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Finals > Gastroenterology and General Surgery > Flashcards

Gastroenterology and General Surgery Flashcards

1
Q

Give the stages of alcoholic liver disease

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

Give the recommended weekly maximum number of units of alcohol

A

14

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3
Q

Describe the CAGE questionnaire

A

Cut down - have you ever thought you should cut down on your drinking?

Annoyed - do you ever get annoyed at others commenting on your drinking?

Guilty - do you ever feel guilty about your drinking?

Eye opener - do you ever drink in the morning to help you get through the day?

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4
Q

What questionnaires can be used to screen for harmful alcohol consumption?

A

CAGE

AUDIT (>8 suggests harmful use)

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5
Q

Give the serious complications of alcohol consumption

A

Cirrhosis

Wernicke-Korsakoff syndrome

Pancreatitis

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6
Q

Give the presentation of alcoholic liver disease

A
  1. Jaundice
  2. Hepatomegaly
  3. Spider naevi
  4. Asterixis (liver flap)
  5. Palmar erythema
  6. Bruising
  7. Ascites
  8. Caput medusae
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7
Q

Give the investigations for alcoholic liver disease

A

FBC - raised MCV
LFT - raised ALT, ALP, gamma-GT, bilirubin. Decreased albumin
Clotting - elevated PT
USS - increased echogenicity
Endoscopy - to treat oesophageal varices
CT/MRI - to assess for cancer
Biopsy - definitive diagnosis

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8
Q

Give the management of alcoholic liver disease

A
  1. Permanent alcohol abstinence
  2. Thiamine (IV pabrinex)
  3. Steroids - aid short term outcome
  4. Liver transplant
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9
Q

Describe the stages of alcohol withdrawal

A

6-12 hours: tremor, sweating, headache, cravings and anxiety

12-24 hours: hallucinations

24-48 hours: seizures

24-72 hours: delirium tremens

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10
Q

Describe the pathophysiology of delirium tremens

A

Excess excitability of neurones due to removal of previous constant inhibitor (alcohol) which they had adapted to

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11
Q

Give the presentation of delirium tremens

A
  1. Acute confusion/agitation
  2. Delusions/hallucinations
  3. Tremor
  4. Tachycardia/hypertension
  5. Ataxia (difficulty with co-ordinated movement)
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12
Q

Give the management of delirium tremens

A
  1. Chlordiazepoxide (benzodiazepine)
  2. IV parbrinex
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13
Q

Describe the pathophysiology of Wernicke-Korsakoff syndrome

A

Alcohol excess causes thiamine (vit B1) deficiency

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14
Q

Describe the presentation of Wernicke’s encephalopathy

A
  1. Confusion
  2. Oculomotor disturbance
  3. Ataxia
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15
Q

Describe the presentation of Korsakoff syndrome

A
  1. Memory impairment
  2. Behavioural changes

Irreversible - patients require round-the-clock care

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16
Q

Describe the pathophysiology of liver cirrhosis

A

Chronic inflammation results in the replacement of normal hepatic tissue with scar tissue (fibrosis), which disrupts blood flow through the liver and causes portal hypertension.

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17
Q

Give the causes of liver cirrhosis

A
  1. Alcoholic liver disease
  2. NAFLD
  3. Hepatitis B & C
  4. Haemochromatosis
  5. Wilson’s disease
  6. Cystic fibrosis
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18
Q

Give the presentation of liver cirrhosis

A
  1. Jaundice
  2. Hepatosplenomegaly
  3. Spider naevi
  4. Palmar erythema
  5. Bruising
  6. Asterixis
  7. Caput medusae
  8. Ascites
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19
Q

Give the investigations for liver cirrhosis

A
  1. Enhanced liver fibrosis blood test - 1st line
  2. USS
  3. Fibroscan
  4. Liver biopsy
  5. Deranged LFTs
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20
Q

Give the complications of liver cirrhosis

A
  1. Malnutrition
  2. Oesophageal varices
  3. Hepatic encephalopathy
  4. Hepatocellular carcinoma
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21
Q

Describe the presentation of oesophageal varices

A
  1. Asymptomatic
  2. Bleeding - patients may bleed out very quickly!
    a) Haematemesis
    b) Meleana
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22
Q

Give the management of oesophageal varices

A
  1. Propranolol - reduced portal hypertension
  2. Elastic band ligation
  3. Sengstaken-Blakemore tube - compresses oesophageal bleeding
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23
Q

Describe the management of ascites

A
  1. Low-sodium diet
  2. Spironolactone
  3. Paracentesis
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24
Q

Describe spontaneous bacterial peritonitis

A

Infection of the ascitic fluid resulting in generalised infective peritonitis.

