GI Flashcards

1
Q

What is haemochromatosis?

A

An iron storage disorder- deposition of iron in tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the inheritance of haemochromatosis?

A

Autosomal recessive mutation on the HFE gene on chromosome 6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

When does haemochromatosis usually present?

A

Age > 40

later in females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Presentation of haemochromatosis

A

Chronic tiredness, joint pain, pigmentation (bronze), hair loss, ED, amenorrhoea, memory and mood problems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Investigations in haemochromatosis

A

High serum ferritin, transferrin saturation
Liver biopsy with Perl’s stain- iron concentration in parenchymal cells
Genetic testing
CT/MRI for iron deposits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Management of haemochromatosis

A

Venesection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complications of haemochromatosis

A
  • Type 1 diabetes
  • Liver cirrhosis, HCC
  • Cardiomyopathy
  • Iron in pituitary + gonads- hypogonadism, infertility
  • Hypothyroidism
  • Pseudogout
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is Wilson’s disease?

A

Excessive accumulation of copper in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the pattern of inheritance of Wilson’s disease?

A

Autosomal recessive

Mutation of ‘Wilson disease protein’ on chromosome 13

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Clinical features of Wilson’s disease

A

Hepatic- chronic hepatitis, liver cirrhosis
CNS- dysarthria, dystonia, Parkinsonism, depression, psychosis
Kayser-Fleischer rings
Haemolytic anaemia, renal tubular acidosis, osteopenia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can be seen in the eyes in Wilson’s disease?

A

Kayser-Fleischer rings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Investigations in Wilson’s disease

A

Serum caeruloplasmin
24hr urine copper assay
Liver biopsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Management of Wilson’s disease

A

Copper chelation- Penicillamine, Trientene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the aetiology of Alpha-1-Antitrypsin deficiency?

A

A1AT inhibits neutrophil elastase –> excessive protease enzymes –> liver cirrhosis and lung disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the inheritance pattern of Alpha-1-Antitrypsin deficiency?

A

Autosomal recessive defect on chromosome 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the 2 key clinical features in Alpha-1-Antitrypsin deficiency?

A

Liver cirrhosis

Pulmonary basal emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is found on liver biopsy in Alpha-1-Antitrypsin deficiency?

A

Acid-Schiff positive staining globules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Management of Alpha-1-Antitrypsin deficiency

A

Stop smoking
Manage symptoms
Organ transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the aetiology of Primary Biliary Cirrhosis?

A

Immune system attacks small bile ducts –> cholestasis –> fibrosis –> cirrhosis –> liver failure
–> decreased excretion of bile acids, bilirubin and cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Clinical features of Primary Biliary Cirrhosis

A
  • Bile acids cause jaundice
  • Bilirubin causes jaundice
  • Cholesterol causes xanthelasma + CV disease
  • GI disturbance, malabsorption, greasy stools
  • Cirrhosis- ascites, splenomegaly, spider naevi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Investigations in Primary Biliary Cirrhosis

A

Raised ALP
Antimitochondrial antibodies
Liver biopsy to diagnose and stain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Management of Primary Biliary Cirrhosis

A

Ursodeoxycholic acid- reduces absorption of cholesterol
Cholestyramine- reduces absorption of bile acids
Liver transplant
Immunosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the aetiology of Primary Sclerosing Cholangitis?

A

Intrahepatic/Extrahepatic ducts become strictured/fibrotic

  • -> Obstruction to flow of bile out of liver and into intestines
  • -> Hepatitis, Cirrhosis + Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Risk factors for Primary Sclerosing Cholangitis

A

Ulcerative colitis
Male
Age 30-40
FH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Presentation of Primary Sclerosing Cholangitis

A
Jaundice
RUQ pain
Pruritus
Fatigue
Hepatomegaly
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

LFTs in Primary Sclerosing Cholangitis

A

ALP most deranged, raised bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Diagnosis of Primary Sclerosing Cholangitis

A

MRCP –> bile duct lesions/strictures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Management of Primary Sclerosing Cholangitis

A

Liver transplant curative
ERCP + stent
Ursodeoxycholic acid, Cholestyramine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Complications of Primary Sclerosing Cholangitis

A

Colorectal cancer
Cholangiocarcinoma
Cirrhosis
Fat-soluble vitamin deficiencies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How do you test for H pylori?

