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Year 3 - Diseases > Gastro 2 > Flashcards

Gastro 2 Flashcards

1
Q

Define appendicectomy

A

Removal of the appendix

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2
Q

Summarise the indications of an appendicectomy

A

Appendicitis -

  • Abdominal pain
  • Fever
  • Clinical signs of localized or diffuse peritonitis
  • Especially if leukocytosis present
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3
Q

List possible complications of appendicectomy

A
  • Surgical wound infection
  • Haemorrhage
  • Ileus
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4
Q

Summarise epidemiology of Crohn’s disease

A
  • 100-200 per 100000 prevalence
  • 10-20/100000 per year incidence
  • Typically presents age 20-40
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5
Q

List signs of Crohns disease

A
  • Perianal lesions (skin tags, fistulae.ect)
  • Bowel obstruction (distention, borborygmi)
  • Fever
  • Fatigue
  • Abdominal tenderness
  • Oral lesions
  • Abdominal mass (teminal ileum in right lower quadrant)
  • Erythema nodosum or pyoderma gangrenosum, uveitis or episcleritis
  • Clubbing
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6
Q

List investigations of Crohns

A
  • FBC (anaemia, Leukocytosis, thrombocytosis)
  • Iron deficiency
  • B12 - normal/low
  • Serum folate (normal/low)
  • Metabolic panel (hypoalbuminaemia, hypocholesterolaemia, hypocalcaemia)
  • CRP and ESR raised
  • Stool testing (C diff should be absent, calprotectin)
  • Y enterolitica
  • Abdominal X ray (small bowel dilation, calcification, sacroilitis, intra-abdominal abscesses)
  • CT abdomen (skip lesions, bowel wall thickening, surrounding inflammation, abscess, fistulae)
  • MRI abdo/pelvis (same as above)
  • Faecal calprotectin
  • Colonoscopy, biopsy
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7
Q

Describe management of Crohn’s disease

A

Mildly active

  • Observation with monitoring or budesonide
  • Prednisolone 40mg + mesalazine, then taper
  • Management of extra-intestinal manifestations

Moderately active

  • Budenoside or corticosteroids, mesalazine (aminosalicylate)
  • Antibiotics + manage extra-intestinal manifestations
  • Alternatively to budenoside, immunomodulator therapy (azathioprine, mercaptopurine, methotrexate) or biological therapy (infliximab, adalimumab)

Severely active

  • Hospitalisation, corticosteroids, surgery plus manage extras plus antibiotics plus immunomodulators and steroids
  • 2nd line biologics
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8
Q

List complications of Crohn’s disease

A
  • Intestinal obstruction
  • Pregnancy complications due to immunosuppressant
  • Intra-abdominal sepsis
  • Sinuses
  • Fistula
  • Toxic megacolon
  • Anaemia
  • Short bowel syndrome
  • Malignancy
  • Kidney stones
  • Methotrexate induced hepatotoxicity or pulmonary fibrosis
  • Malabsorption
  • Metabolic bone disease
  • Cholelithiasis
  • Primary sclerosing cholangitis
  • Hepatic steatosis
  • Liver abscess
  • Granulomatous hepatitis
  • Arthropathy
  • Ocular manifestations
  • Cutaneous manifestations
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9
Q

Describe prognosis of Crohns

A
  • Intermittent exacerbations followed by periods of remission with 10-20%
  • 90% have surgery by 10 years, 50% never require further surgery
  • Up to 1/3rd of patients with gastroduodenal require gastrojejunostomy bypasss
  • Severe disease if age under 40, presence of peri-anal disease, initial requirement for steroids
  • Colon cancer leading cause of disease-related death. Associated with decrease in life expectancy
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10
Q

List causes of hepatomegaly

A
  • Cancer
  • Cirrhosis
  • Cardiac (congestive cardiac failure and pericarditis)
  • Infilration - fatty, haemochromatosis, amyloidosis, sarcoidosis, lymphoroliferative diseases
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11
Q

List causes of splenomegaly

A
  • Portal hypertension
  • Haematological
  • Infection
  • Inflammation
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12
Q

Describe symptoms and signs of AAA

A
  • Pain, epigastric region, radiating to the back
  • Hypotension
  • Grey turners sign if retroperitoneal bleed
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13
Q

Describe differences between acute pancreatitis and chronic pancreatitis

A

Acute

  • Pain
  • High amylase on blood test

Chronic

  • Pain
  • Weight loss
  • Loss of exocrine/endocrine function
  • Normal amylase
  • Fecal elastase in stool
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14
Q

List arteries of the bowel and what they supply

A
  • Coeliac - stomach, spleen, liver, gallbladder, duodenum
  • SMA - SI, right colon
  • IMA - Left colon
  • Ileomesenteric - Rectum
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15
Q

Describe different classifications of ascites and what causes it (2 types of classification)

A
  • Transudate - cirrhosis, cardiac failure, nephrotic syndrome
  • Exudate - malignancy (abdominal, pelvic, mesothelioma), infection (TB, pyogenic), budd-chiari syndrome (portal vein thrombosis)

Serum albumin minus ascites albumin:

  • Over 11g caused by cirrhosis or cardiac failure
  • Less than 11g/L TB, cancer, nephrotic syndrome
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16
Q

List causes of jaundice and their different presentations

A
  • Prehepatic - haemolysis, defective conjugation, high unconjugated bilirubin - pale, yellow skin
  • Hepatic- hepatitis (alcohol, autoimmune, drugs, viruses - dark urine due to high conjugated bilrubin)
  • Post hepatic - CBD obstruction (gallstone, stricture, ca. head of pancreas - decreased stercobilinogen, pale stool)
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17
Q

What is trousseau sign of malignancy?

A
  • In pancreatic cancer

- Migratory thrombophlebitis

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18
Q

List different cancer markers for abdo and pelvis

A
  • ca 19-9 pancreatic
  • CEA colon cancer
  • ca125 ovarian
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19
Q

What is thumbprinting?

A
  • Sign on abdominal X ray

- Thickening of the bowel wall

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20
Q

Describe management of an acute GI bleed

A
  • ABC
  • IV access
  • Fluids
  • G and S
  • OGD
  • Variceal bleed - antibiotics and terlipressin
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21
Q

Describe management of an acute abdomen

A
  • Nil by mouth
  • IV fluids
  • Analgesics
  • Consider antibiotics and antiemetics
  • Consult surgeons
  • Monitor vitals and urine output
    Investigations
  • FBC, U%E, LFT, CRP, Clotting, G&S, X-match
  • Erect CXR
  • CT
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22
Q

List investigations performed in Jaundice

A
  • FBC
  • LFT
  • CRP
  • USS
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23
Q

List investigations in a patient with weight loss and dysphagia/PR bleed

A

Dysphagia

  • OGD
  • Biopsy

PR bleed
- Colonoscopy

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24
Q

List causes of bloody diarrhoea

A
  • Infective collitis
  • Inflammatory colitis
  • Ischaemic colitis
  • Diverticulitis
  • Malignancy
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25
Q

Describe management plan of ascites

A
  1. diuretics
  2. Dietary sodium restriction
  3. fluid restriction if hyponatraemia
  4. Monitor wt
  5. Therapeutic paracentesis (with IV human albulin)
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26
Q

List signs of surgical wound infection

A
  • Erythematosus discharge
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27
Q

List signs of anastomotic leak post surgery

A
  • Diffuse abdominal tenderness
  • Guarding
  • Rigidity
  • Hypotension/tachycardia
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28
Q

List features of pelvic abscess post op

A
  • Pain
  • Fever
  • Sweats
  • Mucus
  • Diarrhoea
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29
Q

Describe presentation and treatment of perianal abscess

A
  • Tender, red swelling

- Incision and drainage

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30
Q

Describe troisiers sign

A

Palpable vircows node

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31
Q

Define primary biliary cirrhosis

A
  • A chronic disease of the small intrahepatic bile ducts that is characterised by progressive bile duct damage (and eventual loss) occurring in the context of chronic portal tract inflammation.
  • Fibrosis develops as a consequence of the original insult and the secondary effects of toxic bile acids retained in the liver, resulting ultimately in cirrhosis.
  • Thought to be autoimmune
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32
Q