Commonly caused by E. coli or klebsiella pneumoniae

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25
Q

Describe the management of spontaneous bacterial peritonitis

A
  1. Culture of ascitic fluid
  2. IV cefotaxime
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26
Q

Describe the pathophysiology of hepatic encephalopathy

A

Build-up of toxins which affect the brain - most commonly ammonia

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27
Q

Describe the presentation of hepatic encephalopathy

A
  1. Confusion
  2. Reduced consciousness
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28
Q

Give the management of hepatic encephalopathy

A
  1. Laxatives (i.e. lactulose) - promote ammonia excretion
  2. Antibiotics (i.e. rifaximin) - reduces the number of ammonia-producing bacteria
  3. Nutritional support
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29
Q

Describe the pathophysiology of NAFLD

A

Deposition of lipids within hepatocytes, which interfere with the normal functioning of the liver - potentially resulting in hepatitis and cirrhosis.

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30
Q

Give the management of small intestine bacterial overgrowth syndrome

A

Rifaximin

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31
Q

Describe the stages of NADLD

A
  1. NAFLD
  2. Non-alcoholic steato-hepatitis
  3. Fibrosis
  4. Cirrhosis
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32
Q

Give the risk factors for NAFLD

A
  1. Obesity
  2. T2DM
  3. High cholesterol
  4. Older age
  5. Smoking
  6. HTN
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33
Q

Describe the components of a liver screen

A

If abnormal LFTs with no identifiable cause, do a liver screen:
1. USS liver
2. Hepatitis B & C serology
3. Autoantibodies (e.g. ANA)
4. Immunoglobulins (for autoimmune hepatitis)
5. Caeruloplasmin
6. Alpha-1-antitrypsin
7. Ferritin and transferrin

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34
Q

Give the managemnt of NAFLD

A
  1. Weight loss
  2. Exercise
  3. Avoid alcohol
  4. Stop smoking
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35
Q

Describe hepatitis

A

Inflammation of the liver - which can lead to large areas of necrosis and liver failure

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36
Q

Describe the causes of hepatitis

A
  1. Alcohol
  2. NAFLD
  3. Viral
  4. Autoimmune
  5. Drug induced 9e.g. paracetamol overdose)
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37
Q

Give the presentation of hepatitis

A
  1. Abdominal pain
  2. Fatigue
  3. Pruritus
  4. Fever (if viral)
  5. N+V
  6. Muscle pain
  7. Jaundice
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38
Q

Describe the presentation of Hepatitis A

A

Cholestasis:
1. Dark urine
2. Pale stool

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39
Q

Describe the management of Hepatitis A

A
  1. Resolves spontaneously in 1-3 months
  2. Basic analgesia
  3. Vaccination
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40
Q

Describe the pathophysiology of Hepatitis B

A

DNA virus conducted via blood or bodily fluids, or via vertical transmission from mother to fetus

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41
Q

Describe the viral markers for Hepatitis B

A

HBsAg - signifies active infection
Anti-HBc - signifies previous infection
Anti-HBs - signifies immunity
Viral load - to assess extent of infection

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42
Q

What pattern of viral markers would be seen in acute/chronic Hepatitis B infection?

A

+ve HBsAg

Chronic Hep B have symptoms for >6 months

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43
Q

What pattern of viral markers would be seen in previous Hepatitis B infection?

A

+ve HBcAg

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44
Q

What pattern of viral markers would be seen in previous Hepatitis B infection if now a carrier?

A

+ve Anti-HBc
+ve HBsAg

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45
Q

What pattern of viral markers would be seen in previous Hepatitis B vaccination?

