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Medicine Year 3 > Week 13 - GI/Liver > Flashcards

Week 13 - GI/Liver Flashcards

1
Q

What is seen on imaging in appendicitis?

A
  • Plain films not useful - can see stone, distended tubular structure
  • Fat stranding on CT- fat around organ more grey and streaky = oedema
  • US best for appendicitis in young + slim
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2
Q

What causes liver cysts? What is the most common liver cyst?

A
  • Usually developmental or degenerative in origin
  • Commonest = Von Meyenberg complex (= simple biliary hamartoma)
    • Important because can resemble metastases by naked eye at operation; often submitted for pathology including urgent intra-operative frozen section
    • No treatment required
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3
Q

Which mutations cause carcinoma of the pancreas?

A
  • Heterogenous tumours w/ wide range of mutations - no standard effective therapy
  • Most common mutations are v common generally e.g. KRAS, P53
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4
Q

What is the acute abdomen?

A

Acute/subacute onset of abdominal pain

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5
Q

What are the consequences of autoimmune gastritis?

A
  • Complete loss of parietal cells with pyloric and intestinal metaplasia
  • Achlorhydria -> bacterial overgrowth
  • Hypergastrinaemia -> endocrine cell hyperplasia /carcinoids
  • Persistent inflammation which can lead to epithelial dysplasia and may lead to cancer
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6
Q

Describe the medical management of ulcerative colitis

A
  • 5-ASA/Mesalazine:
    • Numerous preparations
      • Better tolerated than Sulphasalazine
    • 4.8g > 2.4g daily for induction of remission in moderate UC (ASCEND studies)
    • 2.4g maintenance (minimum 1.2g to ↓ CRC risk)
    • PO and topical > PO alone
    • Topical 5-ASA > topical steroids
  • Medical Escalation:
    • Azathioprine/6MP
      • With a severe relapse/frequently relapsing disease
      • Requiring two or more corticosteroid courses within a 12 month period
      • Those whose disease relapses as the dose of steroid is reduced below 15 mg
      • Relapse within 6 weeks of stopping corticosteroids
      • 20-30% intolerant, risks of lymphoma, NMSC, Ca
  • Biologics/surgery
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7
Q

What causes gastritis?

A
  • Acute
    • Alcohol
    • Medication e.g. NSAIDs
    • Severe trauma
    • Burns (Curling’s ulcers)
    • Surgery
  • Chronic
    • Autoimmune
    • Bacterial (H pylori)
    • Chemical
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8
Q

Describe the macroscopic and microscopic features of ulcerative colitis

A
  • Macroscopic features
    • Diffuse involvement of the lower GIT; terminal ileum can be involved but generally only in severe cases where the whole bowel including the caecum is involved (so-called ‘back-wash ileitis’)
  • Microscopic features
    • Crypt architectural changes are generally very marked
    • Little/no fibrosis
    • No granulomas
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9
Q

Describe the prognosis of colorectal carcinoma based on staging

A
  • Stage 1 (T1/2 N0 M0)
    • 91.7% 5 YS
    • 16% of cases
  • Stage 2 (T3/4 N0 M0)
    • 84.1% 5YS
    • 25% of cases
  • Stage 3 (T and N1/2 M0)
    • 64.9% 5YS
    • 26% of cases
  • Stage 4 (T any N1/2 M1)
    • 10% 5YS
    • 20% of cases
  • Unknown stage
    • 41% survival
    • 14% of cases

Staging dictates what management the patient will undergo e.g. adjuvant therapy in stage 3

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10
Q

Describe the guidelines for variceal bleeding

A
  • Primary prophylaxis - beta-blockers or band ligation
  • Acute bleeding
    • Antibiotics and Terlipressin (in A&E)
    • Banding first lie for oesophageal variceal bleeding
    • TIPS for uncontrolled variceal bleeding
    • Balloon tamponade (as temporary salvage)
  • Prevention of rebleeding
    • Beta-blocker and repeated band ligation
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11
Q

What is faecal calprotectin? How is it used clinically?

A
  • Protein produced in gut as result of any inflammatory process
  • High negative predictive value
  • Differentiate between functional and organic GI disorders in patients presenting w/ lower abd symptoms
  • Sensitive but non-specific, can be elevated due to any cause of underlying inflammation e.g. coeliac, NSAIDs, IBD or infection
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12
Q

Why is stress important in a GI history?

A

Stress can lead to functional GI diseases e.g. IBS

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13
Q

Describe the appearance of the GIT on plain abdominal film

A
  • Colon laterally, small bowel medially, stomach medial LUQ
  • Ascending and descending colon usually fixed, variable transverse and sigmoid
  • Colonic gas - round pockets, shows haustral contractions
  • Midline gas in pelvis = rectum
  • Stomach most superior and medial structure below L hemidiaphragm
  • No gas in small bowel - collapsed or full of fluid (not visible on plain film)
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14
Q

Where are AST/ALT found?

A
  • In liver - hepatocytes
  • Muscle (including cardiac) - check CK
    • E.g. compartment syndrome
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15
Q

Describe the features of pancreatic neuroendocrine tumours

A
  • Rare
  • May secret hormones (functional)
    • Glucagonomas/insulinomas
  • Commonest functional tumour is insulinoma which presents with hypoglycaemia
  • 90% of insulinomas are benign
  • Malignant endocrine tumours have much better prognosis than pancreatic carcinoma
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16
Q

List the types of liver neoplasms

A
  • Benign (5%)
    • Liver cell (hepatocyte) - hepatocellular adenoma
    • Bile duct - bile duct adenoma (rare)
    • Blood vessel - haemangioma
    • Non-liver tissue - N/A
  • Malignant
    • Liver cell (hepatocyte) - hepatocellular carcinoma (HCC)
    • Bile duct - cholangio-carcinoma
    • Blood vessel - angiosarcoma
    • Non-liver tissue - metastases
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17
Q

What are the risk factors for colorectal carcinomas?

A
  • Adenoma - size, number, villous
  • History of IBD (especially Ulcerative colitis patients)
  • Family History (e.g. Polyposis syndromes)
    • Familial adenomatous polyposis syndrome (associated with APC gene)
    • Lynch syndrome (previously called Hereditary Non-Polyposis Colorectal Carcinoma syndrome, HNPCC; associated with mismatch repair defects)
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18
Q

What imaging modalities are used in investigation of an acute abdomen?

A
  • Plain films
  • Ultrasound
  • CT
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19
Q

Describe the absorption of vitamin B12

A
  • Vitamin B12 ingested (meat, eggs, fish, milk)
  • B12 bound to salivary haptocorrin (transcobalamin I) which protects it from gastric acid
  • Haptocorrin is digested in duodenum and ‘free’ B12 then binds to intrinsic factor (IF) produced by gastric parietal cells
  • B12-IF complex then absorbed in terminal ileum
  • B12 then binds to transcobalamin II and is secreted into plasma and transported to liver and other tissues
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20
Q

Describe the pathogenesis of the clinical manifestations of chronic liver disease

A
  • Cirrhosis = higher resistance within liver, raised portal venous pressure
    • Hypersplenism (thrombocytopaenia)
  • Raised portal pressure leads to redistribution of blood and porto-systemic shunting
    • Porto-systemic shunting –> oesophago-gastric varices, encephalopathy (ammonia build up in the brain - liver can’t break down/bypasses)
  • Portosystemic shunting –> release of nitric oxide –> vasodilatation
  • Vasodilatation –> splanchnic vasodilatation (–> raised portal pressure), reduced effective circulating volume
    • Hyperdynamic circulation
  • Reduced effective circulating volume –> compensatory vasopressors (RAAS, catecholamines) –> sodium retention
    • Sodium retention = ascites
  • Reduced effective circulating volume –> compensatory vasopressors (RAAS, catecholamines) –> renal vasoconstriction
    • Renal vasoconstriction = hepato-renal syndrome
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21
Q

Describe the Glasgow Blatchford Score

A
  • Predicts need for intervention or death
  • Uses
    • Blood urea
    • Haemoglobin for men/women
    • Systolic blood pressure
    • Other markers - pulse > 100, melaena, syncope, hepatic disease, cardiac failure
  • GBS <1 identifies those at very low risk of poor outcome - can be discharged for out-patient endoscopy
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22
Q

Describe the immediate management of an upper GI bleed

A
  • Resuscitate
    • Pulse & BP
    • IV access for fluids/blood (check bloods, esp. Hb & urea)
    • Lie flat & give oxygen
  • Risk assessment & timing of endoscopy:
    • High risk: emergency endoscopy
      • Identified by clinical assessment - pulse/BP, age and comorbidities
    • Moderate risk: admit & next day endoscopy
    • Low risk: out-patient management?
  • Drug therapy and transfusion
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23
Q

Describe the histological appearance of Barrett’s mucosa

A
  • No dysplasia
  • Goblet cells imply intestinal differentiation
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24
Q

What are the complications of chronic hepatitis B?

A
  • Development of chronic liver disease in 25%
  • Cirrhosis
  • Decompensation
  • Hepatocellular Carcinoma (HCC)
  • Death
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25
Q

Describe management strategies for Crohn’s disease

A
  • Step-up approach - least to most aggressive treatment
  • Top-down approach - most to least
  1. 5-ASA or sulfasalazine
  2. Prednisone or budesonide
  3. Immunodulators (AZA or 6-MP or MTX)
  4. Biologic agents
  5. Surgery

Nutritional support throughout

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26
Q

How can inflammation in the liver manifest?

A
  • Acute inflammation = agent causes injury but is then removed
    • Days to weeks
      • N.B. “Fulminant” = severe acute, rapidly progressing towards liver failure
  • Chronic inflammation = agent causes injury and then persists
    • Months to years
    • Chronic liver disease = >6 months deranged LFTs
    • Chronic common in liver and may increase connective tissue (fibrosis)
  • “Acute-on-chronic”
    • Chronic liver disease often presents with acute exacerbation plus evidence of underlying chronicity e.g. fibrosis
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27
Q

Describe the transmission of HBV infection

A
  • Mother to baby - vertical transmission, usually at birth
  • Contaminated needles and syringes
  • Organs and tissue transplantation
  • Fluids (blood, semen)
  • Transfusion (blood, blood products)

Worldwide, most infections occur vertically at birth

In the UK, most new infections diagnosed in migrants infected elsewhere, moving into UK

New sexual infections in UK rare

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28
Q

What is the effect of inflammation on liver tissue?

A

Injurious agent causes cell damage and sometimes death, often with inflammatory cell infiltrate

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29
Q

What causes gastric cancer?

A

Strongly associated with chronic gastritis - H. Pylori or autoimmune

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30
Q

List the lab tests used in hepatitis B diagnosis

A
  • sAg - surface antigen - marker of infection
    • Produced by virus into blood - currently infected w/ Hep B
  • sAb - surface antibody - marker of immunity
    • Have had virus/vaccine and mounted an immune response - don’t currently have Hep B
  • cAb - core antibody
    • Made only if been infected with Hep B (vaccine doesn’t contain)
  • eAg - e antigen - suggests high infectivity
  • eAb - e antibody - suggests low infectivity
  • HBV DNA
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31
Q

How is hepatitis A transmitted?

A
  • Faeco-oral
  • Human reservoir - only host
  • Virus can survive for months in contaminated water
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32
Q

What are the criteria for pancreatitis diagnosis?

A
  • Clinical symptoms
  • Biochemistry
  • CT findings

In keeping with pancreatitis

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33
Q

How can liver disease be classified?

A
  • Clinical presentation
  • Histological pattern (of diffuse liver disease: morphology)
  • Specific cause
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34
Q

What are the potential causes of weight loss?

A
  • Malignancy
  • Thyrotoxicosis
  • Infection (TB)
  • Malabsorption
  • Eating disorders
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35
Q

Describe the histological consequences of chemical gastritis

A

Few inflammatory cells. Surface congestion oedema, elongation of gastric pits, tortuosity, reactive hyperplasia / atypia, ulceration

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36
Q

What are the causes of acute hepatitis?