A

C13 urea breath test/Stool antigen test + CLO test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Management of H pylori

A

Triple therapy:

  1. PPI
  2. Amoxicillin
  3. Clarithromycin + Metronidazole
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Achalasia?

A

Disorder of motility of lower oesophageal sphincter –> impaired peristalsis + fails to relax
Often due to an acquired aganglionic segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Presentation of achalasia

A

Dysphagia, regurgitation, chest pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CXR finding in achalasia

A

Dilated oeseophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Gold standard investigation in achalasia

A

Manometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Finding on barium swallow in achalasia

A

Bird’s beak

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Management of achalasia

A

CCB/Nitrates

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Causes of upper GI bleed

A

Peptic ulcer disease
Varices, Mallory-Weiss tear
Malignancy
Drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Investigation required in upper GI bleed

A

Endoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is a Mallory-Weiss tear?

A

Mucosal tear at the oesophago-gastric junction

Caused by persistent vomiting/wretching

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Risk factors for Mallory-Weiss tear?

A

Alcohol, Bulimia, raised ICP, Gastroenteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What are oesophageal varices?

A

Dilated veins at junction between portal and systemic venous circulation
In distal oesophagus/proximal stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Risk factors for oesophageal varices

A

Portal hypertension from chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What score is used for mortality risk in GI bleed?

A

Rockall score

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the 3 types of liver cancer?

A

Hepatocellular carcinoma (80%)
Cholangiocarcinoma
Mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the common primary sites for liver mets?

A

GI, pancreas, breast, melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Risk factors for Hepatocellular carcinoma

A

Hep B/C, Alcohol, NAFLD, chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Presentation of Hepatocellular carcinoma

A

Asymptomatic and presents late

Weight loss, abdo pain, anorexia, N&V, jaundice, pruritus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Tumour marker for Hepatocellular carcinoma

A

AFP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Management of HCC

A

Surgery

+ Sorafenib etc for viral hepatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Risk factors for Cholangiocarcinoma

A

Primary Sclerosing Cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Presentation of Cholangiocarcinoma

A

Painless jaundice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Tumour marker for Cholangiocarcinoma

A

Ca19-9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Investigations for Cholangiocarcinoma

A

Ca19-9
CT/MRI
ERCP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Management of Cholangiocarcinoma

A

Symptomatic management with bile duct stent

Surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is peritonitis?

A

Inflammation of the peritoneum due to blood, air, bacteria or GI contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Causes of peritonitis

A

AEIOU Peritoneum:

  • Appendicitis
  • Ectopic pregnancy
  • Infection with TB
  • Obstruction
  • Ulcer
  • Peritoneal dialysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Aetiology of pancreatitis

A

Pancreatic enzymes destroy pancreas and it’s blood supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Presentation of pancreatitis

A

N&V, epigastric pain radiating to back, relieved on sitting forwards, tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Signs on examination of pancreatitis

A

Cullen’s sign- superficial oedema and bruising around umbilicus
Grey-turner’s sign- bruising of flanks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Raised blood result in pancreatitis

A

Amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Management of pancreatitis

A

IV fluids

pain relief

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Blood derangements in alcoholic liver disease

A

Raised MCV
LFT: Raised AST, ALT, GGT, later on ALP, Low albumin, Raised bilirubin
Clotting: Raised PT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Complications of alcohol

A
Alcoholic liver disease, cirrhosis and HCC
Alcohol dependence and withdrawal
Wernicke-Korsakoff syndrome
Pancreatitis
Alcoholic cardiomyopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Presentation of alcohol withdrawal

A

6-12hrs: tremor, sweating, headache, craving, anxiety
12-24hrs: hallucinations
24-48hrs: seizures
24-72hrs: delirium tremens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Management of alcohol withdrawal

A

Benzodiazepine- Chlordiazepoxide 5-7 days

IV B vitamins- Pabrinex

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the aetiology of delirium tremens?