Describe epidemiology of primary biliary cirrhosis

A
  • 35 per 100000 overall
  • 5 per 100000 per year
  • More common in women (10 times)
  • Peak age 55-65 years
  • Highest risk: european and american women over 50, prevalence of 1 in 750
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33
Q

List symptoms of primary biliary cirrhosis

A
  • Itch
  • Fatigue
  • Dry eyes and mouth
  • Sleep disturbance
  • Dizziness/blackouts
  • Weight loss and other features of malabsorption
  • Memory and concentration problems
  • May be asymptomatic
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34
Q

List signs for primary biliary cirrhosis

A
  • Jaundice
  • Ascites
  • Splenomegaly
  • Skin pigmentation
  • Xanthelasma
  • Hepatomegaly
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35
Q

List risk factors for primary biliary cirrhosis

A
  • Age 45-60
  • Female
  • History of autoimmune disease (family or personal) and primary biliary cholangitis
  • Smoking
  • UTI
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36
Q

List investigations of primary biliary cirrhosis

A
  • Alkaline phosphatase (increased)
  • Gamma GT (increased)
  • Bilirubin (increased)
  • Alanine aminotransferase (increased)
  • Serum albumin (decreased)
  • Antimitochondrial antibody immunofluorescence (present - HALLMARK)
  • Antinuclear antibody
  • Antipyruvate dehydrogenase complex ELISA and anti-M2 ELISA (present)
  • Antiglycoprotein ELISA
  • Anti Sp100 ELISA
  • Abdominal ultrasound scan (no obstructive lesion)
  • MR cholangiopancreatography (no obstructive lesion)
  • Prothrombin time
  • Serum immunoglobulin
  • Liver biopsy (bile duct lesions and granulomata formation, and loss of bile ducts with fibrosis in later stages)
  • Upper GI endoscopy
  • Serum alpha-fetoprotein
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37
Q

Describe FBC in anaemia due to GI bleed

A
  • Low MCV and Hb

- High platelet count

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38
Q

Define cholecystitis

A

Acute gallbladder inflammation, and one of the major complications of cholelithiasis or gallstones

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39
Q

Describe epidemiology of cholecystitis

A
  • Cholelithiasis occurs in approximately 15% of adults.
  • The prevalence rates are relatively low in Africa and Asia.
  • About 1% to 2% of people with asymptomatic gallstones become symptomatic each year.- Acute cholecystitis occurs in about 10% of symptomatic patients.
  • It is 3 times more common in women than in men up to the age of 50 years, and is about 1.5 times more common in women than in men thereafter
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40
Q

Describe aetiology of cholecystitis

A
  • Starvation, total parenteral nutrition, narcotic analgesics, and immobility are predisposing factors for acute acalculous cholecystitis.
  • It has also been described as a rare occurrence during the course of acute Epstein-Barr virus (EBV) infection and can be an atypical clinical presentation of primary EBV infection.
  • Generally due to gallstones
  • Can also occur in helminth infection
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41
Q

List risk factors for cholecystitis

A
  • Gallstones (90%)
  • Previous episode of biliary pain
  • Severe illness
  • Gallbladder dysmotility or ischaemia may occur in critically ill patients, increasing the risk of cholecystitis.
  • Physical activity level
  • Ceftriaxone vauses precipitation of calcium salts into bile.
  • Ciclosporin can decrease bile acid secretion, which may predispose to sludge or stone formation.

Risk factors for acalculous cholecystitis

  • Severe trauma or burns – patients with extensive burns commonly have multiple risk factors for developing acalculous cholecystitis, such as sepsis, dehydration, total parenteral nutrition use, and positive pressure ventilation
  • Major surgery (such as cardiopulmonary bypass)
  • Long-term fasting
  • Total parenteral nutrition
  • Sepsis arising from any infection (including pneumonia)
  • Diabetes mellitus – there is an increased risk of gallbladder disease in people with diabetes[18]
  • Atherosclerotic disease
  • Systemic vasculitis
  • Acute renal failure
  • HIV – cholangiopathy due to infection can occur.
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42
Q

List symptoms of cholecystitis

A
  • Pain in URQ
  • Fever
  • Nausea
  • Right shoulder pain (diaphragm)
  • Anorexia
  • Vomiting
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43
Q

List signs of cholecystitis

A
  • Jaundice
  • Tenderness in URQ (murphys sign - holding breath when you press on gallstone)
  • Palpable mass
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44
Q

List investigations for cholecystitis

A
  • CT or MRI of the abdomen if sepsis suspected (thickening of bladder wall)
  • Abdominal ultrasound if sepsis not suspected - first investigation to identify presence of gallstones (thickened wall, distended, stone - also called hepatic imidodicetic acid scan (HIDA))
  • FBC
  • CRP
  • Bilirubin
  • LFTs (ALP, ALT, bilirubin, GGT raised)
  • Serum lipase or amylase (normal)
  • Blood cultures and/or bile cultures
  • Magnetic resonance cholangiopancreatography (MRCP - if USS has not detected stones)
  • Endoscopic ultrasound (EUS)
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45
Q

Describe management of cholecystitis

A

If associated organ dysfunction

  • IV fluids
  • Antibiotics
  • Analgesia
  • Cholecystectomy

If not associated with organ dysfunction

  • Analgesia
  • IV fluid resusitation
  • Antibiotics
  • Early laproscopic cholecystectomy or percutaneous cholecystectomy
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46
Q

List complications of cholecystitis

A
  • Suppurative cholecystitis (abscess formation)
  • Bile duct injury due to surgery
  • Gallstone ileus (enterotomy)
  • Cholecystoenteric fistula
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47
Q

Describe prognosis of cholecystitis

A
  • Removing the gallbladder and the contained gallstones when biliary pain starts will prevent further biliary attacks and reduce the risk of developing cholecystitis. If the gallbladder perforates, mortality is 30%.
  • Untreated acute acalculous cholecystitis is life-threatening and is associated with up to 50% mortality.
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48
Q

Describe aetiology of acute cholangitis

A
  • The most common aetiology of acute cholangitis is cholelithiasis leading to choledocholithiasis and biliary obstruction. E coli most common pathogen
  • Iatrogenic biliary duct injury, most commonly caused via surgical injury during cholecystectomy, can lead to benign strictures, which can in turn lead to obstruction (with or without secondary sclerosing cholangitis).
  • Other causes of benign biliary stricture include chronic pancreatitis (with stenosis and stricture of the distal common bile duct, which has an intrapancreatic course), radiation-induced biliary injury, or biliary injury as a complication of systemic chemotherapy (e.g., fluorodeoxyuridine).
  • Sclerosing cholangitis causes 24%
  • Malignancy unlikely
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49
Q

List risk factors for acute cholangitis

A
  • Age over 50 years
  • History of cholelithiasis
  • Primary or secondary sclerosing cholangitis
  • Stricture of the biliary tree (benign or malignant)
  • Post-procedure injury of bile ducts (surgical, endoscopic, or radiological intervention with resulting inadequate biliary drainage).
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50
Q

Describe epidemiology of acute cholangitis

A
  • Cholangitis is relatively uncommon, presenting as a complication in about 1% of patients with cholelithiasis.
  • The male-to-female ratio is equal.
  • The median age of presentation is between 50 and 60 years.
  • About 1% to 3% of patients develop cholangitis after endoscopic retrograde cholangiopancreatography, usually due to inadequate steps taken to ensure biliary drainage.
  • Recurrent oriental pyogenic cholangitis is more common in the eastern hemisphere than in the western hemisphere.
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51
Q

List complications of acute cholangitis

A
  • Acute pancreatitis
  • Hepatic abscess
  • Inadequate biliary drainage following radiology, surgery or endoscopy
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52
Q

Describe prognosis of acute cholangitis

A
  • Most patients experience rapid clinical improvement once adequate biliary drainage is achieved, with improvement in haemodynamic parameters and systemic inflammatory response parameters.
  • For patients with significant underlying medical conditions and those in whom decompression is delayed, prognosis is poorer.
  • Predictive factors for poor prognosis include hyperbilirubinaemia, high fever, leukocytosis, older age, and hypoalbuminaemia.
  • Patients requiring emergent surgery have higher rates of morbidity and mortality than those managed acutely with non-operative procedures.
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53
Q

