Es, LFTs, amylase - raised with perf
    1. Erect CXR for air under diaphragm
    2. AXR: shows abnormal gas shadowing
    3. Gastrograffin swallow: for suspected oesophageal perf
  7. Resus: correct fluid and electrolytes, IV abx
    1. Surgical:
      1. large bowel: Id site of perf with peritoneal lavage, resection of perforated section;
      2. gastroduodenal: laparotomy, peritoneal lavage, perf closed with omental patch, gastric ulcers biopsied, H pylori eradication if positive
      3. oesophageal: pleural lavage, repair of ruptured oesophagus
  8. Large and small bowel - peritonitis; oesophagus - mediastinitis, shock, overwhelming sepsis and death
  9. Gastroduodenal: gastric ulcers have higher morbiditiy and mortality than duodenla ulcer, poor prognosis for perf gastric carcinomas
    1. large bowel: hgih risk of faecal peritonitis if left untreated; lead to death via septicaemia for multiorgan failure
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16
Q

GORD

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
  2. Caused by disruption of mechanism that prevents reflux; mechanisms that prevent reflux: lower oesophageal sphincter, acute angle of junction, mucosal rosette, intra-abdominal portion of oesophagus - prolonged oesophageal clearance contributes to 50% of cases
  3. Common, 5-10% of adults
  4. Substernal/epigastric burning discomfort or heartburn; aggravated by: lying supine, bending, large emals, drinking alcohol; relieved by antacid
    1. Waterbrash - regurg of excessive accumulation of saliva from lower part of oesophagus
    2. Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze
    3. Dysphagia - caused by formation of peptic stricture after long-standing reflux
  5. Usually normal; occasionally epigastric tenderness, wheeze on chest auscultation, dysphonia
  6. Clinical dx
    1. Upper GI endoscopy, biopsy, cytological brushings to exclude malignancy
    2. Barium swallow - detects hiatus hernia (repair op = Nissen fundoplication), peptic stricture, extrinsic compression of oesophagus
    3. CXR: not specific for GORD but can lead to finding hiatus hernia = gastric bubble behind the cardiac shadow
    4. 24hr oesophageal pH monitoring: pH probe places in lower oesophagus determining relationship between syx and oesophageal pH
  7. Advice: wt loss, elevating head of bed, avoid provoking factors, stop smoking, lower fat meals, avoid large meals in the evening
    1. Medical: antacids, alginates, H2 antagonists, PPI
    2. Endoscopy: annual endoscopic surveillance looking for barrett’s, neessary for stricture dilation or stenting
    3. Surgery: antireflux surgery if refractory to medical tx
    4. Nissen fundoplication: fundus of stomach is wrapped around lower oesophagus - helps reduce risk of hiatus hernia and reduce reflux
  8. Oesophageal ulceration, peptic stricture, anaemia, barrett’s, oesophageal adenocarcinoma, associated with asthma and chronic laryngitis
  9. 50% respond to lifestyle measures alone; in pts that require drug therapy, withdrawal is often associated with relapse; 20% of pts undergoing endoscopy for GORD have barrett’s
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17
Q

Haemorrhoids

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Anal vascuar cushions become enlarged and engorged with a tendency to protrude, bleed or prolapse in the anal canal; classification:
    1. Internal: arises from superior haemorrhoidal plexus; above dentate line
    2. External: lie below dentate line
    3. Degrees:
      1. 1st degree: haemorrhoids that do NOT prolapse
      2. 2nd: prolapse with defecation but reduce spontaneously
      3. 3rd: prolapse and require manual reduction
      4. 4th: prolapse that can’t be reduced
  2. Exact cause is disputed; caused by disorganisation of the fibromuscular stroma of anal cushions; RF:
    1. Constipation
    2. Prolonged straining
    3. Derangement of internal anal sphincter
    4. Pregnancy
    5. Portal HTN
  3. Common, peak age 45-65yrs
  4. Usually asyx, bleeding (bright red blood on toilet paper and drips into pan after stool/ not mixed in); absence of alarm syx (FLAWS), other syx: itching, anal lumps, prolapsing tissue; external haemorrhoids that have thrombosed can be very painful
  5. 1st or 2nd degree not usually visible on external inspection; internal haemorrhoids NOT normally palpable on DRE unless thrombosed, usually visible on proctoscopy
    1. DDx: anal tags, anal fissures, rectal prolapse, polyps, tumours
  6. DRE, proctoscopy, rigid or flexible sigmoidoscopy: important to exclude rectal/sigmoid bleeding
  7. Conservative: high fibre diet, increase fluid intake, bulk laxatives, topical creams (local anaesthetics)
    1. Injection sclerotherapy: induces fibrosis of the dilated veins
    2. Banding: barron’s bands applied proximal to the haemorrhoids, haemorrhoid will fall off after a few days, BUT may be more painful than injection sclerotherapy
    3. Surgery: reserved for syx 3rd and 4th degree; milligan-morgan haemorrhoidectomy: excision of 3 haemorrhoidal cushions; stapled haemorrhoidectomy is an alternative method; post-op the pt should be given laxatives to avoid constipation
  8. Bleeding, prolapse, thrombosis, gangrene
    1. Injection sclerotherapy: prostatitis, perineal sepsis, impotence, retroperitoneal sepsis, hepatic abscess
    2. Haemorrhoidectomy: pain, bleeding, incontience, anal stricture
  9. Often chronic, high rate of recurrence, surgery can provide long term relief
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18
Q

Inguinal hernia

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Abnormal protrusion of a peritoneal sac through a weakness of the abdo wall in the inguinal region:
    1. Direct inguinal: Protruision of hernial sac directly through a weakness in the transversalis fascia and post wall of inguinal canal, arises medial to inf epigastric vessels and appears through Hesselbach’s triangle
    2. Indirect inguinal: potrusion of hernial sac through the deep inguinal ring, following path of inguinal canal
    3. If both coexist - pantaloon hernia
  2. Congenital: abdo contents enter the inguinal canal through a patent processus vaginalis
    1. Acquired: due to increased intra-abdo pressure along with muscle and transversalis fascia weakness
    2. RF: male, prematurity, age, obesity, raised intra-abdo pressure, constipation, bladder outflow obstruction, intraperitoneal fluid
  3. Common, peak age in adults: 55-85yrs; 9x more common in males
  4. Asyx; lump in groin; cause discomfort and pain, irreducible, may increase in size or have complications
  5. groin lump extending to the scrotum or labia;
    1. distinguishing inguinal and femoral hernias: inguinal - superior and medial to pubic tubercle, femoral - inferior and lateral to pubic tubercle;
    2. check for cough impusle
    3. indirect can be reduced and controlled by applying pressure on the deep inguinal ring
    4. Auscultation - may be bowel sounds over hernia; tenderness if strangulated
    5. hernia may be irreducible; check for sx of complications: bowel obstruction and systemic upset
  6. If acute with painful, irreducible hernia;
    1. Bloods: FBC, U+E, CRP, clotting, group and save for ops, ABG - lactic acidosis from bowel ischaemia
    2. Imagining: erect CXR - check for perf; USS - exclude other causes of groin lump; AXR - check for obstruction
  7. Surgical: usually elective, mesh repair to reinforce defect in transversalis fascia; laproscopic mesh repair; emergency: obstructed or strangulated, laparotomy with bowel restriction may be indicated if bowel is gangrenous
  8. Incarceration, strangulation, bowel obstruction, maydl’s hernia (w-shape strangulation of small bowel); richter’s hernia: strangulation only part of bowel circum
    1. Surgery complications: pain, wound infection, haematoma, penile/scrotal oedema, mesh infection, testicular ischaemia
  9. slowly enlarge if left alone; surgical mesh repair has GOOD outcome
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19
Q

Hiatus hernia

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Prolapse of the upper stomach through the diaphragmatic oesophageal hiatus
  2. Congenital, traumatic, non-traumatic (sliding - moves in and out of chest, paraoesophageal - goes through hole in diaphragm next to oesophagus, mixed) RF: obesity, low-fibre diet, chronic oesophagitis, ascites, pregnancy
  3. Common in western countries, increased freq with age, 70% of pts >70
  4. Most asyx; sliding hernias cause syx; may present with GORD (heartburn, waterbrash) no correlation between size of hernia and severity of syx
  5. Usually no sx
  6. Bloods: FBC for IDA; Radiology: CSR with gastric air bubble seen above diaphragm, barium swallow; endoscopy
  7. Medical: modify lifestyle factors, inhibit acid production, enhance upper GI motility
    1. Surgical: necessary in pt minority, usually performed in pts with complications of reflux disease, despite aggressive med tx or pulm complications;
      1. Nissen fundoplication - stomach pulled down through oesophageal hiatus and part of stomach wrapped 360 degrees around oesophagus to make a new sphincter
      2. Belsey Mark IV fundoplication: 270 degree wrap
      3. Hill repair: gastric cardia is anchored to the posterior abdo wall
  8. Oesophageal: intermittent bleeding, oesophagitis, erosions, barrett’s oesophagus, oesophageal strictures
    1. Non-oesophageal: incarcertion of hiatus hernia, lead to strangulation and perforation
  9. Generally good, sliding hernias have better prognosis than rolling hernias
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20
Q

Infectious colitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx and Sx
  5. Investigations
A
  1. Inflammation of the colon due to bacteria, parasites or viruses
  2. Infection leads to inflammation of the colon; RF: lack of sanitation, drinking contaminated water, Abx use
  3. Quite common
  4. Diarrhoea, blood and mucus in the stools, lower abdo pain, malaise, low-grade fever
  5. Dx largely clinical, stool culture may be used to identify the causative organism
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21
Q

Intestinal ischaemia

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Obstruction of mesenteric vessel, leading to bowel ischaemia and necrosis
  2. Embolus (60%), thrombosis (40%), consequence of volvulus, intussusception, bowel strangulation, failed surgical resection; RF: AF, endocarditis, arterial thrombosis (hypercholesterolaemia, HTN, DM, smoking), venous thrombosis (portal HTN, splenectomy, septic thrombophlebitis, OCP, thrombophilia)
  3. Uncommon, more common in the elderly
  4. Severe acute colicky abdo pain, vomiting, rectal bleeding, hx of chronic mesenteric artery insufficiency: gross wt loss, post-prandial abdo pain; hx of heart/liver disease
  5. Diffuse abdo tenderness, abdo distention, tender palpable mass (ischaemic bowel), bowel sounds may be absent, disproportionate degree of cardiovascular collapse
  6. Dx based on clinical suspicion/after laparotomy;
    1. AXR - thickening of small bowel folds and sx of obstruction;
    2. bloods: ABG (lactic acidosis), FBC, U+Es, LFTs, Clotting, cross-match;
    3. mesenteric angiography: only if stable

Watershed zone - most vulnerable is splenic flexure and sigmoid flexure near superior and inferior mesenteric arteries

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22
Q

Intestinal obstruction

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Obstruction of normal movement of bowel contents; classified according to site: small or large bowel; partial or complete obstruction; simple or strangulated
  2. Extramural: hernia, adhesions, bands, volvulus; intramural: tumours, inflammatory strictures; intraluminal: pedunculated tumours, foreign body
  3. Common, more common in elderly due to increasing incidence of adhesions, hernias and malignancy
  4. Severe gripping colicky pain with periods of ease, abdo distension, frequent vomiting (bile stained/faeculent), absolute constipation
  5. Abdo distention with generalised tenderness; may see visible peristalsis, tinkling bowel sounds, peritonitis (absent bowel sounds, guarding, rebound tenderness), inspect for hernias, look for abdo scars (previous abdo surgery increases the risk of adhesions), inspect for abdo mass
  6. AXR - for dx and localisation, check for valvulae conniventes or haustra; water soluble contrast enema, barium follow through
  7. General: gastric aspiration via NGT if pt is vomiting, IV fluids, electrolyte replacement, monitor vital sx, fluid balance and urine output;
    1. Surgical: emergency laparotomy in acute obstruction
  8. Dehydration, bowel perf, peritonitis, toxaemia, gangrene of ischaemic bowel wall
  9. Variable, dependent on general state of pt and prevalence of complications
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23
Q

IBS

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Functional bowel disorder defined as recurrent episodes of abdo pain/discomfort (absence of detectable organic pathology) for > 6m of the previous year, associated with 2 of the following:
    1. altered stool passage, abdo bloating, syx made worse by eating, passage of mucous
  2. Unknown, could be visceral sensory abnormalities, gut motility abnormalities, psychosocial factors, food intolerance and many more
  3. Common, 10-20% of adults; more common in females, 2:1 ratio
  4. 6+ months of hx of abdo pain, pain is often colicky, lower abdo, relieved by defecation or passing of flatus;
    1. altered bowel frequency (>3 motions per day/<3 motions per week)
    2. abdo bloating
    3. change in stool consistency
    4. passage with urgency or straining
    5. tenesmus
    6. Screen for Red flag syx: wt loss, anaemia, PR bleeding, late onset (>60yrs)
  5. Usually normal on examination, sometimes the abdo may appear distended and be mildly tender on palpitation in one or both iliac fossae
  6. Dx mainly from hx but organic pathology must be excludeed;
    1. blood: FBC (anaemia), LFT, ESR, CRP, TFT, anti-endomysial/anti-tranglutaminase Ab
    2. Stool exam: microscopy and culture for infective cause
    3. US: exclude gallstone disease
    4. Urease breath test: exclude dyspepsia due to h pylori
    5. Endoscopy: if other pathologies suspected
  7. Advice: dietary modification;
    1. Medical: depends on main syx affecting the pt: antispasmodics, prokinetic agents, anti-diarrhoeals, laxatives, low-dose TCA
    2. Psych therapy: CBT, relaxation and psychotherapy
  8. Physical and psych morbidity, increased incidence of colonic diverticulosis
  9. Chronic relapsing and remitting course of disease, often exacerbated by psychosocial stresses
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24
Q

Liver abscesses and cysts

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
A
  1. Abscess: liver infection resulting in a walled off collection of pus; cyst: liver infection resulting in walled off collection of cyst fluid
  2. Pyogenic: E coli, Klebsiella, enterococcus, bacteriodes, strep, staph, 60% caused by biliary tract disease, 15% unknown
    1. Amoebic abscess: caused by entamoeba histolytica
    2. Hydatid cyst: caused by tapeworm, echinococcus granulosis
    3. Other causes: TB
  3. Pyogenic is most common type of liver abscess in industrialised world, amoebic liver abscess - most common worldwide; hydatid cysts - common in sheep rearing countries
  4. Fever, malaise, nausea, anorexia, night sweats, wt loss, RUQ/epigastric pain, referred to shoulder; jaundice, diarrhoea, pyrexia of unknown origin
  5. Fever - continuous or spiking; jaundice, tender hepatomegaly, right lung base - dullness to percussion, reduced breath sounds, due to reactive pleural effusion
  6. Bloods: FBC: mild anaemia, leukocytosis, high eosinophils; LFTs: high ALP, high bilirubin; high ESR/CRP, blood cultures, amoebic and hydatid serology
    1. Stool MC+S for e hystiolytica
    2. Liver US or CT/MRI localises structure of mass
    3. CXR: for right PE o atelactasis, raised hemidiaphragm
    4. Aspiration and culture of abscess material - most pyogenic liver abscesses are polymicrobial, amoebic abscesses have fluid of necrotic hepatocytes and trophozoites
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25
Q