A

Chronic alcohol use –> GABA system up-regulated + glutamate system down-regulated –> opposite when alcohol removed –> excess adrenergic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Presentation of delirium tremens

A

Acute confusion, agitation, delusions, hallucinations, tremor, tachycardia, hypertension, hyperthermia, ataxia, arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Aetiology of Wernicke-Korsakoff syndrome

A

Thiamine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Presentation of Wernicke’s encephalopathy

A

Confusion, oculomotor disturbance, ataxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Presentation of Korsakoff’s syndrome

A

Memory impairment, behavioural changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Causes of liver cirrhosis

A

Alcoholic liver disease, NAFLD, Hep B/C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Presentation of liver cirrhosis

A

Jaundice, hepatosplenomegaly, spider naevi, palmar erythema, gynaecomastia, bruising, ascites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Investigations in liver cirrhosis

A

USS Fibroscan for transient elastography
Liver biopsy confirms diagnosis
Screened for HCC with AFP and USS every 6mth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Scoring systems for Liver cirrhosis

A

Child-Pugh score A, B, C for severity

MELD score for mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Management of liver cirrhosis

A

High protein low sodium diet
Propranolol reduces portal hypertension
Liver transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Complications of liver cirrhosis

A

Malnutrition, portal hypertension, varices, ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy, HCC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Stages of NAFLD

A
  1. NAFLD
  2. Non-alcoholic steatohepatitis
  3. Fibrosis
  4. Cirrhosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Risk factors for NAFLD

A

Obesity, T2DM, hypercholesterolaemia, age, smoking, hypertension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the aetiology of Meckel’s diverticulum?

A

Vestigial remnant of vitello-intestinal duct at distal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Clinical features of Meckel’s diverticulum

A

Asymptomatic/haemorrhage/obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Aetiology of Acute Mesenteric Ischaemia

A

Embolus/Thrombosis reduces blood flow to intestine –> bacterial translocation –> systemic inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Presentation of acute mesenteric ischaemia

A

Severe, colicky, poorly localised pain

No real tenderness/peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How is acute mesenteric ischaemia diagnosed?

A

CT Angiography

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Management of acute mesenteric ischaemia

A

O2, IV fluids
Papverine to relieve spasm
IV Unfractionated Heparin/Surgical angioplasty

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Causes of ischaemic colitis

A

Thrombosis, emboli, reduced cardiac output, shock, trauma, COCP, cocaine, strangulated hernia, vasculitis, clotting disorders

87
Q

Clinical features of ischaemic colitis

A

Acute LIF pain
N&V
Loose stools containing blood

88
Q

What blood gas abnormality is seen in ischaemic colitis?

A

Metabolic acidosis

89
Q

Investigation and finding in ischaemic colitis

A

Colonoscopy- blue swollen mucosa

Barium enema- thumb printing

90
Q

Which blood vessels are affected in ischaemic colitis?

A

Inferior and Superior mesenteric artery

91
Q

Differential diagnosis of malabsorption

A

Coeliac, HIV, Lymphoma, TB, Pancreatic insufficiency, Crohn’s, Amyloidosis, Hyper/pothyroidism, diabetes, eating disorders

92
Q

Define ileus

A

A non-mechanical obstruction of bowel

93
Q

Causes of intestinal obstruction

A

Adhesions, strangulated hernia, malignancy, volvulus, post-operatively, CF, Hirschsprung’s

94
Q

Presentation of intestinal obstruction

A

N&V- faeculant, abdo pain, failure to pass bowel movements or flatus, abdominal distension, high-pitched bowel sounds, dehydration

95
Q

What is heard on auscultation of bowel sounds in intestinal obstruction?