Describe management of gallstones

A

ACUTE
symptomatic cholelithiasis
- 1st line – cholecystectomy

Choledocholithiasis with or without symptoms

  • 1st line – endoscopic retrograde cholangiopancreatography (ERCP)
  • Adjunct – lithotripsy, papillary balloon dilation, or long-term biliary stenting
  • 2nd line – laparoscopic common bile duct exploration

ONGOING
- Asymptomatic cholelithiasis
1st line – observation (watch and wait)

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54
Q

List possible complications of gallstones

A
  • Endoscopic retrograde cholangiopancreatography (ERCP)- associated pancreatitis
  • Iatrogenic bile duct injuries
  • Post-sphincterotomy bleeding
  • Bouveret syndrome
  • Gallstone ileus
  • Cholecystitis
  • Acute (ascending) cholangitis
  • Acute biliary pancreatitis
  • Mirizzi syndrome
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55
Q

Describe prognosis of gallstones

A
  • The outlook for patients with symptomatic cholelithiasis managed by cholecystectomy is favourable.
  • The same holds for patients with choledocholithiasis who undergo endoscopic retrograde cholangiopancreatography (ERCP) with biliary sphincterotomy and stone extraction, followed later by cholecystectomy.
  • Risk factors for recurrent choledochal problems are common with: bile duct dilatation to >15mm; a periampullary diverticulum; brown pigment stones; or the gallbladder being left intact.
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56
Q

List Abdo scars and their uses

A
  • Midline (majority of organ acess)
  • Kocher (gall bladder/biliary tree, open cholecystectomy)
  • Gridiron (appendix)
  • Lanz (appendix)
  • Pfannensteil (Cesarian)
  • Rutherford morrison (access ascending colon)
  • Paramedian (kidneys, spleen, adrenals)
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57
Q

Describe aetiology of haemochromatosis

A

Most common mutations C282Y and H63D in the HFE gene

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58
Q

List risk factors of haemochromatosis

A
  • Middle age
  • Male gender
  • White ancestry
  • Family history
  • Supplemental iron
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59
Q

Describe epidemiology of haemochromatosis

A
  • Type 1 primarily in northern European descent
  • 1 in 10 white people heterozygous for major HFE mutation
  • Equal heterozygote frequency in males and females, but more common condition in men
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60
Q

List investigations for haemochromatosis

A
  • Serum transferrin saturation (over 45%)
  • Serum ferritin (raised)
  • Serum iron raised
  • Decreased total iron binding capacity
  • HFE mutation analysis
  • MRI liver (liver to muscle signal intensity decreased)
  • Liver biopsy (raised iron, shown by prussian blue staining)
  • LFTs (Aminotransferase raised)
  • Fasting blood sugar (raised)
  • Echocardiogram
  • ECG (decreased QRS amplitude and T wave flattening or inversion)
  • Testosterone/FSH/LH (lower)
  • Bone densitometry (osteopenia or osteoporosis, radiograph symptomatic joints)
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61
Q

Define pancreatic cancer

A

Primary pancreatic ductal adenocarcinoma, which accounts for >85% of all pancreatic neoplasms.

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62
Q

Describe epidemiology of pancreatic cancer

A
  • Poor prognosis
  • Median age of diagnosis 70, median age of death 72
  • 7.6 in 100000 people per year in men, 4.9 per 100000 per year in women
  • Overall median survival from diagnosis 4.6 months
  • 128000 deaths in 2018 in europe
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63
Q

Describe aetiology of pancreatic cancer

A
  • Smoking
  • 5-10% of cases inherited component (hereditary pancreatitis, Peutz-Jeghers syndrome, familial atypical multiple mole melanoma, familial breast cancer syndrome, non-polyposis colorectal cancer syndrome)
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64
Q

List risk factors for pancreatic cancer

A
  • Age 65-75
  • Smoking
  • Family history of pancreatic cancer/ other hereditary cancer syndromes
  • Chronic sporadic pancreatitis
  • Diabetes mellitus
  • Obesity
  • Dietary factors
  • Alcohol
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65
Q

List signs and symptoms of pancreatic cancer

A
  • Jaundice
  • Upper abdominal pain or discomfort
  • Weight loss and anorexia
  • Steatorrhoea
  • Thirst, polyuria, nocturia, weight loss (new onset diabetes)
  • Nausea, vomiting, anorexia, mid-epigastric pain
  • Hepatomegaly (metastasis)
  • Epigastric abdominal mass
  • Positive courvoisiers sign (painless palpable gallbladder and jaundice)
  • Petechiae, purpura, bruising (DIC - advanced disease)
  • Trousseaus sign (thrombophlebitis of lower limb)
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66
Q

Describe investigations for pancreatic cancer

A
  • Abdominal ultrasound (pancreatic mass, dilated bile ducts, liver mets), CT CAP
  • Pancreatic protocol CT (mass)
  • LFTs (degree of obstructive jaundice - bilirubin, ALP and GGT raised, animotransferases normal)
  • PT (prolonged)
  • FBC (anaemia in GI bleed, low platelets in DIC)
  • CA19-9 (70-90% sensitivity, 90% specificity)
  • PET
  • ERCP
  • MR cholagiopancreatography
  • Endoscopic ultrasound
  • Staging laparoscopy
  • Biopsy GOLD STANDARD
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67
Q

Define acute liver failure

A
  • a rapid decline in hepatic function characterised by jaundice, coagulopathy (INR >1.5), and hepatic encephalopathy in patients with no evidence of prior liver disease
  • Classified as hyperacute, acute, or subacute
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68
Q

Describe epidemiology of acute liver failure

A
  • 2000 cases anually in the US
  • Most patients women
  • Mean age 38
  • Spontaneous recovery without liver transplant 45%, with 30% overall mortality
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69
Q

Describe aetiology of acute liver failure

A
  • Paracetamol overdose most common cause in the UK and US
  • 66% of cases in UK due to paracetamol
  • Other causes drug induced, acute hep B, autoimmune Hepatitis, ischaemic hepatitis, and acute hep A
  • Viral infection most common in Bangladesh and India (HEV) and Japan (HBV)
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70
Q

List risk factors for acute liver failure

A
  • Chronic alcohol abuse
  • Poor nutritional status
  • Female sex
  • Age >40 years
  • Pregnancy (and hep E)
  • Chronic hepatitis B
  • Chronic pain and narcotic use
  • Complementary and alternative medicine hepatotoxicity
  • Paracetamol and antidepressant therapy
  • Chronic hepatitis C
  • HIV and hepatitis C co-infection
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71
Q

List symptoms of acute liver failure

A
  • Abdominal pain
  • Nausea
  • Vomiting
  • Malaise
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72
Q

List signs of acute liver failure

A
  • Jaundice
  • Hepatic encephalopathy (impaired awareness, sleep alteration, personality change, dyspraxia, strange behaviour)
  • Cerebral oedema (abnormal pupillary reflexes, papilloedema, muscular rigidity)
  • RUQ tenderness
  • Hepatomegaly
  • NO splenomegaly, spider angiomata, palmar erythema, ascites
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73
Q

Describe investigations of acute liver failure

A
  • LFT (high bilirubin and liver enzymes)
  • Prothrombin/INR
  • Basic metabolic panel (elevated urea and creatinine)
  • FBC
  • Blood type and screen
  • ABG (metabolic acidosis)
  • Arterial blood lactate (prognostic in paracetamol associated)
  • Paracetamol
  • Urine toxicology (paracetamol)
  • Factor 5 level (low with hepatic encephalopathy suggests high risk of mortality)
  • Viral hepatitis serology
  • Autoimmune hepatitis markers
  • Pregnancy test
  • CXR (possible aspiration pneumonia)
  • Abdo doppler ultrasound (hepatic vessel thrombosis, hepatomegaly)
  • PCR
  • Serum ceruloplasmin (low in wilsons disease)
  • Serum copper/24hr copper excretion
  • Arterial ammonia
  • HIV test
  • Coombs test (autoimmune haemolysis coombs positive)
  • Liver biopsy (hepatocellular necrosis, microvesicular steatosis, viral inclusions, elevated hepatic copper)
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74
Q

Describe treatment of acute liver failure

A
  • Intensive care management (monitoring, raise head of bed, reduce surrounding stimuli, tracheal intubation in advanced encephalopathy, propofol and fentanyl for analgesia and sedation, IV fluids with caution, nutritional support, PPI)
  • Liver transplantation assessment
  • Neurological status monitoring for advanced encephalopathy
  • Monitoring of blood glucose (every 1-2 hours), electrolytes (twice daily, correct), and cultures