A
  • Hepatitis viruses esp. A & E
  • Hepatitis viruses esp. B & C (& D)
  • Drug injury
  • Autoimmune liver disease
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37
Q

How is a patient with decompensated cirrhosis assessed/managed?

A

Decompensated cirrhosis bundle (first 24 hours)

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38
Q

How is chronic liver disease diagnosed?

A
  • Ultrasound (Cancer, Bile ducts, Blood vessels, Portal hypertension) +/- CT / MRCP
  • Liver ‘screen’
    • Chronic viral hepatitis : HBV, HCV
    • Autoimmune liver disease
      • ANA / SMA / LKM (AIH); AMA (PBC); Immunoglogulins (A –alcohol/NAFLD M – PBC G-AIH)
    • Metabolic liver disease
      • Ferritin (haemochromatosis); Caeruloplasmin (Wilson’s Disease); a1 anti-trypsin deficiency
        • Alpha 1 anti-trypsin deficiency - high in acute phase but low chronically
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39
Q

What is the cause of persistent symptoms in coeliac disease?

A
  • Non-compliant to gluten free diet
    • TTG stays positive with ongoing exposure - can be used as guide to non-compliance
  • Wrong diagnosis – look at differential again
    • Lymphocytic collitis
    • IBS + coeliac
    • T1DM – autonomic neuropathy
  • Refractory coeliac – rare
    • Steroids, chemo, biologics

Repeat OGD and biopsy - evidence of persistent villous atrophy suggests refractory coeliac

Potential for small bowel imaging (investigate possible enteropathy-associated T cell lymphoma)

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40
Q

How can cholecystitis be seen on imaging?

A
  • US best modality - identify stones which cause inflammation
    • Acoustic shadow indicates stones
    • Thickening of GB wall
    • Can identify which area is tender w/ US probe and see corresponding stone/inflammation
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41
Q

Where is GGT found/produced?

A
  • In liver - ALL
  • Alcohol/drug metabolism
  • Smoking can induce a rise in GGT
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42
Q

What are the causes of fatty liver disease (steatosis and steatohepatitis)?

A
  • Drug injury
  • Alcohol
  • Metabolic syndrome e.g. obesity
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43
Q

What would you ask in a patient presenting with PR bleeding?

A
  • Presenting complaint
    • Duration, character of blood, altered bowel habit
  • Systemic enquiry
    • Appetite, weight loss, symptoms of possible anaemia
  • Drug history
    • Any drugs which might cause bleeding e.g. Warfarin, NSAID
  • Family history
    • Colitis or colorectal neoplasia
  • Social history
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44
Q

Describe the transmission of hepatitis D

A
  • Transmission same as Hep B
  • Vertical Tm rare
  • Acquired by:
    • Co-infection with HBV
    • Super-infection of chronic HBV carriers
    • Increases risk of chronic liver disease
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45
Q

Describe the clinical approach to liver disease

A
  • History, symptoms and signs by examination
  • Investigations:
    • Blood tests: LFTs, haematology, viral and autoimmune serology, metabolic tests
    • Radiology: usu. at least ultrasound
  • Usually yields firm diagnosis without biopsy but at least should tell us
    • Diffuse liver disease?
    • Space-occupying lesion?
  • Try to avoid biopsy - complications
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46
Q

Give examples of causes of small bowel obstruction

A
  • Inguinal/obturator foramen hernia
  • Colon cancer - distal small bowel obstruction (caecum)
  • Gallstone ileus - inflamed gallbladder eroded into small bowel, stone moves into ileum and causes obstruction
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47
Q

What are the ‘red flags’ in a lower GI tract history?

A
  • Abd pain
    • Persistent, w/ anaemia, change in bowel habit
  • Blood in stool
  • Weight loss
  • Mass in abd
  • IDA
  • Anal lesions – ulcer, mass
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48
Q

How can the severity of chronic liver disease be assessed?

A

Childs-Turcotte-Pugh Score:

  • Encephalopathy
    • 1 - none
    • 2 - grade 1-2
    • 3 - grade 3-4
  • Ascites
    • 1 - none
    • 2 - slight
    • 3 - moderate
  • Bilirubin
    • 1 - <25
    • 2 - 25-50
    • 3 - >50
  • Albumin
    • 1 - >35
    • 2 - 28-35
    • 3 - <28
  • Prothrombin time prolongation
    • 1 - <4
    • 2 - 4-6
    • 3 - >6

Grade A (5-6) = mild

Grade B (7-9) = moderate

Grade C (10-15) = severe

  • Transplant/end of life care
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49
Q

When should surgery be considered in ulcerative colitis?

A
  • Stool frequency >8/day or >3 and CRP >45 on Day 3 predicts need for colectomy in 85%
  • Consider surgery or rescue medical Rx with Infliximab or Ciclosporin
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50
Q

What is Rigler’s sign?

A
  • Rigler’s sign - gas on both sides of bowel wall indicates pneumoperitoneum
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51
Q

How can a diagnosis of candida oesophagitis be confirmed?

A

PAS stain confirms spores and hyphae of candida albicans

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52
Q

Describe the dysplasia which can develop as a response to Barrett’s oesophagus

A
  • Dysplasia represents a spectrum of morphological changes
    • ‘Indefinite for dysplasia‘
    • Low grade dysplasia
    • High grade dysplasia
  • Dysplastic epithelium is architecturally and cytologically abnormal
  • Inflammation/reactive changes can mimic dysplasia
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53
Q

Describe the classification of the severity of coeliac

A

Marsh Classification

  • Marsh 0 - no change
  • Marsh 1 - increased no. of intra-epithelial lymphocytes
  • Marsh 2 - proliferation of the crypts of Leiberkuhn
  • Marsh 3a - partial villous atrophy
  • Marsh 3b - subtotal villous atrophy
  • Marsh 3c - total villous atrophy
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54
Q

Describe the histological appearance of the oesophageal lining in candida oesophagitis

A

Active chronic inflammation w/ many neutrophils, especially near luminal surface of epithelium

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55
Q

What steps have to be taken for a colorectal cancer specimen to be evaluated in the pathology department?

A
  • Specimen inspected, opened or incised if necessary for good fixation
  • Fixed specimen dissected, tissue samples selected
  • Processed for histology: embedded in paraffin wax
  • Sections cut and stained
  • Interpretation by pathologist
  • Report written, checked, authorised, issued
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56
Q

Describe the types of cholangiocarcinomas

A
  • Classified as intrahepatic / extrahepatic depending on origin
  • Intrahepatic cholangiocarcinoma needs to be distinguished from metastatic adenocarcinoma (which may have similar histology) and hepatocellular carcinoma
  • Extrahepatic cholangiocarcinoma has similar morphology and prognosis to pancreatic carcinoma. Treatment is currently Whipple’s operation to remove common bile duct and involved pancreas/duodenum. Trials likely to start looking at value of neoadjuvant therapy.
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57
Q

What is faecal elastase? How is it used clinically?

A
  • Elastase - pancreatic enzyme
  • Helps to break down connective tissue
  • Present in serum, urine, faeces
  • Doesn’t undergo significant degradation during intestinal transit - useful marker of pancreatic activity
  • Low faecal elastase (<500) indicates pancreatic exocrine insufficiency
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58
Q

What can be seen on plain abdominal film in inflammation of the large bowel?

A
  • Silhouette between gas and bowel wall irregular/lumpy
  • Abnormal haustrations - thickened, oedematous
  • Colonic wall thickening
  • Burnt out colitis - previous chronic inflammation, not currently actively inflamed
    • Hosepipe appearance - straightened, no haustrations
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59
Q

How can the common bile duct be investigated?

A
  • US
  • MRCP
  • Endoscopic US
  • Operative cholangiogram
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60
Q

Describe the anatomy of the biliary system

A
  • R and L hepatic ducts drain bile produced by liver
    • Join to form common hepatic duct
  • Cystic duct connects gallbladder to common hepatic duct, continue as common bile duct
  • Common bile duct + pancreatic duct –> hepatopancreatic ampulla of Vater, empty into the second part of the duodenum
  • Flow of bile/pancreatic fluid controlled by sphincter of Oddi - smooth muscle around ampulla
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61
Q

How long is the incubation period of hepatitis E?

A

40 days

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62
Q

Why is liver disease important?

A

5th most common cause of death in the UK

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63
Q

What causes acute cholestasis or cholestatic hepatitis?

A

Extrahepatic biliary obstruction

Drug injury e.g. antibiotics

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64
Q

List the causes of upper GI bleeding and how prevelant they are

A
  • Peptic ulcer 36%
    • Due to acid, H. Pylori, NSAIDs
  • Oesophagitis 24%
  • Gastritis 22%
  • Duodenitis 13%
  • Varices 11%
  • Malignancy 4%
  • Mallory-Weiss tear 4%
  • Other 3%
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65
Q

How can acute and chronic hepatitis be distinguished histologically?

A

Histological difference between acute and chronic hepatitis = fibrosis

Can be clinically but not histologically chronic

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66
Q

How can patients be protected against Hepatitis A infection?

A
  • Hepatitis A vaccine
    • Inactivated virus
    • 95% efficacy after 4 weeks
      • Immunity for 1 year
    • 2nd dose (booster) gives life protection
    • Pre-exposure
      • Travellers/homosexual men/IVDU/chronic liver disease patients
    • Post-exposure
      • Outbreak control
  • Hepatitis A immune globulin
    • Pooled immunoglobulin
    • Pre-exposure if
      • Vaccine allergic
      • <4 weeks to travel
      • Confers 3-6 months immunity
    • Post-exposure
      • Outbreak control
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67
Q

What are the risk factors for hepatitis C infection?

A
  • IDU (80% of heroin users exposed) includes cocaine / steroids
  • Iatrogenic: blood transfusion ( esp. pre 1991), unsterilised equipment (poorer resourced healthcare environments)
  • Sexual transmission:
    • Multiple partners / anal sex
    • Monogamous couple lower risk
  • Vertical transmission:
    • Approx. 3% rate
  • Needle-stick transmission
    • Approx. 5 - 10% rate

NO RISK FACTORS IN 5-10% OF PATIENTS

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68
Q

What is the significance of venous invasion of cancers?

A

Adverse prognostic feature

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69
Q

Describe the histology of acute cholestasis or cholestatic hepatitis

A

Brown bile (bilirubin) pigment +/- acute hepatitis

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70
Q

What causes acute pancreatitis?

A
  • 30% secondary to gallstones
    • Gallstone blocking ampulla of Vater - bile reflux into pancreatic duct
  • 50% secondary to alcohol abuse
  • 20% other causes including post ERCP (stretches ampulla, risk of backflow), hypercalcaemia, drugs (e.g. azathioprine), mumps
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71
Q

Describe the patterns of drug induced liver disease

A
  • Drugs can cause almost any pattern of liver disease
  • Therefore usually will be in differential diagnosis for cause, esp. acute hepatitis and acute cholestasis/cholestatic hepatitis
    • Most drug hepatotoxicity idiosyncratic (rare but usually single clinical pattern) thus difficult to investigate e.g. Augmentin (co-amoxiclav: may cause acute cholestatic hepatitis)
    • Occasional predictable liver damage e.g. paracetamol, methotrexate
    • Don’t forget non-prescribed drugs e.g. over internet or herbal
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72
Q

How is the severity of hepatic encephalopathy graded?

