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Gastroenterology Flashcards

1
Q

Primary biliary cirrhosis associations?

A
  1. Sjogrens (80%)
  2. RhA, SLE
  3. SS particularly the limited cutaneous subtype (CREST syndrome)
  4. Thyroid disease (hashimoto’s thyroiditis and graves’ d6)
  5. 9F:1M

6.? Coeliac d6

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2
Q

PBC Dx?

A
  1. Immunology = Raised IgM, Anti-Mitochondrial Abs (AMA) M2 subtype (present in about 98% of px, highly specific), ASMA (30%)
  2. Imaging = required before diagnosis to exclude an extrahepatic biliary obstruction (typically a right upper quadrant ultrasound or magnetic resonance cholangiopancreatography (MRCP)
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3
Q

PBC Rx?

A
  1. Ursodeoxycholic Acid (UDCA)
  2. Cholestyramine for pruritis
  3. Fat soluble vitamin supplementation
  4. Liver transplantation e.g. if bilirubin > 100 (recurrence in graft can occur but usually not a problem)
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4
Q

PBC complications?

A
  1. Cirrhosis
  2. Osteomalacia and osteoporosis
  3. HCC (x20)
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5
Q

GORD correlation between symptoms and endoscopy appearance?

A

Poor correlation

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6
Q

Indications for UGI endoscopy?

A
  1. Age >55 y/o
  2. Symptoms > 4 weeks or persistent symptoms despite treatment
  3. Dysphagia
  4. Relapsing symptoms
  5. Weight loss
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7
Q

If GORD and endoscopy negative Ix?

A

24hr oesophageal pH monitoring (gold standard for Dx)

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8
Q

PPI stopped when before endoscopy?

A

2 weeks

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9
Q

Alcoholic liver disease spectrum?

A
  1. Alcoholic fatty liver disease
  2. Alcoholic hepatitis
  3. Cirrhosis
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10
Q

Alcoholic liver disease LFTs?

A
  1. Raised GGT
  2. AST:ALT > 2, >3 = strongly suggestive of acute alcoholic hepatitis
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11
Q

Alcoholic hepatitis management?

A
  1. Prednisolone during acute episode = Maddrey’s discriminant function (DF) is often used during acute episodes to determine who would benefit from glucocorticoid therapy, calculated using PT and bilirubin
  2. Pentoxyphylline sometimes used
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12
Q

UC management classification?

A
  1. Inducing remission
  2. Maintaining remission
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13
Q

UC severity?

A
  1. Mild = < 4 stools/day, small blood
  2. Moderate = 4-6 stools/day, varying blood, no systemic upset
  3. Severe = >6 bloody stools, systemic upset
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14
Q

Inducing remission in mild to moderate colitis classification?

A
  1. Proctitis
  2. Proctosigmoiditis and left sided
  3. Extensive disease
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15
Q

Inducing remission in mild to moderate UC proctitis?

A
  1. Topical aminosalicylate
  2. No improvement after 4 weeks –> add oral aminosalicylate
  3. No improvement –> topical or oral steroid
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16
Q

Inducing remission in mild to moderate UC proctosigmoiditis/left sided UC?

A
  1. Topical aminosalicylate
  2. No improvement after 4 weeks –> add high dose oral aminosalicylate OR switch to a high-dose oral aminosalicylate and a topical corticosteroid
  3. No improvement –> Stop topicals, oral aminosalicylate + oral corticosteroid
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17
Q

Inducing remission in mild to moderate UC extensive disease?

A
  1. Topical AND high dose oral aminosalicylate
  2. No improvement after 4 weeks –> Stop topicals, oral aminosalicylate + oral corticosteroid
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18
Q

Inducing remission in severe colitis?

A
  1. Admit to hospital
  2. IV steroids (IV ciclosporin if steroids C/I)
  3. No improvement after 72h –> consider adding IV ciclosporin/surgery
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19
Q

Maintaining remission following a mild to moderate UC proctitis/proctosigmoiditis flare?

A
  1. Topical aminosalicylate alone (daily or intermittent)
  2. Oral aminosalicylate plus a topical aminosalicylate (daily or intermittent) or
  3. Oral aminosalicylate by itself: this may not be effective as the other two options
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20
Q

Maintaining remission following a mild to moderate UC left sided and extensive UC flare?

A

Low maintenance dose of an oral aminosalicylate

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21
Q

Maintaining remission following a severe relapse or >/2 UC exacerbations in the past year?

A

Oral Azathioprine or Oral Mercaptopurine

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22
Q

Is methotrexate used in Rx of UC?

A

No

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23
Q

C. diff gram and shape?

A

Gram positive rod

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24
Q

C.diff RFs?

A

Abx and PPI

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25
Q

Characteristic C.diff bloods?

A

Raised WCC

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26
Q

C. diff severity scale?

A
  1. Mild = normal WCC
  2. Moderate = WCC <15, 3-5 loose stools per day
  3. Severe = WCC > 15, temp > 38.5, raised creatinine, abdo/radiological signs of severe colitis
  4. Life threatening = hypotension, partial or complete ileus, toxic megacolon/CT evidence of severe disease
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27
Q

C.Diff Dx?

A
  1. C. diff toxin in the stool
  2. C. diff antigen positivity only shows exposure to the bacteria, rather than current exposure
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28
Q

C. diff first episode management?

A
  1. 1st line = Oral vancomycin 10 days
  2. 2nd line = Oral fidoxamicin
  3. 3rd line = Oral vancomycin +/- IV Metronidazole
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29
Q

C. diff recurrent episodes Rx?

A

Recurrent infection occurs in around 20% of patients, increasing to 50% after their second episode
1. Within 12 weeks of symptom resolution = oral fidoxamicin
2. After 12 weeks of symptom resolution = oral vancomycin OR fidoxamacin

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30
Q

Life threatening C.diff infection Rx?