Paracetamol-related or with mild to moderate (grade 1 or 2) hepatic encephalopathy
- Acetylcysteine

With herpes simplex hepatitis
- Aciclovir

With acute fatty liver of pregnancy or the haemolysis, elevated liver enzymes, and low platelet (HELLP) syndrome
- Expedient delivery of the fetus

With suspected Amanita phalloides poisoning

  • Intravenous fluids + gastric lavage + activated charcoal
  • Benzylpenicillin
  • Acetylcysteine

With autoimmune hepatitis
- Methylprednisolone

With acute hepatitis B
- Oral nucleoside or nucleotide analogue

With acute Budd-Chiari syndrome

  • Anticoagulation
  • Transjugular intrahepatic portosystemic shunt (TIPS)

with acute Wilson’s disease
- Measures to decrease serum copper

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75
Q

List complications of acute liver failure

A
  • Rapidly progressing hepatic encephalopathy
  • Coagulopathy
  • Infection
  • Renal failure and haemodynamic changes
  • Metabolic disorders
  • Cerebral oedema
  • Gastrointestinal bleeding
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76
Q

Describe prognosis of acute liver failure

A
  • 75% paracetamol induced recover without liver transplant
  • Hep B, drug induced or indeterminate cause only 25-41% spontaneous recovery
  • Patients who have liver transplant higher risk of death within the first 2 months following transplant, and commonly require retransplant
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77
Q

List symptoms of cirrhosis

A
  • Fagigue, weight loss, weakness
  • Lower extremity swelling
  • Hepatic fetor (smelly breath)
  • Dyspnoea
  • Chest pain
  • Syncope
  • Decreased libido
  • Recurrent infections
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78
Q

List risk factors for cirrhosis

A
  • Alcohol misuse
  • Intravenous drug use
  • Unprotected intercourse
  • Obesity
  • Country of birth (Hep B and C)
  • Blood transfusion
  • Tattooing
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79
Q

Describe epidemiology of cirrhosis

A
  • Liver disease 3rd biggest cause of premature mortality in the UK - 62000 working life years lost
  • 170000 deaths in 2002 in Europ3
  • In US and Europe, most cases caused by viral hepatitis, alcoholic liver disease and NAFLD
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80
Q

Describe investigations for cirrhosis

A
  • Liver function tests (deranged)
  • Gamma-glutamyl transferase (GGT high)
  • Serum albumin (low)
  • Serum sodium (low)
  • Prothrombin time (increased)
  • Platelet count (reduced)
  • Antibodies to hepatitis C virus
  • Hepatitis B surface antigen
  • Total iron (high), total iron binding capacity (TIBC low), transferrin saturation (high), and ferritin (high) - haemochromatosis
  • Antinuclear antibody, antismooth muscle antibody, antimitochondrial antibody
  • Serum ceruloplasmin
  • Plasma alpha-1 antitrypsin
  • Serum protein electrophoresis
  • Abdominal ultrasound
  • Abdominal CT + MRI
  • Upper gastrointestinal endoscopy
  • Liver biopsy
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81
Q

Describe management of cirrhosis

A
  • Treat underlying liver disease and prevent hepatic insult (eg. oral antivirals, avoid alcohol and hepatotoxic drugs, immunise, manage risk factors)
  • Monitoring (ultrasound, endoscopy, CT, MRI)
  • Sodium restriction and diuretic therapy (spironolactone/furosimide)
  • Diagnostic paracentesis of ascites
  • Liver transplant

Encephalopathy

  • Treat precipitating event (antibiotics, GI bleed management)
  • Oral lactulose (reduces ammonia in the gut), phosphate enema
  • Avoid sedatives
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82
Q

List complications of cirrhosis

A
  • Ascites
  • Gastro-oesophageal varices
  • Hepatocellular carcinoma
  • Bleeding and thrombosis
  • Spontaneous bacterial peritonitis
  • Hepatic hydrothorax
  • Portosystemic encephalopathy
  • Acute kidney injury-hepatorenal syndrome (AKI-HRS)
  • Hepatopulmonary syndrome
  • Portopulmonary hypertension
  • Hypogonadism and feminisation
  • Hepatic osteodystrophy
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83
Q

Describe prognosis of cirrhosis

A
  • Median survival 10 years
  • Prongosis depends on disease
  • Compensated 90% 10 year survival, transitions to decompensated in 50%
  • Median survival time in decompensated 2 years
  • Four clinical stages of cirrhosis have been identified and each is associated with a different prognosis.
  • Stage 1 - patients without gastro-oesophageal varices or ascites have a mortality of approximately 1% per year.
  • Stage 2 - patients with gastro-oesophageal varices (but no bleeding) and no ascites have a mortality of approximately 4% per year.
  • Stage 3 - patients with ascites with or without gastro-oesophageal varices (but no bleeding) have a mortality of approximately 20% per year.
  • Stage 4 - patients with GI bleeding due to portal hypertension with or without ascites have a 1-year mortality of 57%.
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84
Q

Describe the mechanism of hepatic encephalopathy

A
  • Liver unable to break down toxins
  • Therefore, increased urea which leads to raised ammonia
  • This leads to ammonia reaching the brain, causing confusion
  • First signs are sleeping during the day
  • Causes asterixis (liver flap)
85
Q

List drugs that can cause hepatitis

A
  • Apsirin
  • Paracetamol
  • Salicylate
  • Anabolic steroids
86
Q

List questions that should be asked in liver history

A
  • History of diabetes, hypertension, high cholesterol
  • Sexual contact, IV drug use, any blood transfusion pre 1992/ outside of england
  • Any vaccinations abroad
  • Dental work outside the UK
  • Piercings/tattoos
87
Q

List risks of liver biopsy

A
  • Haemorrhage
  • Perforation of bowel/ gall bladder
  • Mortality 1 in 9000 so only performed if necessary
88
Q

Describe the mechanism of ascites in liver failure

A
  • Decreased albumin production
  • Loss of oncotic pressure, with maintained hydrostatic pressure leading to gradient causing fluid to leave the vessels
  • Also caused by renal failure (fluid retention, protein loss) and heart failure (backflow of blood)
89
Q

How is ascites investigated?

Discuss results and causes

A
  • Ascitic fluid tap.
  • Investigate for any infection
  • Serum ascites albumin gradient to determine aetiology.
  • High gradient indicates transudate, may be caused by cirrhosis/hepatic failure, cardiac failure, hepatic failure, liver mets (non-peritoneal cause of ascites)
  • Low gradient is exudate indicating malignancy, pancreatitis, nephrotic syndrome, bowel obstruction or infarction
90
Q

How does haemochromatosis cause tanning?

A
  • Deposit of iron in the skin stimulating melanocytes to make more melanin
  • Indirect
91
Q

Define infectious colitis

A

An infection of the colon causing diarrhoea and vomiting

92
Q

Describe aetiology of infectious colitis

A
  • Causes of bacterial colitis include Campylobacter jejuni, Salmonella, Shigella, Escherichia coli, Yersinia enterocolitica, Clostridium difficile, and Mycobacterium tuberculosis, staphylococcus aureaus and bacillus cereus
  • Common causes of viral colitis include Norovirus, Rotavirus, Adenovirus, and Cytomegalovirus
  • Norovirus likely to affect institutions (eg. old peoples home)
  • Shigella or E coli O157 causes dysentry (bloody diarrhoea) in primary schools
  • Campylobacter jejuni post-barbeque
  • S. aureus and bacillus cereus cause sudden onset diarrhoea due to pre-formed toxins
  • C. difficile common after taking antibiotics
  • Yersinia enterocolitica travel history
93
Q

Describe epidemiology of infectious colitis

A
  • Bacterial 47% of diarrhoea cases
  • Campylobacter jejuni is the number one bacterial cause of diarrheal illness worldwide
  • Shigellosis mortality has decreased in the last three decades because of improvement in laboratory diagnosis and treatment.
  • Yersinia enterocolitica colitis commonly presents in young children in the winter.
  • Clostridium difficile infection in hospitalized adults in the United States 8.2 per 1000 cases in 2010 .
  • Amebiasis ranks as the second leading cause of death due to protozoan infection after malaria, Chagas disease, and leishmaniasis.
  • The prevalence of CMV infection in percent colitis is in the range of 21% to 34
94
Q