Liver failure

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy; classified based on time interval between the onset of jaundice and the development of hepatic encephalopathy
    1. Hyperacute = <7d
    2. Acute = 1-4wks
    3. Subacute = 4-12wks
    4. Acute on chronic liver failure = acute deterioration in pts with chronic liver disease
  2. Viral: hep A/B/C/D/E
    1. Drugs: paracetamol OD, idiosyncratic drug reaction
    2. Less common cause: AI hepatitis, budd-chiari syndrome, pregnancy related, malignancy, haemochromatosis, mushroom poisoning, wilson’s disease
    3. Pathogenesis of manifestations of liver failure:
      1. Jaundice - decreased secretion of conjugated bilirubin
      2. Encephalopathy: Nitrogenous products absorbed in gut and goes via portal circulation to the liver, which can’t filter and goes straight to the brain
      3. Coagulopathy: reduced synthesis of clotting factors, reduced platelets, platelet functional abnormalities associated with jaundice or renal failure
  3. Paracetamol overdose counts for 50% of acute liver failure in the UK
  4. May be asyx, fever, nausea, jaundice
  5. Jaundice, encephalopathy, asterixis, fetor hepaticus, ascites and splenomegaly (less common if acute/hyperacute), bruising or bleeding, sx of 2ry causes (bronze skin colour, kayser-fleisher rings), pyrexia - may indicate infection or liver necrosis
  6. ID the cause: viral serology, paracetamol levels, autoAb (ASM, anti-LKM), ferritin (haemochromatosis), caeruloplasmin and urinary copper (wilson’s disease)
    1. bloods: FBC low Hb (GI bleed)/high wcc (infection); U+Es (renal failure); glucose; LFTs: high bilirubin, high AST/ALT/ALP/GGT, low albumin, ESR/CRP, coagulation screen, ABG to determine blood pH, group and save
    2. Liver US/CT
    3. Ascitic Tap: send for MC+S, neutrophils >250/mm3 = spontaneous bacterial peritonitis
    4. Doppler scan of hepatic or portal veins - Budd-chiari syndrome
    5. EEG - monitor encephalopathy
  7. Resus ABC, tx cause if possible - N-acetylcysteine: tx of paracetamol ODs
    1. tx/prevention of complications: monitor - vital sx, PT, pH, creatinine, urine output, encephalopathy
      1. Manage encephalopathy: lactulose and phosphate enemas
      2. Abx and antifungal prophylaxis
      3. hypoglycaemia tx
      4. coagulopathy tx - IV vitamin K, FFP, platelet infusions
      5. gastric mucosa protection PPIs, sucralfate
      6. Avoid sedatives or drugs met by the liver,
      7. cerebral oedema - decrease ICP with mannitol
    2. Renal failure: haemodialysis, nutritional support
    3. Surgical liver transplant
  8. Infection, coagulopathy, hypoglycaemia, disturbance of electrolyte balance and acid-base balance, disturbance of cardiovacular system, hepatorenal syndrome, cerebral oedema, resp failure
  9. Depends on severity and aetiology
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26
Q

Mallory-Weiss tear

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Tearing of the lining of the oesophagus around the junction with the stomach as a result of violent vomiting or straining to vomit
  2. Caused by prolonged violent vomiting; RF: chronic alcohol abuse, bulimia, other causes: trauma, intense coughing, gastritis
  3. Quite rare
  4. Most are asyx, abdo pain, severe vomiting, haematemesis, involuntary retching, black/tarry stools, syx of hypovolaemia if severe blood loss
  5. Malaena, see above
  6. OGD, bloods: FBC to check for anaemia
  7. 80-90% of the time, blleding will stop on its own; surgery: only if bleeding doesn’t stop - injection sclerotherapy, coagulation therapy, arteriography; anti-reflux meds may be prescribed
  8. Boerhaave’s perforation
  9. Good prognosis
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27
Q

Non-alcoholic steatohepatitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Term used to describe range of conditions caused by the build up of fat in the liver due to causes other than excessive alcohol use
  2. Liver may initially become fatty due to alcohol abuse , but tends to resolve over matter of days, but if it persists can cause inflammation and fibrosis; increases risk of DM, MI, stroke
    1. RF: obesity, T2DM, HTN, hypercholesterolaemia, >50, smoking
  3. Most common liver disorder in developed countries, 1/3 of people in UK have early stages
  4. Asyx, incidental finding; occasionally: dull/aching RUQ, fatigue, unexplained wt loss, weakness; syx experienced in most advanced stages
  5. RUQ pain/tenderness, sx of cirrhosis - jaundice, ascites, pruritus
  6. LFTs: elevated AST and ALT; liver US steatosis, liver biopsy
  7. Conservative - control RF: BP, DM, cholesterol, weight, smoking, exercise, alcohol (makes it worse)
  8. Cirrhosis: ascites, oesophageal varices, hepatic encephalopathy, hepatocellular carcinoma, end stage liver failure
  9. 20% with NASH will develop cirrhosis
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28
Q

Acute pancreatitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems; classified as: Mild - minimal organ dysfunction and uneventful recovery; severe - organ failure and/or local complications such as necrosis, abscesses and pseudocysts
  2. Insult will result in activation of pancreatic proenzymes within the pancreatic duct/acini leading to tissue damage and inflammation; causes: GET SMASHED: GALLSTONES, ETHANOL, trauma, steroids, mumps/HIV/coxsackie, AI, scorpion venom, HyperCa/Hypothermia, ERCP, drugs (Na Valproate, steroids)
  3. Common, UK annual incidence, peak age 60yrs; most common: M=alcohol, F=gallstones
  4. Severe epigastric pain, radiating to the back, relieved by sitting forward, aggravated by movement, associated with anorexia, N/V
  5. Epigastric tenderness, fever, shock, decreased bowel sounds, severe pancreatitis: cullen’s sx (periumbilical bruising), grey-turner sx (flank bruising)
  6. Blood: very high serum amylase, high WCC, U+Es, high glucose, high CRP, low Ca, LFTs, ABG
    1. USS: evidence of gallstones in biliary tree
    2. Erect CXR Pleural effusion or bowel perf
    3. AXR: exclude other acute abdo
    4. CT scan
  7. 2 main scales: modified glasgow score (with CRP) and Apache-II score
    1. Medical: fluid and electrolytes resus, urinary catheter and NGT if vomiting, analgesia, blood sugar control, HDU and ITU care, prophylactic ABx
    2. ERCP and sphincterotomy: used for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct - within 72hrs
    3. Early detection and tx of complications: e.g. persistent syx or >30% pancreatic necrosis or sx of sepsis
    4. Surgical: necrotising pancreatitis mx by specialists
  8. Local: pancreatic necrosis, pseudocyst, abscesses, ascites, pseudoaneurysm, venous thrombosis
    1. Systemic: multiorgan dysfunciton, sepsis, renal failure, ARDS, DIC, hypoCa, DM
    2. Long term - chronic pancreatitis
  9. 20% high mortality, infected pancreatic necrosis has 70% mortality; 80% follow milder course
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29
Q

Chronic pancreatitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endo/exocrine function and recurrent abdo pain
  2. Alcohol - 70%, idiopathic 20%; Rare: recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism
    1. Caused by chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilation and cyst and stone formation; pain associated with raised intraductal pressures
  3. 1/100,000 incidece; 3/100,000 prevalence, mean age:40-50yrs in alcohol associated disease
  4. Recurrent severe epigastric pain, radiates to back, relieved by sitting forward, aggravated by eating/drinking alcohol; many yrs -> wt loss, bloating, steatorrhoea
  5. Epigastric tenderness; sx of complications - wt loss, malnutrition
  6. Bloods: high glucose (OGTT), amylase/lipase normal, high Ig
    1. US
    2. ERCP/MRCP: early changes = main duct dilatation and stumping of branches; late changes = duct strictures with alternating dilatation
    3. Abdo XR: calcification of pancreas
    4. CT scan: same as AXR
    5. Test of pancreatic exocrine function: faecal elastase - pacreatic exocrine function
  7. General: mainly syx and supportive - dietary advice, stop smoking/drinking, tx DM, oral pancreatic enzyme replacement, analgesia; chronic pain may need specialist input
    1. Endoscopy: sphincterotomy, stone extraction, dilatation and stenting of strictures, ESWL
    2. Surgical: Lat pancreaticojejunal drainage, panc resection (whipple’s procedure), limited resection of panc head (beger procedure), open panc duct and excavate head of pancreas (Frey)
  8. Local: pseudocysts, biliary duct stricture, duodenal obstruction, pancreatic ascites/carcinoma
    1. Systemic: DM, steatorrhoea, chronic pain syndromes, dependence on strong analgesics
  9. Difficult to predict, surgery improves syx in 60-70% but results not sustained, with life expectancy reduced by 10-20yrs
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30
Q

Peptic ulcer disease and gastritis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Ulceration of areas of GIT caused by exposure to gastric acid and pepsin; most commonly gastric and duodenal ulcers (can occur in oesophagus and Meckel’s diverticulum)
  2. Imbalance between damaging action of acid and pepsin and the mucosal protective mechanisms; strong correlation with H. pylori (common causes w/ NSAIDS)
    1. Rare cause: Zollinger-Ellison syndrome
  3. Common, annual incidence 1-4/1000; more common in males; mean age: duodenal ulcer= 30s, gastric ulcer = 50s
  4. Epigastric pain, relieved by antacids, syx depend on food intake: gastric pain worse soon after eating, duodenal: pain worse several hours after eating; may present with complications
  5. No physical findings, epigastric tenderness, sx of complications
  6. Bloods: FBC, serum amylase, U+Es, clotting screen, LFT, cross match if active bleeding, secretin test if Z-E syndrome suspected - IV secretin causes rise in serum gastrin in these pts
    1. Endoscopy - to rule out malignancy; duodenal not needed
    2. Rockall scoring: severity after GI bleed, <3 good prognosis, >8 high risk of mortality
    3. C13 urea breath test; serology (IgG against H pylori confirms exposure to H pylori but not eradication); campylobacter-like organism test - colour change indicates HP
  7. Acute: fluid resus if ulcer perf/bleeding (IV colloids), close monitoring of vital sx, endoscopy, surgical tx; pts with upper GI bleeds treated with IV PPIs at presentation until bleeding ID
    1. Endoscopy: haemostasis for bleeding ulcer with injection sclerotherapy, laser coag, electrocoag
    2. Surgery: indicated if ulcer perf/bleeding can’t be controlled
    3. H pylori eradication: 3x therapy for 1-2wks, 2Abx and PPI
    4. If not HP: tx with PPIs/H2 antags, stop NSAIDS, use misoprostol if NSAID use necessary
  8. Major complications 1% per year; inc: haemorrhage (haematemesis, malaena, IDA), perf, obstruction/pyloric stenosis (scarring, penetration, pancreatitis)
  9. Overall lifetime risk = 10%; outlook good as HP can be cured by eradication
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31
Q

Perineal abscess and fistula

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Abscess = pus collection in perineal region; fistula = abnormal chronically infected tract communicating between perineal skin and anal canal/rectum
  2. Bacterial infection; fistulae are complication of abscess or CD (pepper pot perineum); RF: IBD, DM, malignancy
  3. Common
  4. Constant throbbing pain in perineum; intermitten discharge (mucus/faecal staining) near anal region; PMH/FH of IBD
  5. Localised tender perineal mass, small skin lesion near anus; DRE = thickened area over abscess/fistula; goodsall’s law: rule that correlates internal with external fistula opening - external is anterior to anal canal then fistula radial and direct to anal canal; fistula 3cm away/opening lying posterior to transverse anal line follows curved path and open internally in post midline
  6. Bloods: FBC, CRP, ESR, blood culture
    1. MRI
    2. Endoanal US
  7. Surgical tx; open drainage of abscess; ABx; laying open of fistula - dye inserted to find internal opening
    1. Low fistula = fistulotomy and care with anal sphincter
    2. High fistula = fistulotomy cause incontinence so NOT performed; seton - suture threaded through fistula to allow drainage
  8. Recurrence, damage to internal anal sphicter, incontinence, persisting pain
  9. High recurrence rate without complete excision
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32
Q

Peritonitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Inflammation of the peritoneal lining of the abdo cavity; localised to oe part of peritoneum or generalised
  2. Localised peritonitis: appendicitis, cholecystitis, diverticulitis, salpingitis
    1. 1ry generalised peritonitis: bacterial infection of the peritoneal cavity without an obvious source (via haematogenous or lymphatic spread/ascending infection
      1. RF: ascites, nephrotic syndroome
    2. 2ry generalised peritonitis: caused by bacterial translocation form a localised focus; could be non-bacterial due to spillage of bowel contents, bile and blood
  3. 1ry peritonitis is rare, usually seen in adolescent females; loaclised and 2ry general peritonitis is common in surgical pts
  4. SOCRATES; inflammation of parietal peritoneum is usually continuous, sharp, locaised, exacerbated by movement and coughing; syx vague in those with liver disease and ascites
  5. Check vital sx and look for sx of dehydration or compromised perfusion;
    1. localised peritonitis: tenderness on examination, guarding, rebound tenderness
    2. Generalised peritonitis: very unwell, systemic sx of toxaemia or sepsis pt lies still, shallow breathing, rigid abdo, generalised abdo tenderness, reduced bowel sounds, DRE may show ant tenderness
  6. Bloods: FBC, U+Es, LFTs, amylase, CRP, clotting, x-match, blood cultures, pregnancy test, ABG
    1. Imaging: erect CXR, AXR, USS/CT abdo, laparoscopy
    2. If ascites: ascitic tap and cell count; SBP: >250 neutrophils/mm3; gram stain and culture
  7. Localised peritonitis: depends on cause, some causes may require surgery, some causes can be treated with Abx
    1. Generalised: may look at risk of death from sepsis or shock, IV fluids/Abx, urinary catheter, NGT, central venous line; laparotomy: to remove infected or necrotic tissue, treat cause, peritoneal lavage; 1ry tx with Abx
    2. Spontaneous bacterial peritonitis: quinolone Abx OR cefuroxime and metronidazole
  8. Early: septic shock, resp failure, multiorgan failure, paralytic ileus, wound infection, abscesses
    1. Late: incisional hernia, adhesions
  9. Localised peritonitis usually resolves with tx of underlying cause; generalised has much higher mortality 30-50%; 1ry peritonitis has a good prognosis with abx tx; SBP has mortality >30% if dx and tx is delayed
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33
Q

Pilonidal sinus

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in natal cleft
  2. Caused by shed or sheared hairs penetrating the skin and inciting and inflam reaction and sinus development; intermitent negative pressure will draw in more hair and perpetuate the cycle
    1. RF: hirsuitism, spending a long time sitting down, occupational (hairdressers may develop interdigital pilodinal sinus)
  3. Common, affects 0.7%
  4. Painful natal cleft, discharging swelling, often recurrent
  5. Midline openings or pits between the buttocks, hairs may protrude from the swelling; if infection/abscess, the swelling will become tender; fluctuant and discharge pus or blood-stained fluid on compression
  6. None needed; bloods for sx of infections: raised WCC, fasting glucose
  7. Acute pilonidal abscess: incision and drainage; chronic pilonidal sinus: excision under GA with exploration; prevention: good hygiene, shaving
  8. Pain, infection, abscess, recurrence
  9. Good with drainage, shaving will cure in most cases, usually resolves by age of 40
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34
Q