A
  1. Oral Vancomycin AND IV Metronidazole
  2. Specialist advice - surgery may be considered
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31
Q

C. diff other therapies?

A
  1. Bezlotoxumab is a monoclonal antibody which targets C. difficile toxin B
  2. Faecal microbiota transplant = may be considered for pts who’ve had 2 or more previous episodes
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32
Q

Achalasia symptoms?

A
  1. Dysphagia of both liquids and solids from the start
  2. Heartburn
  3. Regurgitation of food - may lead to cough, aspiration pneumonia etc.
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33
Q

Pharyngeal pouch mushkies?

A
  1. Older men typically
  2. Posteromedial herniation between thyropharyngeus and cricopharyngeus muscles
  3. Usually not seen but if large then a midline lump in the neck that gurgles on palpation
  4. Dysphagia, regurgitation, aspiration, chronic cough, halitosis
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34
Q

Achalasia LES pressure?

A

Increased

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35
Q

Systemic sclerosis LES pressure?

A

Decreased

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36
Q

Globus hystericus mushkies?

A
  1. History of anxiety
  2. Symptoms are often intermittent and relieved by swallowing
  3. Usually painless - presence of pain should warrant further investigation for organic causes
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37
Q

HBsAg?

A
  1. Ongoing infection (1-6 months)
  2. If present for >6 months implies chronic disease i.e. infective
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38
Q

Anti-HBs?

A
  1. Immunity = either exposure or infection
  2. Is negative in chronic disease
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39
Q

Anti-Hbc?

A
  1. Previous or current infection (caught)
  2. Negative if immunised
  3. IgM anti-HBc appears during acute or recent hepatitis B infection and is present for about 6 months. IgG anti-HBc persists
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40
Q

HBeAg?

A

Results from breakdown of core antigen from infected liver cells as is, therefore, a marker of infectivity. Marker of HBV replication and infectivity

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41
Q

WHO Diarrhoea definition?

A

> 3 loose or watery stools per day

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42
Q

Acute diarrhoea definition?

A

< 14 days

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43
Q

Chronic diarrhoea definition?

A

> 14 days

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44
Q

Urgent (2ww) endoscopy criteria?

A
  1. Dysphagia
  2. Upper abdominal mass consistent with stomach cancer
  3. > 55 who have weight loss AND upper abdominal pain/reflux/dyspepsia
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45
Q

Non-urgent endoscopy criteria?

A
  1. Haematemesis
  2. > 55 who have –>
    a. Treatment-resistant dyspepsia
    b. Upper abdominal pain with low Hb levels
    c. Raised platelet count with N&V/weight loss/reflux/dyspepsia/upper abdominal pain
    d. N&V with: weight loss, reflux, dyspepsia, upper abdominal pain
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46
Q

Undiagnosed dyspepsia management?

A
  1. Review medications
  2. Lifestyle advice
  3. PPI for 1 month OR test and treat approach for H. pylori
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47
Q

H. pylori Dx?

A

Carbon-13 urea breath test or a stool antigen test, or laboratory-based serology ‘where its performance has been locally validated

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48
Q

H. pylori test of cure?

A
  1. No need to check for H. pylori eradication if symptoms have resolved following test and treat
  2. If repeat testing required, then Carbon-13 urea breath test should be used
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49
Q

Causes of B12 deficiency?

A
  1. Pernicious anaemia (most common)
  2. Atrophic gastritis (secondary to H.pylori)
  3. Gastrectomy
  4. Malnutrition (e.g. alcoholism)
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50
Q

Pernicious anaemia pathophysiology?

A

Antibodies to intrinsic factor +/- gastric parietal cells

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51
Q

Vitamin B12 roles and thus malfunction as a result of deficiency?

A
  1. Production of blood cells –> megaloblastic anaemia
  2. Myelination of nerves –> neuropathy
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52
Q

Pernicious anaemia RFs?

A
  1. 6F:1M, middle to old age
  2. Other AI = T1DM, Addisons, RhA, Vitiligo, thyroid disease
  3. More common in blood group A
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53
Q

Pernicious anaemia features?

A
  1. Anaemia = lethargy, pallor, dyspnoea
  2. Neurological features = peripheral neuropathy (pine and needles, numbness, typically symmetrical and affects legs > arms), SCDSC, neuropsychiatric features
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54
Q

SCDSC features?

A
  1. Progressive weakness
  2. Ataxia
  3. Paraesthesias that may progress to spasticity and paraplegia
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55
Q

Other features of pernicious anaemia?

A
  1. Mild jaundice = combined with pallor results in a ‘lemon tinge’
  2. Glossitis = sore tongue
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56
Q

Pernicious anaemia Ix?

A
  1. FBC = macrocytic anaemia, hypersegmented polymorphs on blood film, low WCC and platelets may also be seen
  2. Anti-intrinsic factor antibodies = 95% specificity, 50% sensitivity
  3. Anti-gastric parietal cell antibodies = present in 90%, but low specificity so often not useful clinically
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57
Q

Pernicious anaemia Rx?

A
  1. Vitamin B12 replacement usually IM, no neurological features –> 3 injections per week for 2 weeks followed by 3 monthly injections
  2. More frequent doses given for patients with neurological features
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58
Q

Pernicious anaemia and gastric cancer?