A

+Anti-HBs

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46
Q

Give the management of Hepatitis B

A

Most recover within 2 months, but 10% become chronic carriers

  1. Screen for other blood-borne or sexually transmitted infections
  2. Notify public health
  3. Fibroscan - for cirrhosis
  4. Antivirals
  5. Liver transplant
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47
Q

Give the management of Hepatitis C

A
  1. Notify public health
  2. Stop smoking and drinking alcohol
  3. USS and fibroscan
  4. Direct acting antivirals
  5. Liver transplant
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48
Q

Give the risks of hepatitis C

A

Hepatocellular carcinoma

Cirrhosis

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49
Q

Describe hepatitis D

A

Can only exist alongside hepatitis B, but increases it’s severity

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50
Q

Describe hepatitis E

A

Very mild, self-limiting illness which requires no treatment.

If immunocompromised may progress to hepatitis and liver failure.

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51
Q

Describe autoimmune hepatitis

A

Type 1: seen in adults, associated with ANA, anti-actin and anti-SLA

Type 2: see in children, associated with anti-LKM, anti-LC

Diagnose with biopsy

Manage with prednisolone and azathioprine

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52
Q

Describe haemochromatosis

A

Iron storage disorder resulting in excess total iron with resultant deposition in tissues.

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53
Q

Describe the inheritance pattern seen in haemochromatosis

A

Autosomal recessive

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54
Q

Describe the presentation of haemochromatosis

A
  1. Age >40
  2. Chronic tiredness
  3. Joint pain
  4. Hair loss
  5. Erectile dysfunction
  6. Amenorrhoea
  7. Memory/mood disturbance
  8. Bronze skin pigmentation
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55
Q

Describe the diagnosis of haemochromatosis

A
  1. Serum ferritin and transferrin raised
  2. Genetic testing
  3. Liver biopsy using Perl’s stain
  4. CT/MRI
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56
Q

Describe the complications of haemochromatosis

A
  1. T1DM
  2. Liver cirrhosis
  3. Hypothyroidism
  4. Cardiomyopathy
  5. Hepatocellular carcinoma
  6. Pseudogout
57
Q

Give the management of haemochromatosis

A
  1. Venesection. (decreases total iron)
  2. Monitor serum ferritin
  3. Avoid alcohol
58
Q

Describe Wilson’s disease

A

Excessive accumulation of copper as a result of the mutation in the ‘Wilson disease protein’

59
Q

Describe the inheritance pattern seen in Wilson’s disease

A

Autosomal recessive

60
Q

Describe the presentation of Wilson’s disease

A

Hepatic: hepatitis and cirrhosis

CNS: dysarthria, dystonia, Parkinsonism

Psychiatric: depression, psychosis

Kayser-Fleischer rings
Haemolytic anaemia
Osteopenia
Renal tubular acidosis

61
Q

Describe the diagnosis of Wilson’s disease

A

Serum caeruloplasmin - the protein which carries copper in the blood, would be low

Liver biopsy

Serum copper

62
Q

Give the management of Wilson’s disease

A

Copper chelation therapy:
1. Penicillamine
2. Trientene

Risk of developing psychosis secondary to Wilson’s

63
Q

Give the pathophysiology of alpha-1 antitrypsin deficiency

A

Alpha-1 antitrypsin normally inhibits elastase (produced by neutrophils) which breaks down elastic tissues.

Due to a genetic mutation there is insufficient alpha-1 antitrypsin which results in reduced inhibition of elastase, causing liver cirrhosis, bronchiectasis and emphysema.

64
Q

Describe the diagnosis of alpha-1 antitrypsin deficiency

A
  1. Serum alpha-1 antitrypsin - reduced
  2. Liver biopsy
  3. CT thorax (for pulmonary complications)
65
Q

Describe the management of alpha-1 antitrypsin deficiency

A
  1. Stop smoking (rapidly accelerates emphysema)
  2. Symptomatic management
  3. Organ transplantation
  4. Monitor for complications (incl. HCC)
66
Q

Give the pathophysiology of pellagra

A

Vitamin B3 (niacin) deficiency

67
Q

Give the presentation of pellagra

A

Pellagra: Dermatitis, diarrhoea, dementia/delusions, leading to death

68
Q

Give 1 side effect of sulfasalazine

A

Heinz body anaemia

69
Q

Describe the pathophysiology of primary biliary cirrhosis

A

Autoimmune disorder affecting the small bile ducts within the liver resulting in obstruction, as well as fibrosis, cirrhosis and liver failure due to the back-pressure of bile.