A

High-pitched bowel sounds

96
Q

Management of intestinal obstruction

A

NBM
Fluids
Intestinal decompression- endoscopy/NG tube
Laparotomy +/- stoma

97
Q

What is sigmoid volvulus?

A

Faeces and gas-filled sigmoid loop twists on mesentary

98
Q

Risk factors for sigmoid volvulus

A

Elderly, constipation, megacolon, history of sigmoid volvulus, pregnancy, pelvic masses

99
Q

Presentation of sigmoid volvulus

A

Sudden onset lower abdominal colicky pain, distension, failure to pass flatus or stool, empty rectum

100
Q

What findings are present on AXR of sigmoid volvulus?

A

Coffee-bean sign

101
Q

Management of sigmoid volvulus

A

Urgent admission + decompression

102
Q

What is paralytic ileus?

A

Lack of peristalsis in the bowel due to an autonomic imbalance causing sympathetic overactivity affecting the colon

103
Q

Presentation of paralytic ileus

A

Nausea and faeculant vomiting, NO pain, failure to pass bowel movements or flatus, NO bowel sounds, abdominal distension

104
Q

Risk factors for paralytic ileus

A

Chest infection, MI, stroke, AKI, trauma, elderly

105
Q

What findings are present on AXR of paralytic ileus?

A

Fluid levels, small bowel distension

106
Q

What is the aetiology of diverticular disease?

A

Herniation of mucosa through thickened colonic muscle

107
Q

What are the commonest sites of diverticular disease?

A

Sigmoid and descending colon

108
Q

Risk factors for diverticular disease

A

Age, obesity, low dietary fibre

109
Q

Presentation of uncomplicated diverticular disease

A

Left iliac fossa pain, worse on eating, better on flatus/defaecation, bloating, bleeding, constipation

110
Q

Presentation of diverticulitis

A
Diverticular disease (Left iliac fossa pain, worse on eating, better on flatus/defaecation, bloating, bleeding, constipation
PLUS fever, tachycardia
111
Q

Management of diverticular disease

A

Asymptomatic- high fibre diet
Symptomatic- bulk-forming laxative, paracetamol
Diverticulitis- fluids, antibiotics (Co-amoxiclav 7 days), Surgery

112
Q

Complications of diverticular disease

A

POFASH:

  • Perforation
  • Obstruction
  • Fistula
  • Abscess
  • Stricture
  • Haemorrhage
113
Q

Risk factors for GORD

A

Male, increased abdominal pressure (pregnancy, obesity etc), smoking, hiatus hernia

114
Q

Management of GORD

A

Antacids eg gaviscon

PPI eg Lansoprazole

115
Q

Complications of GORD

A

Peptic stricture, Barrett’s oesophagus

116
Q

What is the transformation in Barrett’s oesophagus?

A

Squamous to columnar epithelium

117
Q

What is the most common location of peptic ulcers?

A

Duodenal/lesser curvature of stomach

118
Q

How do you test for H pylori?

A

Urea breath test

Stool antigen

119
Q

Management of H pylori

A

Triple therapy:

  1. PPI- Lanzoprazole
  2. Clarithromycin
  3. Metronidazole
120
Q

What is the aetiology behind NSAIDs causing peptic ulcers?

A

NSAIDs inhibit prostaglandin production for mucous production –> no mucus to protect stomach

121
Q

What is the aetiology of coeliac disease?

A

Autoimmune gluten-sensitive enteropathy

Gliadin protein –> immune cell reaction at HLADQ8 –> produces toxic T cells –> villous atrophy

122
Q

Presentation of coeliac disease

A

Bloating, FTT, diarrhoea, anaemia

Dermatitis herpetiformis

123
Q

Name of skin condition seen in coeliac disease

A

Dermatitis Herpetiformis

124
Q

Blood tests for coeliac disease

A

Tissue transglutaminase antibodies IgA

Endomysial antibody IgA

125
Q

How long does gluten need to be consumed to test for coeliac disease?