A

Increased risk

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59
Q

Maximum recommended alcohol consumption?

A

14 units for men and women

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60
Q

Calculation of units in a drink?

A

(ml x ABV) / 1000

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61
Q

Haemachromatosis definition?

A

Autosomal recessive disorder of iron absorption and metabolism resulting in iron accumulation. It is caused by inheritance of mutations in the HFE gene on both copies of chromosome 6

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62
Q

Haemachromatosis screening?

A
  1. General population = transferrin saturation is considered the most useful marker. Ferritin should also be measured but is not usually abnormal in the early stages of iron accumulation
  2. Testing family members = genetic testing for HFE mutation
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63
Q

Haemachromatosis diagnostic tests?

A
  1. Molecular testing for C282Y and H63D mutations
  2. Liver biopsy = Perl’s stain
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64
Q

Typical iron study profile in pt with haemachromatosis?

A
  1. Transferrin saturation = >55% in men or >50% in women
  2. Raised ferritin and iron
  3. Low TIBC
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65
Q

Haemachromatosis Rx?

A
  1. 1st line = Venesection, transferrin saturation should be < 50% and ferritin < 50
  2. 2nd line = desferrioxamine
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66
Q

Haemachromatosis joint X-rays?

A

Chondrocalcinosis

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67
Q

Pancreatic cancer associations?

A
  1. Age, smoking, diabetes
  2. Chronic pancreatitis
  3. HNPCC
  4. MEN
  5. BRCA2 gene
  6. KRAS mutation
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68
Q

Courvoisier’s law?

A

In the presence of painless obstructive jaundice, a palpable gallbladder is unlikely to be due to gallstones

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69
Q

Pancreatic cancer Ix?

A
  1. High-resolution CT scan is investigation of choice
  2. US has a sensitivity of 60-90%
  3. Imaging may show double-duct sign = presence of simultaneous dilatation of the common bile and pancreatic ducts
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70
Q

Pancreatic cancer Rx?

A
  1. <20% suitable for surgery at Dx
  2. Whipple’s (pancreaticoduodenectomy) for resectable lesions in the head of the pancreas
  3. Adjuvant chemotherapy usually given following surgery
  4. ERCP with stenting often used for palliation
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71
Q

Whipple’s side effects?

A
  1. Dumping syndrome
  2. Peptic ulcer disease
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72
Q

Urea breath test important note?

A

Should not be performed within 4w of antibacterial or 2w of PPI

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73
Q

When should IBS diagnosis be considered?

A

Had the following for 6 months (ABC):
1. Abdominal pain
2. Bloating
3. Change in bowel habit

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74
Q

IBS Diagnosis?

A

Abdominal pain relieved by defecation or associated with altered bowel frequency and stool form, in addition to 2 of the following 4 features:
1. Altered stool passage (straining, urgency, incomplete evacuation)
2. Abdominal bloating, distension or hardness
3. Symptoms made worse by eating
4. Passage of mucus

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75
Q

IBS Ix?

A
  1. FBC, ESR/CRP
  2. Coeliac disease screen (anti-TTG)
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76
Q

Diabetes medication causing cholestasis?

A

Sulphonylureas e.g. Gliclazide

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77
Q

Classification of drug-induced liver disease?

A
  1. Hepatocellular
  2. Cholestatic
  3. Mixed
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78
Q

3 drugs causing liver cirrhosis?

A
  1. Methotrexate
  2. Methyldopa
  3. Amiodarone
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79
Q

TIBC in anaemia?

A

High

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80
Q

TIBC in ACD?

A

Low/normal

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81
Q

Ferritin in IDA?

A

Low

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82
Q

TIBC in pregnancy?

A

Raised

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83
Q

Transferrin saturation equation?

A

Serum iron/TIBC

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84
Q

Obesity with abnormal LFTs?

A

NAFLD (Non-alcoholic fatty liver disease)

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85
Q

Most common cause of liver disease in the developed world?

A

NAFLD

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86
Q

Key mechanism leading to steatosis in NAFLD?

A

Insulin resistance

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87
Q

NASH definition?

A

Non-alcoholic steatohepatitis (NASH) is a term used to describe liver changes similar to those seen in alcoholic hepatitis in the absence of a history of alcohol abuse. It is relatively common and thought to affect around 3-4% of the general population. The progression of disease in patients with NASH may be responsible for a proportion of patients previously labelled as cryptogenic cirrhosis.

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88
Q

NAFLD ALT and AST?

A

ALT > AST

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89
Q

NAFLD Ix?

A
  1. No screening, management based on incidental findings on liver ultrasound
  2. Enhanced lived fibrosis (ELF) blood test to check for advanced fibrosis
  3. Fibroscan can be used
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90
Q

NAFLD Rx?

A
  1. Lifestyle changes
  2. Research ongoing for gastric banding and insulin-sensitising drugs e.g. metformin, pioglitazone
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91
Q

Triggers of UC flare?

A
  1. No known trigger
  2. Stress
  3. NSAIDs/Abx
  4. Smoking cessation
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92
Q

When is smoking cessation bad?

A

Can trigger a UC flare

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93
Q

GI complication of systemic sclerosis?

A

Malabsorption syndrome = B12 and folate deficiency, low iron and low albumin

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94
Q

Malabsorption features?

A
  1. Diarrhoea
  2. Steatorrhoea
  3. Weight loss
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95
Q

Classification of malabsorption?

