Week 13 Flashcards

1
Q

What are the broad causes of injury to the liver?

A
drugs and toxins including alcohol
abnormal nutrition / metabolism
infection
obstruction to bile or blow flow
autoimmune liver disease
genetic/deposition disease
neoplasia
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2
Q

What is meant by fulminant hepatitis?

A

severe acute, rapidly progressing towards liver failure

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3
Q

What is the definition of cirrhosis?

A

end stage liver disease

diffuse process with fibrosis and nodule formation

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4
Q

What is the clinical approach to liver disease?

A

History, symptoms and signs by examination
investigations - bloods, LFTS, haematology, viral and autoimmune serology, metabolic tests
radiology - ultrasound

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5
Q

What are some of the types of diffuse liver disease?

A
acute hepatitis
acute cholestsis
fatty liver disease
chronic hepatitis
chronic biliary disease
hepatic vascular disease 
deposition / genetic disease
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6
Q

What is the appearance of acute hepatitis?

A

Diffuse hepatocyte injury seen as swelling, some cell death. spotty necrosis. There is an inflammatory cell infiltrate in all areas - portal tracts, interface and parenchyma

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7
Q

What are the causes of acute cholestasis or cholestatic hepatitis?

A

extrahepatic biliary obstruction

drug injury - antibiotics

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8
Q

What is the appearance of acute cholestasis in histology?

A

brown bile (bilirubin) pigment, +/- acute hepatitis

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9
Q

Describe hepatitis B on pathology

A

acute hepatitis plus fibrosis

ground glass cytoplasm in hepatocytes

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10
Q

What are the causes of chronic biliary / cholestatic disease?

A

primary biliary cholangitis

primary sclerosing cholangitis

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11
Q

What is the historical appearance of chronic biliary disease?

A

focal, portal predominant inflammation and fibrosis with bile duct injury
Granulomas in PBC

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12
Q

What are the causes of genetic/deposition liver disease?

A

haemochromatosis
wilson’s disease
alpha 1 antitrypsin

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13
Q

What are the non neoplastic space occupying lesions (focal liver lesions)?

A

developmental/degenertive cysts

inflammatory - abscess

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14
Q

What is the commonest form of liver cyst?

A

Von Meyenberg complex (simple biliary hamartoma)

can resemble metastases by naked eye operation

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15
Q

What are the benign and malignant names of liver cell neoplasms?

A
hepatocellular adenoma
hepatocellular carcinoma (HCC)
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16
Q

What are the benign and malignant names of bile duct neoplasms?

A

bile duct adenoma (rare)

cholangio-carcinoma

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17
Q

What are the benign and malignant names of blood vessels neoplasms in liver?

A

haemangioma

angiosarcoma

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18
Q

Describe a haemangioma

A

benign blood vessel tumour

biopsy avoided because risk of bleeding

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19
Q

Describe a hepatic adenoma

A

rare
mainly young women, often associated with hormonal therapy
risk of bleeding and rupture so excision if large

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20
Q

Describe hepatocellular carcinoma

A

most common primary liver tumour
usually arises in cirrhosis and associated with elevated serum alpha feto-protein
screening available

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21
Q

What are the normal functions of the liver?

A
protein, carbohydrate and fat metabolism
plasma protein and enzyme synthesis
production of bile
detoxification
storage of protein, glycogen, vitamins and metals
immune function
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22
Q

How is the actual function of the liver assessed?

A

albumin
bilirubin
prothrombin time

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23
Q

How should chronic liver disease be investigated?

A
ultrasound 
viral hepatitis serlogy
AI - ANA/SMA/LKM (AIH), AMA (PBC)
metabolic liver disease- ferritin (haemachromatosis)
caeruloplasmin (wilsons)
alpha 1 antitrypsin deficiency
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24
Q

How should acute liver injury be investigated?

A

ultrasound
acute viral hepatitis serology
autoimmune liver disease (ANA, AMA, LKM (AIH), immunoglobulins”
paracetamol levels

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25
Q

What are the most common causes of abnormal liver blood tests?