70
Q

Describe the presentation of primary biliary cirrhosis

A
  1. Xanthelasma - cholesterol deposits within the skin
  2. Pruritus
  3. Jaundice
  4. Pale stools
  5. GI disturbance and abdo pain
71
Q

Describe the investigations for primary biliary cirrhosis

A

LFTs - raised ALP, ALT and bilirubin

Autoantibodies - e.g. AMA, ANA

ESR - raised

IgM - raised

Liver biopsy

72
Q

Give the management of primary biliary cirrhosis

A
  1. Ursodeoxycholic acid
  2. Colestyramine
  3. Steroids (for immunosuppression)
  4. Liver transplant
73
Q

Describe the pathophysiology of primary sclerosing cholangitis

A

Where the intra/extra-hepatic ducts become strictured and fibrotic, causing an obstruction to the outflow of bile

74
Q

Give the risk factors for primary sclerosing cholangitis

A
  1. UC
  2. FHx
  3. Male
  4. Age 30-40

Infection can trigger in those who are predisposed

75
Q

Give the presentation of primary sclerosing cholangitis

A
  1. Jaundice
  2. Chronic RUQ pain
  3. Pruritus
  4. Fatigue
  5. Hepatomegaly
76
Q

Give the investigations for primary sclerosing cholangitis

A

pANCA, ANA, aCL autoantibodies positive

Raised ALP and bilirubin

GOLD STANDARD: MRCP (magnetic resonance cholangiopancreatography)

77
Q

Give the management of primary sclerosing cholangitis

A
  1. Liver transplant
  2. ERCP (endoscopic retrograde cholangiopancreatography)
  3. Colestyramine - helps with pruritus
78
Q

Give the two types of liver cancer

A
  1. Hepatocellular carcinoma
  2. Cholangiocarcinoma
79
Q

Give the risk factors for hepatocellular carcinoma

A
  1. Viral hepatitis
  2. Alcohol
  3. NAFLD
80
Q

Give the risk factors for cholangiocarcinoma

A
  1. Primary sclerosing cholangitis
  2. Parasitic infection (liver flukes)
81
Q

Give the presentation of hepatocellular carcinoma

A
  1. Non-specific Sx, e.g. weight loss, abdo pain, anorexia, pruritus
  2. Liver dysfunction
82
Q

Give the investigations for hepatocellular carcinoma

A
  1. Alpha-fetoprotein - tumour marker
  2. Liver USS
  3. CT/MRI (for diagnosis or staging)
83
Q

Give the management of hepatocellular carcinoma

A
  1. Surgical resection
  2. Liver transplant possible
  3. Sorafenib
84
Q

Describe the pathophysiology of GORD

A

Stomach acid regurgitates through the lower oesophageal sphincter and irritates the oesophageal epithelium

85
Q

Give the presentation of GORD

A
  1. Heartburn (retrosternal/epigastric pain)
  2. Acid regurgitation
  3. Hoarse voice
  4. Nocturnal cough
86
Q

Give the referral indications for endoscopy in GORD

A
  1. Dysphagia
  2. Age >55
  3. Weight loss
87
Q

Give the management of GORD

A
  1. Lifestyle advice (lose weight, smaller and lighter meals)
  2. Gaviscon & Rennie etc.
  3. PPI
  4. Ranitidine (as ALTERNATIVE to PPI if not tolerated) - e.g. H2 receptor antagonist
88
Q

Describe the H. pylori bacterium

A

Gram -ve aerobic bacterium

89
Q

Give the investigations for H. pylori

A
  1. Urea breath test (no PPI for 2 weeks prior) - best for testing following eradication therapy
  2. Stool antigen test
90
Q

Give the management of H. pylori

A

Triple therapy:
1. PPI
2. Amoxicillin
3. Clarithromycin

91
Q

Describe the pathophysiology of Barretts oesophagus

A

Constant reflux results in metaplasia - conversion of oesophageal squamous epithelium to columnar epithelium.