A
  1. Intestinal = Coeliac, Crohn’s, Whipple’s, tropical sprue, Giardiasis, brush border enzyme deficiency e.g. lactase insufficiency
  2. Pancreatic = chronic pancreatitis, CF, pancreatic cancer
  3. Biliary = obstruction, PBC
  4. Other = Bacterial overgrowth (systemic sclerosis, diverticulae, blind loop), short bowel syndrome, lymphoma
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96
Q

PSC definition?

A

A biliary disease of unknown aetiology characterised by inflammation and fibrosis of intra and extra-hepatic bile ducts

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97
Q

PSC associations?

A
  1. UC (4% with UC have PSC, 80% with PSC have UC)
  2. Crohn’s (much less common than UC)
  3. HIV
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98
Q

PSC Ix?

A
  1. ERCP/MRCP gold standard, beaded appearance
  2. pANCA +ve
  3. Onion skin on liver biopsy
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99
Q

PSC complications?

A
  1. Cholangiocarcinoma in 10%
  2. Colorectal cancer
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100
Q

Coeliac disease HLA associations?

A

HLA-DQ2 (95%) and HLA-DQ8 (80%)

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101
Q

Coeliac disease complications?

A
  1. Anaemia = iron, folate and B12 deficiency (folate most common)
  2. Hyposplenism
  3. Osteoporosis, osteomalacia
  4. Lactose intolerance
  5. Enteropathy-associated T-cell lymphoma of small intestine
  6. Subfertility, unfavourable pregnancy outcomes
  7. Rare = oesophageal cancer
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102
Q

Ischaemia to lower GI tract types?

A
  1. Acute mesenteric ischaemia
  2. Chronic mesenteric ischaemia
  3. Ischaemic colitis
103
Q

Acute mesenteric ischaemia features?

A
  1. Typically small bowel e.g. SMA, due to embolism, sudden onset severe symptoms out of keeping with examination findings
  2. High mortality, needs urgent surgery
104
Q

Chronic mesenteric ischaemia mushkies?

A

Rare clinical diagnosis due to non-specific features, colicky intermittent abdominal pain, ‘intestinal angina’

105
Q

Ischaemic colitis mushkies?

A
  1. Large bowel, multifactorial, bloody diarrhoea, transient and less severe symptoms
  2. Thumbprinting on AXR due to mucosal oedema/haemorrhage
  3. Conservative management
  4. An acute but transient compromise in blood flow to the large bowel, watershed areas e.g. splenic flexure
  5. Rx = usually supportive, surgery if generalised peritonitis/perforation/ongoing haemorrhage
106
Q

Murphy’s sign?

A

Acute cholecystitis, arrest of inspiration on palpation of RUQ

107
Q

Cholangiocarcinoma mushkies?

A
  1. Courvoisier’s sign
  2. Sister Mary Joseph nodes = periumbilical lymphadenopathy
  3. Virchow’s node
  4. Persistent biliary colic symptoms associated with anorexia, jaundice and weight loss
108
Q

Most common type of oesophageal cancer?

A

Adenocarcinoma

109
Q

Oesophageal adenocarcinoma mushkies?

A
  1. Most common type in UK/US
  2. Lower 1/3rd near GOJ
  3. RFs = GORD, Barrett’s, smoking, achalasia, obesity
110
Q

Oesophageal SCC mushkies?

A
  1. Most common type in developing world
  2. Upper 2/3rds
  3. RFs = Smoking, alcohol, achalasia, Plummer-Vinson syndrome, diets rich in nitrosamines
111
Q

Oesophageal cancer Ix?

A
  1. Upper GI endoscopy with biopsy
  2. Endoscopic US is preferred for locoregional staging
  3. CT CAP for initial staging (FDG-PET for detecting occult metastases if not seen on initial staging CT scans)
  4. Laparoscopy is sometimes performed to detect occult peritoneal disease
112
Q

Oesophageal cancer Rx?

A
  1. Operable disease –> Ivor-Lewis type oesophagectomy
  2. Many pts will have adjuvant chemoterapy
113
Q

Biggest surgical challenge of oesophageal cancer?

A

Anastomotic leak –> intrathoracic anastomosis –> mediastinitis

114
Q

PPI s/e?

A
  1. Hyponatraemia, hypomagnesaemia
  2. Osteoporosis –> increased fracture risk
  3. Microscopic colitis
  4. Increased risk of C.diff
115
Q

Most common SBP organism?

116
Q

SBP Paracentesis cell count?

117
Q

SBP Rx?

A

IV Cefotaxime

118
Q

When is Abx prophylaxis given to ascites pts?

A
  1. Have had an episode of SBP
  2. Fluid protein <15g/l and either a Child-Pugh of at least 9 or hepatorenal syndrome
  3. Oral ciprofloxacin or norfloxacin
119
Q

GORD definition?

A

Symptoms of oesophagitis secondary to refluxed gastric contents

120
Q

GORD management classification?

A
  1. Endoscopically proven
  2. Endoscopically negative
121
Q

Endoscopically proven GORD Rx?

A
  1. Full dose PPI for 1-2 months
  2. If response then low dose treatment as required
  3. If no response then double PPI dose for 1 month
122
Q

Endoscopically negative reflux disease?

A
  1. Full dose PPI for 1 month
  2. If response then offer low dose treatment, possibly on an as-required basis, with a limited number of repeat prescriptions
  3. If no response then H2RA or prokinetic for 1 month
123
Q

Ascites classification?

A
  1. SAAG > 11g/L (portal hypertension)
  2. SAAG < 11g/L
124
Q

Raised SAAG Ascites causes?