A

6 weeks

126
Q

Investigations for coeliac disease

A

Tissue transglutaminase antibodies IgA
Endomysial antibody IgA
FBC for anaemia
Duodenal biopsy

127
Q

What is found on duodenal biopsy in coeliac disease?

A

Villous atrophy and crypt hyperplasia

128
Q

What criteria is used to diagnose coeliac disease on duodenal biopsy?

A

Marsh criteria

129
Q

Complications of Coeliac disease

A

Vitamin D/Iron deficiency
Osteoporosis
Infertility
Malignancy

130
Q

IBD affecting whole GI tract, skip lesions, no blood/mucus, transmural inflammation

A

Crohn’s disease

131
Q

IBD with continuous inflammation, limited to colon and rectum, blood and mucus

A

Ulcerative colitis

132
Q

Features of Crohn’s disease

A

NESTS:

  • No blood or mucus
  • Entire GI tract
  • Skip lesions
  • Terminal ileum/Transmural inflammation
  • Smoking is RF
133
Q

Features of Ulcerative Colitis

A

CLOSE UP:

  • Continuous inflammation
  • Limited to colon and rectum
  • Only superficial mucosa
  • Smoking protective
  • Excrete blood and mucus
  • Use aminosalicylates (Sulfasalazine)
  • Primary sclerosing cholangitis
134
Q

Which of Crohn’s and UC is smoking a risk factor and which is smoking protective for?

A

Crohn’s- smoking is a risk factor

UC- smoking is protective

135
Q

Presentation of IBD

A

Diarrhoea, abdominal pain, bloating, pasing blood

136
Q

Investigations of IBD

A

CRP, faecal calprotectin for inflammation

Endoscopy and biopsy diagnostic

137
Q

Management of Crohn’s

A

Acute: Steroids (oral prednisolone), Immunosuppressant (eg Azathioprine)
Maintain remission: Azathioprine, Mercaptopurine

138
Q

Management of Ulcerative Colitis

A

Aminosalicylate- Sulfasalazine, Corticosteroids
Azathioprine
Panproctocolostomy + ileostomy

139
Q

Presentation of IBS

A

Diarrhoea, constipation, fluctuating bowel habit, abdo pain, bloating
Symptoms worse after eating, improves after defaecation

140
Q

Criteria for IBS

A
Abdo pain/discomfort relieved on opening bowels or associated with a change in bowel habit
AND 2 of...
- Abnormal stool passage
- Bloating
- Worse after eating
- PR mucus
141
Q

Management of IBS

A
Lifestyle: fluid intake, limit caffeine/alcohol intake, low FODMAP diet, probiotic supplement
1st line meds: 
- Loperamide for diarrhoea
- Laxatives for constipation
- Antispasmodic- Hyoscine bromide
2nd line: Amitriptylline
142
Q

Common causative organisms of infective diarrhoea

A

Viral- rotavirus, norovirus, adenovirus
Bacteria- Campylobacter jejuni, E coli, Salmonella, Shigella
Parasite- Giardia lamblia

143
Q

Risk factors for gastric cancer

A

Age, male, H pylori, diet, smoking, FH

144
Q

Most common location of gastric cancer

A

50% pylorus

145
Q

Types of gastric cancer by location

A

Cardia/GO junction- adenocarcinoma

Distal- carcinoma

146
Q

Presentation of gastric cancer

A

Dyspepsia, Dysphagia, weight loss, anaemia, vomiting

147
Q

Investigations of gastric cancer

A

FBC, LFT

Endoscopy/sigmoidoscopy + biopsy

148
Q

Common sites of metastasis of gastric cancer

A

Lung, liver, ovary

149
Q

Management of gastric cancer

A

Surgery + pre-op chemo with 5-FU

150
Q

What condition are gastrointestinal stromal tumours associated with?