A

fatty liver - alcohol in non
chronic viral hepatitis - C
autoimmune liver disease - primary biliary cholangitis, autoimmune hepatitis
haemochromatosis

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26
Q

Describe the progression of alcoholic liver disease

A

alcoholic steatosis
alcoholic hepatitis
alcoholic cirrhosis

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27
Q

Describe the progression of non-alcoholic fatty disease

A

steatosis
non-alcoholic steatitic hepatitis
NAFLD cirrhosis

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28
Q

What are the main associations with NAFLD?

A

obesity, type 2 diabetes and hyperlipidaemia

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29
Q

How can ALD and NAFLD be differentiated with LFTs?

A

AST:ALT ratio

AST is much higher in ALD

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30
Q

What are the essential features on alcoholic hepatitis?

A
excess alcohol within 2 months 
bilirubin >80 for less than 2 months 
exclusion of other liver disease 
treatment of sepsis / GI bleeding 
AST >500 (AST:ALT ration >1.5)
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31
Q

What are the characteristic features of alcoholic hepatitis?

A

hepatomegaly, fever, leucocytosis and hepatic bruit

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32
Q

What are signs of chronic liver disease?

A

stigmata: spiders, foetor, encephalopathy

synthetic dysfunction - prolonged prothrombin time, hypoalbuminaemia

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33
Q

What are the signs of portal hypertension?

A

caput medusa
hypersplenisms
thrombocytopaenia

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34
Q

Describe the cell count in the assessment of ascites

A

> 500 WBC/cm3 and 250 neutrophils/cm3 suggests spontaneous bacterial peritonitis
inflammatory conditions can also increase WBC count
lymphocytosis suggests TB or peritoneal carcinomatosis

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35
Q

Describe the albumin in the diagnosis of ascites

A

serum ascites albumin gradient (SAAG) = serum albumin - ascitic albumin
if SAAG >11g/l = portal hypertension

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36
Q

What is the management of ascites?

A
low salt diet 
spironolactone
furosemide 
paracentesis
transjugular intrahepatic portosystemic shunt
liver transplant
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37
Q

What are common precipitating factors for hepatic encephalopathy?

A
gastrointestinal bleeding
infections
constipation
electrolyte inbalance 
excess dietary (especially animal) protein
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38
Q

how can hepatic encephalopathy be treated?

A

lactulose and rifaximin

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39
Q

Describe lithogenic bile

A

bile becomes lithogenic for cholesterol if there is excessive secretion of cholesterol or decreased secretion of bile salts
excessive secretion of bilirubin (haemolytic anaemia) can cause its precipitation in concentrated bile in the gallbladder

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40
Q

Describe acute cholecystitis

A

severe RUQ pain, tenderness and fever
leukocytosis and normal serum amylase
usually resolves spontaneously but can progress to empyema, gangrene and rupture
initiated by stone obstruction of cystic duct causing supersaturation of bile and chemical irritation

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41
Q

Describe chronic cholecystitis

A

may be a sequel to repeated attacks of acute cholecystitis
gallstones are virtually always present
inflammation secondary to chemical damage (supersaturated bile)
rather than bacterial infection

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42
Q

How does acute pancreatitis present?

A

severe RUQ pain
fever
leukocytosis
raised serum amylase

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43
Q

Describe pancreatic abscess

A

potential complication of acute pancreatitis
infected pancreatic necrosis
avascular haemorrhagic pancreas good culture medium
drainage or necrosectomy plus antibiotics

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44
Q

Describe a pancreatic pseudocyst

A
potential complication of acute pancreatic
no epithelial lining 
commonly in lesser sac
high concentration of pancreatic enzymes
may resolve spontaneously 
may be drained into stomach
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45
Q

What are the differentials of pancreatic pseuodocysts

A

mucinous cystic neoplasm - ovarian type
intraductal papillary mucinuos neoplasm
serous cystadenoma

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46
Q

What are the risk factors for pancreatic cancer?