A

Conn Score (West Haven Classification) for Grading Mental State in hepatic encephalopathy:

  • Grade 0 - no personality or behavioural abnormality detected
  • Grade 1 - lack of awareness, euphoria or anxiety, shortened attention span, impaired performance of addition
  • Grade 2 - lethargy or apathy, minimal disorientation for time or place, subtle personality change, inappropriate behaviour, impaired performance of subtraction
  • Grade 3 - somnolence to semi-stupor, but responsive to verbal stimuli, confusion, gross disorientation
  • Grade 4 - coma (unresponsive to verbal or noxious stimuli)
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73
Q

Describe the lymphatic spread and treatment of head/neck cancers

A
  • Head and neck cancers may spread to LN in neck, usually ipsilateral
  • Radical neck dissection - 20 LN removed
  • No carcinoma cells identified in any of the removed LN - chemo/radiotherapy not given
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74
Q

How are structures seen on plain abdominal film?

A
  • Structures outlined by fat allows visualisation = silhouette sign (differences in densities outlines structures)
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75
Q

What are the risk factors for head/neck cancers?

A
  • Smoking and alcohol - not strictly causal
  • HPV in some cases - tonsil, oropharynx
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76
Q

How is coeliac diagnosed?

A
  • Serology
    • Coeliac specific markers
    • Blood film - Howell-Jolly bodes indicated functional hyposplenism
    • Iron, B12, folate, Mg, Ca - malabsorption
    • CRP, ESR - inflammation
    • TFTs, U+Es, LFTs, FBC - rule out differential, check organ function
  • Stool culture
    • Rule out infective gastroenteritis
    • Ask about travel history
  • Faecal elastase - rule out pancreatic insufficiency
  • Occult blood/Qfit test - blood in stool
    • Crohns/UC, malignancy
  • Calprotectin - non-specific marker for gut inflammation
  • CXR - exclude malignancy/TB
  • OGD and duodenal biopsy
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77
Q

What are the potential sites for upper GI bleeding?

A

Due to bleeding source from oesophagus, stomach or duodenum

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78
Q

How prevalent is the presentation of an acute abdomen?

A

5-10% ER attendances

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79
Q

Describe the use of blood products in UGI bleeding

A
  • Transfuse blood once Hb <7-8g/dL
  • Transfuse platelets if actively bleeding and platelet count <50x10^9/L
  • FFP if INR > 1.5
  • Prothrombin complex concentrate (PCC) if on warfarin and active bleeding
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80
Q

Describe the prevalence of Crohn’s disease

A
  • Smoking (2x commoner in smokers)
    • Stopping reduces relapse rate, need for immunosuppression and surgery
  • Female = Male
  • Peak incidence 15-25y
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81
Q

Describe the clinical features of hepatitis E

A
  • Similar to Hepatitis A plus rare reports of neurological effects
    • Diarrhoeal illness, hepatitis
  • Case-fatality rate: 1 - 3%, higher in Pregnant women for some genotypes (genotype 1)
  • Treatment: Supportive
  • No Vaccine
  • Chronic Hep E is seen in very immunosuppressed patients, e.g. bone marrow transplants. Treatment with Ribavirin
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82
Q

Which imaging modalities are used to see inflammation in the abdomen?

A
  • AXR useful for colitis
  • AXR signs not specific in other inflammatory conditions
  • US for cholecystitis (and appendicitis if young and slim)
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83
Q

What does the eAg indicate about HBV infection?

A
  • eAg +ve (early disease)
    • High Viral Load
    • High risk of CLD and HCC
    • Highly infectious
  • eAg –ve (late disease)
    • Low viral load
    • Lower risk of CLD and HCC
    • Less infectious
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84
Q

What guidelines are available for management of upper GI bleeding?

A
  • UK (NICE) guidelines 2012
  • European guidelines 2015
  • Asia-Pacific guidelines 2018
  • UK (BSG) varices guidelines 2015
  • European varices guidelines 2015
  • USA varices guidelines 2017
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85
Q

Describe the risk of colorectal cancer in ulcerative colitis

A
  • 5 years - 1%
  • 10 years - 5%
  • 30 years - 20%

Depends on extent, inflammation, pseudopolyps and FH

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86
Q

Describe the features of diffuse gastric cancer

A
  • Individual malignant cells with mucin vacuoles (‘signet ring’ cells)
  • May invade extensively without being endoscopically obvious, so called linitis plastica (‘leather bottle stomach’)
  • Weaker link with gastritis.
  • Metastasis to ovaries (‘Krukenberg tumour’)
  • Supraclavicular lymph node (‘Virchow’s node’)
  • ‘Sister Joseph’s nodule’ (umbilical metastasis)
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87
Q

How is an acute abdomen diagnosed?

A
  • Careful clinical assessment paramount
    • History
    • Physical examination
    • Blood workup
    • Then think imaging
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88
Q

What are the signs/symptoms of carcinoma of the pancreas?

A
  • Painless obstructive jaundice
    • Painless more worrying than painful - bile duct can’t contract against obstruction, more worrying than painful jaundice
  • New onset diabetes
  • Abdominal pain due to pancreatic insufficiency or nerve invasion.
  • Tumours in head may obstruct pancreatic duct and bile duct – “double duct sign” on radiology
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89
Q

How can H. Pylori infection be identified histologically?

A

Cresyl violet stain

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90
Q

List the most common types colorectal cancers

A
  • Not all malignant intestinal tumours are adenocarcinomas, but majority are
  • Other epithelial tumours are found less frequently
    • E.g. Neuroendocrine neoplasms, squamous cell carcinoma, metastatic carcinoma, adenosquamous carcinoma
  • Non-epithelial tumours can also be encountered
    • E.g. Gastro intestinal stromal tumours (GISTs), melanoma and lymphomas may all occur as primary tumours arising in small or large intestines
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91
Q

Describe the surgical management of Crohn’s disease

A
  • 70% lifetime risk of surgery
    • LyRIC trial suggests outcomes = biologics
  • Recurrence common (50% further surgery)
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92
Q

Describe the prevalence of hepatitis B

A
  • 300 million carriers worldwide
  • 2 million deaths per year
  • Vaccine preventable since 1981
    • HBV vaccination included in immunisation schedule in most countries
  • 0.3% UK population (180,000) infected
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93
Q

What are colorectal polyps?

A
  • Polyp = exophytic protuberant growth
  • Example of bowel polyps include
    • Hamartomatous polyps
    • Inflammatory polyps
    • Hyperplastic polyps
    • Adenomas
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94
Q

What are the causes of painless jaundice?

A
  • Pre-hepatic
    • Haemolytic causes – malaria, haemolytic anaemia etc.
    • Gilbert’s syndrome
  • Intrahepatic
    • Hepatitis – viral, AI, drug-induced
    • Alcoholic liver disease
    • Wilson’s disease, haemochromatosis
    • Hepatocellular carcinoma
    • Iatrogenic – medication
    • Primary biliary cirrhosis (young men), primary sclerosing cholangitis (older women w/ RA)
  • Post-hepatic
    • Gallstones
    • Pancreatic tumours
    • Abd lymphoma
    • Cholangiocarcinoma
    • Drug induced
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95
Q

Describe the diagnosis of AI hepatitis

A
  • Transaminases + immunoglobulins raised, negative for viral hepatitis, high titres for circulating autoantibodies (>1:40)
  • Do liver biopsy to confirm – serious complications if undiagnosed/untreated
    • Unless serious co-morbidity or contraindication
  • Interface hepatitis - inflammation of hepatocytes at junction of portal tract and hepatic parenchymal - is typical
  • Grade of inflammation and stage of fibrosis in liver biopsy are described using validated pathological index
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96
Q

Describe the clinical features of hepatitis A

A
  • Incubation period ≈30 days
  • Age is main determinant of severity
    • Mostly asymptomatic in children < 5 yrs
    • Mortality rate 1.5% if > 50 year
  • No specific treatments
  • Maintain hydration, avoid alcohol
  • Usually self-limiting illness
  • No role for Vaccine or IgG as treatment
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97
Q

Describe the clinical spectrum of alcoholic liver disease

A
  • Malaise
  • Nausea
  • Itch
  • Hepatomegaly
  • Fever
  • Jaundice
  • Sepsis
  • Encephalopathy
    • Liver failure
  • Ascites
  • Renal failure
  • Death

From incidental –> clinical

Steatosis/hepatitis –> cirrhosis

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98
Q

What risk scores are used for upper GI bleeding?

A
  • Endoscopic
    • Rockall
  • Clinical
    • ‘Admission’ Rockall
    • Glasgow Blatchford
    • AIMS 65
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99
Q

What is the model for end-stage liver disease?

A
  • Model for End-Stage Liver Disease (MELD) originally used for post-TIPSS prognosis.
  • Now used to allocate donor organs in USA for liver transplant.
  • Adjusted formula with Sodium (low = bad) used in UK

‘Mild’: <10 ‘Moderate’: 10-15 ‘Severe’: >15

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100
Q

How can progression of Barrett’s oesophagus be prevented?

A
  • Role of surveillance / screening controversial
    • Four biopsies (aka Seattle Protocol) every 2cm effective at finding dysplasia, but laborious
    • Targeted biopsy may eventually replace it with improvements in endoscopy
  • Endoscopic treatments may avoid need for radical surgery
    • Radiofrequency ablation - reduced cancer risk
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101
Q

What is hepatic encephalopathy?

A

Hepatic encephalopathy is a disease caused by the failure of the cirrhotic liver to remove toxins (nitrogenous - ammonia) from the blood, which ultimately negatively affects the brains function

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102
Q

Describe metastatic liver tumours

A
  • Most common form of liver tumour
  • From colon, rectum, pancreas, stomach, oesophagus, breast, lung, melanoma etc.
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103
Q

When should a patient with IBD be admitted to hospital?

A

Stools >6/day and systemic upset

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104
Q

Describe fat necrosis happen in acute pancreatitis

A
  • E.g. omentum
  • Autodigestions of tissue by pancreatic enzymes
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105
Q

How long is the incubation period of hepatitis C?

A

Average 6-7 weeks

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106
Q

Describe the macroscopic findings seen in Crohn’s disease

A
  • Small bowel stricture
  • Cobblestone like intestinal surface
  • Fissure
  • Thickened wall
  • Fat wrapping
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107
Q

How does acute pancreatitis present?

A
  • Severe upper abdominal pain
  • Fever
  • Leukocytosis
  • Raised serum amylase
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108
Q

Describe the treatment of Crohn’s disease

A
  • 5-ASA/Masalazine
    • Cochrane review - no benefit vs placebo for inducing remission or response in active SB Crohn’s
    • May be a role in post-operative prophylaxis and prevention of CRC
  • Thiopurines
    • Azathioprine and 6-Mercaptopurine
      • Induction of remission - no benefit vs placebo
      • Maintenance Rx - OR 2.32, NNT = 6
  • Methotrexate
    • Induction
      • 25mg/wk IM 16/52
      • 39.4% remission vs 19.1% placebo
    • Maintenance
      • 15mg/wk IM
      • ?PO
  • Biologics
    • TNF alpha anatagonists
      • Infliximab/adalimumab (biosimilars)
    • Anti-integrins (alpha4beta7)
      • Vedolizumab
    • Anti-il12/23
      • Ustekinumab
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109
Q

Describe the histological appearance of acute hepatitis

A
  • Diffuse hepatocyte injury seen as swelling
  • Some cell death described as spotty necrosis
  • Inflammatory cell infiltrate in all areas - portal tracts, interface and parenchyma
  • Higher power can see dying hepatocytes (called acidophil bodies) and plasma cells prominent in the inflammatory cells
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110
Q

Define cirrhosis

A
  • = End-stage liver disease
  • Definition is three-fold:
    • Diffuse process with
    • Fibrosis &
    • Nodule formation
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111
Q

Describe the features of clinically relevant alcoholic hepatitis

A
  • Essential Features
    • Excess alcohol within 2 months
    • Bilirubin > 80mmol/l for less than 2 months
    • Exclusion of other liver disease
    • Treatment of Sepsis/ GI Bleeding
    • AST < 500 (AST: ALT ratio >1.5)
  • Characteristic Features
    • Hepatomegaly ± fever ± leucocytosis ± hepatic bruit
  • SHORT-TERM MORTALITY AS HIGH AS 60%
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112
Q

What specific points would you look for when examining a patient presenting with PR bleeding?