A
  1. Liver = cirrhosis, acute liver failure, metastases
  2. Cardiac = HF, constrictive pericarditis
  3. Other = Budd-chiari, portal vein thrombosis, veno-occlusive disease, myxoedema
125
Q

Low SAAG ascites causes?

A
  1. Infection = TB
  2. Hypoalbuminaemia = nephrotic syndrome, Kwashiorkor
  3. Metastases
  4. Other = Pancreatitis, bowel obstruction, serositis in CTD
126
Q

Ascites Rx?

A
  1. Conservative = reduce dietary sodium, fluid restriction if Na < 125
  2. Aldosterone antagonist (spironolactone), can add loop diuretic if needed
  3. Drainage if tense
  4. Prophylactic Abx (ciprofloxacin) if cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved
  5. TIPSS may be considered
127
Q

Most common cause of HCC worldwide?

A

Chronic Hepatitis B

128
Q

Most common cause of HCC in Europe?

A

Chronic Hepatitis C

129
Q

HCC marker?

130
Q

HCC Screening?

A

With US +/- AFP for high risk groups:
1. Liver cirrhosis secondary to Hep B/C or haemachromatosis
2. Men with liver cirrhosis secondary to alcohol

131
Q

HCC Rx?

A
  1. Early disease = surgical resection
  2. Liver transplantation
  3. RFA
  4. Transarterial chemoembolisation
  5. Sorafenib: a multikinase inhibitor
132
Q

Most common extra-intestinal feature in IBD?

133
Q

Most prominent Crohn’s symptom in children?

A

Abdominal pain

134
Q

Most prominent Crohn’s symptoms in adults?

135
Q

Episcleritis more common in UC or CD?

136
Q

Uveitis more common in UC or CD?

137
Q

IBD crypt abscesses?

138
Q

IBD goblet cells and granulomas?

139
Q

Best first line management for NAFLD?

A

Weight loss

140
Q

Causes of haematemesis?

A
  1. Oesophageal = varices, oesophagitis, cancer, mallory-weiss tear
  2. Gastric = ulcer, cancer, dieulafoy lesion, diffuse erosive gastritis
  3. Duodenal = ulcer, aorto-enteric fistula
141
Q

Aorto-enteric fistula mushkies?

A

In patients with previous abdominal aortic aneurysm surgery aorto-enteric fistulation remains a rare but important cause of major haemorrhage associated with high mortality

142
Q

Upper GI bleed scoring?

A
  1. Glasgow-Blatchford at first assessment (Rockall after endoscopy)
143
Q

Blatchford score components?

A

HUSO
1. Hb
2. Urea
3. SBP
4. Other = pulse, melaena, syncope, hepatic disease, cardiac failure

144
Q

Common Upper GI Bleed Rx?

A
  1. ABC, wide bore access x 2
  2. Platelet transfusion if actively bleeding and < 50
  3. FFP if fibrinogen <1 or PT/APTT x1.5 normal
  4. PCC if on warfarin and actively bleeding
  5. Endoscopy = immediately after resus in severe bleed, all pts should have endoscopy within 24 hours
145
Q

Management of non-variceal bleeding?

A
  1. Do not recommend PPIs before endoscopy
  2. If further bleeding then repeat endoscopy, IR and surgery
146
Q

Management of variceal bleeding?

A
  1. Terlipressin and prophylactic Abx
  2. Band ligation for oesophageal varices
  3. N-butyl-2-cyanoacrylate injection for gastric varices
  4. TIPS if bleeding from varices not controlled with above measures
147
Q

NICE guidance before coeliac testing?

A

Reintroduce gluten for at least 6 weeks prior to testing

148
Q

Coeliac Ix?

A
  1. Serology = TTG (IgA) 1st line, anti-endomysial (IgA), anti-casein sometimes found
  2. Endoscopic intestinal biopsy is gold standard, duodenal/jejunal
149
Q

Coeliac histology?

A
  1. Villous atrophy
  2. Crypt hyperplasia
  3. Increase in intraepithelial lymphocytes
  4. Lamina propria infiltration with lymphocytes
150
Q

Crohn’s general points?

A
  1. Stop smoking
  2. Increased risk of relapse secondary to NSAIDs and the combined oral contraceptive pill but evidence is patchy
151
Q

Crohn’s inducing remission?

A
  1. Glucocorticoids (budesonide is an alternative in certain subgroups)
  2. Enteral feeding with an elemental diet may be used in addition to or instead of other measures to induce remission, particularly if there is concern regarding the side-effects of steroids (for example in young children)
  3. 5-ASA second line but not as effective
  4. Azathioprine or mercaptopurine may be used as add-on to induce remission but is not used as monotherapy (Methotrexate is an alternative to AZA)
  5. Infliximab is useful in refractory disease and fistulating Crohn’s. Patients typically continue on azathioprine or methotrexate
  6. Metronidazole is often used for isolated peri-anal disease
152
Q

Crohn’s maintaining remission?

A
  1. Stop smoking
  2. AZA or 6-MP first line (TPMT should be assessed before starting)
  3. Methotrexate is 2nd line
153
Q

Crohn’s surgery mushkies?

A
  1. 80% will eventually have surgery
  2. Stricturing terminal ileal disease –> ileocaecal resection
  3. Segmental bowel resections
  4. Stricturoplasty
  5. Perianal disease see cards
154
Q

Perianal fistulae mushkies?