A
gremlin mutations (BRCA) account for small proportion
smoking is by far the biggest risk factor
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47
Q

What are the signs and symptoms of pancreatic cancer?

A

painless obstructive jaundice
new onset diabetes
abdominal pain due to pancreatic insufficiency or nerve invasion
tumours in head may obstruct pancreatic duct and bile duct - double duct sign on radiology

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48
Q

Describe pancreatic endocrine tumours

A

rare
may secrete hormones
commonest functional tumour is insulinoma which presents with hypoglycaemia, mainly benign
malignant endocrine tumours have a much better prognosis than pancreatic carcinoma

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49
Q

Describe cholagniocarcinoma

A

classified as intrahepatic or extra hepatic depending on origin
intrahepatic has to be distinguished from metastatic adnenocarcinoma and HCC
Extrahepatic has similar morphology and prognosis to pancreatic carcinoma,.

50
Q

Describe carcinoma of the gallbladder

A

rare
gallstones usually present
adenocarcinoma
dismal prognosis unless incidentally found in a gallbladder removal for chronic cholecystitis
local infiltration may make gallbladder seem abnormally stuck down at theatre

51
Q

Describe the exocrine function of the pancreas

A

ductal cells release alkaline fluid in response to secretin
acinar cells secrete digestive enzymes in response to secreaogues (CCH, secretin, substance P, VIP, acetylcholine, bombesin)
starch and glycogen breakdown
triglycerides
protein and polypeptides

52
Q

describe cholelithasis

A

gallstones
most common cause of RUQ pain
abdominal ultrasound /EUS, MRCP

53
Q

Describe acute cholecystitis

A

mainly secondary to gallstones
risk factors -female, fat, increasing age, rapid weight loss, pregnancy, drugs
persistent gallbladder neck or cystic duct obstruction
pain may radiate to right shoulder
Murphy’s sign
associated with fever and nausea
LFTs often deranged - elevated transaminases, ALP, mild hyperbilirubinaemia, mild hypermylasaemia

54
Q

Describe biliary sepsis

A

cholangitis
chacots triad - fever, jaundice and RUQ pain
causes - gallstones, biliary manipulation, hepatobiliary malignancy
obstructive LFTs
may have raised amylase
positive blood cultures 50%
broad spectrum antibiotics and ERCP/PTC

55
Q

Describe the presentation of acute pancreatitis

A

acute severe upper abdominal pain
50% radiates to back
partially relieved by sitting or bending forward
severe pancreatico - multi-organ failure, pleural effusions, ascites
5-10% painless
jaundice may be present if gallstones disease

56
Q

What are the two signs of AP?

A

Cullen’s

Grey Turner

57
Q

Describe the diagnosis of AP

A
elevated serum amylase >3 times ULN
amylase rises within 6-12 hours
has a short half life 
alcoholic and hypertriglyceride pancreatitis - amylase may be lower
serum lipase - elevated for longer
imaging -Ct
58
Q

What is the aetiology of AP?

A
I GET SMASHED 
idiopathic 
gallstones 
ethanol
trauma
steroids
mumps / malignancy 
autoimmune
scorpion sting 
hyperlipidaemia, hypercalcaemia
ERCP / EUS
drugs (azathioprine)
59
Q

How can AP be classified?

A

internal oedematous acute pancreatiis
necrotising acute pancreatitis
mild (no organ failure or complications)
moderately severe (organ failure <48 hours or local complications)
severe acute pancreatitis (persistent rogan failure >48 hours)

60
Q

What is the management of acute pancreatitis?

A

supportive in mild cases - fluid replacement, pain control, PO/enteral nutriotion, antibiotics (only if sepsis)
treat underlying cause
persistant symptomatic fluid collections >4 weeks may need drainage

61
Q

Describe chronic pancreatis

A
inflammatory condition
parenchyma replaced with fibrous tissue
pain
malnutrition
diabetes
increased risk of pancreatic cancer
62
Q

What are the the risk factors for CP?