A

Any signs of anaemia (general pallor, conjunctiva, palmar creases, tongue, nails

Abdomen - any palpable masses? Is the liver palpable? Any evidence of malnutrition?

Digital rectal examination.

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113
Q

How is portal fibrosis viewed histologically?

A

Masson stain

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114
Q

How does the ileocaecal valve determine how colonic obstruction will present?

A
  • Colonic obstruction - ileocaecal valve open, gas fills small bowel
  • If ileocaecal valve not open caecum will distend
  • Longer obstruction before presentation
    • Abdominal pain and constipation, maybe vomiting because small bowel distended
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115
Q

Describe the structure and function of the oesophagus

A
  • Food + saliva from pharynx to stomach
  • 4 layers
    • Mucosa - non-keratinising stratified squamous
      • Muscularis mucosae
    • Submucosa
    • Muscularis propria
    • Adventitia
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116
Q

What causes chronic biliary/cholestatic disease?

A
  • Primary biliary cholangitis (PBC)
  • Primary sclerosing cholangitis (PSC)
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117
Q

Describe the features of hepatocellular carcinomas

A
  • Most common primary liver tumour
  • Usually arises in cirrhosis and associated with elevated serum AFP (alpha feto-protein)
  • Screening available
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118
Q

How can NAFLD and ALD be distinguished based on:

  1. Weight
  2. Fasting plasma glucose/HbA1c
  3. Reported daily alcohol intake
  4. ALT
  5. AST
  6. ALT:AST ratio
  7. GGT
  8. Triglycerides
  9. HDL cholesteriol
  10. Mean corpuscular volume?
A
  • Weight
    • NAFLD - elevated
    • ALD - variable
  • Fasting plasma glucose or HbA1c
    • NAFLD - often elevated
    • ALD - usually normal
  • Reported daily alcohol intake
    • NAFLD - <20g female and <30g male
    • ALD - >20g female and >30g male
  • ALT
    • NAFLD - elevated or normal
    • ALD - elevated or normal
  • AST
    • NAFLD - normal
    • ALD - elevated
  • AST/ALT ratio
    • NAFLD - <0.8 (>0.8 more advanced disease)
    • ALD - >1.5
  • GGT
    • NAFLD - elevated or normal
    • ALD - markedly elevated
  • Triglycerides
    • NAFLD - elevated
    • ALD - variable, may be markedly elevated
  • HDL cholesterol
    • NAFLD - low
    • ALD - elevated
  • Mean corpuscular volume
    • NAFLD - normal
    • ALD - elevated
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119
Q

How can acute hepatitis C infection progress?

A
  • Newly infected (acute) - 25% symptomatic
    • Chronic infection 70%
    • Clear infection 30%
  • Chronic infection
    • Cirrhosis 25%
    • HCC 1-5%
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120
Q

What information can a pathologist provide about resected colorectal cancers?

A
  • Confirmation of the diagnosis
  • Evaluation of whether complete resection had been achieved (margins)
  • Quality of surgery
    • Complete excision
    • Number of lymph nodes in specimen
  • Evaluation of response by the carcinoma to chemotherapy
  • Pathological staging and other prognostic information
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121
Q

What are the aims of investigation in diffuse liver disease?

A
  • Establish diagnosis in terms of pattern (morphology) of disease
  • Establish cause, if possible
  • If appropriate, establish grade of disease (severity = activity of inflammation)
  • If chronic liver disease, establish stage (severity of fibrosis i.e. how far towards cirrhosis)
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122
Q

How can GI perforations be imaged?

A
  • CXR sensitive for free gas (80% sensitive down to few mls of free gas)
  • AXR less so - can be very subtle
  • CT to confirm and look for cause
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123
Q

Describe the prognosis of carcinoma of the pancreas

A
  • I in 8 patients alive I year after diagnosis
  • 5 year survival is only 7 %
  • No change in 5 year survival expectancy in past 40 years
  • Predicted to be 3rd most common cause of cancer deaths by 2030
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124
Q

Describe the prevalence of upper GI bleeding in the UK

A
  • 1993 4%
  • 2007 8%
  • Due to rise in - alcohol, hepatitis C and non-alcoholic fatty liver disease
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125
Q

What pathologies can affect the oesophagus?

A
  • Infections
    • Candida albicans (fungus)
    • Herpes simplex virus
  • Inflammation – chemicals
    • Peptic oesophagitis / GORD: reflux of acid, bile
    • Caustics: lye (NaOH, caustic soda)
    • Pills: iron, bisphosphonates, tetracyclines, etc
      • If not swallowed properly can irritate oesophageal lining
  • Diverticula, achalasia, Schatzki ring, systemic sclerosis, hiatus hernia etc.
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126
Q

Describe the sensitivity of imaging modalities in the diagnosis of Crohn’s disease

A
  • MRI - 90.5%
  • CT - 95.2%
  • SBE/Ba M&FT - 74-82%
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127
Q

Where is alkaline phosphatase found?

A
  • In liver - canaliculi
  • Bone e.g. growing, pregnancy, bone disorders e.g. Paget’s, bone mets
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128
Q

How does the age at time of infection of hepatitis B effect the outcome?

A
  • Age at the time of infection determines:
    • Severity of acute illness
    • Risk of Chronic HBV Infection (CHB)
  • Infection at birth/young child is usually asymptomatic but leads to chronic infection
  • Infection as an adults is usually symptomatic but is cleared
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129
Q

What are the symptoms of hepatocellular carcinoma?

A
  • Weight loss, abdo pain, fever
  • Cachexia
  • Mass in abdomen
  • Bloody ascites
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130
Q

What are the components of gallstones?

A
  • Can be pure - cholesterol or bile pigment
  • Most are mixed
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131
Q

How is the severity of ulcerative colitis classified?

A

Truelove and Witts classification of severity of UC

  • Number of bloody stools per day
    • Mild - <4
    • Moderate - 4-6
    • Severe - >6
  • Temperature
    • Mild - afebrile
    • Moderate - intermediate
    • Severe - >37.8
  • Heart rate (bpm)
    • Mild - normal
    • Moderate - intermediate
    • Severe - >90
  • Haemoglobin (g/dl)
    • Mild - >11
    • Moderate 10-5-11
    • Severe - <10.5
  • ESR (mm/h)
    • Mild - <20
    • Moderate - 20-30
    • Severe - >30
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132
Q

Describe the histological appearance and LFTs which would be seen in massive necrosis of the liver. What could cause this?

A
  • E.g. due to paracetamol overdose
  • AST/ALT very high e.g. 8000
  • More severe - confluent necrosis (spotty necrosis joined - more severe impact on liver function, AST/ALT high - release transaminases when they die)
133
Q

Describe the prevalence of AI hepatitis

A
  • 10-17/100,000 in Europe
  • F:M 3:1
  • Young more commonly affected, but can be any age group
  • 30-50% have other AI disease
134
Q

Describe the stages of ALD vs NAFLD

A

ALD:

Alcoholic steatosis –> alcoholic hepatitis –> alcoholic cirrhosis

NAFLD:

Steatosis –> NASH –> NAFLD cirrhosis

135
Q

Describe the appearance of colon distention on plain abdominal film

A
  • Loss of haustral folds
  • Irregular margin
  • Mucosal thumb printing = colitis
  • Abnormal haustrations - thickened, oedematous = diffuse colitis
136
Q

What is included in an AI panel for liver disease?

A
  • ANA, AMA, ASMA, LKM
  • Immunoglobulins
137
Q

Describe the prevalence of hepatitis E

A
  • More common than Hep A in the UK
    • Risk increasing - used to be only due to travel, now majority are catching it within UK
138
Q

How can GI ischaemia be viewed on imaging?

A
  • AXR usually non-specific
  • Positive signs usually mean advanced ischaemia
    • E.g. gas in wall
  • CT first choice test but <60% sensitive
139
Q

How is acute liver disease diagnosed?

A
  • HISTORY AND EXAMINATION (Timing/Alcohol/Meds/Family/BMI)
    • Medication - new, OTC, herbal, recreational
  • ACUTE LIVER INJURY (days /weeks)
    • Ultrasound (Cancer, Bile ducts, Blood vessels)
    • Acute viral hepatitis
    • HAV, HBV, (HCV), HEV, CMV, EBV (other infections)
    • Autoimmune liver disease
    • ANA / SMA / LKM (AIH); Immunoglobulins
    • Paracetamol levels
140
Q

What are the differential diagnoses of pancreatic cysts?

A
  • Intraductal papillary mucinous neoplasm – in continuity with main pancreatic duct or side branch duct, dysplastic papillary lining secreting mucin
    • Dysplasia can progress to pancreatic cancer
    • Enlarge >3cm consider operating
  • Mucinous cystic neoplasm – mucinous lining, “ovarian-type” stroma (in women)
  • Serous cystadenoma – no mucin production; (almost always) benign
141
Q

Describe the transmission of hepatitis E

A
  • Faeco-oral
  • Pork products
  • Minimal person-to-person transmission
142
Q

What are the causes of acute cholestasis or cholestatic hepatitis?

A
  • Hepatitis viruses esp. A & E
  • Hepatitis viruses esp. B & C (& D)
  • Drug injury
  • Autoimmune liver disease
  • Extrahepatic biliary obstruction
143
Q

List the commonest types of oesophageal cancer and the risks associated with each

A
  • Squamous carcinoma associated with smoking and drinking
  • Adenocarcinoma associated with gastro-oesophageal reflux (GORD) and obesity
144
Q

What is seen on CT in cholecystitis?

A

CT often done when don’t suspect cholecystitis

  • Stones (60-70% sensitivity)
  • Oedema - fat stranding, wall thickening
  • Gas within wall = ischaemia
145
Q

What is the target of inflammation in the liver?

A
  • Liver injury often mainly to parenchyma (hepatocytes); but bile ducts or rarely blood vessels can be the main target
  • Parenchyma, bile ducts, blood vessels and connective tissue are inter-dependent, so damage to one damages the others
146
Q

Describe the prevalence of carcinoma of the cancer

A
  • 5% of cancer deaths
  • 66% in head of pancreas
  • Ductal adenocarcinoma most common subtype
147
Q

How are oesophageal varices treated?

A
  • Endoscopic banding TIPS or B-blocker drugs
148
Q

How can NAFLD be reversed?

A

Reduction of body weight >10% esp. if this takes them under BMI 25 - reversal of changes completely or to some extent

149
Q

What are the potential complications of coeliac disease?

A
  • If non-compliant to gluten-free diet - risk of small bowel enteropathy-associated T cell lymphoma (even if gluten doesn’t give symptoms/symptoms are mild)
  • Osteoporosis
  • IDA
  • Functional hyposplenism (indicated by Howell-Jolly bodies on blood film)
    • Need vaccinations
150
Q

How is uncontrolled variceal bleeding controlled?

A
  • Sengstaken tube
  • TIPS useful ‘rescue’ procedure for failed endoscopy and drug therapy
    • High mortality
  • Surgical shunt/transection (very rarely used)
151
Q

Describe the histological appearance of the lining of the oesophagus in reflux oesophagitis and what are the clinical/pathological consequences

A
  • Acid and digestive enzymes injure squamous epithelium lining oesophagus
  • Increased no. of inflammatory cells, basal zone of squamous epithelium is hyperplastic
  • Ulceration/oesophagitis - stricture formation, dysphagia can be presenting feature
152
Q

Which areas have a high prevalence of hepatitis A?

A
  • Africa
  • Asia
  • Middle East
  • South America
  • Greenland

In UK mostly acquire outside of UK and return with infection - incidence increasing

153
Q

How is pancreatic cancer imaged?

A

CT - chest/abd/pelvis

Gives staging information

154
Q

What is the most common cause of colonic obstruction?