A
  1. MRI is the investigation of choice for suspected perianal fistulae - can be used to determine if there (is an abscess and if the fistula is simple (low fistula) or complex (high fistula that passes through or above muscle layers)
  2. Symptomatic –> given oral metronidazole
  3. Anti-TNF agents such as infliximab may also be effective in closing and maintaining closure of perianal fistulas
  4. Draining seton used for complex fistulae
155
Q

Perianal abscess Rx?

A
  1. Requires I&D and Abx
  2. Draining seton may be placed if tract is identified
156
Q

Crohn’s complications?

A
  1. Small bowel cancer x40
  2. Colorectal cancer x2
  3. Osteoporosis
157
Q

Variceal haemorrhage acute management?

A
  1. ABC = resus prior to endoscopy
  2. Correct clotting = FFP, Vitamin K
  3. Terlipressin (or octreotide)
  4. IV Abx, quinolones
  5. Endoscopy = band ligation superior to sclerotherapy
  6. Sengstaken-Blakemore tube if uncontrolled haemorrhage
  7. TIPS if uncontrolled haemorrhage
158
Q

Prophylaxis of variceal haemorrhage?

A
  1. Propranolol
  2. Endoscopic band ligation is superior to sclerotherapy (PPI cover given to prevent EVL-induced ulceration)
159
Q

Gastric cancer RFs?

A
  1. H. pylori
  2. Atrophic gastritis
  3. Diet
  4. Smoking
  5. Blood group
160
Q

Sister Mary Joseph’s node?

A

Periumbilical node in gastric cancer

161
Q

Gastric cancer Ix?

A
  1. Dx = endoscopy with biopsy
  2. Staging = CT
162
Q

Gastric cancer histology?

A

Signet ring cells. High numbers associated with worse prognosis.

163
Q

Gastric cancer Rx?

A
  1. Surgery = endoscopic mucosal resection, partial/total gastrectomy
  2. Chemotherapy
164
Q

Melanosis coli?

A

Disorder of pigmentation of the bowel wall. Histology shows pigment-laden macrophages. Associated with laxative abuse, especially senna.

165
Q

Swinging pyrexia and right upper quadrant pain?

A

Gallbladder abscess

166
Q

Gallstone ileus Rx?

A

Laparotomy and removal of the gallstone from small bowel, the enterotomy must be made proximal to the site of obstruction and not at the site of obstruction. The fistula between the gallbladder and duodenum should not be interfered with.

167
Q

Acalculous cholecystitis Rx?

A

If patient fit then cholecystectomy, if unfit then percutaneous cholecystostomy

168
Q

Asymptomatic gallstone in gallbladder Rx”

169
Q

Asymptomatic gallstone in CBD management?

A

Surgical management

170
Q

ERCP risks?

A
  1. Bleeding
  2. Duodenal perforation
  3. Cholangitis
  4. Pancreatitis
171
Q

Peutz-Jeghers syndrome definition?

A

An autosomal dominant condition characterised by numerous hamartomatous polyps in the gastrointestinal tract. It is also associated with pigmented freckles on the lips, face, palms and soles. Although the polyps themselves don’t have malignant potential, around 50% of patients will have died from another gastrointestinal tract cancer by the age of 60 years.

172
Q

Peutz-Jeghers genetics?

A
  1. AD
  2. Gene encodes serine threonine kinase LKB1 or STK11
173
Q

Peutz-Jeghers features?

A
  1. Hamartomatous polyps in the GI tract (mainly small bowel) -
  2. SBO is a common presenting complaint often due to intussuscpetion, GI bleeding
  3. Pigmented lesions on lips, oral mucosa, face, palms and soles
174
Q

Peutz-Jeghers Rx?

A

Conservative unless complications develop

175
Q

Barrett’s oesophagus definition?

A

Metaplasia of the lower oesophageal mucosa, with the usual squamous epithelium being replaced by columnar epithelium. There is an increased risk of oesophageal adenocarcinoma, estimated at 50-100 fold. There are no screening programs for Barrett’s - it’s typically identified when patients have an endoscopy for evaluation of upper gastrointestinal symptoms such as dyspepsia.

176
Q

Barrett’s classification?

A

Barrett’s can be subdivided into short (<3cm) and long (>3cm). The length of the affected segment correlates strongly with the chances of identifying metaplasia.

177
Q

Barrett’s histology?

A

Columnar epithelium may resemble that of either the cardiac region of the stomach or that of the small intestine (e.g. with goblet cells, brush border)

178
Q

Barrett’s RFs?

A
  1. GORD
  2. 7M:1F
  3. Smoking
  4. Central obesity
179
Q

Is alcohol an independent RF for Barrett’s?

180
Q

Barrett’s Rx?

A
  1. High dose PPI
  2. Endoscopic surveillance with biopsies (for pts with metaplasia (but not dysplasia) endoscopy is recommended every 3-5 years)
  3. If dysplasia of any grade is identified, endosopic intervention is offered –> RFA first line, endoscopic mucosal resection also
181
Q

Achalasia definition?

A

Failure of oesophageal peristalsis and of relaxation of the lower oesophageal sphincter (LOS) due to degenerative loss of ganglia from Auerbach’s plexus i.e. LOS contracted, oesophagus above dilated. Achalasia typically presents in middle-age and is equally common in men and women.

182
Q

Achalasia features?

A
  1. Dysphagia of both liquids and solids
  2. Malignant change in small number of patients
  3. Regurgitation of food may lead to cough/aspiration pneumonia
183
Q

Achalasia Ix?