A

TIGAR - O
Toxic/metabolic - alcohol tobacco, hyperlipidaemia, CKD
Idiopathic
genetic
Autoimune
RAP/SAP associated - post necrotic, vascular, post -irradiation
obstructive

63
Q

Describe the diagnosis of CP

A

calcification on imagine
aspiration of duodenal secretions post secretin / CCK at ERCP
secretin enchanted MRCP
EUS
labelled carbon breath test
wedge biopsy or section of resected pancreas

64
Q

What is the treatment of CP?

A
potent analgesia
duct drainage
address exocrine and endocrine needs
smoking cessation
alcohol cessation
surgery -
65
Q

What are the mechanisms of exocrine pancreas insufficiency?

A

reduced secretion due to pancreatic disease
low CCK released to duodenal disease
acidic duodenal pH due to gastric hyper secretion or low bicarb secretion
abnormal aboral transit due to surgery

66
Q

What are the causes of PEI?

A
acute pancreatitis
chronic pancreatitis
cystic fibrosis
pancreatic cancer
diabetes myelitis 
pancreatectomy
gastrectomy
coeliac disease
IBD
Zollinger-Ellision syndromw
67
Q

What are the clinical consequences of PEI?

A

malnutrition is main clinical consequence - more pain episodes, more hospitalisation, cardiovascular events, fracture risk, infection risk

68
Q

How is PEI diagnosed?

A

confirmation with tests not always essential
direct, indirect, faecal
consider a trial off PERT in suspected PEI patients

69
Q

What are the aims of PEI theraoy

A

to avoid
steatorrhoea
weight loss
maldigestion related symptoms

to ensure a normal nutritional status

70
Q

What are the layers of the oesophagus?

A
mucosa (non-keratinised stratified squamous)
muscularis mucosae 
submucosa
muscularis proproa
adventitia
71
Q

What is the appearance of reflux oesophagitis?

A

acid and digestive enzymes injure squamous epithelium lining oesophagus. increased numbers of inflammatory cells and basal layer. proliferative zone of the squamous epithelium is hyperplastic

72
Q

What can cause infections of the oesophagus?

A
candida albicans (fungus)
herpes simplex virus
73
Q

What chemicals can cause oesophagitis?

A

reflux of acid, bile
caustics - cleaning products (NaOH)
Pills: iron, bisphosphonates, tetracyclines

74
Q

What are other causes of oesophagitis?

A

diverticula, achalasia, schatzki ring, systemic sclerosis, hiatus hernia

75
Q

Describe eosinophilic oesophagitis

A

overlap with reflux oesophagitis
causes dysphasia
eosinophils infiltrate epithelium. Allergic aetiology. Responsive to steroids
may be possible to identify dietary sensitisers
fluticasone sometimes used in treatment

76
Q

Describe oesophageal cancre

A

late presentation - high lethality
squamous carcinoma - associated with smoking and drinking
adenocarcinoma- associated with gastro-oesophageal reflux disease and obesity

77
Q

Describe Barrett’s oesophagus

A

metaplastic response to mucosal injury - squamous becomes glandular
usually intestinal with goblet cells
associated with benign strictures but also with adenocarcinomas

78
Q

Describe dysplasia

A

architecturally and cytologically abnormal
low grade - cells polarised, nuclei stratified
high grade - polarity lost, nuclei rounder, vesicular, prominent nucleoli, abnormal mitoses, necrosis

79
Q

What are the causes of acute gastritis?

A

alcohol, NSAIDs, severe trauma

80
Q

What are the causes of chronic gastritis?