A

Undiagnosed cancer

155
Q

Which tests indicate liver function?

A
  • Not reflected by degree of abnormality of transaminases (AST or ALT)
  • ‘Function’ indicated by:
    • ALBUMIN
    • BILIRUBIN
    • PROTHROMBIN TIME
    • Liver Failure (High Bil/PT and Encephalopathy = <25% function)
156
Q

How does a pathologist tell the difference between UC and Crohn’s?

A

Clues in the:

  1. Distribution of inflammation
  2. Type of inflammation
  3. Clinical context/scope findings

Other things we need to know:

  • If the patient has established diagnosis of CIBD then what type/how long for?
  • Is the patient on treatment?
  • Have the patient’s symptoms worsened recently?
157
Q

What is the cause of gas density outside the abdomen/pelvis on plain abdominal film?

A

Herniation - inguinoscrotal

158
Q

What are the ‘red flags’ in an upper GI history?

A
  • Dysphagia
  • Haematemesis
  • Lymphadenopathy – Virchow’s
  • Loss of appetite
  • Unintentional weight loss
  • Dyspepsia
    • >55 y/o, treatment resistant
    • Raised platelets
  • Jaundice
  • IDA
159
Q

What is autoimmune hepatitis? What are the consequences of untreated AI hepatitis?

A

Chronic inflammatory disease of liver (–> cirrhosis, liver failure, death)

160
Q

What are the causes of chronic biliary/cholestatic disease?

A
  • Extrahepatic biliary obstruction
  • Chronic biliary disease e.g. PBC
  • Genetic/deposition e.g. haemochromatosis, Wilson’s
161
Q

How is choledocholithiasis treated?

A
  • ERCP
  • Lap cholecystectomy and bile duct imaging/clearance
    • Likely to have more stones in GB
162
Q

Describe the prevalence of ischaemic colitis

A
  • Increasing incidence (x4)
    • Elderly, CV disease, heart failure
163
Q

How is hepatitis C diagnosed?

A
  • Mostly asymptomatic
  • Most diagnosed by screening of high risk groups
    • Drug users
    • Immigrants to UK from high prevalence countries
  • Anti HCV IgG positive = chronic infection or cleared infection
  • PCR or Antigen positive = current infection / viraemia
164
Q

How does oral cancer classically present?

A
  • Ulcer which will not heal
  • Ulcer which persists without definite, identifiable cause - think cancer
165
Q

How is acute hepatitis B treated?

A
  • No treatment. Usually resolves and clears
  • Acute rarely go into liver failure - need transplant
166
Q

When is Whipple’s resection used? How effective is it?

A
  • Only for tumours of head of pancreas
  • Only about 10% of these patients suitable for operation
  • 75% incompletely excised
  • Average life expectancy following operation 20 months
167
Q

What is the main aim of the management of chronic hepatitis?

A

Trying to avoid progression to cirrhosis is main aim of diagnosing and treating chronic hepatitis

168
Q

How is chronic hepatitis B treated?

A
  • Most do not require treatment
    • Only 1/4 to 1/4 are treated
  • Only treat those with liver inflammation (LFT or Biopsy) or fibrosis (on Fibroscan or Biopsy)
  • Aim of treatment is NOT to cure
  • Aim is to suppress viral replication and prevent further liver damage
  • Two different types of treatment:
    • Immuno-modulatory - Interferon
    • Suppress viral replication – Tenofovir or Entecavir
169
Q

Describe the types of colorectal adenomas

A
  • All colorectal adenomas are dysplastic by defintion
    • Adenomatous dysplasia can be either
      • High grade
      • Low grade
    • Architecture of adenoma can be
      • Villous
      • Tubulovillous
      • Tubular
170
Q

Can hepatitis C infection be prevented?

A
  • No vaccine, no post exposure prophylaxis
  • No reliable immunity after infection
171
Q

What do these lab results indicate?

HBV sAg - positive

Anti-HBV core IgG - positive

Anti-HB core IgM - positive

A
  • Currently infected with Hep B - surface antigen positive
  • Recently acquired infection - IgM acute
  • Likely to clear virus within 6 months
172
Q

Describe the normal structure of the bowel wall

A
  • Mucosa
    • Simple columnar epithelium
    • Lamina propria - supporting scaffold of connective tissue containing a few inflammatory cells
    • Regular arrangement of glands
    • Muscularis mucosae
  • Submucosa
  • Muscularis
  • Sub-serous
173
Q

Describe the prevalence of NAFLD

A

Western populations, prevalence 20-30%, 90% in morbidly obese

174
Q

Describe the presentation of R colon cancer

A

Anaemia, weight loss, obstruction

175
Q

How is gastric cancer morphologically classified?

A

Via Lauren classification into intestinal or diffuse types

176
Q

What are the options for management of gallstones?

A
  • Conservative
    • E.g. if unsuitable for surgery
    • Avoid fatty foods - less CCK + contraction of GB
  • Operative
    • Keyhole surgery, 1 in 20 need open surgery
    • 1 in 100 risk of bile leak
    • Damage to bile duct, need further surgery to fix (1 in 1000)
177
Q

List the normal components of the liver

A
  • Vasculature
    • Incoming portal vein and hepatic artery
    • Outgoing hepatic vein
  • Parenchymal liver cells
  • Biliary system
  • Connective tissue matrix
  • All arranged as portal tracts and parenchyma
178
Q

Describe the appearance of ischaemia on imaging

A
  • Linear gas in GIT wall
  • Unusual gaseous appearance - be suspicious of ischaemia
  • Stage before ischaemia
    • Does bowel enhance normally?
    • Blurry looking thick walled bowel
  • Stenosis of vessels e.g. splanchnic
179
Q

What is Chilaiditi syndrome?

A
  • Gas where it shouldn’t be
  • Colon in abnormal position (usually below liver) - between liver and hemidiaphragm
  • Presents w/ acute abdominal pain
180
Q

How are the APRI/FIB-4 scores calculated?

A

APRI = ((AST level/AST (upper limit of normal))/platelet count) x 100

FIB-4 = (age (years) x AST (U/L))/(platelet count (10^9/L) x root ALT (U/L))

181
Q

Compare the pathology of Crohn’s vs UC

A
  • Crohn’s:
    • Small and Large bowel inflammation
    • Tends to involve proximal large bowel
    • Patchy inflammation resulting in macroscopic ‘skip lesions’
    • Transmural, deeply ulcerating inflammation
    • Granulomas
    • Peri-anal disease e.g. fistulas / sinus tracts
  • Ulcerative Colitis:
    • Large bowel inflammation only
    • Tends to extend from rectum to involve left side of bowel
    • Confluent, diffuse inflammation
    • Inflammation centred on mucosa
182
Q

How long is the incubation period of acute hepatitis B?

A
  • Incubation 2-6 months
183
Q

Are acute vs chronic hepatitis usually symptomatic?

A
  • Acute Hepatitis
    • Usually symptomatic
  • Chronic hepatitis
    • Hepatitis virus present for more than 6 months. Usually asymptomatic by this stage
184
Q

Describe palliative treatment of pancreatic cancer

A
  • Creon - pancreatic enzymes in capsule
  • Prognosis - months
  • Stent at ERCP for jaundice (resolve blockage of liver)
  • Brushings to confirm diagnosis if chemotherapy being considered dependant on performance status
185
Q

Describe the appearance an aneurysm on imaging

A
  • Plain abdominal film
    • Calcific density in curved area medially = aneurysm
    • Psoas muscles hard to see - burst aneurysm
  • CT
    • Burst aneurysm - haemorrhage obscuring psoas muscle
    • Don’t need contrast to see
    • Wall more dense - about to burst
186
Q

How can early detection of colorectal cancer be improved?

A
  • Bowel Cancer Screening Programme
    • qFIT testing of >50-74 year olds in Scotland every 2y (+ve –> colonoscopy)
  • Patient education of symptoms
    • PR bleeding
    • Change in bowel habit
187
Q

Describe the used of IV PPIs in upper GI bleeding

A
  • Not beneficial prior to endoscopy
  • Reduced rebleeding and mortality if given post-endoscopy to the high risk patients who required endoscopic therapy
188
Q

What kind of virus is hepatitis B?

A

DNA virus

189
Q

What is caecum volvulus?

A
  • Misplacement of caecum
  • Caecum twists, becomes ischaemic
  • Blocks bowel and blood supply (obstruction and ischaemia)
190
Q

Where is bilirubin found/produced (conjugated/unconjugated)?

A
  • In liver - hepatocytes conjugate bilirubin, excreted in bile
  • Unconjugated bilirubin from haem (haemolysis)
191
Q

How should patients on antiplatelets/anticoagulants be managed following a GI bleed?

A
  • Aspirin and NSAIDs
    • Continue low dose aspirin after UGI bleeding once haemostasis achieved (+ add PPI)
    • Stop NSAIDs
  • Clopidogrel, warfarin and DOACs
    • Once haemostasis achieved, assess risks vs benefits but generally aim to restart these medications as mortality high from CVD
192
Q

Describe the management of acute variceal bleeding

A
  • Resuscitation
    • Restore circulating volume
    • Transfuse once Hb<7 g/dL
    • Consider airway protection
  • Diagnosis
    • Endoscopy
  • Therapy
    • Antibiotics early
    • Vasopressors (Terlipressin) early
    • Endoscopic band ligation
    • ….rescue TIPS
      • Trans-jugular intrahepatic stent shunt
193
Q

What are the standard liver function tests?

A
  • Bilirubin; Aspartate Aminotransferase (AST);
  • Alanine Aminotransferase (ALT);
  • Gamma Glutamyl transferase (GGT);
    • Parenchymal
  • Alkaline Phosphatase (ALP);
    • Bile duct cells
  • Albumin
194
Q

Why can LFTs be difficult to interpret?

A
  • Advanced cirrhosis may have normal blood tests
    • Can’t produce enough for high results
  • Some proteins / enzymes not isolated to liver
195
Q

Describe the mutations which cause colorectal cancer

A

Progressive acquisition of mutations, actual sequence probably less important than the accumulation of effects

  1. Loss/mutation in tumour suppressor genes like APC (adenomatous polyposis Coli) and TP53 (p53 can stall cell cycle at checkpoints to allow for DNA repair or initiate apoptosis). Due to point mutations or chromosomal deletions but increasing awareness of the importance of hypermethylation of promoter regions as mechanism for transcriptional silencing of tumour suppression genes
  2. Activation of oncogenes e.g. RAS genes with mutated Ras proteins leading to persistent cell signalling and drive cell proliferation
  3. Defective DNA repair e.g. mismatch repair genes such as MSH2 and MSH6 can be mutated in Lynch syndrome or can be silenced through promoter methylation
196
Q

Describe the use of infliximab in ulcerative colitis

A
  • Monoclonal antibody to TNF-alpha
  • 14/24 avoided colectomy after a single dose IFX 5mg/kg vs 7/21 placebo
    • Sub-group analysis suggested more effective in patients with partial response treated at days 5-7
197
Q

What are haemangiomas and hepatic adenomas? Why are they important?

A
  • Importance because of differential diagnosis with metastases
    • Haemangioma
      • Benign blood vessel tumour
      • Biopsy avoided because of risk of bleeding
    • Hepatic adenoma
      • Rare
      • Mainly young women, often associated with hormonal therapy
      • Risk of bleeding and rupture so excision if large
198
Q

What treatments are available in colorectal cancer?