Portal Hypertension

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Abnormally hgih pressure within the hepatic portal vein; clinically significant defined as hepatic venous pressure gradient >10mmHg
  2. Cirrhosis most common cause; others:
    1. Pre-hepatic: blockage of portal vein before the liver - congenital stenosis, portal vein thrombosis, splenic vein thrombosis, extrinsic compression
    2. Hepatic: Cirrhosis, chronic hepatitis, schistosomiasis, myeloprolif disease
    3. Post-hepatic: blockage of hepatic veins or venules - Budd-chiari syndrome (hepatic vein obstruction), constrictive pericarditis, right HF
  3. Common consequences of cirrhosis
  4. Features of liver disease: jaundice, hx of alcohol abuse, RF of viral hepatitis (tattoos, unprotected sex, IV drug use, travel abroad and blood transfusion), FHX
    1. Complications of portal HTN: haematemisis, melaena, lethargy, irritability, changes in sleep, abdo distention, abdo pain and fever, pulm involvement
  5. sx of PHTN: caput medusae, splenomegaly, ascites; sx of Liver failure: jaundice, spider naevi, palmar erythema, confusion, asterixis, fetor hepaticus, enlarged/small liver, gynaecomastia, testicular atrophy
  6. Bloods: LFTs, U+Es, blood glucose, FBC, clotting screen
    1. Specific tests: ferritin - haemochromatosis, hepatitis serology, autoAb, a1-antitrypsin levels, caeruloplasmin - wilson’s disease
    2. Imaging: abdo US, doppler Us, CT/MRI, endoscopy (oesophageal varices); measure hepatic venous pressure gradient; liver biopsy
  7. difficult to tx specifically; tx mainly focused on tx underlying cause where possible;
    1. conservative = salt restriction, diuretics
    2. Tx oesophageal varices
    3. non-selective b-blocker to reduce portal pressure and reduce risk of variceal bleed
    4. Terlipressin to reduce portal venous pressure
    5. TIPS - surgical shunt between hepatic portal vein and hepatic vein to ease congestion in portal vein
    6. Liver transplant
  8. Bleeding from oesophageal varices
    1. Ascites and complications of ascites: spontaneous bacterial peritonitis, hepatorenal syndrome (rapid deterioration in kidney function), hepatic hydrothorax (Pleural eff in pts with PHTN w/no underlying cause)
    2. Pulm complications: portopulm HTN, hepatopulm syndrome (hepatic dysfunction, hypoxaemia, extreve vasodilation)
    3. Liver failure
    4. Hepatic encephalopathy
    5. Cirrhotic cardiomyopathy
  9. Depends on underlying cause, variceal haemorrhages have 40% 1yr mortality
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35
Q

Primary Biliary Cirrhosis

  1. Definition
  2. Aetiollogy/RF
  3. Epidemiology
  4. Presenting syx
  5. Presenting sx
  6. Investigations
A
  1. Chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts > cholestasis and cirrhosis
  2. Unknown, AI, genetic/env factors involved; env trigger causes bile duct epithelial injury then leading to T cell mediated AI response directed against bile duct cells
  3. Middle aged women 9F:1M
  4. Incidental finding on bt; insidious onset with vague syx like fatigue, wt loss, pruritus; rarely RUQ discomfort and complication of liver decompensation (jaundice, ascites); many present with syx of associated conditions (Sjorgen’s, arthritis, Raynaud’s)
  5. Early - no sx; Late: jaundice, skin pigmentation, scratch marks, xanthomas, hepatomegaly, ascites, sx of chronic liver disease
  6. Bloods: LFT -> high ALP+GGT, bilirubin high/ormal; ALT/AST normal initially then increase as cirrhosis develops; clotting: prolonging PT; Antimitochondrial Ab, high IgM/cholesterol; TFTs as associated with AI thyroid disease
    1. USS: exclude extrahepatic biliary obstruction
    2. Liver biopsy: chronic inflammatory cells and granulomas, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes
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36
Q

Primary sclerosing cholangitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting sx
  6. Investigations
A
  1. Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts;
    1. pathology: periductal inflammation with periductal concentric fibrosis, portal oedema, bile duct prolif, expansion of portal tracts, progressive fibrosis, development of biliary cirrhosis
  2. Unknown, possible immune and genetic predisposition with env triggers, close association with IBD (UC - 70% of PSC)
  3. Present between 25-40yrs
  4. Asyx, dx after persistently raised ALP; present with intermittent jaundice, pruritis, RUQ pain, wt loss, fatigue; may present with episodes of fever and rigors caused by acute cholangitis
  5. May have no sx, jaundice, hepatosplenomegaly, spider naevi, palmar erythema, ascites
  6. Bloods: LFTs - high ALP and GGT, mildly elevated ALT and AST, low albumin, high bilirubin
    1. serology: IgG high in children, IgM high in adults, ASMA/ANA in 30%, Anti-mitochondrial Ab ABSENT, pANCA present in 70%
    2. ERCP: stricturing and interdispersed dilation of intrahepatic and extrahepatic bile ducts, small diverticuli on common bile duct may be seen
    3. MRCP: enables non-invasive imaging of biliary tree
    4. Liver biopsy: confirm dx and allows staging
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37
Q

Rectal prolapse

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting sx
  6. Investigation
A
  1. Abnormal protrusion of the full thickess of rectum through the anus
  2. Straining, abnormal rectal anatomy/physiology (poor fixation of rectum to sacrum or reduced anal sphincter pressure, pelvic floor weakness)
    1. RF: constipation, causes of increased straining, cystic fibrosis (children), previous trauma to the anus/perineum, neurological conditions (cauda equina syndrome, MS)
  3. Relatively common, mostly children < 3yrs, elderly
  4. Protruding anal mass, initially associated with defecation, may require digital replacement, constipation, faecal incontinence, PR mucus/bleeding, EMERGENCY if irreducible/strangulated prolapse
  5. Prolapse may be seen on straining, may be ulcerated/necrotic if the vascular supply is compromised, reduced anal sphincter tone
  6. Imaging: proctosigmoidoscopy, defecating proctogram or barium enema
    1. Other: anal sphincter manometry, pudendal nerve studies
    2. Sweat chloride test to check for CF
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38
Q

Ulcerative Colitis

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting sx
  6. Investigation
  7. Management
  8. Complications
  9. Prognosis
A
  1. Chronic relapsing and remitting inflammatory disease affecting the large bowel
  2. Unknown, possible genetic susceptibility, other factors: immune response to bacterial/self-Ag, env factors, altered neutrophil function and abnormality in epithelial integrity, positive FHx in 15%; associations: pANCA, primary sclerosing cholangitis (70% of pts)
  3. Higher prevalence in Ashkenazi jews, caucasians; uncommon before 10yrs; peak onset: 20-40yrs, equal M:F until 40 then higher in M
  4. Bloody/mucous diarrhpea, tenesmus and urgency, crampy abdo pain before passing stool, wt loss, fever, extra GI manifestations (uveitis, scleritis, erythema, nodosum, pyoderma gangrenosum)
  5. Sx of IDA, dehydration, clubbing, abdo tenderness, tachycardia, blood, mucus and tenderness on PR examination, extra GI manifestations
  6. Bloods: FBC - low Hb, high WCC; high ESR or CRP, low albumin
    1. Stool: infectious colitis is DDx so stool culture useful; faecal calprotectin allows differentiation of of IBS from IBD
    2. AXR: rule out toxic megacolon
    3. Flexible sigmoidoscopy/colonoscopy: determines severity, histological confirmation, detection of dysplasia
    4. Barium enema: mucosal ulceration with granular appearance and filling defects, narrow colon, loss of haustral pattern - leadpipe appearance - colonoscopy may be dangerous during acute exacerbation - risk of perf
  7. Markers of diseae activity: decreased Hb/albumin, increased ESR/CRP, diarrhoea freq: <4 is mild, 4-6 mod, 6+ severe; bleeding, fever
    1. Mx of acute exacerbation: IV rehydration/corticosteroids, ABx, bowel rest, parenteral feeding may be necessary, DVT prophylaxis: toxic megacolon - proctolectomy because it has high mortality
    2. Mx of mild disease: oral/rectal 5-ASA derivatices and/or rectal steroids
    3. Mx of moderate/severe disease: oral steroids, oral 5-ASA, immunosuppression (azathioprine, cyclosporine, 6-MPU)
    4. Advice: pt education/support, treat complications, regular colonoscopic surveillance
    5. Surgical: Proctolectomy with ileostomy, ileoanal pouch formation
  8. GI complications: haemorrhage, toxic megacolon, perf, colonic carcinoma, gallstones, 1ry sclerosing cholangitis
    1. Extra-GI manifestations: uveitis, renal calculi, arthropathy, sacroilitis, ankspond, erythema nodosum, pyoderma gangrenosum, osteoporosis, amyloidosis
  9. Normal life expectancy; poor prognostic factors: low albumin (<30g/L), PR blood, Raised CRP, dilated loops of bowel, 8+ bowel movements per day, fever
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39
Q

Viral Hepatitis A and E

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Hepatitis caused by infection with the RNA viruses, hep A and E that follow acute course without progression to chronic carriage
  2. HAV = picornavirus, HEV = calicivirus; transmitted via faecal-oral route; both viruses replicate within hepatocytes and secreted into bile; liver inflammation and hepatocyte necrosis caused by immune response; infected cells targeted by CD8+ T cells and NK cells
    1. Histological: inflammatory cell infiltration of portal tracts, zone 3 necrosis, bile duct prolif
  3. HAV is endemic in developing world, infection often occurs sub-clinically; better in sanitation in the developed world means that it is less common, age of exposure is higher, pts more likely to be syx; HEV is endemic in Asia, Africa and central america
  4. Incubation period of HAV/HEV: 3-6wks; prodromal period: malaise, anorexia, fever, N/V
    1. Hepatitis syx: dark urine, pale stools, jaundice lasting around 3 wks; occasionally itching and jaundice may last several weeks in HAV infection
  5. Pyrexia, jaundice, tender heptomegaly, spleen may be palpable, ABSENCE of stigmata of chronic liver disease
  6. Bloods: LFTs - high ALT/AST/ALP and bilirubin, high ESR, low albumin, high platelets
    1. Vital serology:
      1. hep A: anti-HAV IgM (after 3-5m disappears), anti-HAV IgG (recovery phase and lifelong persistence)
      2. Hep E: anti-HEV IgM (raised 1-4wks after onset); anti-HV IgG
    2. Urinalysis: +ve for bilirubin, raised urobilinogen
  7. No specific mx, bed rest, syx tx (antipyretics/antiemetics/cholestyramine)
    1. Prevention and control: public health - safe water, sanitation, food hygeine; notifiable disease, immunisation available for HAV - passive immunisation with IM human Ig (effective for short time), active immunisation with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas and high risk individuals
  8. Fulminant hep failure (very small proportion, mainly pregnant women; cholestatic hep with prolonged jaundice and pruritus after HAV infection; post-hep syndrome: continued malaise for weeks to months
  9. Recovery within 3-6m, occasionally pts may relapse during recovery, no chronic sequelae, fulminant hepatic failure has mortality of 80%
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40
Q

Viral hepatitis B and D

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Hepatitis caused by infection with hep B virus, which may follow an acute or chronic course - chronic defined as viraemia and hep inflammtion continuing for >6m
    1. Hep D virus is defective and only co-infects with HBV or superinfect people who are carriers of HBV
  2. HBV is eveloped/partially double stranded DNA virus; transmits via sexual contact, blood, vertical transmission; viral proteins: core Ag (HBcAg), surface Ag (HBsAg), e Ag (HBeAg) -> marker of high infectivity; HDV is single-stranded RNA coated with HBsAg
    1. Ab and cell-mediated response to viral replication leads to liver inflamamtion and hepatocyte necrosis; histology = mild/severe inflammation and changes to cirrhosis
    2. RF= IV drug use, unscreened blood and blood products, infants of HBeAg+ve mothers, sexual contact with HBV carriers, younger individuals are more likely to become chronic carriers, genetic factors are associated with varying rates of viral clearance
  3. Common, 1-2 million deaths annually; common in SE asia, africa and mediterranean countries, HDV is worldwide
  4. Incubation 3-6m;
    1. 1-2wks prodrome = malaise, headache, anorexia, N/V, diarrhoea, RUQ pain, serum sickness type illness (fever, arthralgia, polyarthritis, urticaria, maculopapular rash)
    2. Jaundice with dark urine
    3. Recovery 4-8wks
    4. 1% get fulminant liver failure; chronic carriage dx after routine LFT testing or if cirrhosis or decompensation develops
  5. Acute: jaundice, pyrexia, tender hepatomegaly, splenomegaly, cervical lymphadenopathy, occasionally: urticaria and maculopapular rash
    1. Chronic: no findings, or sx of chronic liver disease or decompensation
  6. Viral serology: Acute HBv: HbsAg+ and IgM anti-HBcAg; Chronic HBV: HBsAg +ve, IgG anti-HBcAg, HBeAg+/-; HBV cleared/vaccinated: anti HBsAg Ab+, IgG anti HBcAg; HDV infection: detected by IgM/G against HDV, PCR used for detection
    1. LFTs: high AST/ALT/ALP/bilirubin
    2. Clotting: high PT (severe disease)
    3. Liver biopsy
  7. Prevention: blood screening, safe sex, instrument sterilisation;
    1. passive immunisation: hep B Ig following acute exposure and to neonates born to HBeAg+ mothers
    2. Active immunisation: recombinant HBsAg vaccine for individuals at risk and neonates born to HB
    3. Acute HBV hepatitis: syx tx (antipyretics, antiemetics and cholestyramine) and bed rest, notifiable disease
    4. Chronic HBV: Interferon alpha causing side effects: flu-like syx such as fevers, chills, myalgia, headaches, bone marrow suppression and depression; nucleoside/sucleotide analogues (adefovir, entecavir, telbivudine, tenofovir
  8. 1% get fulminant hepatic failure, chronic HBV infection (10% of adults, much higher in neonates), cirrhosis, HCC, extrahepatic immune complex disorders, superinfection with HDV may lead to acute liver failure or more rapidly progressive disease
  9. Adults: 10% of infections become chonic, of chronic infections 20-30% get cirrhosis
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41
Q

Viral hepatitis C

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigations
  7. Management
  8. Complications
  9. Prognosis
A
  1. Hepatitis caused by infection with hep C virus, often following a chronic course in 80% of cases
  2. HCV is small, enveloped, single stranded RNA virus - poor fidelity of replication, so mutation rates are high, so lots of HCV in one pt; PARENTERAL transmission - sexual/vertical
    1. At risk pts: recipients of blood and blood products, IV drug users, non-sterile acupuncture, tattooing, haemodialysis, health care workers
    2. Pathology: not thought to be directly hepatotoxic, humoral and cell mediated responses to viral infeciton that leads to hepatic inflammation and necrosis; biopsy shows: chronic hepatitis, lymphoid follicles in portal tracts, fatty change, cirrhosis may be present
  3. Common, different genotypes of HCV have different geo prevalence
  4. 90% of acute infections are asyx, 10% become jaundiced with mild flu-like illness, may be dx after incidental abnormal LFT
  5. May be no sx, may be sx of chronic liver disease if long standing infection; extra-hepatic manifestations (rare): skin rash, renal dysfunction (due to glomerulonephritis)
  6. Bloods: HCV serology: anti-HCV Ab - IgM(acute) IgG (chronic); reverse transcriptase PCR: allows detection and genotyping of HCV; LFT: acute - high ALT/AS/bilirubin, chronic infection: 2-8x elevation of AST+ALT
    1. Liver biopsy: assess degree of inflammation and liver damage, useful for dx cirrhosis
  7. Prevention: screen blood, blood products and organ donors, needle exchange scheeme for IV drug users, instrument sterilisation, NO VACCINE AVAILABLE
    1. Medical: Acute - mainly supportive (antipyretics, antiemetics, cholestyramine; chronic: pegylated interferon Alpha, Ribavirin for genotype 1/4: 24-48wks, for genotype 2/3: 12-24wks; regular USS of liver needed if cirrhosis
  8. Fulminant hepatic failure, chronic carriage of HCV, hepatocellular carcinoma, less common: porhpyria cutanea tarda, cryoglobulinaemia, glomerulonephritis
  9. 80% of exposed will progress to chronic carriage; of these 20-30% develop cirrhosis over 10-20yrs
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42
Q