List risk factors for infectious colitis

A
  • Poorly cooked/stored food
  • Travel
  • Antibiotics
  • Crowding/exposure to people with the illness
95
Q

List signs and symptoms of infectious colitis

A
  • Onset of diarrhoea and/or vomiting.
  • May be bloody
  • Abdo pain
  • Fever
  • Chills
  • Sweating
  • Patients with colitis associated with sexually transmitted disease present with anorectal pain, with a purulent, mucoid or bloody discharge, tenesmus, or urgency. Sexual history is vital in evaluating these patients.
  • Dehydration (dry skin, sunken eyes, furry tongue)
96
Q

Describe investigations for infective colitis

A
  • ABC - check for shock.
  • Analyse feces if concerned about disease (eg. c.difficile)
  • FBC
  • U&Es (assess kidney function, hydration).
  • Sodium and pottassium (dehydration)
  • If severe, abdo radiographs, lactate measurements, surgical review in case of toxic megacolon or perforation
97
Q

Describe management of infectious colitis

A
  • Fluids (oral or IV if severely dehydrated. Fluid challenge to raise BP, maintenance fluids/replacement fluids)
  • Antibiotics if C.difficile
  • Isolation may be required in the hospital
  • Advise on methods to prevent transmission
  • Stay at home for 48 hours after last episode of vomiting
98
Q

List possible complications of infectious colitis

A
  • Intestinal perforation
  • Toxic megacolon
  • Pseudo-membrane formation
  • Hemorrhagic colitis (enteroinvasive E. coli, enterohemorrhagic E. coli)
  • Hemolytic-uremic syndrome (enterohemorrhagic E coli, Campylobacter jejuni, Shigella)
  • Post-infectious irritable bowel syndrome, dyspepsia
  • Guillain-Barre syndrome
  • Encephalitis, seizure (Shigella)
  • Reactive arthritis (Shigella, Campylobacter jejuni, Yersinia enterocolitica colitis)
  • Pancreatitis, cholecystitis, meningitis, purulent arthritis (Campylobacter jejuni)
  • Septic shock and death (Shigella, Clostridium difficile)
  • Renal failure, shock (Clostridium difficile)
  • Patients with CMV colitis complicating inflammatory bowel disease may develop severe hemorrhage, megacolon, fulminant colitis, or colon perforation; these complications contribute to the high risk of mortality
99
Q

Describe prognosis of infectious colitis

A
  • C difficile has 1 in 4 chance of returning, usually gone within 2 weeks with antibiotic treatment. 4-6% mortality
  • Generally lasts up to 7 days, though symptoms can persist for a few weeks in some cases
100
Q

List extra-intestinal manifestations of IBD

A
  • Clubbing of nails
  • Anterior uveitis, episcleritis, scleritis
  • Erythema nodosum (inflammation of subcut fat), pyoderma gangrenosum (inflammatory ulceration and necrosis of skin)
  • Ankylosing spondylitis and UC (HLA-B27)
  • Iron deficiency anaemia, folate or B12 deficiency
  • Primary sclerosing cholangitis associated with UC, cholesterol gallstones
  • Kidney stones (reduced Ca allows oxalate to form stones)
  • Amyloidosis
101
Q

Describe aetiology of crohns

A
  • Genetic factors (CARD 15)
  • Environmental factors (smoking, oral contraceptive pill, diet high in refined sugar, nutritional deficiencies (especially zinc), and infectious agents)
102
Q

List stages of hepatic encephalopathy

A
  • Overexcited
  • Talk rubbish
  • Loose idea of where they are
  • Fall asleep
103
Q

Define coeliac disease

A

A systemic autoimmune response where there is a T cell response to gluten in the small bowel causing villous atrophy and malabsorption (GLIADIN)

104
Q

List symptoms of coeliac disease

A
  • Stinking stools - steatorrhoea
  • Diarrhoea
  • Abdo pain, bloating
  • Nausea and vomiting
  • Weight loss
  • Fatigue
  • Weakness
105
Q

Describe prognosis of coeliac disease

A
  • Up to 90% complete symptom resolution with diet changes
  • Ongoing gluten exposure, lactose intolerance, and irritable bowel syndrome account for most of the 10% of cases with persistent symptoms.
  • Fewer than 1% of patients can be expected to develop refractory coeliac disease
106
Q

Describe management of oesophageal varices

A
  • Band ligation or sclerotherapy

- Long term management with B blocker

107
Q

How are patients with cirrhosis screened?

A
  • Measure alpha-fetoprotein and ultrasound liver every 6 months
108
Q

Describe ABG appearance in metabolic acidosis

A
  • Low pH
  • Low HCO3-
  • Low BE
  • Low CO2 if resp compensation
109
Q

List causes of metabolic acidosis

A
  • Diarrhoea
  • AKI
  • Diabetic ketoacidosis
  • Lactic acodisis
  • Aspirin overdose
  • Addisons
110
Q

Describe ABG appearance in metabolic alkalosis

A
  • High pH
  • High HCO3-
  • High BE
  • High CO2 if compensation
111
Q

List causes of metabolic alkalosis

A
  • Vomiting
  • Diuretics, nephrotic syndrome, Conns, cirrhosis
  • Iatrogenic
112
Q

List causes of mixed respiratory and metabolic acidosis

A
  • Cardiac arrest

- Multi organ failure

113
Q

List causes of mixed respiratory and metabolic alkalosis

A
  • Liver cirrhosis + diuretic
  • Hyperemesis gravidarum
  • Excessive ventillation in COPD
114
Q

Define hernia

A
  • A condition where part of an organ is displaced and protrudes through the wall of the vacity containinging
  • Incisional hernias occur around incision sites after surgery
  • Hiatus hernias happen at the gastro-oesophageal junction
  • Spigelian hernias occur on the linea semilunaris of the abdomen
115
Q

Define hiatus hernia

A
  • Herniation of part of the abdominal contents through the oesophageal aperture of the diaphragm
  • Sliding are 85-95%, where the gastrooesophageal junction slides up into the thoracic cavity
  • Rolling is where the junction stays in place but part of the stomach herniates into the chest
116
Q

Describe epidemiology of hiatus hernia

A
  • The prevalence of hiatus hernia can only be estimated, because most of these hernias cause mild or no symptoms and diagnostic criteria may vary.
  • Clinical estimates of the prevalence of hiatus hernia in western populations range up to 50%
  • Males more commonly affected
117
Q

Describe aetiology of hiatus hernia

A
  • Widening of diaphragmatic hiatus
  • Pulling up of the stomach due to oesophageal shortening
  • Pushing up of the stomach by increased intra-abdominal pressure
118
Q

List symptoms of hiatus hernia

A

Sliding

  • Asymptomatic
  • Retrosternal burning/heartburn
  • GORD
  • Dysphagia

Rolling

  • Asymptomatic
  • Chest pain
  • Epigastric pain or fulness
  • Nausea
119
Q

List risks for hiatus hernia

A
  • Obesity, female
  • Pregnancy
  • Ascites
  • Age over 50
120
Q

List signs of hiatus hernia

A
  • Tender abdomen

- Bowel sounds heard

121
Q

List investigations for hiatus hernia

A
  • CXR (retrocardiac bubble)
  • Barium studies
  • Endoscopy (dysplagia)
122
Q

Describe management of hiatus hernia

A
  • Lifestyle changes
  • PPIs, H2 receptor antagonists
  • Surgery for symptomatic sliding hernias using laparoscopic fundoplication
123
Q

List complications of hiatus hernia

A
  • Bloating
  • Dysphagia
  • Recurrence
  • Volvulus
  • Barretts oesophagus
124
Q

Describe prognosis of hiatus hernia

A
  • Symptomatic relief with medial/surgical treatment

- Morbidity and mortality higher in over 70s

125
Q

Define inguinal hernia

A
  • Protrusion of abdominal or pelvic contents through a dilated internal inguinal ring or attenuated inguinal floor.
  • Indirect through internal and sometimes external inguinal ring
  • Direct directly through the muscle
126
Q

Describe epidemiology of inguinal hernia

A
  • Most common type of hernia
  • Less commonly strangulated
  • Younger patients
127
Q