A
  • Loco-regional treatments
    • Surgery - still a mainstay of colorectal cancer treatment - site dependent
      • Right hemi-colectomy
      • Excision of ascending / transverse / descending / sigmoid depending on tumour location
      • Anterior or abdomino-perineal resection* of rectal cancers
  • A colostomy may be needed temporarily or permanently. AP resection will mean a permanent colostomy
  • Chemotherapy (neo-adjuvant or adjuvant)
  • Radiotherapy
199
Q

Describe the histology of hepatitis B

A
  • Hepatitis B pathology may look like acute hepatitis plus fibrosis
  • Specific feature of hepatitis B virus = ground glass cytoplasm in hepatocytes
    • Accumulation of surface antigen - one of three main HB viral antigens
200
Q

Describe the pathogenesis of gastritis and peptic ulceration due to H. Pylori infection

A
  • H. pylori colonises gastric mucosa causing active chronic inflammation; IL-8 from epithelial cells attracts neutrophils
  • After exposure to H pylori the resulting gastritis can occur in 2 patterns
    • Antral-predominant gastritis -> hypergastrinaemia and duodenal ulceration
    • Pangastritis -> hypochlorhydria, multifocal atrophic gastritis, intestinal metaplasia, cancer
  • Microbe-host interface is thought to be the reason 2 patterns emerge; patients with higher IL-8 production tend to get pangastritis, lower IL-8 levels are associated with antral gastritis
  • Peptic ulceration isn’t solely due to ‘too much’ acid, again host/microbe interface is important
    • Impaired mucosal defense (due to NSAID interfering with mucosal prostaglandin synthesis; bile reflux)
    • Microbe factors (CagA + variants associated with more severe inflammation)
201
Q

Define megacolon vs toxic megacolon

A
  • Megacolon
    • Diameter >5.5cm or caecum >9cm
  • Toxic megacolon
    • Megacolon and signs of systemic toxicity
    • Emergent colectomy
202
Q

Compare the features of compensated and decompensated cirrhosis

A
  • Compensated
    • Liver biopsy/fibroscan
    • Might have clinical signs of liver disease/portal HTN
    • NO features of decompensation (but risk of)
  • Decompensation
    • Jaundice (on background of cirrhosis)
    • Ascites
    • Spontaneous bacterial peritonitis
    • Encephalopathy
    • Bleeding varices
    • Hepatocellular cancer
    • Deteriorating synthetic function
    • High Bil/low Alb/high PT
203
Q

What can cause high serum amylase with an acute abdomen?

A
  • Perforation in duodenum and pancreatic/bile fluid leaks
  • Embolic/thrombotic event, loss of barrier in gut, bile/pancreatic fluid absorbed systemically
  • Acute pancreatitis - produces highest serum amylase
204
Q

Which countries have a high prevalence of hepatitis C?

A

Egypt, Middle Eastern countries

205
Q

What are the most common causes of abnormal LFTs?

A
  • FATTY LIVER
    • Alcoholic Liver Disease
    • Non-alcoholic Fatty Liver Disease (NAFLD)
  • CHRONIC VIRAL HEPATITIS
    • Chronic Hepatitis C
  • AUTOIMMUNE LIVER DISEASE
    • Primary Biliary Cholangitis
    • Autoimmune Hepatitis
  • HAEMOCHROMATOSIS
  • DRUGS
206
Q

How can the progression of fibrosis in liver disease be predicted?

A

Limiting plate inflammation used to predict progression of liver disease in terms of fibrosis - more active/aggressive treatment

207
Q

When is imaging used in the diagnosis of pancreatitis?

A
  • CT shows pancreatitis - oedema, fat stranding
  • Don’t do CT unless patient is deteriorating on standard treatment (fluids, analgesia) - check if pancreas is necrotic/ischaemic
208
Q

Describe steroid treatment in ulcerative colitis

A
  • High dose IV corticosteroids such as methylprednisolone 60mg daily or hydrocortisone 100mg 6-hourly
209
Q

What non-invasive tests can be done to determine liver fibrosis? How are the results interpreted?

A
  • Fibroscan:
    • Shear wave velocity measures liver ‘stiffness’ = extent of fibrosis
      • Cirrhosis >12.5kPa
      • Portal hypertension >20kPa
  • Blood based assessment of liver fibrosis
    • Fibroscans not always available e.g. in GP
    • APRI, FIB-4 and NAFLD fibrosis score
  • Commercially available blood tests
    • Enhanced liver fibrosis test (ELF)
      • Hyaluronic acid - produce more in liver fibrosis
    • Fibrotest
210
Q

What are the consequences of hepatitis A infection?

A
  • Virus shed via biliary tree into gut
  • No chronic carriage
  • Good immunity after infection or vaccination
    • Most people in high prevalence countries will catch as children, have mild illness then be immune for life
    • In other countries need immunity from vaccination
211
Q

What does gas in the rectum indicate in bowel obstruction?

A

Not completely obstructed

212
Q

How is ascites managed?

A
  • No added salt diet
  • Diuretics
    • Spironolactone (blocks ALDOSTERONE)
      • Start 100mg/day. Max effect 3days. Max dose 400mg/day (divided doses)
      • Side-effects e.g. gynaecomastia, hyperkalaemia, hyponatraemia, impotence
    • Frusemide (Furosemide) (LOOP DIURETIC)
      • Max 160mg/day (divided doses)
      • Side-effects e.g. hyponatraemia
  • Paracentesis
  • Transjugular intrahepatic portosystemic shunt (TIPSS)
  • Liver transplant
  • SBP Prophylaxis (secondary)
  • Aim for weight loss of 0.5-1 kg/day.
  • Monitor renal function and electrolytes
213
Q

Describe Rutgeerts Score and its clinical implications

A

i0 = No lesions

i1 ≤ 5 aphthous lesions (A)

i2 > 5 aphthous lesions with normal mucosa between the lesions (B)

i3 Diffuse aphthous ileitis (C)

i4 Diffuse inflammation with larger ulcers, and/or narrowing (D)

Clinical recurrence at 3 years

A - 5%

B - 15-20%

C - 40%

D - 90%

214
Q

How can the bile ducts be imaged?

A
  • CT - hard to see stones
  • MCRP - MRI weighted so bile shows up white w/ black stones (90% sensitivity)
  • Endoscopic ultrasound - gold standard, can see small stones missed by other imaging
  • Ultrasound (40-60% sensitivity)
215
Q

Why can polyps result in glandular tissue within the GI wall?

A
  • Gland displacement due to pressure from peristalsis - neoplastic epithelium down stalk into GI wall
  • Clues to gland displacement/pseudoinvasion as opposed to true invasion
    • Presence of haemorrhage and/or haemosiderin (old haemorrhage)
    • Lack of desmoplastic cancer stroma
    • Location in sigmoid colon
216
Q

What is autoimmune gastritis?

A

Autoimmune destruction of parietal cells due to auto-antibodies against intrinsic factor and parietal cell antibodies in blood

217
Q

What are the risks for high mortality in alcoholic hepatitis?

A
  • GAHS >9
  • Non-responders to steroids - 50% in hospital mortality
  • Continuing to drink is biggest risk
218
Q

How is hepatitis D treated?

A
  • Treatment with Peg IFN only
  • Drugs against Hep B e.g. Tenofovir useless
219
Q

What are the risk factors for carcinoma of the pancreas?

A

Germline mutations (e.g. BRCA) account for small proportion of patients, but SMOKING is by far biggest risk factor

220
Q

What is the upper limit of normal distention in the colon?

A

7/8cm

221
Q

How can the exposure of a plain abdominal film be identified?

A

Psoas muscles outlined by fat = silhouette sign (differences in densities outline structures)

Ability to see psoas muscles indicates good exposure

222
Q

How is UC monitored for risk of colorectal cancer?

A
  • Screening colonoscopy at 10 years (preferably in remission, pancolonic dye-spray)
  • Lower risk
    • Extensive colitis with NO ACTIVE endoscopic/histological inflammation
    • OR left sided colitis
    • OR Crohn’s colitis of <50% colon
    • Repeat every 5 years
  • Intermediate risk
    • Extensive colitis with mild active endoscopic/histological inflammation
    • OR post-inflammatory polyps
    • OR family history CRC in FDR aged 50+
    • Repeat every 3 years
  • Higher risk
    • Extensive colitis with moderate/severe active endoscopic/histological inflammation
    • OR stricture in past 5 years
    • OR dysplasia in past 5 years declining surgery
    • OR PSC/transplant for PSC
    • OR family history CRC in FDR aged <50
    • Repeat in 1 year
223
Q

What do these lab results indicate?

HBV sAg negative

Anti-HBV sAb positive

Anti-HB core IgG negative

Anti-HB core IgM negative

Anti-HAV IgM positive

A
  • Has been vaccinated against hepatitis B - sAb positive
  • Acute infection Hepatitis A - anti-HAV IgM positive
224
Q

Describe the structure and function of the small bowel

A
  • Approximately 3-7m in length
    • Duodenum (26cm)
    • Jejunum (3.5m)
    • Ileum (1.5m)
  • Major site of digestion/absorption
  • Absorbs approx. 6 litres of fluid daily (+ fat/protein/electrolytes)
225
Q

Describe the symptoms of bowel obstruction

A

Distal obstruction = constipation, distention

Proximal obstruction = vomiting

226
Q

What are the causes of hepatic vascular injury?

A
  • Drug injury
  • Vascular disease e.g. venous obstruction
227
Q

Describe the prevalence of hepatitis C

A
  • 0.7% of Scottish population infected, 30% unaware
  • 300,000 die from HCV per year worldwide
228
Q

Describe the use of natalizumab in Crohn’s disease

A
  • Effective
  • Patient died in open-label study from PML secondary to JC virus
  • Still used in Rx of MS but not Crohn’s
229
Q

Describe the neurological manifestations of Hepatitis E

A
  • May be GT 3 associated
  • 5% patients affected in one series
    • Guillain Barre syndrome
    • Encephalitis
    • Ataxia
    • Myopathy
230
Q

What makes bile lithogenic (stone forming)?

A
  • Bile becomes lithogenic for cholesterol if there is excessive secretion of cholesterol or decreased secretion of bile salts
  • Excessive secretion of bilirubin (e.g. haemolytic anaemia) can cause its precipitation in concentrated bile in the gallbladder
231
Q

How can obstruction of the colon due to a tumour be decompressed?

A

Contrast enema to place metallic stent through obstructing colon tumour to allow gas to decompress, followed by surgery to resect colon

232
Q

How can hepatitis B be prevented?

A
  • Education (safe sex, injecting etc)
  • Immunisation
    • HBV sAg Vaccine
      • All newborn in UK from Autumn 2017 – 3 doses
      • At risk groups
  • Prevention of Mother to Child Transmission
  1. HBV vaccination to newborn – 6 doses in first year
  2. HBV Immunoglobulin if eAg + or high VL
  3. Tenofovir during the last trimester if high Viral Load
233
Q

How does a pancreatic abscess form secondary to acute pancreatitis? How is it managed?

A
  • Potential complications of acute pancreatitis
  • Infected pancreatic necrosis
  • Avascular haemorrhagic pancreas good culture medium
  • Drainage or necrosectomy plus antibiotics
234
Q

How is Crohn’s disease diagnosed?

A
  • Faecal calprotectin
  • MR or CT enterography/enteroclysis
  • Ileocolonoscopy and Bx
  • Capsule endoscopy/enteroscopy
235
Q

What do these lab results indicate?

HBV sAg - positive

Anti-HBc IgG - positive

Anti-HBc IgM - negative

HBV eAg - positive

A
  • Is infected with Hep B - surface antigen +ve
  • Not an acute infection - IgM -ve
  • eAg - highly infectious, high risk of developing liver cirrhosis/cancer
236
Q

Describe the investigations/treatment of ischaemic colitis

A
  • CT may show segmental colitis in watershed areas
  • Treatment usually conservative
    • IV fluids +/- antibiotics
237
Q

Describe the montreal classification of IBD

A
  • Montreal L category
    • L1 - terminal ileum
    • L2 - colon
    • L3 - ileocolon
    • L4 - upper GI tract
    • L4 + L3 - upper GI tract and distal disease
  • Montreal B category
    • B1 - without stricutre formation, non-penetrating
    • B2 - stricturing
    • B3 - penetrating
    • B3p - perianally penetrating
238
Q

Describe the endoscopy timing in upper GI bleeding

A
  • Most patients: endoscope within 24 hrs (even at weekend)
  • Very low risk (GBS≤1): can be discharged for out-patient endoscopy
  • Very high risk (haemodynamic instability or severe ongoing bleeding): emergency endoscopy
239
Q

What are the risk factors for severe Crohn’s disease?