A

Autoimmune
Bacterial (H. pylori)
Chemical

81
Q

Describe the absorption of B12

A

B12 bound to salivary haptocorrin is protected from gastric acid
haptocorrin is digested in duodenum
B12 binds to Intrinsic factor secreted by gastric parietal cells. Absorbed in terminal ileum via specialised receptor

82
Q

Describe autoimmune gastritis

A

autoimmune destruction of parietal cells
anti-parietal cell antibodies in blood
eventual complete loss of parietal cells with pyloric and intestinal metaplasia
achlorydia - bacterial overgrowth
hypergastrinaemia - endocrine cell hyperplasia / carcinoids
persistent inflammation can lead to dysplasia and to cancer

83
Q

Describe Zollinger-Ellison syndrome

A

Hypersecretion of gastrin by an endocrine tumour (gastrinoma) in pancreas or duodenum leads to increased gastric acid output and severe peptic ulceration

84
Q

Describe H.Pylori gastritis

A

potentially lifelong. colonises gastric mucosa and leads to chronic inflammation: IL8 attracts neutrophils

85
Q

Describe antral-predominant gastritits

A

hypergastrinaemia and duodenal ulceration

86
Q

Describe pangastriits

A

hypochlorhydria, multifocal atrophic gastritis, IM, cancer (intestinal type)

87
Q

What are the causes of chemical gastritis?

A

bile reflux, NSAIDs, ethanol, oral iron

88
Q

Describe gastric cancer

A

historically more distal than proximal
strongly associated with chronic gastritis - H.pylori or autoimmune
background atrophic mucosa, chronic inflammation, intestinal metaplasia, dysplasia
intestinal versus diffuse
proximal (reflux) vs distal (infectious)

89
Q

Describe diffuse gastric cancer

A

individual malignant cells with mucin vacuoles: signet ring cells
may invade extensively without being endoscopically obvious - linitis plastica
weaker link with gastritis
metastasis to ovaries (Krukenberg tumour)
supraclavicular lymph node (Virchows)
Sister Joseph’s nodule - umbilical

90
Q

Describe familial gastric cancer

A

CDH1 (E.cadherin) mutation
Penetrance - 70-80% lifelong
small intamucosal foci of diffuse gastric cancer may be numerous
prophylactic gastrectomy
increased risk lobular carcinoma of breast

91
Q

Describe giardiasis

A

waterborne protozoal infection
rare in Glasgow
usually a chronic infection
diarrhoea, malabsorption, weight loss but often asymptomatic
associated with immunodeficiency - can then be very serious
treated with metronidazole

92
Q

Describe cytomegalovirus infection in the GI tract

A

presents with severe pain, weight loss, weakness, remitting fever
gastrointestinal lesions are erosive ulcerous or ulceronephrotic
infection and viral replication, mostly occurs in ulcerative disease of the intestine - IBD

93
Q

Describe Whipple’s disease

A
very rare
affects middle aged men
weight loss, arthralgia, diarrhoea, abdominal pain
Diagnosed by biopsy
tropheryma whipplei
94
Q

Describe a tropical sprue

A

also called post-infectious sprue
affects people living in or visiting the tropics
endemic and epidemic features
may be due to E.coli or haemophilus.
Presents in a similar fashion to coeliac disease
can be successfully treated with a long course of tetracycline

95
Q

What are the intestinal diseases of entamoeba histolytica infection?

A

asymptomatic
dysentery
acute necrotising colitis with perforation
toxic megacolon
ameboma
perianal ulceration with fistula formation

96
Q

Describe the histopathology of coeliac disease

A

villous atrophy
crypt hyperplasia
increased number of intraepithelial lymphocytes
increased number of plasma cells in lamina propria

97
Q

What should prompt serological testing for coeliac disease?

A

persistent unexplained abdominal or GI symptoms
faltering growth
prolonged fatigue
unexplained weight loss
severe or persistent mouth ulcers
unexplained iron, vitamin B12 or folate deficiency
type 1 diabetes at diagnosis
autoimmune thyroid disease at diagnosis
irritable bowel syndrome
first degree relatives of people with coeliac disease

98
Q

What can malabsorption lead to?

A

iron deficiency anaemia
fatty diarrhoea, bulky, pale, greasy, offensive
weight loss
reduced bone density with increased risk of fracture

99
Q

What are the complications of acute appendicitis?