Describe aetiology of inguinal hernia

A
  • Congenital indirect due to processus vaginalis failing to undergo regression
  • Acquired defects sue to changes in the inguinal wall, or weakness in the posterior wall
128
Q

List risk factors for inguinal hernia

A
  • Male sex
  • Old age
  • Smoking
  • Family history
  • Prematurity
  • AAA
  • Previous right lower quadrant pain
  • Marfan/Ehlers Danlos
  • Heavy lifting
  • Pregnancy
129
Q

List symptoms and signs of inguinal hernia

A
  • Groin discomfort or pain with bulge.
  • Groin mass superomedial to pubic tubercle
  • Abdo pain and vomiting if strangulated
130
Q

List investigations of inguinal hernia

A
  • Clinical diagnosis (reduce hernia, place finger over deep inguinal ring, ask patient to cough, if reappears must be direct)
  • USS
  • CT scan
  • Herniography
  • MRI of groin
131
Q

Describe treatment of inguinal hernia

A
  • If strnagulated, surgical repair, prophylactic antibiotic therapy
  • If small asymptomatic watch and weight
  • If large or symptomatic open mesh or laproscopic repair
  • Laparoscopic prefered if non-complicated, open prefered if complicated
132
Q

List complications of inguinal hernia

A
  • Strangulated (lack of blood supply)
  • Obstructed (bowel obstruction)
  • Urinary retention post op
  • Wound seroma post op
  • Inguinal wound haematoma post op
  • Scrotal haemotoma post op
  • Wound infection post op
133
Q

Compare location of direct and indirect inguinal hernias

A
  • Inguinal outside of hesslebach triangle
  • Direct in hesslebach traingle
  • Hesslebach triangle rectus abdominis, inferior epigastric vessels, inguinal ligament
134
Q

Describe prognosis of inguinal hernias

A
  • Good prognosis after surgical repair
  • Recurrent hernia with mesh repair less than 2%
  • Chronic pain in 10-12% of patients after repair
135
Q

Define femoral hernia

A

Bowel enters the femoral canal presenting as a mass in the upper medial thigh or above the inguinal ligament towards the leg

136
Q

Describe epidemiology/risks of femoral hernia

A
  • More common in females
  • Rarer than inguinal hernia (5% of all hernias)
  • More commonly strangulated
  • More common in older patients
  • Obesity, chronic cough, straining
137
Q

Describe signs and symptoms of femoral hernia

A
  • Mass lateral and inferior to pubic tubercle
  • Abdo discomfort
  • Appears on coughing
  • May be reducible, but likely to be irreducible
  • If strangulated, tender, red, colicky abdo pain, distention, vomiting
138
Q

Describe diagnosis of femoral hernia

A
  • Clinical diagnosis

- Groin ultrasound

139
Q

Describe management of femoral hernia

A
  • Non-complicated elective surgical repair with mesh hernioplasty
  • Complicated herniorrhaphy non mesh repair
140
Q

List complications of femoral hernia

A
  • Incarceration (irreducible)

- Strangulation (necrosis of hernia contents)

141
Q

Describe prognosis of femoral hernia

A
  • Strangulation must be treated through emergency surgery

- Generally patients recover well

142
Q

Describe intestinal obstruction

A

A broad condition resulting from the blockage of flow of the intestines

143
Q

Describe aetiology of intestinal obstruction

A

Small bowel

  • Adhesions from prior operations
  • Herniae
  • Malignancy
  • Gallstone ileus
  • Foreign body
  • Pathogen: ascaris lumbricoides

Large bowel

  • Colorectal malignancies
  • Sigmoid or caecal volvulus
  • Intussuseption
  • Paralytic ileus
  • Diverticular disease
  • Faecal impaction
  • Foreign body
  • Postoperative ileus
  • Pathogen: ascaris lumbricoides
144
Q

List risks for intestinal obstruction

A
  • Previous abdo surgery
  • Hernias
  • Crohns
  • Malignnacy
  • Appendicitis
  • Foreign body ingestion
  • Gallstone ileus
  • Malrotation of gut
  • Intusseption
  • Volvulus
145
Q

Describe epidemiology of intestinal obstruction

A
  • 20% asmissions with acute abdo pain
  • 20% large bowel obstruction
  • 15-29% occurence in colorectal cancer
146
Q

List symptoms of intestinal obstruction

A
  • Constipation
  • Intermittent abdo pain
  • Vomiting, nausea, anorexia
  • Pyrexia
147
Q

List signs of intestinal obstruction

A
  • Abdo tenderness
  • Tinkling bowel sounds
  • Absent bowel sounds
  • Abdomass
  • Rectal mass
  • Perotinitis (laying still)
  • Pyrexia, sweating
148
Q

Describe investigations of intestinal obstruction

A
  • CT/ X ray (riglers sign ie air on both sides of the bowel wall, volvulus)
  • Gastrograffin for SBO to identify point of issue
  • FBC
  • U and E
  • CRP
  • Glucose
  • Clotting, group and save
  • ABG
149
Q

Describe management of intestinal obstruction

A
  • Drip and suck (IV drip and NG tube)
  • Rigid sigmoidoscope decompression for sigmoid volvulus
  • Laparotomy (esp. if haemodynamically unstable)
150
Q

Describe prognosis of intestinal obstruction

A

Small bowel mortality 25% with delayed surgery, under 36 hours drops to 8%

151
Q

List complications of intestinal obstruction

A
  • Necrosis
  • Sepsis
  • Multi organ failure
  • Abscess
  • Perforation
152
Q

List classification of liver disease

A
  • Hyperacute less than 7 days to get jaundice and encephalopathy, commonly paracetamol
  • Acute 8-28 days, poorer prognosis than hyperaccute. Often caused by repeated insults to liver, eg. staggered paracetamol overdose
  • Subacute 29 days -3 months, tend to be autoimmune. Generally dont do well and require transplant
  • Chronic over 3 months
153
Q

Define zollinger ellison syndrome

A

A syndrome of gastric acid hypersecretion caused by a gastrin secreting neuroendocrine tumour

154
Q

List signs and symptoms of peptic ulcer disease

A
  • Abdo pain (pointing sign)
  • Related to eating
  • Nocturnal
  • Nausea and vomiting, early satiety, weight loss
  • Epigastric tenderness
155
Q

Describe how to differentiate between gastric and duodenal ulcer

A
  • Gastric peak in 5th and 6th decade
  • Duodenal in 4th and 5th
  • Gastric more commonly NSAID, duodenal more commonly H. pylori
  • Gastric pain shortly after eating, duodenal pain a few hours after eating
  • Pain may radiate to the back in duodenal
156
Q

Describe epidemiology of achalasia

A
  • Median age at diagnosis 53

- 8-27 per 100000

157
Q

Describe aetiology/risks of achalasia

A
  • Autoimmunity (Ab and T cells in myenteric plexus)
  • Chagas disease
  • Genes
  • Allgrove syndrome (triple A syndrome, a multisystem disorder with triad of achalasia, alacrima, and adrenal insufficiency)
158
Q

List symptoms and signs of achalasia

A
  • Dysphagia to solids and liquids
  • Posuring to aid swallowing
  • Retrosternal pressure/pain
  • Regurgitation
  • Weight loss (gradual)
159
Q

Define liver abscess

A
  • Purulent collections in the liver parenchyma that result from bacterial, fungal, or parasitic infection.
  • Infection can spread to the liver through the biliary tree, hepatic vein, or portal vein, by extension of an adjacent infection, or as a result of trauma.
160
Q

Describe epidemiology of liver abscess

A
  • Uncommon
  • 3.6 per 100000 in the UK
  • Increases with age, more common in men
  • Increasing incidence and decreasing mortality
161
Q

Describe aetiology of liver abscess

A
  • Pyogenic liver abscess polymicrobial
  • E coli, Klensiella, streptococccus constellatus, anginosus and intermedius
  • S aureus and pseudomonas less common
  • Recurrent pyogenic cholangitis due to salmonella typhi may cause pyogenic liver abscess
  • Amoebic may occur following E histolytica infection
162
Q