A
  • Young onset
  • Smoking
  • Perianal disease
  • Stricturing SB disease
240
Q

Describe the Rockall Score for upper GI bleeding

A
  • Predicts mortality
    • Age
    • Shock
    • Comorbidity
    • Stigmata of recent haemorrhage
    • Diagnosis
241
Q

How is hepatitis A diagnosed?

A
  • Acute Hep A - IgM positive or HAV RNA in blood or stool
  • Previous Hep A or vaccinated - IgG positive
242
Q

What are the common causative agents of infective gastroenteritis?

A
  • Salmonella
  • Campylobacter
  • Shigella
243
Q

Describe the gross appearance of carcinoma of the pancreas

A
  • Normal - lobulated, cream/yellow
  • Carcinoma
    • Whiter, loss of lobulation
    • Strong fibrotic reaction around cancer
244
Q

How is hepatitis C transmitted?

A
  • Injecting drugs
  • Transfusion + Transplant
  • Sexual/vertical rare
245
Q

How is chronic HBV diagnosed using lab results?

A

HBV infection is diagnosed if sAg or DNA are detectable

246
Q

Describe the appearance of diverticuli on imaging

A
  • CT
    • Outpouching on side of bowel
    • Whole bowel thickened, extensive oedema and fat stranding
    • Can lead to abscess in wall of mucosa - perforation = peritonitis
247
Q

Describe the components of bile

A
  • Bile is 97% water and 500mls is secreted by liver daily
  • Cholesterol secreted in bile is not water soluble and is kept in solution by micelles containing bile acids and phospholipid
  • Colour of bile is caused by the bile pigment, bilirubin which is a breakdown product of haemoglobin
248
Q

How can ascites be investigated?

A

Diagnostic tap

  • Cell count
    • >500 WBC/ cm3 and/ or >250 neutrophils/cm3 suggest spontaneous bacterial peritonitis (SBP)
    • Inflammatory conditions also increase WBC count
    • Lymphocytosis - TB or peritoneal carcinomatosis
  • Albumin
    • Serum ascites albumin gradient (SAAG) = serum albumin MINUS ascitic albumin g/l
      • LOW PROTEIN ASCITES (SAAG >11g/l) = portal hypertension
  • SBP diagnosed in 20% cirrhotics admitted to hospital, and 2-3% attending for outpatient paracentesis
    • Ascitic fluid should be cultured
249
Q

What causes IBD?

A
  • Environmental factors
  • Genetic predisposition
  • Gut microbiota
  • Host immune response (innate/adaptive)
250
Q

What are the causes of chronic hepatitis?

A
  • Hepatitis viruses esp. B & C (& D)
  • Autoimmune liver disease
  • Genetic/deposition e.g. haemochromatosis, Wilson’s
251
Q

What is Barrett’s oesophagus?

A
  • Metaplastic response to mucosal injury e.g. from long term GORD
  • Squamous epithelium becomes glandular, usually intestinal w/ goblet cells
  • Associated w/ development of benign strictures, but also adenocarcinoma
252
Q

Give examples of the causes of calcification outside of the kidney in the abdomen

A
  • Calcified lymph node secondary to TB
  • Calcification in faecal material
  • Appendicitis
  • Porcelain GB (increased risk of cancer)
253
Q

Describe the increasing burden of alcoholic liver disease

A
  • 41% increase in discharges with alcoholic liver disease 1997/8 to 2002/3
  • 236% increase in alcohol-related deaths 1980 - 2002
  • Alcohol related deaths decrease as alcohol affordability decreases
    • 60 fewer deaths per year, 1000s fewer admissions - not yet evaluated
  • Minimum unit pricing - reduction in alcohol intake
254
Q

How can hepatic encephalopathy be avoided when managing a patient with chronic liver disease?

A
  • Avoid regular sedation
  • Caution with opiates
  • Avoid hyponatraemia
  • Non-absorbable disaccharides (i.e. lactulose)
    • Aim for 2-3 soft stool/day
  • Non (minimally)-absorbably antibiotics
    • Gut ‘decontamination’ reduces urease and protease activity
255
Q

List the functions of the liver

A
  • Filtration of blood from GI tract
    • Metabolism/ detox of toxins / medications
    • Production of bile (excretion / digestion – fat/fat soluble vit)
  • Storage – Glycogen / proteins / vitamins / metals
  • Synthesis
    • Proteins / Carbohydrates / Fats
    • Clotting factors
  • Immune system (makes CRP, has APCs)
    • End stage liver disease - CRP may not rise as you would expect

LIVER FUNCTION NOT THE SAME AS ABN LFTs

256
Q

What kind of virus is hepatitis C?

A
  • RNA virus
  • Multiple genotypes
257
Q

Describe (neo)adjuvant therapy in carcinomas of the pancreas

A
  • Folfirinox chemotherapy associated with (limited) improvement in metastatic disease
  • Early data suggests that neoadjuvant therapy improves margin status and may be associated with longer survival
258
Q

Which areas are high risk for hepatitis B infection?

A

Africa, the Western Pacific, South East Asia, the Indian sub-continent and the Eastern Mediterranean

259
Q

Where is albumin found/produced?

A
  • Hepatocyte synthesis (low is abnormal)
  • Low in infection/inflammation/renal loss
    • Acute phase protein
260
Q

Describe the features of low and high grade dysplasia from Barrett’s oesophagus

A
  • Dysplastic epithelium is architecturally and cytologically abnormal
    • Low grade
      • Cells polarised
      • Nuclei stratified
    • High grade
      • Polarity lost
      • Nuclei rounder, vesicular
      • Prominent nucleoli
      • Abnormal mitoses
      • Necrosis
261
Q

How does upper GI bleeding present?

A
  • Major acute medical emergency
  • Presents w/
    • Haematemesis - coffee ground
    • Vomiting
    • Malena
262
Q

Describe the Glasgow Alcoholic Hepatitis Score

A
  • Age
    • <50 - score 1
    • >50 - score 2
  • WCC (10^9/l)
    • <15 - score 1
    • >15 - score 2
  • Urea (mmol/l)
    • <5 - score 1
    • >5 - score 2
  • PT ratio/INR
    • <1.5 - score 1
    • 1.5-2.0 - score 2
    • >2.0 - score 3
  • Bilirubin (mmol/l)
    • <125 - score 1
    • 125-250 - score 2
    • >250 - score 3
263
Q

Which part of the stomach is mostly affected by chemical gastritis?

A

Seen more commonly in antrum than corpus

264
Q

What are the histological features of gastric cancer?

A

Background atrophic mucosa, chronic inflammation, intestinal metaplasia, dysplasia

265
Q

What lab results indicate HBV infection?

A

HBV infection is diagnosed if sAg or DNA are detectable

266
Q

What are the risks of mortality/rebleeding following an upper GI bleed?

A
  • Mortality 10%
  • Rebleeding 13%
267
Q

Describe the treatment of autoimmune hepatitis

A
  • Treatment – immunosuppressant glucocorticoids +/- azathioprine
    • Remission can be achieved in up to 60-80% of case and long-term immunosuppression often required
268
Q

How is a OGD and duodenal biopsy carried out in the investigation of coeliac disease?

A
  • Gluten rich diet for 4-6 weeks before
  • Take 4 biopsies from distal duodenum for maximal yield as changes may be patchy
269
Q

Describe the classification of focal/space occupying liver lesions

A
  • Neoplastic
    • Benign
    • Malignant
  • Non-neoplastic
    • Developmental/degenerative e.g. cysts
    • Inflammatoy e.g. abscess
      • More common w/ instrumentation/infection e.g. streptococcus
270
Q

What is sigmoid volvulus?

A
  • Coffee bean appearance
  • Doesn’t tend to cause obstructive symptoms, more abdominal distention and pain
  • Sigmoid twists around mesentery
271
Q

Describe the appearance of a small bowel obstruction on plain abdominal film

A
  • Minimal colon gas
    • High grade - no gas
    • Incomplete SBO - some colon gas
272
Q

List the signs of chronic liver disease and/or portal hypertension

A
  • Chronic
    • Spider naevi
    • Palmar erythema
    • Loss of male hair pattern
    • Gynaecomastia - altered oestrogen metabolism
    • Foetor
    • Sarcopenia - breakdown of muscle, can’t rely on liver glycogen store
    • Bruising (PT/Plt)
    • Scratching (itch)
  • Portal Hypertension
    • Caput medusa
    • Hypersplenism
      • Thrombocytopaenia (Pancytopaenia)
  • Decompensation
    • Jaundice
    • Hepatic flap
    • Ascites
    • Peripheral oedema
273
Q

What are the risks associated with Barrett’s oesophagus?

A
  • Dysplasia can progress to carcinoma over years
  • Males > Females. Increasing.
  • Cancer risk ~ 0.4% per annum in BE
  • Definite LGD or HGD: increased risk but progression to cancer still slow, but pathologists do not always agree. LGD agreed by 3 pathologists nearly same cancer risk as HGD
274
Q

Describe the histological appearance of herpes simplex infection in the oesophageal lining

A
  • Atypical squamous cells
  • Inflammatory exudate and cells (‘slough’)
275
Q

What can the consequences of colonic wall thickening be?

A

Bowel wall splitting - ischaemia/perforation

276
Q

Describe the mortality associated with variceal bleeding

A

30-40%

277
Q

What dermatological symptom can indicate coeliac disease?

A

Herpetiformis dermatitis - rash on extensor surfaces

278
Q

Where is non-keratinising stratified squamous epithelium found?

A

Oral cavity, oesophagus, larynx, cervix, vagina

279
Q

List the broad categories of causes of injury to the liver

A
  • Drugs or toxins incl. alcohol
  • Abnormal nutrition/metabolism
  • Infection
  • Obstruction to bile or blood flow
  • Autoimmune liver disease
  • Genetic/deposition disease
  • Neoplasia
  • Others
280
Q

List the pathological changes which occur in acute/chronic IBD

A
  • Acute changes:
    • Acute inflammation (plasma cells, lymphocytes, neutrophils)
    • Ulceration
    • Loss of Goblet cells
    • Crypt abscess formation
  • Chronic changes:
    • Architectural changes
    • Paneth cell metaplasia
    • Chronic inflammatory infiltrates in lamina propria
    • Neuronal hyperplasia
    • Fibrosis
281
Q

Describe the prevalence of gallstones

A

1 in 10 of population

282
Q

Give examples of genetic/deposition liver diseases

A
  • Haemochromatosis (iron)
    • Excess iron is shown by (blue) Perl’s stain: normally no blue stain present
    • Most common genetic liver disease in Scotland
  • Wilson’s disease (copper)
  • Alpha-1-antitrypsin deficiency
283
Q

Describe the features of a carcinoma of the ampulla of Vater

A
  • Presents when smaller than carcinoma of pancreas
  • May arise from pre-existing adenoma
  • 25% 5 year survival following Whipples’ resection
284
Q

How are bowel obstructions viewed on imaging?

A
  • AXR useful
  • Look for
    • Small and/or large bowel dilatation?
    • How much gas in colon?
    • Any gas in rectum?
    • Any complications - ischaemia, perforation?
  • CT to look for cause
285
Q

Describe the histological staging of fatty liver disease

A
  • Macrovesicular steatosis with lipid vacuole filling the hepatocyte cytoplasm.
  • Steatohepatitis: neutrophils and lymphocytes surrounding hepatocytes with Mallory hyaline.
  • Pericellular fibrosis as well as bands of fibrous tracts between portal tracts.
286
Q

How can acute hepatitis and acute cholestatic hepatitis be distinguished?