A

Neurofibromatosis type 1

151
Q

Management of gastrointestinal stromal tumour

A

Complete surgical resection + Imatinib

152
Q

Presentation of gastrointestinal stromal tumour

A

Early satiety, bloating, fever, weight loss, night sweats

153
Q

What type of cancer is a gastrointestinal stromal tumour

A

Soft tissue sarcoma

154
Q

What is the aetiology of MALT Lymphoma?

A

Mucosa-associated lymphoid tissue

Extra-nodal type of Non-Hodgkin’s lymphoma

155
Q

Where is MALT Lymphoma most common?

A

Gastric

156
Q

What infections is MALT Lymphoma associated with?

A

H pylori

Campylobacter jejuni

157
Q

Presentation of MALT Lymphoma

A

Dyspepsia, fever, nausea, constipation, weight loss, pain, ulcer

158
Q

Management of MALT Lymphoma

A

Eradication of H pylori may induce remission

Rituximab + chemo + radio +/- surgery

159
Q

Presentation of Topical Sprue

A

Diarrhoea, weight loss, steatorrhoea, fatigue

Deficiency of iron, folate, vit B12, vit A/D/K

160
Q

Investigations in Topical Sprue

A

Bloods: Deficiency of iron, folate, vit B12, vit A/D/K

Jejunal biopsy: incomplete villous atrophy

161
Q

What does jejunal biopsy show in topical sprue?

A

Incomplete villous atrophy

162
Q

Management of topical sprue

A

Fluids
Tetracycline
Nutritional supplements- folic acid, B12, iron

163
Q

Risk factors for acute mesenteric ischaemia

A

Age > 50, MI, endocarditis, atherosclerosis, hypotension, vasodepressive drugs, hypercoagulability disorders (Protein C+S deficiency), intra-abdominal infection

164
Q

Aetiology of chronic mesenteric ischaemia

A

Chronic atherosclerotic disease of vessels supplying intestine

165
Q

Presentation of chronic mesenteric ischaemia

A

Colicky/constant poorly localised pain
Weight loss, post-prandial pain and fear of eating
N&V

166
Q

Investigations of chronic mesenteric ischaemia

A

Arteriography gold standard

167
Q

Management of chronic mesenteric ischaemia

A

Asymptomatic: smoking cessation, antiplatelet
Symptomatic: open or endovascular revascularisation

168
Q

Aetiology of ischaemic colitis

A

Compromise of blood supply to colon

169
Q

Management of ischaemic colitis

A

Bowel rest + supportive care
Broad spectrum abx
Laparotomy and removal of necrotic part

170
Q

Peak age for appendicitis

A

Age 10-20

171
Q

Presentation of appendicitis

A

Abdo pain- central then settles in RIF
Loss of appetite, N&V, guarding, rebound and percussion tenderness
Tender in McBurney’s point
Rovsing’s sign

172
Q

What is Rovsing’s sign?

A

Palpation of the LIF causes RIF pain

173
Q

Management of appendicitis

A

Diagnostic laparoscopy + appendicectomy

174
Q

Define cholestasis

A

Blockage to the flow of bile

175
Q

Define cholelithiasis

A

Presence of gallstones

176
Q

Define choledocholelithiasis

A

Gallstones in the bile duct

177
Q

What is biliary colic?

A

Intermittent RUQ pain caused by gallstones irritating bile ducts

178
Q

Define cholecystitis

A

Inflammation of gallbladder

179
Q

Define cholangitis

A

Infection and obstruction of biliary system

180
Q

What is gallbladder empyema?

A

Pus in the gallbladder

181
Q

Investigation/Management of suspected Gallstones

A
  1. LFT + USS- raised bilirubin
  2. MRCP- if USS doesn’t show stones
  3. ERCP- down to sphincter of oddi to remove stones from bile duct
  4. Cholecystectomy
182
Q

What is the significance of a raised bilirubin in biliary disease?