Volvulus

  1. Definition
  2. Aetiology/Risk Factors
  3. Presenting syx
  4. Presenting sx
  5. Investigations
A
  1. Rotation of a loop of small bowel around the axis of its mesentery; results in bowel obstruction and potential ischaemia -> affected: sigmoid colon (65%), caecum (30%), volvulus neonatorum (typically midgut in neonates)
  2. Anatomical factors (long mesentery); RF: Adults = long sigmoid colon, long mesentery, mobile caecum, chronic constipation, adhesion, chagas disease, parasitic infections; neonatal: malrotation
  3. Severe colicky abdo pain and swelling, absolute constipation, vomiting, hx of transient attack with spontaneous reduction of volvulus; neonatal volvulus around 3m
  4. Sx of bowel obstruction with abdo distention and tenderness; absent or tinkling bowel sounds; fever; tachycardia; sx of dehydration
  5. AXR, erect CXR if perf suspected; water soluble contrast enema, shows site of obstruction; CT scan
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43
Q

Wilson’s disease

  1. Definition
  2. Aetiology/RF
  3. Epidemiology
  4. Presenting Syx
  5. Presenting Sx
  6. Investigation
A
  1. Autosomal recessive disorder characterised by reduced biliary excretion of copper and accumulation of copper in the liver and brain, especially in the basal ganglia. Also known as hepatolenticular degeneration
  2. Mutation in a gene on chromosome 13 that codes for copper transporting ATPase in hepatocytes;
    1. interferes with transport of Cu into the intracellular compartments for incorporation into caeruloplasmin (normally secreted into plasma/excreted in bile),
    2. excess copper damages hepatocyte mitochondria, leading to cell death and release of free copper into plasma,
    3. which then gets deposited in tissues and impairs tissue function
  3. Liver disease may present in children; neuro disease usually presents in young adults
  4. Liver: hepatitis, liver failure, cirrhosis; syx: jaundice, easy bruising, variceal bleeding, encephalopathy
    1. Neuro: dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia
    2. Psych:conduct disorder, personality change, psychosis
  5. Liver: hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia;
    1. Eyes:Kayser-fleischer rings, sunflower cataract (Cu accumulation in the lens, seen with slit lamp)
  6. Bloods: LFTs = high AST/ALT/ALP; low serum caeruloplasmin (acute phase protein, false negative if underlying infection), serum copper
    1. 24hr urinary Cu levels increased in wilson’s disease
    2. Liver biopsy: increased copper content
    3. Genetic analysis: wilson’s wide variety of gene mutations so there isn’t a simple genetic test that can be done
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44
Q

Spontaneous bacterial peritonitis

  1. Definition
  2. S+S
  3. Dx
  4. Prevention
  5. Tx
A
  1. Development of bacterial infection in peritoneum causing peritonitis, with no obvious cause for infection.
    1. Occurs almost exclusively in pts with portal HTN due to cirrhosis of liver; also with nephrotic syndrome
  2. Fevers, chills, N/V, abdo tenderness, malaise, abdo pain/worsening ascites. hep encephalopathy may be only manifestation of SBP
  3. Paracentesis - if fluid has neutrophils >250 cells/mm3, with no known reason for it
  4. Pts with cirrhosis may benefit from Abx if previous SBP or if admitted to hospital and have oesophageal varices
  5. ABx: cefotaxime IV, IV albumin
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45
Q

Definition

Achalasia

A
  1. normal musc activity of the oesophagus is disturbed due to failure or incomplete relaxation of the lower oesophageal sphincter;
  2. leads to delay in the passage of swallowed material into the stomach
  3. Caused by degeneration of the ganglion cells of the myenteric plexus in the oesophagus due to unknown cause;
  4. oesophageal infection with trypanosoma cruzi seen in central/south america, produces a similar disorder - chagas disease
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46
Q

S+S

Achalasia

A
  1. Insidious onset: intermittent dysphagia, difficulty belching, regurg, heart burn, chest pain (atypical/cramping, retrosternal), weight loss
  2. Complication sx: aspiration pneumonia, malnutrition, weight loss
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47
Q

Investigations

Achalasia

A
  1. CXR: widened mediastinum, double right heart border, air fluid level in upper chest, absence of normal gastric air bubble
  2. Barium swallow: dilated oesophagus, smooth taper down to the sphincter
  3. Endoscopy to exclude malignancy, mimic achalasia
  4. Manometry: to assess pressure at LOS = elevated resting LOS pressure, incomplete LOS relaxation, absence of peristalsis in SM portion of oesophagus
  5. Can do serology for Ab for chagas disease
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48
Q

Definition

Acute cholangitis

A
  1. Infection of the bile duct
  2. Due to: obstruction of gallbladder/bile duct due to stones, ERCP, tumours, bile duct structure or stenosis, oarasitic infection
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49
Q

S+S

Acute cholangitis

A
  1. Charcot’s triad: RUQ pain, jaundice, fever with rigors;
  2. with 2 others: mental confusion and septic shock Reynold’s pentad;
  3. may also have pruritus
  4. Fever, RUQ tenderness, mild hepatomegaly, jaundice, mental status changes, sepsis, hypotension, tachycardia, peritonitis
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50
Q

Investigations

Acute cholangitis

A
  1. Bloods: FBC high WCC, CRP/ESR ?raised, LFTs: obstructive jaundice so raised ALP and GGT;
  2. U+Es:sx of renal dysfunction;
  3. blood culture for sepsis;
  4. amylase raised if lower part of common bile duct involved
  5. Imaging: XR KUB for stones;
  6. Abdo USS for stones and dilation of common bile duct;
  7. contrast enhanced CT/MRI for dx;
  8. MRCP: necessary for non-calcified stones
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51
Q

Management

Acute cholangitis

A
  1. Resus if in septic shock
  2. Broad spec Abx: give after culture and those effective against anaerobes and GNB: cefuroxime and metronidazole
  3. Endoscopic biliary drainage usually required to treat underlying obstruciton
  4. Depends on severity:
  5. Stage 1: anti-microbial therapy, percutaneous, endoscopic, operative intervention for non-responders
  6. Stage 2: early percutaneous or endoscopic drainage (biliary is recommended)
  7. Stage 3: Severe includes shock, conscious disturbance, acute lung injury, AKI, hepatic injury or DIC;
    1. tx of organ failure with ventilatory support, VP;
    2. urgent percutaneous or endoscopic drainage
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52
Q

Definition

Alcoholic hepatitis

A
  1. Inflammatory liver injury caused by chronic heavy intake of alcohol
  2. 3 types on the spectrum: alcoholic steatosis, hepatitis and chronic cirrhosis;
  3. histopath features of alcohol hepatitis:
    1. Centrilobular ballooning
    2. Degeneration and necrosis of hepatocytes
    3. Steatosis
    4. neutrophilic inflammation
    5. Cholestasis
    6. Mallory hyaline inclusions
    7. Giant mitochondria
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53
Q

S+S

Alcoholic hepatitis

A
  1. May be asyx and undetected, or mild with: nausea, malaise, epigastric pain, right hypochondrial pain, low-grade fever;
  2. more severe: Jaundice, abdo discomfort or swelling, swollen ankles, GI bleeding ->15-20 yr hx of drinking
  3. Alcohol excess: malnourished, palmar erythema, dupuytren’s contracture, facial telngiectasia, parotid enlargment, spider naevi, gynaecomastia, testicular atrophy, hepatomegaly, easy bruising
  4. Severe alcoholic hepatitis: febrile, tachycardia, jaundice, bruising, encephalopathy (liver flap, drowsiness, disorientation), ascites, hepato/splenomegaly
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54
Q

Investigations

Alcoholic hepatitis

A
  1. Bloods: FBC: low Hb, high MCV, high WCC, low platelets;
    1. LFTS: high AST/ALT, high bilirubin, high ALP/GGT, low albumin;
    2. U+Es: urea and K tend to be low;
    3. clotting: prolong PT
  2. US: other liver impairment causes
  3. Upper GI endoscopy: investigate varices
  4. Liver biopsy: distinguish from other causes of hepatitis
  5. EEG: slow wave activity = encephalopathy
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55
Q

Management

Alcoholic hepatitis

A
  1. Acute: thiamine, vit C and multivits (pabrinex), monitor and correct K/Mg/glucose;
  2. adequate urine output;
  3. encephalopathy tx with oral lactulose or phosphate enemas;
  4. ascites with diuretics (spirono and frusemide);
  5. therapeutic paracentesis;
  6. glypressing and N-acetylcysteine for hepatorenal syndrome
  7. nutrition: via oral/NG feeding;
  8. protein restriction avoided unless ecephalopathic;
  9. nutritional supplementation and vit (B group, thiamine and folic acid) should be started parenterally initially and continued orally
  10. Steroid therapy: reduce short term mortality for severe alcoholic hepatitis
  11. NB:hepatorenal syndrome (dev of renal failure in pts with advanced chronic liver disease - RAS activated and vasoconstriction of vessels in kidney leads to kidney failure
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56
Q

Definition

Anal fissure

A
  1. A painful tear in the squamous lining of the lower anal canal - 90% of anal fissures are posterior (ant occur after childbirth
  2. Affects 1/10 people during their lifetime, both sexes are affected equally, can occur at any age;
  3. most cases occur in children and young adults - 10-30yrs
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57
Q

S+S

Anal fissure

A
  1. Tearing pain when passing stools;
  2. may be a little bit of blood in the faeces or on the paper;
  3. pruritus ani
  4. Tears in the squamous lining on the anus on examination
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58
Q

Management

Anal fissure

A
  1. Conservative: high fibre diet, softening the stools (laxative), good hydration
  2. Medical: lidocaine ointment, GTN ointment and diltiazem (relaxing anal sphincter and promoting healing), botulinum toxin injection
  3. Surgical: lateral sphincterotomy, relax anal sphincter and promotes healing but has complication, so reserved for non-tolerant pts to non-surgical tx
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59
Q

Definition

Appendicitis

A
  1. Inflammation of appendix
  2. Gut organisms invade appendix wall after lumen obstruction;
  3. leads to oedema, ischaemic necrosis and perforation
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60
Q

S+S

Appendicitis

A
  1. Periumbilical pain that moves to right iliac fossa, anorexia, vomiting, constipation, diarrhoea
  2. General sx: tachycardia, fever, furred tongue, lying still, coughing hurts, foetor w/w/out flushing, shallow breaths
  3. RIF: guarding, rebound/percussion tenderness, PR pain on RHS (sx of low-lying pelvic appendix)
  4. Special sx:
    1. Rovsing’s sign: palpation of the left iliac fossa causes more pain in the right iliac fossa than the left
    2. Psoas sx: pain on extending hip
    3. Cope sx: pain on flexion and internal rotation of the hip
  5. Variations in clincal picture: inflammation of retrocaecal/retroperitoneal appendix may cause flank/RUQ pain; child would have vague abdo pain and won’t eat; shocked confused 80+ year old not in any pain
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61
Q

Investigations

Appendicitis

A
  1. Bloods: high WCC and CRP;
  2. US may help;
  3. CT for dx
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62
Q

Management

Appendicitis

A

Prompt appendicectomy; ABx: cefuroxime, metronidazole; laparoscopy - dx and therapuetic advantages

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63
Q

Definition

Autoimmune hepatitis

A
  1. Chronic hepatitis of unknown aetiology, characterised by autoimmune features, hyperglobulinaemia and the presence of circulating autoAb
  2. Genetically predisposed individual and env agent may lead to hepatocyte expression of HLA ag, which then become the focus of a principally T-cell-mediated autoimmune attack;
  3. Raised titre of ANA and anti-SM Ab, anti-liver/kidney microsomes are NOT thought to directly injure the liver;
  4. 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 cirrhosis
  5. Type 1: ANA, ASMA, anti-actin Ab, anti-soluble liver Ag
  6. Type 2: ab to liver/kidney microsomes, antibodies to liver cytosol Ag
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64
Q

S+S

Autoimmune hepatitis

A
  1. Asyx and discovered incidentally through abnormal LFT;
  2. insidiously present with: malaise, fatigue, anorexia, weight loss, nausea, jaundice, amenorrhoea, epistaxis
  3. Acute hepatitis (25%): fever, anorexia, jaundice, N/V/D, RUQ pain, some present with serum sickness = arthralgia, polyarthritis, maculopapular rash
  4. Check for FHx of other AI diseases;
  5. full Hx important to rule out other causes of hepatitis
  6. Stigmata of chronic liver disease, ascites, oedema, hepatic encephalopathy are late features;
  7. cushingoid features may be present even before the admin of steroids
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65
Q

Investigations

Autoimmune hepatitis

A
  1. Bloods: LFTs: high: AST/ALT/GGT/ALP/bilirubin, low: albumin (severe);
  2. Clotting: high PT;
  3. FBC: low Hb, platetes and WCC;
  4. hypergammaglobulinaemia: presence of ANA, ASMA and anti-LKM Ab
  5. Liver biopsy: needed to establish dx and check hepatitis vs cirrhosis
  6. Rule out other causes of liver disease: viral serology, urinary copper/caeruloplasmin, ferritin and transferrin saturation, alpha-1 antitrypsin, anti-mitochondrial antibodies
  7. US/CT/MRI of liver and abdo: visualise structural lesions
  8. ERCP: rule out PSC
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66
Q

Definition

Barrett’s oesophagus

A
  1. 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;
  2. metaplastic change from squamous -> columnar;
  3. main problem: barrett’s could progress to oesophageal adenocarcinoma
  4. Reflux will occur if the cardiac sphincter is not working properly; hiatus hernia makes GORD more likely
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67
Q

S+S

Barrett’s oesophagus

A
  1. Heartburn,
  2. nausea,
  3. waterbrash,
  4. bloating,
  5. belching,
  6. burning pain when swallowing
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68
Q

Management

Barett’s oesophagus

A
  1. Premalignant/high grade dysplasia: oesophageal resection, eradicative mucosectomy
  2. Other techniques: endoscopic targeted mucosectomy, mucosal ablation by epithelial laser, radiofrequency or photodynamic ablation
  3. Low-grade dysplasia: annual endoscopic surveillance is recommend
  4. No pre-malingant changes found: surveillance endoscopy and biopsy performed every 1-3yrs, anti-reflux measures
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69
Q

Investigations

Barrett’s oesophagus

A

OGD and biopsy: show replacement of squamous epithelium with columnar epithelium

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70
Q

Definition

Biliary colic

A
  1. Pain resulting from obstruction of the gallbladder or common bile duct, usually by a stone;
  2. pain which is very severe, is usually felt in upper abdo but can also be poorly localised due to its visceral nature
  3. Occurs due to contractions of the biliary tree in an attempt to relieve an obstruction; risk factors of gallstones:
  4. Fair, fat, fertile, 40, female
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71
Q

S+S

Biliary colic

A
  1. Crampy RUQ pain, N/V, pain may radiate to right scapula;
  2. pain doesn’t fluctuate and has tendency to persist;
  3. individuals may present with pain following ingestion of fatty meal
  4. RUQ pain and epigastric tenderness
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72
Q

Investigations

Biliary colic

A
  1. Urinalysis, CXR, ECG to exclude other causes;
  2. US: look for dilatation of CBD, gallbladder wall may be thickened;
  3. LFT; ERCP dx and therapeutically;
  4. CT: may be useful if other forms of imaging have been insufficient
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73
Q

Management

Biliary colic

A
  1. Analgesia, IV fluids, NBM;
  2. surgical: laproscopic cholecystectomy;
  3. ERCP can also be used to help remove stones or stent a blocked bile duct
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74
Q

Definition

Cholecystitis

A
  1. Inflammation of the gallbladder
  2. Types of stones: Mixed stones (80%) - contains cholesterol, Ca bilirubinate, PO4 and protein;
    1. form due to imbalance between bile salts, PL, cholesterol, nucleation factors and gallbladder motility
  3. Pure cholesterol stones
  4. Pigment stones - black stones made of calcium bilirubinate, form due to increased bilirubin
  5. RF: age, female, fat, DM, drugs (OCP, octreotide), Fhx, ethnicity, pigment stone risk factors: haemolytic disorders
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75
Q

S+S

Cholecystitis

A
  1. systemically unwell,
  2. fever,
  3. prolonged abdo pain,
  4. pain may be referred to right shoulder due to diaphragmatic irritation
  5. Tachycardia,
  6. pyrexia,
  7. RUQ pain or epigastric tenderness,
  8. murphy’s sign positive
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76
Q