A

Both inflammation affecting parenchymal cells but acute bile stasis more marked in cholestasis/cholestatic hepatitis

287
Q

How can gallstones be diagnosed on imaging?

A
  • Most by ultrasound
  • 10% have sufficient calcium to be seen on plain X-rays
288
Q

Why not just CT every patient presenting with an acute abdomen?

A
  • RADIATION DOSE
    • CXR 0.02 mSv
    • AXR 0.5 mSv
    • CT abdomen/pelvis 6-10mSv
  • 10 mSv = 1:1000 life time risk of fatal cancer (for adult age 30-39)
  • 5 times increase in this risk for given dose at age 20 years compared to 80 years
  • “COINCIDENTALOMAS”
    • Up to 25% in >70’s
    • Some need further investigation but are not relevant to original presentation
289
Q

What are the aims of management of diffuse liver disease?

A
  • Management aims to reduce symptoms, reduce inflammation and prevent or slow progression of fibrosis
  • Treatment may include:
    • Specific treatment against cause e.g. removal of alcohol or drug, weight loss, optimal diabetic control, specific antivirals or immunosuppression, and/or…
    • Supportive treatment e.g. for severe acute hepatitis or for cirrhosis in general
290
Q

What are the complications of UC?

A
  • Local complications
    • Haemorrhage
    • Toxic dilation (aka toxic megacolon)
  • Systemic complications
    • Skin - erythema nodosum, pyoderma gangrenosum
    • Liver - sclerosing cholangitis, cholangiocarcinoma
    • Eyes - iritis, uveitis, episcleritis
    • Ankylosing spondylitis
  • Malignancy
291
Q

Describe the histology of chronic biliary/cholestatic disease

A

Histology: Focal, portal-predominant inflammation and fibrosis with bile duct injury; granulomas in PBC

292
Q

What kind of virus is hepatitis A?

A
  • RNA virus
293
Q

Describe the presentation of infective colitis

A
  • Short history of diarrhoea +/- vomiting
  • Abrupt onset +/- resolution of symptoms
  • Systemic upset and fevers prominent
  • Travel
  • Unwell contacts
  • Immunocompromised
294
Q

Describe the histological stages of liver fibrosis

A
  • 0 = none
  • 1 = mild
    • Portal fibrosis
  • 2 = moderate
    • Portal fibrosis with septa
  • 3 = severe
    • Bridging fibrosis
    • Focal, diffuse or marked
  • 4 = cirrhosis
295
Q

What can be tested in the laboratory diagnosis of viral hepatitis?

A
  • Detection of specific immune response (IgM or IgG)
    • IgM - new infection, recently acquired
    • IgG - later infection, previous infection (months after)
  • Viral nucleic acid detection (RNA or DNA) or antigen detection (HBV and HCV)
    • Blood or stool
296
Q

How is severe colitis investigated?

A
  • Abdominal X-ray - helps assess disease extent and severity
  • Endoscopy?
    • Flexible sigmoidoscopy > colonoscopy
    • BSG guidelines suggest
      • Within 72 hours (ideally 24 hours)
      • Pathology within 5/7
297
Q

List the signs/symptoms of Crohn’s disease

A
  • Features
    • Abdominal pain (if central think small bowel)
    • Diarrhoea (watery > bloody)
    • Weight loss
    • Fistulae, abscesses, oropharyngeal, gastroduodenal
  • Extra-intestinal symptoms
    • Eyes (episcleritis, uveitis)
    • Joints (sacroiliitis, inflammatory arthropathy)
    • Skin (erythema nodosum)
298
Q

Describe the features of carcinoma of the pancreas

A
  • Perineural invasion
    • Hard to clear
  • Pre-malignant PanIN asymptomatic
    • Present late
299
Q

What imaging results suggest Crohn’s disease?

A
  • CT/MRI - terminal ileal thickening/changes
    • Enterography/enteroclysis
  • Activity
  • Extraluminal detail - collection, fistulae
300
Q

List the classification of liver disease by specific causes

A
  • Hepatitis viruses esp A & E - acute
  • Hepatitis viruses esp B & C (& D) – acute/chronic
  • Drug injury
  • Autoimmune liver disease
  • Extrahepatic biliary obstruction
  • Alcohol
  • Metabolic syndrome e.g. obesity
  • Chronic biliary disease e.g. PBC
  • Vascular disease e.g. venous obstruction
  • Genetic/deposition e.g. haemochromatosis
301
Q

What are the common precipitating factors for hepatic encephalopathy? What effect do they have?

A
  • GI bleeding
  • Infections
  • Constipation
  • Renal and electrolyte imbalance
  • Excess dietary (esp. animal) protein
  • Medications
    • Psychoactive
  • Deterioration of liver function

Lead to -

  • Reduction of hepatic or cerebral function
  • Stimulation of an inflammatory response
  • Increasing ammonia levels
302
Q

What are the potential causes of an acute abdomen?

A
  • Something has/is
    • Burst
    • Blocked
    • Inflamed
    • Lost its blood supply
  • One or combination
  • Or nothing to do with abdomen
    • Myocardial infarction
    • Pneumonia
303
Q

What are the consequences of peptic ulceration?

A
  • Haemorrhage
  • Perforation
  • Fibrosis (leading to stenosis)
304
Q

What is the relevancy of a family history including AI disease?

A

Raises possibility of other AI diseases e.g. thyroid, Addison’s, coeliac etc.

305
Q

What are the causes of acute hepatitis?

A
  • Infections
    • Hepatitis A, B, C, D, E
    • EBV, CMV, toxoplasmosis
    • Leptospirosis (water borne)
    • Q fever
    • Syphilis
    • Malaria
  • Toxins
  • Drugs
  • Alcohol
  • Autoimmune
  • Wilsons
  • Haemochromatosis
306
Q

What endoscopic therapy can be used in an upper GI bleed?

A
  • Adrenaline injection
  • Heater probe
  • Endoscopic clips
  • Haemostatic powders
  • (thrombin, laser)
307
Q

Describe the appearance of the bladder on plain abdominal film

A

Usually can’t see unless enlarged

308
Q

Describe the staging of colorectal carcinomas

A

T1 - invasion into submucosa

T2 - invasion intro, but not through, muscularis propria

T3 - invasion through muscularis propria, into subserosa or non-peritonealised pericolic/perirectal tissue

T4 - invasion of visceral peritoneum (T4a) and/or other organs (T4b)

N0 - no regional LN mets

N1 - 1-3 regional LN mets

N2 - 4+ regional LN mets

M0 - no distant mets

M1 - distant mets

309
Q

Describe the prevalence of oral cancers

A
  • Oral cancer rates increasing
  • Rarer in young people but keep open mind
310
Q

Describe the classification of diffuse liver disease by histological pattern

A
  • Acute hepatitis
  • Acute cholestasis or cholestatic hepatitis
  • Fatty liver disease (steatosis and steatohepatitis)
  • Chronic hepatitis
  • Chronic biliary/cholestatic disease
  • Genetic/deposition disease
  • Hepatic vascular disease
311
Q

What kind of virus is hepatitis D?

A
  • Single strand RNA virus
  • Requires HBV to replicate
312
Q

Describe the investigation/treatment of infective colitis

A
  • Stool Cx/CDT
    • Need 4 for 90% sensitivity
  • Treatment usually conservative if immunocompetent
    • Even if bacterial gastroenteritis confirmed (e.g. Campylobacter)
313
Q

Describe the features of carcinomas of the gallbladder

A
  • Rare
  • Gallstones present in 80% of cases
  • Adenocarcinoma
  • Dismal prognosis unless found incidentally in a gallbladder removed for chronic cholecystitis
  • Local infiltration may make gallbladder seem abnormally stuck down at theatre
314
Q

How can serology aid the diagnosis of coeliac?

A
  • TTG/anti-endomysial antibodies
    • TTG more sensitive, anti-endomysial antibodies more specific
  • Immunoglobulins?
    • Selective IgA deficiency in 2-5% of coeliac disease which can lead to false negative test
  • HLA DQ2/8 + in 95% in coeliac
    • Sensitive but non-specific, useful in difficult cases
315
Q

Why do polyps develop with long stalks?

A

Over a long period of time waves of peristalsis repeatedly attempt to expel the polyp, and eventually drags out a lengthy stalk. Pressures in the sigmoid colon are high, and the polyp may be significantly traumatised, with bleeding into its stalk.

316
Q

What blood tests would you do in PR bleeding?

A
  • FBC, platelets
  • U&Es
  • LFTs - liver metastases?
317
Q

Describe the appearance of pneumoperitoneum on plain film imaging

A
  • Crescent of lucency below hemidiaphragm
  • If see structure of diaphragm - gas between it and stomach
318
Q

Which diseases are associated with NAFLD?

A

Main associations are Obesity, Type 2 diabetes and hyperlipidaemia

319
Q

Describe the appearance of gas in the large vs small bowel on plain abdominal film

A
  • Mottled appearance - mixture of gas and faeces in colon
  • Small bowel - continuous gas, no haustrations, centrally placed, cross hatching
320
Q

How is hepatitis C treated?

A
  • Direct Acting Antiviral (DAAs) inhibit different stages of the replication cycle
  • Cure rates of >95% with 8 – 12 weeks of oral treatment
  • DAA regimen is decided according to Genotype and degree of fibrosis / cirrhosis
  • DAAs are often dispensed from Community pharmacies with methadone on daily observed basis
  • Cost of DAAs is falling rapidly and many are Pan-Genotypic
  • Will probably be GP led treatment within 5-10 years
321
Q

What factors are related to the progression of hepatitic C?

A
  • Male sex
  • Age >40 at time of acquisition
  • Alcohol >50g/week
  • Duration of infection
    • 20% cirrhosis after 20 years
    • 50% cirrhosis after 50 years
322
Q

Describe the presentation of ischaemic colitis

A
  • Abrupt onset pain and bloody diarrhoea +/- SIRS
  • Hypoperfusion > embolic
323
Q

Describe the use of faecal calprotectin in the diagnosis of Crohn’s disease

A
  • Calcium-binding protein, predominantly derived from neutrophil
  • Single 20g sample, stable for 5 days
  • ‘Normal’ <50 but studies in GGC suggest results <200 rarely indicate organic pathology
  • Useful test to differentiate between IBD/IBS and assess activity in IBD
  • Sensitive but not disease specific
324
Q

Describe the prevalence of IBD

A
  • 0.5-1.5% population prevalence
  • Crohns
    • Highest prevalence in women/men aged 20-29
  • UC
    • Highest prevalence in women 20-29, men 60-79
325
Q

What kind of virus is hepatitis E?

A
  • RNA virus
  • 4 genotypes
326
Q

What causes gas in the liver seen on plain abdominal film?

A

Gas in liver - biliary gas or portal venous gas (more sinister)

  • Portal venous gas - bowel ischaemia, gas leaks through ischaemic wall into mesenteric vessels into liver
  • Different biliary gas - gas pushed more peripherally from portal vein, biliary tree gas stays more central
327
Q

What are the causes of chemical gastritis?

A

Causes include bile reflux, NSAIDs, ehtanol, oral iron

328
Q

Describe the appearance of gastric parietal cells on H&E

A

Big pink cells with abundant cytoplasm

329
Q

How do gastro-oesophageal varices form?

A
  • Cirrhosis - increased hepatic resistance
    • Mechanical
      • Architectural changes
      • Fibrosis
      • Vascular occlusion
    • Dynamic
      • Endothelial dysfunction
      • Increased vascular tone
  • Increased portal inflow
    • Splanchnic vasodilation
      • Increased NO, CO, glucagon, endocannabinoids
      • Hyperkinetic syndrome

= Increased portal pressure

–> Porto-systemic shunts and varices form

Medicine Year 3 (15 decks)

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