A

transmural gangrene leading to perforation
generalised peritonitis
right iliac fossa abscess

100
Q

Describe the pathology of UC

A
chronic inflammation
usually confined to large intestine
rectum always involved
inflammation confined to mucosa and submucosa
no granulomas
101
Q

Describe the pathology of Crohn’s disease

A

mouth - anus
commonly affects terminal ileum
inflammation commonly transmural
granulomas are diagnostic

102
Q

What are the causes of ischaemic gut?

A
mesenteric artery or vein thrombosis 
mesenteric artery embolus
hypotension 
stragulated hernia
volvulus
103
Q

Describe the history for IBD

A

stool frequency, constancy, urgency, blood
abdo pain, malaise, fever
weight loss
extra intestinal symptoms (joint, eyes, skin)
Travel
family history
smoking

104
Q

Describe the examination for IBD

A
weight
pulse
temperature
anaemia 
abdominal tenderness
perineal examination
105
Q

Describe erythema nodosum

A

perniculitis
usually on shins
exquisitely tender- associated with strep, sarcoid and IBD

106
Q

Describe pyoderma gangrenosum

A
central ulceration surrounded by purple
not painful
does tend to heal without much scarring 
will respond to immunomodilatory therapy 
sometimes topical steroids
107
Q

Describe the investigations for IBD

A
FBC, ESR
U&amp;E, LFTS
CRP
stool cultures + C.dif toxin
faecal calprotectin 
AXR
rigid sigmoidoscopy
colonoscopy 
small bowel radiology 
labelled WCC scanning
108
Q

Describe the categories of treatment for IBD

A
corticosteroids
thiopurines
biologics
UC - 5ASAs
Crohns - methotrexate, immune modulating diets
109
Q

Describe the main roles of aminosalicylates

A

induction of remission in mild-moderate ulcerative colitis
maintenance of remission in UC
maintenance therapy may reduce cancer risk
renal impairment

110
Q

Describe thiopurines

A

azothioprine and mercaptopurine are unliscenced in IBD therapy
effective as maintenance therapy for both
prevent T cell clonal expansion
need to checkTPMT
monitoring of FBC and LFT important

111
Q

What are the side effects of thiopurines

A
leucopenia
nausea, vomiting
arthralgia
pancreatitis
hepatitis
squamous skin cancres
haematological malignancy
112
Q

What are the side effects of methotrexate?

A
GI upset
hepatotoxicity
immunosuppression
sepsis
pulmonary fibrosis
113
Q

What is the treatment for acute severe colitis?

A

prophylactic LMW heparin
IV hydrocortisone 100mg QDS or methylprednisalone 30mg BD
treat for 72 hours if no improvement - reduce therapy

114
Q

What is the rescue therapy for acute severe colitis?

A

ciclosporin
infliximab
surgery

115
Q

How does upper GI bleeding present?

A

haematemesis

coffee ground vomiting or malaena

116
Q

What are the causes of upper GI bleeding?

A
peptic ulcer
oesophagitis 
gastritis 
duodenitis 
varices
malignancy 
mallory-weiss tear 
other
117
Q

Describe the management of upper GI bleeding

A

resuscitate if required - pulse and BP, IV access - fluid /bloods, check hb, urea, lie flat, give oxygen
risk assessment and timing of endoscopy
drug therapy and transfusion

118
Q

Describe endoscopic therapy of upper GI bleed

A

adrenaline injection
heater probe
endoscopic clips

119
Q

Describe the use of blood products in upper GI bleedss

A

restrictive transfusion if Hb <7-8
transfuse platelets if actively bleeding and count <50
FFP if INR >1.5
prothrombin complex concentrate if on warfarin and active bleeding

120
Q

Describe the management of acute variceal bleeding

A
resucitation - 
diagnosis - endoscopy
therapy - antibiotics early 
vasopressors early
endoscopic banding treatment
121
Q

What is used to prevent rebreeding of varices?

A

beta blockers and banding