Investigations

Cholecystitis

A
  1. Bloods: FBC - high WCC in cholecystites and cholangitis;
  2. LFT high ALP/GGT;
  3. blood cultures;
  4. amylase
  5. US: show gallstones, increased thickness of gallbladder wall, dilatation of biliary tree
  6. AXR: but only 10% of gallstones are radioopaque
  7. Other imaging - to exclude differentials
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77
Q

Management

Cholecystitis

A
  1. Conservative - mild biliary colic, follow low-fat diet
  2. Medical: NBM, IV fluids, analgesia, anti-emetics,
  3. Abx; if obstruction: urgent biliary drainage by ERCP or via percutaenous route is necessary
  4. Surgical: laproscopic cholecytectomy
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78
Q

Definition

Cirrhosis

A
  1. End stage of chronic liver damage with replacement of normal liver architecture with diffuse fibrosis and nodules of regenerating hepatocytes;
  2. cirrhosis is considered decompensated if complicated by: ascites, jaundice, encehalopathy, GI bleed;
  3. can be precipitated by infection, GI bleeding, constipation, high-protein meal, electrolyte imbalances, alcohol and drugs, tumour development or portal vein thrombosis
  4. Causes:
    1. Chronic alcohol misuse,
    2. chronic viral hepatitis,
    3. autoimmune hepatitis,
    4. drugs, inherited (alpha1 antitrypsin def, haemochromatosis, wilson’s disease, galactosaemia, cystic fibrosis),
    5. vascular (budd-chiari syndrome, hepatic venous congestion),
    6. chronic biliary diseases (PBC, PSC, biliary atresia),
    7. unknown,
    8. non-alocholic steatohepatitis (obesity, DM, total parenteral nutrition, short bowel syndromes, hyperlipidaemia, drugs)
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79
Q

S+S

Cirrhosis

A
  1. Early non specific syx: anorexia, nausea, fatigue, weakness, weight loss
  2. Syx due to decreased liver synthetic function: easy bruising, abnormal swelling, ankle oedema
  3. Syx due to reduced detoxification function: jaundice, personality change, altered sleep pattern, amenorrhoea, galactorrhoea
  4. Syx due to portal HTN: abdo swelling, haematemesis, PR bleeding or maelena
  5. Asterixis, bruises, clubbing, dupuytren’s contracture, palmar erythema, jaundice, gynaecomastia, leukonychia, parotid enlargement, spider naevi, scratch mark, ascites, enlarged liver, testicular atrophy, caput medusae, splenomegaly
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80
Q

Investigations

Cirrhosis

A
  1. Bloods: FBC: low pts+Hb, LFTs: normal but often high AST/ALT/ALP/GGT/bilirubin, low albumin;
  2. clotting: prolonged PT;
  3. serum AFP: raised chronic liver disease, high levels suggest hepatocellular carcinoma
  4. To determine cause: viral serology, A1anti-trypsin, caeruloplasmin, iron studies for haemochromatosis, anti-mitochondrial Ab, ANA/ASMA
  5. Ascitic tap: MC+S, biochem, cytology, ascitic tap w/neutrophils >250/mm3 = spontaneous bacterial peritonitis
  6. Liver biopsy: performed percutaneously, transjugular;
  7. histopathological features of cirrhosis: periportal fibrosis, loss of normal liver architecture, nodular appearance;
  8. Grade: indicates degree of inflammation;
  9. Stage: degree of architectural distortion
  10. Imaging: US, CT, MRI for ascites, HCC, hepatic/portal vein thrombosis, exclude biliary obstruction; MRCP
  11. Endoscopy - varices
  12. Child pugh grading: score for estimating prognosis in chronic liver disease/cirrhosis: albumin, bilirubin, PT, ascites encephalopathy;
  13. cirrhosis divided into classes using: Class A: 5-6, Class B: 7-9, Class C: 10-15
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81
Q

Management

Cirrhosis

A
  1. Tx the cause; avoid alcohol, sedative, opiates, NSAIDs and drugs that affect the liver, nutrition is important, enteral supplements should be given, NG feeding may be indicated;
  2. Tx complications:
    1. Encephalopathy: tx infections, exclude GI bleed, use lactulose and phosphate enemas, avoid sedation
    2. Ascites: Diuretics, dietary Na restriction, therapeutic paracentesis, monitor weight, fluid restrict if plasma Na <120 mmol/L, avoid alcohol and NSAIDs
    3. Spontaneous bacterial peritonitis: Abx, prophylaxis against recurrent SBP with ciprofloxacin
    4. Surgical: consider Transjugular intrahepatic portosystemic shunt, helps reduce portal HTN;
    5. liver transplant is only curable method
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82
Q

Definition

Coeliac disease

A
  1. An inflammatory disease caused by intolerance to gluten, causing chronic intestinal malabsorption -> subtotal villous atrophy and crypt hyperplasia
  2. Due to sensitivity to gliadin component of gluten, which triggers an immuno reaction in the small intestine leading to mucosal damage and loss of villi;
  3. 10% risk of 1st degree relatives affected;
  4. clear genetic susceptibility associated with HLA-B8/DR3/DQW2 haplotypes
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83
Q

S+S

Coeliac disease

A
  1. May be asyx;
  2. abdo discomfort, pain and distention;
  3. steatorrhoea (pale bulky stool, with offensive smell and difficult to flush away), diarrhoea, tiredness,
  4. malaise, weight loss, failure to thrive in children,
  5. amenorrhoea in young adults
  6. Sx of anaemia: pallor;
  7. sx of malnutrition: short stature, abdo distention, wasted buttocks in children, triceps skinfold thickness indicates fat stores)
  8. sx of vit/mineral deficiencies: OM, easy bruising
  9. Intense, itchy blisters on elbow, knees and buttocks
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84
Q

Investigations

Coeliac disease

A
  1. Blood: FBC (low Hb, iron, folate), U+Es, albumin, calcium, Phosphate
  2. Serology: IgG anti-gladin Ab, IgA and IgG anti-endomysial tranglutaminase Ab can be dx;
    1. IgA def quite common
  3. Stool: culture to exclude infection, faecal fat tests for steatorrhoea
  4. D-xylose test: reduced urinary excretion after oral xylose indicates small bowel malabsorption
  5. Endoscopy: direct visualisation of vilous atrophy in the small intestine, villous atrophy and crypt hyperplasia in duodenum
85
Q

Management

Coeliac disease

A
  1. Advice: avoid gluten
  2. Medical: vit and mineral supplements, oral corticosteroids if disease doesn’t subside with avoidance of gluten
86
Q

Definition

Crohn’s disease

A
  1. Chronic granulomatous inflammatory disease that can affect any part of the GIT; grouped with UC and known, together, as IBD
  2. Cause unknown but thought to be due to interplay between genetic and env factors;
  3. though inflammation can occur anywhere from mouth to anus;
  4. 40% involves the terminal ileum
87
Q

S+S

Crohn’s disease

A
  1. Crampy abdo pain, diarrhoea, fever, malaise, weight loss, syx of complications, sometimes RIF pain due to inflammation of terminal ileum
  2. Weight loss, clubbing, sx of anaemia, aphthous ulcers in mouth, perianal skin tags, fistulae and abscesses, uveitis, erythema nodosum, pyoderma gangrenosum
88
Q

Investigations

Crohn’s disease

A
  1. Blood: FBC - low Hb, high platelets, high WCC; U+Es, LFTs - low albumin; high ESR, CRP may be high or normal
  2. Stool microscopy and culture: exclude infective colitis
  3. AXR to show toxic megacolon; erect CXR if there is a risk of perf
  4. Small bowel barium follow through - fibrosis/strictures, deep ulceration, cobblestone mucosa
  5. Endoscopy and biopsy: for UC vs CD;
    1. useful for monitoring malignancy and disease progression;
    2. show mucosal oedema and ulceration with rose thorn fissures;
    3. fistulae and abscesses;
    4. transmural chronic inflammation of macrophages, lymphocytes and plasma cells;
    5. granulomas with epitheliod giant cells may be seen in blood vessels and lymphatics
  6. Radionuclide labelled neutrophil scan: can localise the inflammation
89
Q

Management

Crohn’s disease

A
  1. Acute exacerbation: fluid restriction, IV/oral corticosteroids, 5-ASA analogues, analgesia, parenteral nutrition may be necessary, monitor markers of disease activity
  2. Long term:
    1. Steroids for acute exacerbation
    2. 5-ASA analogues - decreases freq of relapses
    3. Immunosuppression: using steroid sparing agents reduces freq of relapses
    4. Anti-TNF agents: very effective at inducing/maintaining remission
  3. General advice: stop smoking, dietician referral
  4. Surgery indicated if: medical tx fails, failure to thrive in children with complications;
  5. involves resection of affected bowel and stoma formation
90
Q

Definition

Diverticular disease

A
  1. Duverticulosis: presence of diverticulae outpouchings of the colonic mucosa and submucosa through the muscular wall of large bowel
  2. Diverticular disease: diverticulosis with complications
  3. Diverticulitis: acute inflammation and infection of colonic diverticulae
  4. Hinchey classificaion of acute diverticulitis:
    1. Ia phlegmon,
    2. Ib and II: localised abscesses,
    3. III: perf and purulent peritonitis,
    4. Iv: faecal peritonitis
  5. Aetiology: low fibre diet = loss of stool bulk leads to high colonic intraluminal pressures to propel stool out, leading to herniation of the mucosa and submucosa through the muscularis
  6. Pathogenesis: Found in sigmoid and descending colon, might be right sided; found at sites of nutrient artery penetration;
  7. diverticular obstruction by thickened faeces can lead to bacterial ovegrowth, toxin production and mucosal injury ->
  8. leading to:
  9. diverticulitis, perforation, pericolic phlegmon, abscess, ulceration and fistulation or stricture formation
91
Q

S+S

Diverticular disease

A
  1. Often Asyx (80-90%); complications lead to syx like:
    1. PR bleed,
    2. diverticulitis causing LIF and lower abdo pain and fever;
    3. diverticular fistulation (causing pneumaturia, faecaluria and recurrent UTI)
  2. diverticulitis: tender abdomen and sx of local or generalised peritonitis if diverticulum has perf
92
Q

Investigations

Diverticular disease

A
  1. Bloods: FBC increased WCC and CRP, check clotting and cross-match if bleeding
  2. Barium enema: shows presence of diverticulae (saw tooth appearance of lumen);
  3. reflects psuedohypertrophy of circular muscle
  4. Flexible sigmoidoscopy and colonoscopy: diverticulae can be visualised and other pathology can be excluded
  5. ACUTE: CT scan for evidence of disease and complications may be performed
93
Q

Management

Diverticular disease

A
  1. Asyx: soluble high fibre diet, some drugs for preventing recurrent flares of diverticulitis
  2. GI bleed: PR bleeeding usually managed conservatively with IV rehydration, Abx, blood transfusion if necessary;
  3. angiography and embolism or surgery if severe
  4. Diverticulitis: IV Abx, fluid rehydration, bowel rest, abscesses may be drained by radiologically sited drains
  5. Surgery: pt with recurrent attacks or complications; open: hartmann’s procedure leaving stoma, one-stage resection and anastamosis;
  6. laproscopic drainage, peritoneal lavage and drain placement can be effective
94
Q

Definition

Gastroenteritis

A
  1. Acute inflammation of the lining of the GIT, manifested by N/V/diarrhoea/abdo discomfort
  2. Viral: rotavirus, adenovirus, astrovirus, calcivirus, norwalk virus;
  3. Bacterial: campylobacter jejuni, e. coli, salmonella, shigella, vibrio cholerae, listeria, yersinia enterocolitica
  4. Protozoal: entamoeba histolytica, cryptosporidium parvum, giardia lamblia
  5. Toxins from: staph aureus, clostridium botulinum/perfringens, bacillus cereus, mushrooms, heavy metals, seafood
  6. Commonly contaminated foods: improperly cooked meat, old rice, eggs and poultry, milk and cheeses, canned food
95
Q

S+S

Gastroenteritis

A
  1. Sudden onset N/V/anorexia, diarrhoea (bloody/watery), abdo pain or discomfory, fever and malaise, (ASK recent travel, Abx use and recent food intake)
  2. Time of onset: toxins = early 1-24hrs, bacterial/viral/protozoal = 12+hrs
  3. Pay attention to the other effects of toxins: botulinum causes paralysis, mushrooms cause fits, renal or liver failure
  4. Diffuse abdo tenderness, abdo distention;
  5. bowel sounds often increased;
  6. severe gastroenteritis: pyrexia, dehydration, hypotension and peripheral shutdown;
  7. DEHYDRATION
96
Q

Investigations

Gastroenteritis

A
  1. Bloods: FBC, blood culture, U+Es
  2. Stool: faecal microscopy, analysis for toxins, pseudomembranous colitis
  3. AXR/US: exclude other causes of abdo pain
  4. Sigmoidoscopy: usually unnecessary unless IBD excluded
97
Q

Management

Gastroenteritis

A
  1. Bed rest, fluid and electrolyte replacement with oral rehydration solution;
  2. IV rehydration may be necessary with severe vomiting;
  3. most are self-limiting;
  4. Abx tx only if severe or if infective agent identified
98
Q

Definition

Gastrointestinal perforation

A
  1. Perforation of the wall of GIT with spillage of bowel contents
  2. Large bowel: Common: diverticulitis, colorectal cancer, appendicitis; others: volvulus, UC (toxic megacolon)
  3. gastroduodenal: common: perf duodenal or gastric ulcer;
  4. or gastric cancer
  5. Small bowel (rare): trauma, infection, crohn’s
  6. Oesophagus: boerhaave’s perf
  7. RF of cause: NSAIDs, steroids, bisphosphonates
99
Q

S+S

Gastrointestinal perforation

A
  1. Large bowel: peritonitic abdo pain;
  2. rule out AAA rupture
  3. Gastroduodenal: sudden-onset severe epigastric pain, worse on movement, pain becomes generalised gastric malignancy with wt loss and N/V
  4. Oesophageal: severe pain following episode of violent vomiting; neck/chest pain and dysphagia develop soon afterwards
  5. Very unwell, sx of shock, pyrexia, pallor, dehydration, sx of peritonitis (guarding, rigidity, rebound tenderness, absent bowel sounds, loss of liver dullness due to overlying gas
100
Q

Investigations

Gastrointestinal perforation

A
  1. Bloods: FBC, U+Es, LFTs, amylase - raised with perf
  2. Erect CXR for air under diaphragm
  3. AXR: shows abnormal gas shadowing
  4. Gastrograffin swallow: for suspected oesophageal perf
101
Q

Management

Gastrointestinal perforation

A
  1. Resus: correct fluid and electrolytes, IV abx
  2. Surgical:
  3. large bowel: Id site of perf with peritoneal lavage, resection of perforated section;
  4. gastroduodenal: laparotomy, peritoneal lavage, perf closed with omental patch, gastric ulcers biopsied, H pylori eradication if positive
  5. oesophageal: pleural lavage, repair of ruptured oesophagus
102
Q

Definition

GORD

A
  1. Inflammation of the oesophagus caused by reflux of gastric acid and/or bile
  2. Caused by disruption of mechanism that prevents reflux;
  3. mechanisms that prevent reflux: lower oesophageal sphincter, acute angle of junction, mucosal rosette, intra-abdominal portion of oesophagus - prolonged oesophageal clearance contributes to 50% of cases
103
Q

S+S

GORD

A
  1. Substernal/epigastric burning discomfort or heartburn; aggravated by: lying supine, bending, large emals, drinking alcohol;
  2. relieved by antacid
  3. Waterbrash - regurg of excessive accumulation of saliva from lower part of oesophagus
  4. Aspiration - may result in hoarseness, laryngitis, nocturnal cough and wheeze
  5. Dysphagia - caused by formation of peptic stricture after long-standing reflux
  6. Usually normal;
  7. occasionally epigastric tenderness, wheeze on chest auscultation, dysphonia
104
Q