A

Obstruction of the bile duct

Stone/head of pancreas tumour/cholangiocarcinoma

183
Q

What does a raised AST/ALT suggest?

A

Hepatocellular injury

184
Q

What is Murphy’s sign?

A

RUQ pain exacerbated by deep inspiration –> gallbladder pathology

185
Q

What is Charcot’s triad?

A
  1. RUQ pain
  2. Fever
  3. Jaundice
186
Q

What is the name of the group of symptoms which suggest cholangitis?

A

Charcot’s triad

  1. RUQ pain
  2. Fever
  3. Jaundice
187
Q

Causes of Hepatitis

A

Alcoholic hepatitis, NAFLD, viral hepatitis, autoimmune hepatitis, drug-induced hepatitis (paracetamol)

188
Q

Presentation of hepatitis

A

Abdo pain, fatigue, pruritus, muscle and joint aches, N&V, jaundice, fever (viral)

189
Q

What happens to LFTs in hepatitis?

A

Raised AST/ALT

Raised bilirubin

190
Q

Which is the most common viral hepatitis worldwide?

A

Hepatitis A

191
Q

How is Hepatitis A transmitted?

A

Faeco-orally

192
Q

Management of Hepatitis A

A

Resolves without treatment in 1-3mths
Analgesia
Vaccine prevention

193
Q

How is Hepatitis B transmitted?

A

Blood/bodily fluids + vertical transmission

194
Q

What do each of the following proteins show in Hepatitis B?

  • HBsAg
  • HBeAg
  • HBcAb
  • HBsAb
  • Hep B virus DNA
A
  • HBsAg- active infection
  • HBeAg- high infectivity
  • HBcAb- past or current infection
  • HBsAb- vaccination or past or current infection
  • Hep B virus DNA- viral load
195
Q

What does the Hepatitis B vaccine contain?

A

Hep B surface antigen- then testing for HBsAb to confirm response

196
Q

Investigations in Hepatitis B

A

Fibroscan for cirrhosis and USS for HCC

197
Q

Management of Hepatitis B

A

Antivirals- Tenofovir

Liver transplant

198
Q

How is Hepatitis C transmitted?

A

Blood + bodily fluids

199
Q

What proportion of people infected with Hepatitis C become chronic?

A

75%

200
Q

How is Hepatitis C diagnosed?

A

Hep C antibody screening test

Hep C RNA testing to confirm diagnosis

201
Q

Management of Hepatitis C

A

Antivirals- Pegylated interferon/Ribavirin

Liver transplant

202
Q

How is Hepatitis D transmitted?

A

Can only survive in patients with Hep B as attaches to HBsAg to survive

203
Q

How is Hepatitis E transmitted?

A

Faeco-oral route

204
Q

Management of Hepatitis E

A

Usually self-limiting within 1 month

205
Q

What type of cell response is autoimmune hepatitis?

A

T-cell mediated response

206
Q

What is an important step in management of all viral hepatitis?

A

NOTIFICATION of public health

207
Q

Describe the types of autoimmune hepatitis

A

Type 1: adults (40/50s)- fatigue + features of liver disease- most chronic
Type 2: children/teenage/early 20s- acute hepatitis with rise in AST/ALT and jaundice- more acute

208
Q

Which antibodies are found in type 1 autoimmune hepatitis?

A

ANA, anti-actin, anti-soluble liver antigen

209
Q

Which antibodies are found in type 2 autoimmune hepatitis?

A

Anti-LKM1, Anti-LC1

210
Q

Diagnosis of autoimmune hepatitis

A

Liver biopsy

211
Q

Management of autoimmune hepatitis

A

High dose prednisolone + azathioprine

Liver transplant

212
Q

What are the 2 types of volvulus and how do they differ?

A

Sigmoid- anticlockwise

Caecum- clockwise

213
Q

Investigations in volvulus

A

AXR- coffee bean sign

CT scan to confirm diagnosis

214
Q

Complications of volvulus

A

Obstruction, ischaemia, perforation