Considered pre-malignant

92
Q

Give the presentation of Barretts oesophagus

A
  1. Improvement in GORD symptoms
93
Q

Give the management of Barretts oesophagus

A
  1. Major risk factor for oesophageal adenocarcinoma - regular endoscopy to identify early
  2. PPI
  3. Ablation treatment - destroys the epithelium so it is replaced with normal cells
94
Q

Describe the pathophysiology of peptic ulcers

A

Ulceration of the gastric or duodenal mucosa, commonly caused by NSAIDs, steroids and H. pylori

95
Q

Give the presentation of peptic ulcers

A
  1. Epigastric discomfort/pain
  2. N+V
  3. Dyspepsia
  4. Haematemesis (“coffee-ground” appearance)
  5. Iron deficiency anaemia
96
Q

Give the impact of eating on gastric/duodenal ulcers

A

Gastric: pain worsens

Duodenal: pain improves

97
Q

Give the management of peptic ulcers

A

Triple therapy (PPI + amoxicillin + clarithromycin)
- if no H. pylori then PPI only

98
Q

Give the diagnosis of peptic ulcer disease

A

Endoscopy

(+ H. pylori testing)

99
Q

Give the complications of peptic ulcer disease

A
  1. Bleeding - may be life threatening
  2. Perforation - may present with acute abdomen and peritonitis
100
Q

Describe the boundaries of the upper GI tract

A

Mouth -> ligament of Treitz (in duodenum)

101
Q

Give the causes of upper GI bleed

A
  1. Oesophageal varices
  2. Mallory-Weiss tear
  3. Ulcers
  4. Cancer
102
Q

Give the presentation of an upper GI bleed

A
  1. Haematemesis
  2. Meleana
  3. Haemodynamic instability
103
Q

Give the management of an upper GI bleed

A

ABATED:
A- ABCDE
B- bloods (coagulation, crossmatch)
A- access
T- transfuse
E- endoscopy
D- drugs (stop anticoagulant and NSAID)

Oesophagogastroduodenoscopy - provides interventions to stop bleeding

104
Q

What features are seen in Crohn’s but not UC

A

NESTS:
N- no blood or mucus
E- entire GI tract
S- skip lesions
T- transmural (full-thickness)
S- smoking is a risk factor

Anal strictures and fistulas are seen

105
Q

Give the management of infected strictures/fistulas in Crohn’s

A

Metronidazole

106
Q

Give the features seen in UC but not Crohn’s

A

CLOSEUP:
C- continuous inflammation
L- limited to colon and rectum
O- only superficial mucosa affected
S- smoking is protective
E- excrete blood and mucus
U- use aminosalicylates (e.g. mesalazine/sulfasalazine)
P- primary sclerosing cholangitis

Drainpipe colon on AXR

107
Q

Give the presentation of IBD

A
  1. Diarrhoea
  2. Weight loss
  3. Abdominal pain
  4. Passing blood
108
Q

Give the diagnostic investigations for IBD

A
  1. Endoscopy with biopsy
  2. Faecal calprotectin
  3. CRP
109
Q

Give the management of Crohn’s for inducing remission

A

1st line: oral prednisolone/IV hydrocortisone
2nd line: steroids PLUS azathioprine/methotrexate/infliximab

110
Q

Give the management of Crohn’s for maintaining remission

A

1st line: azathioprine
2nd line: methotrexate/infliximab

111
Q

Give the surgical management of Crohn’s

A

Resection of distal ileum if affected in isolation

112
Q

Give the management of UC for inducing remission

A

1st line: aminosalicylate (e.g. mesalazine)
2nd line: prednisolone

If severe disease:
1st line: IV hydrocortisone
2nd line: IV ciclosporin

113
Q

Give the management of UC for maintaining remission

A
  1. Aminosalicylate (e.g. mesalazine)
  2. Azathioprine
114
Q

Give the surgical management of UC

A

Panproctocolectomy (removal of colon and rectum with permanent ileostomy)

115
Q

Give the pathophysiology of IBS

A

Functional bowel disorder with no discernable organic cause i.e. abnormal functioning of an otherwise normal bowel