List risk factors for liver abscess

A
  • Biliary tract disease
  • Age >50 years
  • Underlying malignancy
  • Diabetes mellitus
  • Interventional biliary or hepatic procedures
  • Living in or visiting area endemic for amoebiasis
  • Cirrhosis
  • Liver transplantation
  • Alcoholism
  • Male sex
  • Cardiopulmonary disease
  • Immunocompromised state
  • Penetrating abdominal trauma
  • Inflammatory bowel disease, pancreatitis, appendicitis, diverticulitis, or peritonitis
  • Bacteraemia, endocarditis, or other intravascular infection
163
Q

List signs and symptoms of liver abscess

A
  • Fevers and chills
  • RUQ tenderness
  • Hepatomegaly
  • Weight loss
  • Fatigue
  • Abdo pain
  • Nausea and vomiting
  • Cough, SOB, chest pain
  • Jaundice
  • Signs of PE in right lower zone
  • Signs of shock
  • Ascites
164
Q

List investigations for liver abscess

A
  • FBC (leukocytosis, anaemia)
  • LFTs (raised alk phos, low albumin)
  • Blood culture
  • PT and aPTT
  • Liver ultrasound (variably echoic lesion, can guide aspiration)
  • Contrast enhanced abdo CT (hypodense liver lesion)
  • Gram stain and culture aspirated abscess fluid
165
Q

Compare choledocholithiasis and cholithiasis

A
  • Choledocholithiasis is gallstones in the bile duct

- Cholelithiasis stones are contained in the gall bladder

166
Q

Describe epidemiology of wilsons disease

A
  • 30 cases per million
  • 1 in 30000- 1 in 40000 births
  • Clinical disease appears from 10-40 years
167
Q

Describe aetiology of Wilsons

A
  • Autosomal recessive caused by ATP7B gene mutations

- Impaired copper excretion

168
Q

Compare MRCP and ERCP

A
  • MRCP imaging only, diagnostic tool where die is injected into the ampulla of vata and images taken
  • ERCP is therapeutic, images are taken and then tools used to break up stones
169
Q

How is C difficile treated?

A

Metronidazole and vancomycin

170
Q

Define B12 and folate deficiency

A
  • Vitamin B12 deficiency is a common condition that can manifest with neurological, psychiatric, and haematological disorders.
  • Megaloblastic anaemia without neuropathy is the classic manifestation of folate deficiency
171
Q

Describe epidemiology of B12 and folate deficiency

A
  • B12 prevalence in the UK is estimated to be around 6% in people under 60 years and closer to 20% in people aged over 60. 11% of vegans
  • Pernicious anaemia age 40-70, most common cause of B12 deficiency. More women than men affected, risk of gastric cancer
  • Folate 5%
172
Q

Describe aetiology of B12 deficiency

A
  • B12 stores in the body sufficient to last 2-5 years
  • Vitamin B12 combines with intrinsic factor (IF), which is produced by parietal cells in the stomach, to form an IF–B12 complex. The complex binds to surface receptors for IF in the distal ileum, which then allows absorption of vitamin B12 to take place.
  • Pernicious anaemia (an autoimmune disorder which results in reduced production of IF) is the most common cause of severe vitamin B12 deficiency.
  • Drugs — colchicine, metformin, nitrous oxide, protein pump inhibitors, H2-receptor antagonists.
  • Gastric — total or partial gastrectomy, congenital intrinsic factor deficiency or abnormality, Zollinger-Ellison syndrome.
  • Inherited — intrinsic factor receptor deficiency (Imerslund Gräsback syndrome), congenital intrinsic factor deficiency (juvenile pernicious anaemia), cobalamin mutation, transcobalamin deficiency.
  • Intestinal — malabsorption (for example gluten-induced enteropathy), ileal resection, Crohn’s disease, blind loop syndrome, parasites (for example, giardiasis, fish tapeworm).
  • Nutritional — malnutrition, vegan diet.
173
Q

Describe aetiology of folate deficiency

A
  • Folate is usually absorbed through the upper part of the small intestine and body stores are around 10–12 mg, which is sufficient for around 4 months.
  • Folate deficiency is often caused by problems with dietary intake alone, or in a combination with increased folate usage, or malabsorption.
  • Drugs — alcohol, anticonvulsants, nitrofurantoin, sulfasalazine, methotrexate, trimethoprim.
  • Increased requirements, for example, due to:
  • Pregnancy and lactation, prematurity.
  • Malignancy (for example leukaemia, carcinoma, or lymphoma).
  • Blood disorders (for example haemolytic anaemias, sickle cell anaemia, myelofibrosis).
  • Inflammatory diseases (for example tuberculosis, Crohn’s disease, or malaria).
  • Exfoliative skin diseases.
  • Excessive urinary excretion (for example due to congestive heart failure, acute liver damage, or chronic dialysis).
  • Liver disease.
  • Malabsorption — due to coeliac disease, tropical sprue, congenital specific malabsorption, jejunal resection, or inflammatory bowel disease.
  • Nutrition — alcoholism or dietary fads.
174
Q

List symptoms of B12 and folate deficiency

A
  • Cognitive changes.
  • Dyspnoea.
  • Headache.
  • Indigestion.
  • Loss of appetite.
  • Palpitations.
  • Tachypnoea.
  • Visual disturbance.
  • Weakness, lethargy.
175
Q

List signs of B12 and folate deficiency

A
  • Anorexia.
  • Angina (in older people).
  • Angular cheilosis.
  • Brown pigmentation affecting nail beds and skin creases (but not mucous membranes).
  • Congestive heart failure (in older people).
  • Episodic diarrhoea.
  • Glossitis — red smooth and shiny tongue, perhaps with ulcers.
  • Heart murmurs.
  • Liver enlargement.
  • Mild jaundice — a lemon-yellow tint.
  • Mild pyrexia.
  • Oropharyngeal ulceration.
  • Pallor of mucous membranes or nail beds.
  • Tachycardia.
  • Weight loss.
176
Q

List investigations for B12 and folate deficiency

A
  • A full blood count to determine mean cell volume (MCV), haematocrit and haemoglobin levels, and a blood film — which help to identify megaloblastic anaemia.
  • Measurement of serum cobalamin and folate levels — to determine the cause of anaemia.
  • Test for anti-parietal cell antibodies (pernicious anaemia)
  • Additional investigations, such as liver function tests, gamma-glutamyl transpeptidase, and/or thyroid function tests — to identify the underlying cause.
  • Reticulocyte count
177
Q

Define peritonitis

A
  • Spontaneous bacterial peritonitis: : infection of the ascitic fluid in the absence of any focal intraabdominal, surgically treatable source of infection
  • Secondary bacterial peritonitis: inflammation of the peritoneum caused by bacterial infection from a surgically treatable intraabdominal source
178
Q

Describe epidemiology of peritonitis

A
  • Most common bacterial infection in patients with cirrhosis
  • 30% of bacterial infections in hospitalised cirrhosis patients
  • Prevalence among asymptomatic outpatients with decompensated cirrhosis 3.5%
179
Q

List risk factors/aetiology for peritonitis

A
  • Cirrhosis and ascites (most common cause E coli)
  • Post operative due to anastamotic leakage
  • Burst stomach ulcer
  • Burst appendix
  • Pancreatitis
  • Pelvic inflammatory disease
  • Diverticulitis
  • Penetrating wound
180
Q

List signs and symptoms of peritonitis

A
  • Diffuse abdominal pain/tenderness
  • Fever and chills
  • Worsening ascites
  • New-onset or worsening encephalopathy
  • Nausea, vomiting
  • Constipation or diarrhea (peristaltic signs sparse or absent in cases of ileus)
  • Patient laying completely still
181
Q

Describe investigations for peritonitis

A
  • Ascitic fluid neutrophil count over 250/mm3, SAAG
  • Obtain 2 sets of blood cultures before administering antibiotics
  • CT/MRI
  • X ray for pneumoperitoneus
  • ESR, CRP,
182
Q

Describe management of peritonitis

A
  • Antibiotics - most common cause E coli, continue for at least 5-7 days (eg. cephalosporin or carbapenem
  • May need IV beta blockers, discontinue duretics and avoid using nephrotoxic drugs
  • Replace electrolytes, anaglestics, antipyretics, IV fluids
183
Q

List complications of peritonitis

A
  • Sepsis, septic shock, death
  • Acute or chronic liver failure
  • AKI and/or hepatorenal syndrome
  • Hepatic encephalopathy
  • GI bleed
  • Worsening ascites
184
Q