Investigations

GORD

A
  1. Clinical dx
  2. Upper GI endoscopy, biopsy, cytological brushings to exclude malignancy
  3. Barium swallow - detects hiatus hernia (repair op = Nissen fundoplication), peptic stricture, extrinsic compression of oesophagus
  4. CXR: not specific for GORD but can lead to finding hiatus hernia = gastric bubble behind the cardiac shadow
  5. 24hr oesophageal pH monitoring: pH probe places in lower oesophagus determining relationship between syx and oesophageal pH
105
Q

Management

GORD

A
  1. Advice: wt loss, elevating head of bed, avoid provoking factors, stop smoking, lower fat meals, avoid large meals in the evening
  2. Medical: antacids, alginates, H2 antagonists, PPI
  3. Endoscopy: annual endoscopic surveillance looking for barrett’s, neessary for stricture dilation or stenting
  4. Surgery: antireflux surgery if refractory to medical tx
  5. Nissen fundoplication: fundus of stomach is wrapped around lower oesophagus - helps reduce risk of hiatus hernia and reduce reflux
106
Q

Definition

Haemorrhoids

A
  1. Anal vascuar cushions become enlarged and engorged with a tendency to protrude, bleed or prolapse in the anal canal;
  2. classification:
    1. Internal: arises from superior haemorrhoidal plexus; above dentate line
    2. External: lie below dentate line
  3. Degrees:
    1. 1st degree: haemorrhoids that do NOT prolapse
    2. 2nd: prolapse with defecation but reduce spontaneously
    3. 3rd: prolapse and require manual reduction
    4. 4th: prolapse that can’t be reduced
  4. Exact cause is disputed; caused by disorganisation of the fibromuscular stroma of anal cushions;
  5. RF:
    1. Constipation
    2. Prolonged straining
    3. Derangement of internal anal sphincter
    4. Pregnancy
    5. Portal HTN
107
Q

S+S

Haemorrhoids

A
  1. Usually asyx, bleeding (bright red blood on toilet paper and drips into pan after stool/ not mixed in);
  2. absence of alarm syx (FLAWS),
  3. other syx: itching, anal lumps, prolapsing tissue;
  4. external haemorrhoids that have thrombosed can be very painful
  5. 1st or 2nd degree not usually visible on external inspection;
  6. internal haemorrhoids NOT normally palpable on DRE unless thrombosed, usually visible on proctoscopy
  7. DDx: anal tags, anal fissures, rectal prolapse, polyps, tumours
108
Q

Investigations

Haemorrhoids

A
  1. DRE,
  2. proctoscopy,
  3. rigid or flexible sigmoidoscopy: important to exclude rectal/sigmoid bleeding
109
Q

Management

Haemorrhoids

A
  1. Conservative: high fibre diet, increase fluid intake, bulk laxatives, topical creams (local anaesthetics)
  2. Injection sclerotherapy: induces fibrosis of the dilated veins
  3. Banding: barron’s bands applied proximal to the haemorrhoids, haemorrhoid will fall off after a few days, BUT may be more painful than injection sclerotherapy
  4. Surgery: reserved for syx 3rd and 4th degree;
  5. milligan-morgan haemorrhoidectomy: excision of 3 haemorrhoidal cushions;
  6. stapled haemorrhoidectomy is an alternative method;
  7. post-op the pt should be given laxatives to avoid constipation
110
Q

Definition

Inguinal hernia

A
  1. Abnormal protrusion of a peritoneal sac through a weakness of the abdo wall in the inguinal region:
  2. Direct inguinal: Protruision of hernial sac directly through a weakness in the transversalis fascia and post wall of inguinal canal, arises medial to inf epigastric vessels and appears through Hesselbach’s triangle
  3. Indirect inguinal: potrusion of hernial sac through the deep inguinal ring, following path of inguinal canal
  4. If both coexist - pantaloon hernia
  5. Congenital: abdo contents enter the inguinal canal through a patent processus vaginalis
  6. Acquired: due to increased intra-abdo pressure along with muscle and transversalis fascia weakness
  7. RF: male, prematurity, age, obesity, raised intra-abdo pressure, constipation, bladder outflow obstruction, intraperitoneal fluid
111
Q

S+S

Inguinal hernia

A
  1. Asyx; lump in groin; cause discomfort and pain, irreducible, may increase in size or have complications
  2. groin lump extending to the scrotum or labia;
  3. distinguishing inguinal and femoral hernias: inguinal - superior and medial to pubic tubercle, femoral - inferior and lateral to pubic tubercle;
  4. check for cough impulse
  5. indirect can be reduced and controlled by applying pressure on the deep inguinal ring
  6. Auscultation - may be bowel sounds over hernia;
  7. tenderness if strangulated
  8. hernia may be irreducible;
  9. check for sx of complications: bowel obstruction and systemic upset
112
Q

Investigations

Inguinal hernias

A
  1. If acute with painful, irreducible hernia;
  2. Bloods: FBC, U+E, CRP, clotting, group and save for ops, ABG - lactic acidosis from bowel ischaemia
  3. Imagining: erect CXR - check for perf;
  4. USS - exclude other causes of groin lump;
  5. AXR - check for obstruction
113
Q

Management

Inguinal hernias

A
  1. Surgical: usually elective, mesh repair to reinforce defect in transversalis fascia;
  2. laproscopic mesh repair;
  3. emergency: obstructed or strangulated, laparotomy with bowel restriction may be indicated if bowel is gangrenous
114
Q

Definition

Hiatus hernia

A
  1. Prolapse of the upper stomach through the diaphragmatic oesophageal hiatus
  2. Congenital, traumatic, non-traumatic (sliding - moves in and out of chest, paraoesophageal - goes through hole in diaphragm next to oesophagus, mixed)
  3. RF: obesity, low-fibre diet, chronic oesophagitis, ascites, pregnancy
115
Q

S+S

Hiatus hernia

A
  1. Most asyx;
  2. sliding hernias cause syx;
  3. may present with GORD (heartburn, waterbrash) no correlation between size of hernia and severity of syx
  4. Usually no sx
116
Q

Investigations

Hiatus hernia

A
  1. Bloods: FBC for IDA;
  2. Radiology: CSR with gastric air bubble seen above diaphragm, barium swallow;
  3. endoscopy
117
Q

Management

Hiatus hernia

A
  1. Medical: modify lifestyle factors, inhibit acid production, enhance upper GI motility
  2. Surgical: necessary in pt minority, usually performed in pts with complications of reflux disease, despite aggressive med tx or pulm complications;
  3. Nissen fundoplication - stomach pulled down through oesophageal hiatus and part of stomach wrapped 360 degrees around oesophagus to make a new sphincter
  4. Belsey Mark IV fundoplication: 270 degree wrap
  5. Hill repair: gastric cardia is anchored to the posterior abdo wall
118
Q

Definition

Infectious colitis

A
  1. Inflammation of the colon due to bacteria, parasites or viruses
  2. Infection leads to inflammation of the colon;
  3. RF: lack of sanitation, drinking contaminated water, Abx use
119
Q

S+S

Infectious colitis

A
  1. Diarrhoea, blood and mucus in the stools,
  2. lower abdo pain,
  3. malaise,
  4. low-grade fever
120
Q

Investigations

Infectious colitis

A
  1. Dx largely clinical,
  2. stool culture may be used to identify the causative organism
121
Q

Definition

Intestinal ischaemia

A
  1. Obstruction of mesenteric vessel, leading to bowel ischaemia and necrosis
  2. Embolus (60%), thrombosis (40%),
  3. consequence of volvulus, intussusception, bowel strangulation, failed surgical resection;
  4. RF: AF, endocarditis, arterial thrombosis (hypercholesterolaemia, HTN, DM, smoking), venous thrombosis (portal HTN, splenectomy, septic thrombophlebitis, OCP, thrombophilia)
122
Q

S+S

Intestinal ischaemia

A
  1. Severe acute colicky abdo pain, vomiting, rectal bleeding,
  2. hx of chronic mesenteric artery insufficiency: gross wt loss, post-prandial abdo pain;
  3. hx of heart/liver disease
  4. Diffuse abdo tenderness,
  5. abdo distention,
  6. tender palpable mass (ischaemic bowel),
  7. bowel sounds may be absent,
  8. disproportionate degree of cardiovascular collapse
123
Q

Investigations

Intestinal ischaemia

A
  1. Dx based on clinical suspicion/after laparotomy;
  2. AXR - thickening of small bowel folds and sx of obstruction;
  3. bloods: ABG (lactic acidosis), FBC, U+Es, LFTs, Clotting, cross-match;
  4. mesenteric angiography: only if stable
124
Q

Definition

Intestinal obstruction

A
  1. Obstruction of normal movement of bowel contents;
  2. classified according to site: small or large bowel;
  3. partial or complete obstruction;
  4. simple or strangulated
  5. Extramural: hernia, adhesions, bands, volvulus;
  6. intramural: tumours, inflammatory strictures;
  7. intraluminal: pedunculated tumours, foreign body
125
Q

S+S

Intestinal obstruction

A
  1. Severe gripping colicky pain with periods of ease, abdo distension, frequent vomiting (bile stained/faeculent), absolute constipation
  2. Abdo distention with generalised tenderness;
  3. may see visible peristalsis,
  4. tinkling bowel sounds,
  5. peritonitis (absent bowel sounds, guarding, rebound tenderness),
  6. inspect for hernias,
  7. look for abdo scars (previous abdo surgery increases the risk of adhesions),
  8. inspect for abdo mass
126
Q

Investigations

Intestinal obstruction

A
  1. AXR - for dx and localisation,
  2. check for valvulae conniventes or haustra;
  3. water soluble contrast enema,
  4. barium follow through
127
Q

Management

Intestinal obstruction

A
  1. General: gastric aspiration via NGT if pt is vomiting, IV fluids, electrolyte replacement, monitor vital sx, fluid balance and urine output;
  2. Surgical: emergency laparotomy in acute obstruction
128
Q

Definition

IBS

A
  1. Functional bowel disorder defined as recurrent episodes of abdo pain/discomfort (absence of detectable organic pathology) for > 6m of the previous year, associated with 2 of the following:
  2. altered stool passage, abdo bloating, syx made worse by eating, passage of mucous
  3. Unknown, could be visceral sensory abnormalities, gut motility abnormalities, psychosocial factors, food intolerance and many more
129
Q

S+S

IBS

A
  1. 6+ months of hx of abdo pain, pain is often colicky, lower abdo, relieved by defecation or passing of flatus;
  2. altered bowel frequency (>3 motions per day/<3 motions per week)
  3. abdo bloating
  4. change in stool consistency
  5. passage with urgency or straining
  6. tenesmus
  7. Screen for Red flag syx: wt loss, anaemia, PR bleeding, late onset (>60yrs)
  8. Usually normal on examination, sometimes the abdo may appear distended and be mildly tender on palpitation in one or both iliac fossae
130
Q

Investigations

IBS

A
  1. Dx mainly from hx but organic pathology must be excludeed;
  2. blood: FBC (anaemia), LFT, ESR, CRP, TFT, anti-endomysial/anti-tranglutaminase Ab
  3. Stool exam: microscopy and culture for infective cause
  4. US: exclude gallstone disease
  5. Urease breath test: exclude dyspepsia due to h pylori
  6. Endoscopy: if other pathologies suspected
131
Q

Management

IBS

A
  1. Advice: dietary modification;
  2. Medical: depends on main syx affecting the pt: antispasmodics, prokinetic agents, anti-diarrhoeals, laxatives, low-dose TCA
  3. Psych therapy: CBT, relaxation and psychotherapy
132
Q

Definition

Liver abscesses and cysts

A
  1. Abscess: liver infection resulting in a walled off collection of pus; cyst: liver infection resulting in walled off collection of cyst fluid
  2. Pyogenic: E coli, Klebsiella, enterococcus, bacteriodes, strep, staph, 60% caused by biliary tract disease, 15% unknown
  3. Amoebic abscess: caused by entamoeba histolytica
  4. Hydatid cyst: caused by tapeworm, echinococcus granulosis
  5. Other causes: TB
133
Q

S+S

Liver abscesses and cysts

A
  1. Fever, malaise, nausea, anorexia, night sweats, wt loss,
  2. RUQ/epigastric pain, referred to shoulder;
  3. jaundice, diarrhoea, pyrexia of unknown origin
  4. Fever - continuous or spiking;
  5. jaundice, tender hepatomegaly,
  6. right lung base - dullness to percussion,
  7. reduced breath sounds,
  8. due to reactive pleural effusion
134
Q

Investigations

Liver abscesses and cysts

A
  1. Bloods: FBC: mild anaemia, leukocytosis, high eosinophils; LFTs: high ALP, high bilirubin;
  2. high ESR/CRP, blood cultures, amoebic and hydatid serology
  3. Stool MC+S for e hystiolytica
  4. Liver US or CT/MRI localises structure of mass
  5. CXR: for right PE or atelactasis, raised hemidiaphragm
  6. Aspiration and culture of abscess material - most pyogenic liver abscesses are polymicrobial, amoebic abscesses have fluid of necrotic hepatocytes and trophozoites
135
Q

Definition

Liver failure

A
  1. Severe liver dysfunction leading to jaundice, encephalopathy and coagulopathy;
  2. classified based on time interval between the onset of jaundice and the development of hepatic encephalopathy
    1. Hyperacute = <7d
    2. Acute = 1-4wks
    3. Subacute = 4-12wks
    4. Acute on chronic liver failure = acute deterioration in pts with chronic liver disease
  3. Causes:
    1. Viral: hep A/B/C/D/E
    2. Drugs: paracetamol OD, idiosyncratic drug reaction
    3. Less common cause: AI hepatitis, budd-chiari syndrome, pregnancy related, malignancy, haemochromatosis, mushroom poisoning, wilson’s disease
  4. Pathogenesis of manifestations of liver failure:
    1. Jaundice - decreased secretion of conjugated bilirubin
    2. Encephalopathy: Nitrogenous products absorbed in gut and goes via portal circulation to the liver, which can’t filter and goes straight to the brain
    3. Coagulopathy: reduced synthesis of clotting factors, reduced platelets, platelet functional abnormalities associated with jaundice or renal failure
136
Q

S+S

Liver failure

A
  1. May be asyx, fever, nausea, jaundice
  2. Jaundice,
  3. encephalopathy,
  4. asterixis,
  5. fetor hepaticus,
  6. ascites and splenomegaly (less common if acute/hyperacute),
  7. bruising or bleeding,
  8. sx of 2ry causes (bronze skin colour, kayser-fleisher rings),
  9. pyrexia - may indicate infection or liver necrosis
137
Q

Investigations

Liver failure

A
  1. ID the cause: viral serology, paracetamol levels, autoAb (ASM, anti-LKM), ferritin (haemochromatosis), caeruloplasmin and urinary copper (wilson’s disease)
  2. bloods: FBC low Hb (GI bleed)/high wcc (infection); U+Es (renal failure); glucose; LFTs: high bilirubin, high AST/ALT/ALP/GGT, low albumin, ESR/CRP, coagulation screen, ABG to determine blood pH, group and save
  3. Liver US/CT
  4. Ascitic Tap: send for MC+S, neutrophils >250/mm3 = spontaneous bacterial peritonitis
  5. Doppler scan of hepatic or portal veins - Budd-chiari syndrome
  6. EEG - monitor encephalopathy
138
Q