116
Q

Give the presentation of IBS

A
  1. Diarrhoea/constipation
  2. Fluctuating bowel habit
  3. Abdo pain/bloating/PR mucus

Sx worst after eating and improved by opening bowels

117
Q

Give the investigations for IBS

A
  1. Faecal calprotectin - to exclude IBD
  2. Anti-TTG - to exclude coeliac
  3. Normal blood results otherwise
118
Q

Give the management of IBS

A
  1. Low FODMAP diet
  2. Probiotic supplements
  3. General healthy diet and exercise
  4. Loperamide - for diarrhoea
  5. Laxatives - for constipation (but avoid lactulose)
  6. Hyoscine butylbromide - for cramps

Can also give amitryptiline, SSRI or CBT

119
Q

Give the pathophysiology of coeliac disease

A

Autoimmune condition in which exposure to gluten causes an autoimmune reaction resulting in inflammation of the small bowel

120
Q

Give the antibodies involved in coeliac disease

A
  1. Anti-TTG
  2. Anti-EMA
121
Q

Give the histological changes seen in coeliac disease

A
  1. Villous atrophy
  2. Crypt hyperplasia

These lead to malabsorption

122
Q

Give the presentation of coeliac disease

A
  1. Anaemia - secondary to B12/iron/folate deficiency
  2. Dermatitis herpetiformis - itchy blistering rash typically on the abdomen
  3. Weight loss
  4. Diarrhoea
  5. Fatigue
  6. Mouth ulcers
  7. Failure to thrive in young children
123
Q

Give the management of coeliac disease

A

Gluten-free diet

124
Q

Give the investigations for coeliac disease

A
  1. Anti-TTG + Anti-EMA + Total IgA (must compare to total IgA as in general IgA deficiency the other antibodies will also be reduced)
  2. Endoscopy and intestinal biopsy

Tests must be conducted while patient on a gluten-containing diet

125
Q

Give the presentation of peritonitis

A
  1. Guarding
  2. Rigidity
  3. Rebound tenderness
  4. Percussion tenderness
  5. Abdo pain on coughing
126
Q

Give the three types of peritonitis

A
  1. Localised - caused by underlying organ inflammation
  2. Generalised - rupture of abdominal organ causes widespread inflammation
  3. Spontaneous bacterial peritonitis - infection of ascites in a patient with liver disease
127
Q

Give the pathophysiology of appendicitis

A

Pathogens become trapped in appendix due to obstruction, leading to inflammation, gangrene and rupture.

If rupture occurs, faeces and infective material are released into the peritoneal cavity, causing a generalised peritonitis.

128
Q

Give the presentation of appendicitis

A
  1. Anorexia (not eating)
  2. Abdo pain (initially central, then shifting to RIF)
  3. N+V
  4. Low-grade fever
  5. Guarding
  6. Rebiund tenderness
  7. Percussion tenderness
129
Q

Describe Rovsing’s sign

A

Palpation of LIF causes pain in RIF

Seen in appendicitis

130
Q

Describe the location of McBurney’s point

A

1/3 distance from ASIS to umbilicus

Tenderness at this point suggests appendicitis

131
Q

Give the diagnosis of appendicitis

A

Clinical picture alongside raised inflammatory markers

USS and urine b-hCG - excludes ectopic pregnancy

CT - excludes other causes if they are more likely

132
Q

Give the management of appendicitis

A

Appendicectomy

133
Q

Give the management of peritonitis

A
  1. ABCDE
  2. Nil by mouth (in case surgery needed)
  3. NG tube (if bowel obstruction or vomiting)
  4. IV fluids
  5. IV Abx (e.g. tazocin in sepsis)
  6. Analgesia
  7. Blood crossmatch
134
Q

Which oesophageal malignancy does Barrett’s oesophagus increase the risk of?

A

Adenocarcinoma

135
Q

Which oesophageal malignancy does achalasia increase the risk of?

A

Squamous cell carcinoma

136
Q

Give 1 risk factor for C. diff infection

A

PPIs

137
Q

Give the first line therapy for C. diff

A

Oral vancomycin

138
Q

Give a histological sign of gastric adenocarcinoma

A

Signet ring cells

Finals (11 decks)

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