Describe prognosis of peritonitis

A
  • Depends on the cause
  • If appendicitis is the cause, good prognosis
  • If long standing liver disease poor prognosis
185
Q

Define gastrointestinal perforation

A
  • A full-thickness loss of bowel wall integrity that results in perforation peritonitis
  • Perforation of a duodenal ulcer is the most common cause of perforation peritonitis
186
Q

Describe aetiology of GI perforation

A
  • Peptic ulcer disease (usually duodenal perforate)
  • Malignancy
  • IBD
  • Diverticulitis
  • Appendicitis
  • Typhoid
  • Toxic megacolon
  • Bowel obstruction
  • Acute mesenteric ischaemia
  • Trauma
  • Foreign body ingestion, post transplant, drug induced
187
Q

Describe epidemiology of gastrointestinal perforation

A
  • Duodenal ulcer perforations most common (2-3 times more common than gastric)
  • 1/3 gastric perforations due to carcinoma
  • 10-15% of patietns with acute diverticulitis perforation
188
Q

List symptoms of gastrointestinal perforation

A
  • Pain (sudden sharp stabbing painfollowed by diffuse abdo pain)
  • Abdominal distention
  • Nausea, comiting
  • No gas or stools passed
  • RLQ pain appendicitis eprforated, LLQ pain perforated diverticulitis, diffuse free intraperitoneal perforation
189
Q

List signs of gastrointestinal perforation

A
  • Fever
  • Tachycardia, tachypnoea, hypotension
  • Decreased or absent bowel sounds
  • Loss of liver dullness
  • Signs of perotinitis (tenderness, laying still)
190
Q

Describe investigations for gastrointestinal perforation

A
  • FBC (raised WCC), electrolytes, creatinine, LFT, lactate, amylase or lipase
  • CRP
  • Erect CXR showing pneumoperitoneum or pneumomediastinum
  • May also be presence of abscess or fistula on AXR. Rigler and psoas sign
  • CT to look for gas
  • Neck imaging to look for surgical emphysema
  • May perform endoscopy, ultrasound
191
Q

Describe management of bowel perforation

A
  • IV fluids, stp oral intake
  • Broad spectrum antibiotics
  • Drainage, gastrostomy, NG tube
  • Antiemetics, analgesics
  • Surgical exploration (if patient has sepsis, perotinitis, ischaemia, or bowel obstruction. Culture peritoneal fluid, close perforation with anastomosis or stoma)
192
Q

List complications of gastrointestinal perforation

A
  • Peritonitis
  • Bacteraemia
  • Sepsis
  • Multi-organ dysfunction
  • Intra-abdominal abscess
  • Intra-abdominal adhesiions
  • Subhepatic abscess
  • Pyogenic liver abscess
  • Pelvic abscess
  • Postoperative complications
193
Q

Describe prognosis of gastrointestinal perforation

A
  • Life threateining, high morbidity and mortality
  • Over all mortality rate 30%
  • Mortality if diffuse peritonitis 70%
194
Q

Define portal hypertension

A
  • Pathological elevation of portal venous pressure resulting from obstructions in portal blood flow, which may be pre hepatic, hepatic or posthepatic
  • Hepatic venous pressure gradient of over 6mmHg
  • Over 10mmHg is cinically significant, over 12mmHg is associated with complications
195
Q

Describe aetiology of portal hypertension

A

Prehepatic

  • Portal vein thrombosis
  • Splenic vein thrombosis

Intrahepatic

  • Cirrhosis including fibrous proliferation (most common western)
  • Hepatosplenic schistosomiasis (most common worldwide)
  • Massive hepatic mets
  • Hepatic sinusoidal obstruction syndrome

Post hepatic

  • Budd-Chiari syndrome (hepatic vein obstruction
  • Right sided heart failure
  • Constrictive pericarditis
196
Q

Describe signs and symptoms of portal hypertension

A
  • Depends on te cause (acute from vein thrombosis, chronic from cirrosis)
  • Caput meduseae
  • Haemorrhoids or anorectal varices
  • Oesophageal varices, gastric varices, splenomegaly
  • Upper GI bleed (meleana, haematemesis)
  • Ascites
197
Q

Describe investigations for portal hypertension

A
  • FBCs, LFT, U and E, glucose, clotting screen, liver screen (ferritin, hepatitis serology, autoantibodies, ceruloplasmin.ect)
  • Ultrasound (cavernous transformation of the portal vein indicates thrombosis, while portal vein dilated over 13mm unspecific)
  • Duplex ultrasonography may show increased blood flow
  • Fibroscan for fibrosis
  • Abdo CT for portal vein thrombosis
  • OGD to assess for and treat varices
  • Measure hepatic venous pressure gradient
198
Q

Describe epidemiology of portal hypertension

A
  • 25000 cases per 100000 with NAFLD
  • Non-cirrhotic 15000 cases per 100000 individuals with portal hypertension
  • Schistosomiasis most common cause worldwide
199
Q

Describe management of portal hypertension

A
  • Non selective beta blocker (propanolol or nadolol, prevent variceal bleeding)
  • Portosystemic shunts (Transjugular intrahepatic portosystemic shunt if ascites, acute thrombosis, hepatorenal syndrome, recurrent bleeding; total portosystemic shunt; selective portal systemic shunt still allows portal perfusion)
  • Nitrates
  • Vasoactive drugs (terlipressin control acute bleeding)
200
Q

List complications of portal hypertension

A
  • Variceal bleed (sengstaken blakemore tube, endoscopic band ligation)
  • Gastropathy
  • Ascites
  • Spontaneous bacterial peritonitis
  • Hepatorenal syndrome
  • Pulmonary complications of portal hypertension
  • Cardiac cirrhosis
201
Q

Describe prognosis of portal hypertension

A
  • Depends on underlying disease and outcome of complications
  • Child-Pugh score in cirrhosis, MELD.
  • Child pugh one-year survival in class A is 100%; class B 81%; class C 45%.
  • 90% cirrhosis patients develop varices, only 30% bleed.
  • Variceal haemorrhage one year mortality rate of 40%
202
Q

Define pilonidal sinus

A
  • Pilonidal sinus is caused by the forceful insertion of hairs into the skin of the natal cleft in the sacrococcygeal area (ingrown hairs, 6cm above anus).
  • This promotes a chronic inflammatory reaction, causing an epithelialised sinus, may form secondary tracks and absesses.
  • Sinuses may be multiple and communicate via a deep cavity.
203
Q

Describe epidemiology of pilonidal sinus

A
  • 10:1 male to female ratio
  • More common in obese caucasians and patients who are from Asia, Middle east and the meditteranian
  • Common, mean age at presentation 20 years
  • Patients often hirsute
204
Q

Describe aetiology and risks of pilonidal sinus

A
  • Caused by hair in the natal cleft, more common in hirsute people
  • Increased risk depending on hair type, force of insertion, vulnerability of tissues to hair insertion
  • Multiple, loose stiff hairs within a deep narrow natal cleft with macerated or broken skin are theoretically most at risk
  • Family history
205
Q

List symptoms and signs of pilonidal disease

A
  • Sacrococcygeal discharge (offensive)
  • Sacrococcygeal pain and swelling (particularly sitting)
  • Sacrococcygeal sinus tracts
  • Skin maceration
  • Acutely increased natal cleft pain and swelling (where superinfection occurs - abscess)
  • Fever or toxaemia
206
Q

Describe investigations for pilonidal disease

A

Clinical diagnosis

207
Q

Describe management of pilonidal disease

A

If asymptomatic

  • Hair removal and local hygiene
  • Shaving/laser depilation

SYmptomatic no abscess

  • Surgery (off midline closure, asymmetric flap)
  • Antibiotic therapy (amoxicillin)
  • Hair removal

Symptomatic with abscess

  • Surgery (incision, drainage, healing by secondary intention)
  • Antibiotic (amoxicillin)
  • Pain relief (paracetamol/ibuprofen)

Recurrent disease - repeat

208
Q

List complications of pilonidal disease

A
  • Suppurative, post op collection deep to sutures (suture removal for drainage)
  • Necrotising fasciitis (urgent admission)
209
Q

Describe prognosis of pilonidal disease

A
  • Recurrence 6.9%
  • Less likely to occur if secondary intention rather than primary
  • Off midline closure has an advantage

Year 3 - Diseases (27 decks)

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