Management

Liver failure

A
  1. Resus ABC, tx cause if possible - N-acetylcysteine: tx of paracetamol ODs
  2. tx/prevention of complications: monitor - vital sx, PT, pH, creatinine, urine output, encephalopathy
  3. Manage encephalopathy: lactulose and phosphate enemas
  4. Abx and antifungal prophylaxis
  5. hypoglycaemia tx
  6. coagulopathy tx - IV vitamin K, FFP, platelet infusions
  7. gastric mucosa protection PPIs, sucralfate
  8. Avoid sedatives or drugs met by the liver,
  9. cerebral oedema - decrease ICP with mannitol
  10. Renal failure: haemodialysis, nutritional support
  11. Surgical liver transplant
139
Q

Definition

Mallory-Weiss tear

A
  1. Tearing of the lining of the oesophagus around the junction with the stomach as a result of violent vomiting or straining to vomit
  2. Caused by prolonged violent vomiting;
  3. RF: chronic alcohol abuse, bulimia,
    1. other causes: trauma, intense coughing, gastritis
140
Q

S+S

Mallory-Weiss tear

A
  1. Most are asyx,
  2. abdo pain,
  3. severe vomiting,
  4. haematemesis,
  5. involuntary retching,
  6. black/tarry stools,
  7. syx of hypovolaemia if severe blood loss
  8. Malaena, see above
141
Q

Investigations

Mallory weiss tear

A
  1. OGD,
  2. bloods: FBC to check for anaemia
142
Q

Management

Mallory Weiss tear

A
  1. 80-90% of the time, bleeding will stop on its own;
  2. surgery: only if bleeding doesn’t stop - injection sclerotherapy, coagulation therapy, arteriography;
  3. anti-reflux meds may be prescribed
143
Q

Definition

Non-alcoholic steatohepatitis

A
  1. Term used to describe range of conditions caused by the build up of fat in the liver due to causes other than excessive alcohol use
  2. Liver may initially become fatty due to alcohol abuse, but tends to resolve over matter of days, but if it persists can cause inflammation and fibrosis;
  3. increases risk of DM, MI, stroke
  4. RF: obesity, T2DM, HTN, hypercholesterolaemia, >50, smoking
144
Q

S+S

Non-alcoholic steatohepatitis

A
  1. Asyx, incidental finding;
  2. occasionally: dull/aching RUQ, fatigue, unexplained wt loss, weakness;
  3. syx experienced in most advanced stages
  4. RUQ pain/tenderness, sx of cirrhosis - jaundice, ascites, pruritus
145
Q

Investigations

Non-alcoholic steatohepatitis

A
  1. LFTs: elevated AST and ALT;
  2. liver US steatosis,
  3. liver biopsy
146
Q

Management

Non-alcoholic steatohepatitis

A
  1. Conservative - control
  2. RF: BP, DM, cholesterol, weight, smoking, exercise, alcohol (makes it worse)
147
Q

Definition

Acute pancreatitis

A
  1. Acute inflammatory process of the pancreas with variable involvement of other regional tissues or remote organ systems; classified as:
    1. Mild - minimal organ dysfunction and uneventful recovery;
    2. severe - organ failure and/or local complications such as necrosis, abscesses and pseudocysts
  2. Insult will result in activation of pancreatic proenzymes within the pancreatic duct/acini leading to tissue damage and inflammation;
  3. causes: GET SMASHED:
    1. GALLSTONES,
    2. ETHANOL,
    3. trauma,
    4. steroids,
    5. mumps/HIV/coxsackie,
    6. AI,
    7. scorpion venom,
    8. HyperCa/Hypothermia,
    9. ERCP,
    10. drugs (Na Valproate, steroids)
148
Q

S+S

Acute pancreatitis

A
  1. Severe epigastric pain, radiating to the back, relieved by sitting forward, aggravated by movement, associated with anorexia, N/V
  2. Epigastric tenderness, fever, shock, decreased bowel sounds,
  3. severe pancreatitis: cullen’s sx (periumbilical bruising), grey-turner sx (flank bruising)
149
Q

Investigations

Acute pancreatitis

A
  1. Blood: very high serum amylase, high WCC, U+Es, high glucose, high CRP, low Ca, LFTs, ABG
  2. USS: evidence of gallstones in biliary tree
  3. Erect CXR Pleural effusion or bowel perf
  4. AXR: exclude other acute abdo
  5. CT scan
150
Q

Management

Acute pancreatitis

A
  1. 2 main scales: modified glasgow score (with CRP) and Apache-II score
  2. Medical: fluid and electrolytes resus, urinary catheter and NGT if vomiting, analgesia, blood sugar control, HDU and ITU care, prophylactic ABx
  3. ERCP and sphincterotomy: used for gallstone pancreatitis, cholangitis, jaundice or dilated common bile duct - within 72hrs
  4. Early detection and tx of complications: e.g. persistent syx or >30% pancreatic necrosis or sx of sepsis
  5. Surgical: necrotising pancreatitis mx by specialists
151
Q

Definition

Chronic pancreatitis

A
  1. Chronic inflammatory disease of the pancreas characterised by irreversible parenchymal atrophy and fibrosis leading to impaired endo/exocrine function and recurrent abdo pain
  2. Alcohol - 70%, idiopathic 20%;
  3. Rare: recurrent acute pancreatitis, ductal obstruction, pancreas divisum, hereditary pancreatitis, tropical pancreatitis, autoimmune pancreatitis, hyperparathyroidism
  4. Caused by chronic inflammation and fibrosis, calcification, parenchymal atrophy, ductal dilation and cyst and stone formation; pain associated with raised intraductal pressures
152
Q

S+S

Chronic pancreatitis

A
  1. Recurrent severe epigastric pain, radiates to back, relieved by sitting forward, aggravated by eating/drinking alcohol;
  2. many yrs -> wt loss, bloating, steatorrhoea
  3. Epigastric tenderness;
  4. sx of complications - wt loss, malnutrition
153
Q

Investigations

Chronic pancreatitis

A
  1. Bloods: high glucose (OGTT), amylase/lipase normal, high Ig
  2. US
  3. ERCP/MRCP: early changes = main duct dilatation and stumping of branches;
  4. late changes = duct strictures with alternating dilatation
  5. Abdo XR: calcification of pancreas
  6. CT scan: same as AXR
  7. Test of pancreatic exocrine function: faecal elastase - pacreatic exocrine function
154
Q

Management

Chronic pancreatitis

A
  1. General: mainly syx and supportive - dietary advice, stop smoking/drinking, tx DM, oral pancreatic enzyme replacement, analgesia; chronic pain may need specialist input
  2. Endoscopy: sphincterotomy, stone extraction, dilatation and stenting of strictures, ESWL
  3. Surgical: Lat pancreaticojejunal drainage, panc resection (whipple’s procedure), limited resection of panc head (beger procedure), open panc duct and excavate head of pancreas (Frey)
155
Q

Definition

Peptic ulcer disease and gastritis

A
  1. Ulceration of areas of GIT caused by exposure to gastric acid and pepsin;
  2. most commonly gastric and duodenal ulcers (can occur in oesophagus and Meckel’s diverticulum)
  3. Imbalance between damaging action of acid and pepsin and the mucosal protective mechanisms;
  4. strong correlation with H. pylori (common causes w/ NSAIDS)
  5. Rare cause: Zollinger-Ellison syndrome
156
Q

S+S

Peptic ulcer disease and gastritis

A
  1. Epigastric pain, relieved by antacids, syx depend on food intake: gastric pain worse soon after eating,
  2. duodenal: pain worse several hours after eating;
  3. may present with complications
  4. No physical findings, epigastric tenderness, sx of complications
157
Q

Investigations

Peptic ulcer disease and gastritis

A
  1. Bloods: FBC, serum amylase, U+Es, clotting screen, LFT, cross match if active bleeding, secretin test if Z-E syndrome suspected - IV secretin causes rise in serum gastrin in these pts
  2. Endoscopy - to rule out malignancy; duodenal not needed
  3. Rockall scoring: severity after GI bleed, <3 good prognosis, >8 high risk of mortality
  4. C13 urea breath test; serology (IgG against H pylori confirms exposure to H pylori but not eradication);
    1. campylobacter-like organism test - colour change indicates HP
158
Q

Management

Peptic ulcer disease and gastritis

A
  1. Acute: fluid resus if ulcer perf/bleeding (IV colloids), close monitoring of vital sx, endoscopy, surgical tx; pts with upper GI bleeds treated with IV PPIs at presentation until bleeding ID
  2. Endoscopy: haemostasis for bleeding ulcer with injection sclerotherapy, laser coag, electrocoag
  3. Surgery: indicated if ulcer perf/bleeding can’t be controlled
  4. H pylori eradication: 3x therapy for 1-2wks, 2Abx and PPI
  5. If not HP: tx with PPIs/H2 antags, stop NSAIDS, use misoprostol if NSAID use necessary
159
Q

Definition

Perineal abscess and fistula

A
  1. Abscess = pus collection in perineal region;
  2. fistula = abnormal chronically infected tract communicating between perineal skin and anal canal/rectum
  3. Bacterial infection;
  4. fistulae are complication of abscess or CD (pepper pot perineum);
  5. RF: IBD, DM, malignancy
160
Q

S+S

Perineal abscess and fistula

A
  1. Constant throbbing pain in perineum;
  2. intermittent discharge (mucus/faecal staining) near anal region;
  3. PMH/FH of IBD
  4. Localised tender perineal mass, small skin lesion near anus;
  5. DRE = thickened area over abscess/fistula;
  6. goodsall’s law: rule that correlates internal with external fistula opening - external is anterior to anal canal then fistula radial and direct to anal canal;
  7. fistula 3cm away/opening lying posterior to transverse anal line follows curved path and open internally in post midline
161
Q

Investigations

Perineal abscess and fistula

A
  1. Bloods: FBC, CRP, ESR, blood culture
  2. MRI
  3. Endoanal US
162
Q

Management

Perineal abscess and fistula

A
  1. Surgical tx;
  2. open drainage of abscess;
  3. ABx;
  4. laying open of fistula - dye inserted to find internal opening
  5. Low fistula = fistulotomy and care with anal sphincter
  6. High fistula = fistulotomy cause incontinence so NOT performed; seton - suture threaded through fistula to allow drainage
163
Q

Definition

Peritonitis

A
  1. Inflammation of the peritoneal lining of the abdo cavity;
  2. localised to oe part of peritoneum or generalised
  3. Localised peritonitis: appendicitis, cholecystitis, diverticulitis, salpingitis
  4. 1ry generalised peritonitis: bacterial infection of the peritoneal cavity without an obvious source (via haematogenous or lymphatic spread/ascending infection
  5. RF: ascites, nephrotic syndroome
  6. 2ry generalised peritonitis: caused by bacterial translocation form a localised focus;
  7. could be non-bacterial due to spillage of bowel contents, bile and blood
164
Q

S+S

Peritonitis

A
  1. SOCRATES; inflammation of parietal peritoneum is usually continuous, sharp, localised, exacerbated by movement and coughing; syx vague in those with liver disease and ascites
  2. Check vital sx and look for sx of dehydration or compromised perfusion;
  3. localised peritonitis: tenderness on examination, guarding, rebound tenderness
  4. Generalised peritonitis: very unwell, systemic sx of toxaemia or sepsis pt lies still, shallow breathing, rigid abdo, generalised abdo tenderness, reduced bowel sounds, DRE may show ant tenderness
165
Q

Investigations

Peritonitis

A
  1. bloods: FBC, U+Es, LFTs, amylase, CRP, clotting, x-match, blood cultures, pregnancy test, ABG
  2. Imaging: erect CXR, AXR, USS/CT abdo, laparoscopy
  3. If ascites: ascitic tap and cell count;
  4. SBP: >250 neutrophils/mm3;
  5. gram stain and culture
166
Q

Management

Peritonitis

A
  1. Localised peritonitis: depends on cause, some causes may require surgery, some causes can be treated with Abx
  2. Generalised: may look at risk of death from sepsis or shock, IV fluids/Abx, urinary catheter, NGT, central venous line;
  3. laparotomy: to remove infected or necrotic tissue, treat cause, peritoneal lavage;
  4. 1ry tx with Abx
  5. Spontaneous bacterial peritonitis: quinolone Abx OR cefuroxime and metronidazole
167
Q

Definition

Pilonidal sinus

A
  1. Abnormal epithelium-lined tract filled with hair that opens onto the skin surface, most commonly in natal cleft
  2. Caused by shed or sheared hairs penetrating the skin and inciting and inflam reaction and sinus development;
  3. intermitent negative pressure will draw in more hair and perpetuate the cycle
  4. RF: hirsuitism, spending a long time sitting down, occupational (hairdressers may develop interdigital pilodinal sinus)
168
Q

S+S

Pilonidal sinus

A
  1. Painful natal cleft, discharging swelling, often recurrent
  2. Midline openings or pits between the buttocks,
  3. hairs may protrude from the swelling;
  4. if infection/abscess, the swelling will become tender;
  5. fluctuant and discharge pus or blood-stained fluid on compression
169
Q

Investigations

Pilonidal sinus

A
  1. None needed;
  2. bloods for sx of infections: raised WCC, fasting glucose
170
Q

Management

Pilonidal sinus

A
  1. Acute pilonidal abscess: incision and drainage;
  2. chronic pilonidal sinus: excision under GA with exploration;
  3. prevention: good hygiene, shaving
171
Q

Definition

Portal HTN

A
  1. Abnormally hgih pressure within the hepatic portal vein; clinically significant defined as hepatic venous pressure gradient >10mmHg
  2. Cirrhosis most common cause; others:
  3. Pre-hepatic: blockage of portal vein before the liver - congenital stenosis, portal vein thrombosis, splenic vein thrombosis, extrinsic compression
  4. Hepatic: Cirrhosis, chronic hepatitis, schistosomiasis, myeloprolif disease
  5. Post-hepatic: blockage of hepatic veins or venules - Budd-chiari syndrome (hepatic vein obstruction), constrictive pericarditis, right HF
172
Q

S+S

Portal HTN

A
  1. Features of liver disease: jaundice, hx of alcohol abuse, RF of viral hepatitis (tattoos, unprotected sex, IV drug use, travel abroad and blood transfusion), FHX
  2. Complications of portal HTN: haematemisis, melaena, lethargy, irritability, changes in sleep, abdo distention, abdo pain and fever, pulm involvement
  3. sx of PHTN: caput medusae, splenomegaly, ascites; sx of Liver failure: jaundice, spider naevi, palmar erythema, confusion, asterixis, fetor hepaticus, enlarged/small liver, gynaecomastia, testicular atrophy
173
Q

Investigations

Portal HTN

A
  1. Bloods: LFTs, U+Es, blood glucose, FBC, clotting screen
  2. Specific tests: ferritin - haemochromatosis, hepatitis serology, autoAb, a1-antitrypsin levels, caeruloplasmin - wilson’s disease
  3. Imaging: abdo US, doppler Us, CT/MRI, endoscopy (oesophageal varices); measure hepatic venous pressure gradient; liver biopsy
174
Q

Management

Portal HTN

A
  1. difficult to tx specifically;
  2. tx mainly focused on tx underlying cause where possible;
  3. conservative = salt restriction, diuretics
  4. Tx oesophageal varices
  5. non-selective b-blocker to reduce portal pressure and reduce risk of variceal bleed
  6. Terlipressin to reduce portal venous pressure
  7. TIPS - surgical shunt between hepatic portal vein and hepatic vein to ease congestion in portal vein
  8. Liver transplant
175
Q

Definition

Primary biliary cirrhosis

A
  1. Chronic inflammatory liver disease involving progressive destruction of intrahepatic bile ducts > cholestasis and cirrhosis
  2. Unknown, AI, genetic/env factors involved; env trigger causes bile duct epithelial injury then leading to T cell mediated AI response directed against bile duct cells
176
Q

S+S

Primary biliary cirrhosis

A
  1. Incidental finding on bt; insidious onset with vague syx like fatigue, wt loss, pruritus;
  2. rarely RUQ discomfort and complication of liver decompensation (jaundice, ascites);
  3. many present with syx of associated conditions (Sjorgen’s, arthritis, Raynaud’s)
  4. Early - no sx;
  5. Late: jaundice, skin pigmentation, scratch marks, xanthomas, hepatomegaly, ascites, sx of chronic liver disease
177
Q