A
  1. Oesophageal manometry = excessive LOS tone which doesnt relax on swallowing, most important test
  2. Barium swallow = birds beak
  3. CXR = wide mediastinum, fluid level
184
Q

Achalasia Rx?

A
  1. Pneumatic dilation 1st line
  2. Surgical intervention with Heller’s cardiomyotomy if recurrent/persistent symptoms
  3. Intra-sphincteric injection of botulinum if high surgical risk
  4. Drugs e.g. nitrates, CCBs has a role but is limited by side effects
185
Q

What medication should be avoided in bowel obstruction?

A

Metoclopramide

186
Q

Metoclopramide MOA?

A

D2 receptor antagonist

187
Q

Metoclopramide uses?

A
  1. GORD
  2. Prokinetic
  3. With analgesics for migraine treatment (migraine attacks result in gastroparesis, slowing the absorption of analgesics)
188
Q

Metoclopramide s/e?

A
  1. EPSE e.g. acute dystonia, tardive dyskinesia, parkinsonism
  2. Diarrhoea
  3. Hyperprolactinaemia
189
Q

Weight loss predominant IBD?

190
Q

Gallstones predominant IBD?

A

Crohn’s due to reduced bile acid reabsorption

191
Q

IBD skip lesions?

192
Q

IBD pseudopolyps?

193
Q

IBD cobblestones?

194
Q

Crohn’s radiological investigation?

A

Small bowel enema
1. High sensitivity and specificity for examination of the terminal ileum
2. Strictures: Kantor’s string sign
3. Proximal bowel dilatation
4. Rose thorn ulcers
5. Fistulae

195
Q

UC radiological investigation?

A

Barium enema
1. Loss of haustrations
2. Superficial ulceration, pseudopolyps
3. Long standing disease: colon is narrow and short -‘drainpipe colon’

196
Q

Pharyngeal pouch Ix?

A

Barium swallow combined with dynamic video fluoroscopy

197
Q

Pharyngeal pouch Rx?

198
Q

Causes of Vitamin B6 deficiency?

A

Isoniazid therapy

199
Q

Vitamin B6 AKA?

A

Pyridoxine

200
Q

Consequences of Vitamin B6 deficiency?

A
  1. Peripheral neuropathy
  2. Sideroblastic anaemia
201
Q

Autoimmune hepatitis mushkies?

A

Autoimmune hepatitis is condition of unknown aetiology which is most commonly seen in young females. Recognised associations include other autoimmune disorders, hypergammaglobulinaemia and HLA B8, DR3. Three types of autoimmune hepatitis have been characterised according to the types of circulating antibodies present

202
Q

Types of autoimmune hepatitis?

A
  1. Type I = ANA/ASMA, adults and children
  2. Type II = Anti-LKM1, children
  3. Type III = soluble liver-kidney antigen, middle aged adults
203
Q

Autoimmune hepatitis mushkie in women?

A

Often presents with amenorrhoea

204
Q

Autoimmune hepatitis liver biopsy?

A

‘Piecemeal necrosis = inflammation extending beyong limiting plate

205
Q

Autoimmune hepatitis Rx?

A
  1. Steroids, AZA
  2. Liver transplantation
206
Q

Bile acid malabsorption Rx?

A

Cholestyramine

207
Q

Bile acid malabsorption Ix?

A

SeHCAT –> scans done 7 days apart to assess retention/loss of radiolabelled SeHCAT

208
Q

Bile acid malabsorption causes?

A
  1. Primary = excessive bile acid production, underlying GI disorder
  2. Secondary = cholecystectomy, coeliac disease, small intestine bacterial overgrowth
209
Q

Bile acid malabsorption presentation?

A
  1. Steatorrhoea
  2. ADEK malabsorption
210
Q

Vitamin A deficiency symptom?

A

Night blindness

211
Q

What vitamin is teratogenic in high doses?

212
Q

Haemachromatosis epidemiology?

A
  1. 1 in 10 people of European descent carry a mutation in the genes affecting iron metabolism, mainly HFE
  2. Prevalence in people of European descent = 1 in 200, making it more common than cystic fibrosis
213
Q

Haemachromatosis presenting features?

A
  1. Fatigue, erectile dysfunction and arthralgia (often of the hands)
  2. ‘Bronze’ skin pigmentation
  3. DM
  4. Liver disease
  5. Heart = DCM
  6. Hypogonadism = 2nd to cirrhosis and pituitary dysfunction - hypogonadotrophic hypogonadism
214
Q

Reversible complications of haemachromatosis?

A
  1. Cardiomyopathy
  2. Skin pigmentation
215
Q

Irreversible complications of haemachromatosis?

A
  1. Liver cirrhosis
  2. DM
  3. Arthropathy
  4. Hypogonadotrophic hypogonadism
216
Q

Ferritin function?

A

An intracellular protein that binds iron and stores it to be released in a controlled fashion at sites where iron is required

217
Q

Increased ferritin levels thresholds in men and women?

A
  1. > 300 in men/postmenopausal women
  2. > 200 in premenopausal women
218
Q

Classification of raised ferritin?

A
  1. With iron overload (10%)
  2. Without iron overload (90%)
219
Q

Causes of raised ferritin with iron overload?

A
  1. Primary = HH
  2. Secondary = repeated transfusions
220
Q

Causes of raised ferritin without iron oveload?

A
  1. Inflammation
  2. EtOH XS
  3. Liver disease
  4. CKD
  5. Malignancy
221
Q

How to tell if there is iron overload?

A

Raised transferrin saturation

222
Q

How to tell if IDA is due to iron deficiency state?