Investigations

Primary biliary cirrhosis

A
  1. Bloods: LFT -> high ALP+GGT, bilirubin high/ormal;
  2. ALT/AST normal initially then increase as cirrhosis develops;
  3. clotting: prolonging PT;
  4. Antimitochondrial Ab, high IgM/cholesterol;
  5. TFTs as associated with AI thyroid disease
  6. USS: exclude extrahepatic biliary obstruction
  7. Liver biopsy: chronic inflammatory cells and granulomas, destruction of bile ducts, fibrosis and regenerating nodules of hepatocytes
178
Q

Definition

Primary sclerosing cholangitis

A
  1. Chronic cholestatic liver disease characterised by progressive inflammatory fibrosis and obliteration of intrahepatic and extrahepatic bile ducts;
  2. pathology: periductal inflammation with periductal concentric fibrosis, portal oedema, bile duct prolif, expansion of portal tracts, progressive fibrosis, development of biliary cirrhosis
  3. Unknown, possible immune and genetic predisposition with env triggers, close association with IBD (UC - 70% of PSC)
179
Q

S+S

Primary sclerosing cholangitis

A
  1. Asyx, dx after persistently raised ALP; present with intermittent jaundice, pruritis, RUQ pain, wt loss, fatigue;
  2. may present with episodes of fever and rigors caused by acute cholangitis
  3. May have no sx, jaundice, hepatosplenomegaly, spider naevi, palmar erythema, ascites
180
Q

Investigations

Primary sclerosing cholangitis

A
  1. Bloods: LFTs - high ALP and GGT, mildly elevated ALT and AST, low albumin, high bilirubin
  2. serology: IgG high in children, IgM high in adults, ASMA/ANA in 30%, Anti-mitochondrial Ab ABSENT, pANCA present in 70%
  3. ERCP: stricturing and interdispersed dilation of intrahepatic and extrahepatic bile ducts, small diverticuli on common bile duct may be seen
  4. MRCP: enables non-invasive imaging of biliary tree
  5. Liver biopsy: confirm dx and allows staging
181
Q

Definition

Rectal prolapse

A
  1. Abnormal protrusion of the full thickess of rectum through the anus
  2. Straining, abnormal rectal anatomy/physiology (poor fixation of rectum to sacrum or reduced anal sphincter pressure, pelvic floor weakness)
  3. RF: constipation, causes of increased straining, cystic fibrosis (children), previous trauma to the anus/perineum, neurological conditions (cauda equina syndrome, MS)
182
Q

S+S

Rectal prolapse

A
  1. Protruding anal mass, initially associated with defecation, may require digital replacement, constipation, faecal incontinence, PR mucus/bleeding, EMERGENCY if irreducible/strangulated prolapse
  2. Prolapse may be seen on straining, may be ulcerated/necrotic if the vascular supply is compromised, reduced anal sphincter tone
183
Q

Investigations

Rectal prolapse

A
  1. Imaging: proctosigmoidoscopy, defecating proctogram or barium enema
  2. Other: anal sphincter manometry, pudendal nerve studies
  3. Sweat chloride test to check for CF
184
Q

Definition

Ulcerative colitis

A
  1. Chronic relapsing and remitting inflammatory disease affecting the large bowel
  2. Unknown, possible genetic susceptibility,
  3. other factors: immune response to bacterial/self-Ag, env factors, altered neutrophil function and abnormality in epithelial integrity, positive FHx in 15%;
  4. associations: pANCA, primary sclerosing cholangitis (70% of pts)
185
Q

S+S

Ulcerative colitis

A
  1. Bloody/mucous diarrhoea, tenesmus and urgency, crampy abdo pain before passing stool, wt loss, fever, extra GI manifestations (uveitis, scleritis, erythema, nodosum, pyoderma gangrenosum)
  2. Sx of IDA, dehydration, clubbing, abdo tenderness, tachycardia, blood, mucus and tenderness on PR examination, extra GI manifestations
186
Q

Investigations

Ulcerative colitis

A
  1. Bloods: FBC - low Hb, high WCC; high ESR or CRP, low albumin
  2. Stool: infectious colitis is DDx so stool culture useful;
  3. faecal calprotectin allows differentiation of of IBS from IBD
  4. AXR: rule out toxic megacolon
  5. Flexible sigmoidoscopy/colonoscopy: determines severity, histological confirmation, detection of dysplasia
  6. Barium enema: mucosal ulceration with granular appearance and filling defects, narrow colon, loss of haustral pattern - leadpipe appearance - colonoscopy may be dangerous during acute exacerbation - risk of perf
187
Q

Management

Ulcerative colitis

A
  1. Markers of diseae activity: decreased Hb/albumin, increased ESR/CRP, diarrhoea freq: <4 is mild, 4-6 mod, 6+ severe; bleeding, fever
  2. Mx of acute exacerbation: IV rehydration/corticosteroids, ABx, bowel rest, parenteral feeding may be necessary, DVT prophylaxis: toxic megacolon - proctolectomy because it has high mortality
  3. Mx of mild disease: oral/rectal 5-ASA derivatices and/or rectal steroids
  4. Mx of moderate/severe disease: oral steroids, oral 5-ASA, immunosuppression (azathioprine, cyclosporine, 6-MPU)
  5. Advice: pt education/support, treat complications, regular colonoscopic surveillance
  6. Surgical: Proctolectomy with ileostomy, ileoanal pouch formation
188
Q

Definition

Viral Hep A and E

A
  1. Hepatitis caused by infection with the RNA viruses, hep A and E that follow acute course without progression to chronic carriage
  2. HAV = picornavirus, HEV = calicivirus;
  3. transmitted via faecal-oral route; both viruses replicate within hepatocytes and secreted into bile;
  4. liver inflammation and hepatocyte necrosis caused by immune response; infected cells targeted by CD8+ T cells and NK cells
  5. Histological: inflammatory cell infiltration of portal tracts, zone 3 necrosis, bile duct prolif
189
Q

S+S

Viral Hep A and E

A
  1. Incubation period of HAV/HEV: 3-6wks;
  2. prodromal period: malaise, anorexia, fever, N/V
  3. Hepatitis syx: dark urine, pale stools, jaundice lasting around 3 wks; occasionally itching and jaundice may last several weeks in HAV infection
  4. Pyrexia, jaundice, tender heptomegaly, spleen may be palpable, ABSENCE of stigmata of chronic liver disease
190
Q

Investigations

Viral Hep A and E

A
  1. Bloods: LFTs - high ALT/AST/ALP and bilirubin, high ESR, low albumin, high platelets
  2. Vital serology:
  3. hep A: anti-HAV IgM (after 3-5m disappears), anti-HAV IgG (recovery phase and lifelong persistence)
  4. Hep E: anti-HEV IgM (raised 1-4wks after onset); anti-HV IgG
  5. Urinalysis: +ve for bilirubin, raised urobilinogen
191
Q

Management

Viral Hep A and E

A
  1. No specific mx, bed rest, syx tx (antipyretics/antiemetics/cholestyramine)
  2. Prevention and control:
    1. public health - safe water,
    2. sanitation, food hygeine;
    3. notifiable disease,
    4. immunisation available for HAV - passive immunisation with IM human Ig (effective for short time),
    5. active immunisation with attenuated HAV vaccine offers safe and effective immunity for those travelling to endemic areas and high risk individuals
192
Q

Definition

Viral Hep B and D

A
  1. Hepatitis caused by infection with hep B virus, which may follow an acute or chronic course - chronic defined as viraemia and hep inflammtion continuing for >6m
  2. Hep D virus is defective and only co-infects with HBV or superinfect people who are carriers of HBV
  3. HBV is eveloped/partially double stranded DNA virus; transmits via sexual contact, blood, vertical transmission;
  4. viral proteins: core Ag (HBcAg), surface Ag (HBsAg), e Ag (HBeAg) -> marker of high infectivity; HDV is single-stranded RNA coated with HBsAg
  5. Ab and cell-mediated response to viral replication leads to liver inflamamtion and hepatocyte necrosis; histology = mild/severe inflammation and changes to cirrhosis
  6. RF= IV drug use, unscreened blood and blood products, infants of HBeAg+ve mothers, sexual contact with HBV carriers, younger individuals are more likely to become chronic carriers, genetic factors are associated with varying rates of viral clearance
193
Q

S+S

Viral Hep B and D

A
  1. Incubation 3-6m;
  2. 1-2wks prodrome = malaise, headache, anorexia, N/V, diarrhoea, RUQ pain, serum sickness type illness (fever, arthralgia, polyarthritis, urticaria, maculopapular rash)
  3. Jaundice with dark urine
  4. Recovery 4-8wks
  5. 1% get fulminant liver failure; chronic carriage dx after routine LFT testing or if cirrhosis or decompensation develops
  6. Acute: jaundice, pyrexia, tender hepatomegaly, splenomegaly, cervical lymphadenopathy, occasionally: urticaria and maculopapular rash
  7. Chronic: no findings, or sx of chronic liver disease or decompensation
194
Q

Investigations

Viral Hep B and D

A
  1. Viral serology: Acute HBv: HbsAg+ and IgM anti-HBcAg;
  2. Chronic HBV: HBsAg +ve, IgG anti-HBcAg, HBeAg+/-;
  3. HBV cleared/vaccinated: anti HBsAg Ab+, IgG anti HBcAg;
  4. HDV infection: detected by IgM/G against HDV, PCR used for detection
  5. LFTs: high AST/ALT/ALP/bilirubin
  6. Clotting: high PT (severe disease)
  7. Liver biopsy
195
Q

Management

Viral Hep B and D

A
  1. Prevention: blood screening, safe sex, instrument sterilisation;
  2. passive immunisation: hep B Ig following acute exposure and to neonates born to HBeAg+ mothers
  3. Active immunisation: recombinant HBsAg vaccine for individuals at risk and neonates born to HB
  4. Acute HBV hepatitis: syx tx (antipyretics, antiemetics and cholestyramine) and bed rest, notifiable disease
  5. Chronic HBV: Interferon alpha causing side effects: flu-like syx such as fevers, chills, myalgia, headaches, bone marrow suppression and depression;
  6. nucleoside/sucleotide analogues (adefovir, entecavir, telbivudine, tenofovir
196
Q

Definition

Viral hep C

A
  1. Hepatitis caused by infection with hep C virus, often following a chronic course in 80% of cases
  2. HCV is small, enveloped, single stranded RNA virus - poor fidelity of replication, so mutation rates are high, so lots of HCV in one pt;
  3. PARENTERAL transmission - sexual/vertical
  4. At risk pts: recipients of blood and blood products, IV drug users, non-sterile acupuncture, tattooing, haemodialysis, health care workers
  5. Pathology: not thought to be directly hepatotoxic, humoral and cell mediated responses to viral infeciton that leads to hepatic inflammation and necrosis;
  6. biopsy shows: chronic hepatitis, lymphoid follicles in portal tracts, fatty change, cirrhosis may be present
197
Q

S+S

Viral Hep C

A
  1. 90% of acute infections are asyx, 10% become jaundiced with mild flu-like illness, may be dx after incidental abnormal LFT
  2. May be no sx, may be sx of chronic liver disease if long standing infection;
  3. extra-hepatic manifestations (rare): skin rash, renal dysfunction (due to glomerulonephritis)
198
Q

Investigations

Viral Hep C

A
  1. Bloods: HCV serology: anti-HCV Ab - IgM(acute) IgG (chronic);
  2. reverse transcriptase PCR: allows detection and genotyping of HCV;
  3. LFT: acute - high ALT/AS/bilirubin, chronic infection: 2-8x elevation of AST+ALT
  4. Liver biopsy: assess degree of inflammation and liver damage, useful for dx cirrhosis
199
Q

Management

Viral Hep C

A
  1. Prevention: screen blood, blood products and organ donors, needle exchange scheme for IV drug users, instrument sterilisation,
  2. NO VACCINE AVAILABLE
  3. Medical: Acute - mainly supportive (antipyretics, antiemetics, cholestyramine;
  4. chronic: pegylated interferon Alpha, Ribavirin for genotype 1/4: 24-48wks, for genotype 2/3: 12-24wks;
  5. regular USS of liver needed if cirrhosis
200
Q

Definition

Volvulus

A
  1. Rotation of a loop of small bowel around the axis of its mesentery;
  2. results in bowel obstruction and potential ischaemia -> affected: sigmoid colon (65%), caecum (30%), volvulus neonatorum (typically midgut in neonates)
  3. Anatomical factors (long mesentery);
  4. RF: Adults = long sigmoid colon, long mesentery, mobile caecum, chronic constipation, adhesion, chagas disease, parasitic infections;
    1. neonatal: malrotation
201
Q

S+S

Volvulus

A
  1. Severe colicky abdo pain and swelling,
  2. absolute constipation,
  3. vomiting,
  4. hx of transient attack with spontaneous reduction of volvulus;
  5. neonatal volvulus around 3m
  6. Sx of bowel obstruction with abdo distention and tenderness;
  7. absent or tinkling bowel sounds;
  8. fever;
  9. tachycardia;
  10. sx of dehydration
202
Q

Investigations

Volvulus

A
  1. AXR, erect CXR if perf suspected;
  2. water soluble contrast enema, shows site of obstruction;
  3. CT scan
203
Q

Definition

Wilson’s disease

A
  1. Autosomal recessive disorder characterised by reduced biliary excretion of copper and accumulation of copper in the liver and brain, especially in the basal ganglia.
  2. Also known as hepatolenticular degeneration
  3. Mutation in a gene on chromosome 13 that codes for copper transporting ATPase in hepatocytes;
  4. interferes with transport of Cu into the intracellular compartments for incorporation into caeruloplasmin (normally secreted into plasma/excreted in bile),
  5. excess copper damages hepatocyte mitochondria, leading to cell death and release of free copper into plasma,
  6. which then gets deposited in tissues and impairs tissue function
204
Q

S+S

Wilson’s disease

A
  1. Liver: hepatitis, liver failure, cirrhosis;
  2. syx: jaundice, easy bruising, variceal bleeding, encephalopathy
  3. Neuro: dyskinesia, rigidity, tremor, dystonia, dysarthria, dysphagia, drooling, dementia, ataxia
  4. Psych:conduct disorder, personality change, psychosis
  5. Liver: hepatosplenomegaly, jaundice, ascites/oedema, gynaecomastia;
  6. Eyes:Kayser-fleischer rings, sunflower cataract (Cu accumulation in the lens, seen with slit lamp)
205
Q

Investigations

Wilson’s disease

A
  1. Bloods: LFTs = high AST/ALT/ALP;
  2. low serum caeruloplasmin (acute phase protein, false negative if underlying infection),
  3. serum copper
  4. 24hr urinary Cu levels increased in wilson’s disease
  5. Liver biopsy: increased copper content
  6. Genetic analysis: wilson’s wide variety of gene mutations so there isn’t a simple genetic test that can be done
206
Q

Definition

Spotaneous Bacterial peritonitis

A
  1. Development of bacterial infection in peritoneum causing peritonitis, with no obvious cause for infection.
  2. Occurs almost exclusively in pts with portal HTN due to cirrhosis of liver;
  3. also with nephrotic syndrome
207
Q

S+S

Spontaneous Bacterial peritonitis

A
  1. Fevers,
  2. chills,
  3. N/V,
  4. abdo tenderness,
  5. malaise,
  6. abdo pain/worsening ascites
  7. hep encephalopathy may be only manifestation of SBP
208
Q

Investigations

Spontaneous bacterial peritonitis

A
  1. Paracentesis - if fluid has neutrophils >250 cells/mm3, with no known reason for it
209
Q

Management

Spontaneous bacterial peritonitis

A
  1. ABx: cefotaxime IV,
  2. IV albumin

Year 3 (13 decks)

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