A

Low ferritin (because iron and ferritin are bound)

223
Q

What Abx classically associated with C.diff?

A

Clindamycin

224
Q

Problem drinking screening?

A
  1. AUDIT
  2. FAST
  3. CAGE
225
Q

AUDIT mushkies?

A
  1. 10 items
  2. Score 0- 40
  3. > 8 men/>7 women = harmful
  4. > 15 men/>13 women = dependence
  5. AUDIT-C is abbreviated form consisting of 3 questions
226
Q

FAST mushkies?

A
  1. 4 items
  2. Score 0 - 16
  3. > 3 = hazardous
  4. If answer to first question is ‘never’ then the pt is not misusing alcohol
  5. If answer to first question is weekly/daily then is hazardous/harmful/dependent
227
Q

CAGE mushkies?

A
  1. Cute down, annoyed, guilty, eye opener
  2. > =2 is positive
228
Q

ICD 10 diagnosis of problem drinking?

A

3 or more of:
1. Compulsion
2. Difficulties controlling
3. Physiological withdrawal
4. Tolerance
5. Neglect of alternative activities
6. Persistent use despite harm

229
Q

Carcinoid syndrome features?

A
  1. Flushing (earliest)
  2. Diarrhoea
  3. Bronchospasm
  4. Hypotension
  5. Right heart valvuler stenosis
  6. ACTH and GHRH ma also be secreted –> Cushing’s
  7. Pellagra can rarely develop as dietary tryptophan is diverted to serotonin by the tuour
230
Q

Carcinoid tumour Ix?

A
  1. Urinary 5-HIAA
  2. Plasma chromagranin Ay
231
Q

Carcinoid tumour Rx?

A
  1. Somatostatin analogue e.g. octreotide
  2. Diarrhoea = cyproheptadine may help
232
Q

Anti-HBs levels after immunisation aim?

A

Aim >100, but >10 generally accepted

233
Q

Aminosalicylate mushkies?

A

5-aminosalicyclic acid (5-ASA) is released in the colon and is not absorbed. It acts locally as an anti-inflammatory. The mechanism of action is not fully understood but 5-ASA may inhibit prostaglandin synthesis

234
Q

Aminosalicylate examples?

A
  1. Sulphasalazine
  2. Mesalazine
  3. Olsalazine
235
Q

Sulphasalazine s/e?

A

These are NOT seen with mesalazine = rashes, oligospermia, headache, Heinz body anaemia, megaloblastic anaemia, lung fibrosis

236
Q

Aminosalicylate s/e?

A

Agranulocytosis

237
Q

Mesalazine s/e?

A

Pancreatitis

238
Q

Liver failure clotting factors?

A

All low except for Factor 8 which is supra-normal (because factor VIII is synthesised in endothelial cells throughout the body, unlike the other clotting factors which are synthesised purely in hepatic endothelial cells)

239
Q

Metabolic acidosis with normal or low glucose?

A

Likely alcoholic ketoacidosis

240
Q

Alcoholic ketoacidosis Rx?

A

Saline and Thiamine

241
Q

IBD phenomena related to disease activity?

A
  1. Arthritis: pauciarticular, asymmetric
  2. Erythema nodosum
  3. Episcleritis
  4. Osteoporosis
242
Q

IBD phenomena unrelated to disease activity?

A
  1. Arthritis = polyarticular, symmetric
  2. Uveitis
  3. Pyoderma gangrenosum
  4. Clubbing
  5. PSC
243
Q

Liver and neurological disease?

A

Wilson’s

244
Q

Wilson’s disease definition?

A

An autosomal recessive disorder characterised by excessive copper deposition in the tissues. Metabolic abnormalities include increased copper absorption from the small intestine and decreased hepatic copper excretion. Wilson’s disease is caused by a defect in the ATP7B gene located on chromosome 13

245
Q

Wilson’s disease onset?

A

10-25 years (children usually present with liver disease, young adults usually present with neurological disease)

246
Q

Wilson’s disease features?

A
  1. Liver = hepatitis, cirrhosis
  2. Neuro = basal ganglia deterioration, neuropsychiatric
  3. Renal = tubular acidosis, esp. Fanconi’s syndrome
  4. Kayser-Fleisher rings
  5. Haemolysis, blue nails
247
Q

Wilson’s Ix?

A
  1. Slit lamp = Feyser=Fleischer rings
  2. Low caeruloplasmin, low total serum copper
  3. Free (non-caeruloplasmin bound) serum is increased, increased 24hr urinary copper excretion
  4. Diagnosis confirmed by genetic analysis of ATP7B gene
248
Q

Wilson’s Rx?

A
  1. Penicillamine 1st line
  2. Trientine hydrochloride is alternative
249
Q

Cyclical vomiting syndrome mushkies?

A
  1. Rare, more common in children, F>M
  2. Aetiology = unknown, 80% children and 25% adults have migraines
250
Q

CVS presentation?

A
  1. Severe nausea and sudden vomiting lasting hours to days
  2. Prodromal intense sweating and nausea
  3. Well in between episodes
251
Q

CVS Dx?

A

Clinical diagnosis, pregnancy test in women, routine blood tests to exclude any underlying conditions

252
Q

CVS Rx?

A
  1. Avoidance of triggers
  2. Prophylaxis = amitriptyline, propranolol and topiramate
  3. Acute = Ondansetron, prochlorperazine and triptans
253
Q

1st line to maintain remission in CD?

A

Azathioprine or 6-MP

Focused 1 (25 decks)

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