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Week 13 Flashcards

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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
What are the most common causes of abnormal liver blood tests?
fatty liver - alcohol in non chronic viral hepatitis - C autoimmune liver disease - primary biliary cholangitis, autoimmune hepatitis haemochromatosis
26
Describe the progression of alcoholic liver disease
alcoholic steatosis alcoholic hepatitis alcoholic cirrhosis
27
Describe the progression of non-alcoholic fatty disease
steatosis non-alcoholic steatitic hepatitis NAFLD cirrhosis
28
What are the main associations with NAFLD?
obesity, type 2 diabetes and hyperlipidaemia
29
How can ALD and NAFLD be differentiated with LFTs?
AST:ALT ratio | AST is much higher in ALD
30
What are the essential features on alcoholic hepatitis?
``` 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) ```
31
What are the characteristic features of alcoholic hepatitis?
hepatomegaly, fever, leucocytosis and hepatic bruit
32
What are signs of chronic liver disease?
stigmata: spiders, foetor, encephalopathy | synthetic dysfunction - prolonged prothrombin time, hypoalbuminaemia
33
What are the signs of portal hypertension?
caput medusa hypersplenisms thrombocytopaenia
34
Describe the cell count in the assessment of ascites
>500 WBC/cm3 and 250 neutrophils/cm3 suggests spontaneous bacterial peritonitis inflammatory conditions can also increase WBC count lymphocytosis suggests TB or peritoneal carcinomatosis
35
Describe the albumin in the diagnosis of ascites
serum ascites albumin gradient (SAAG) = serum albumin - ascitic albumin if SAAG >11g/l = portal hypertension
36
What is the management of ascites?
``` low salt diet spironolactone furosemide paracentesis transjugular intrahepatic portosystemic shunt liver transplant ```
37
What are common precipitating factors for hepatic encephalopathy?
``` gastrointestinal bleeding infections constipation electrolyte inbalance excess dietary (especially animal) protein ```
38
how can hepatic encephalopathy be treated?
lactulose and rifaximin
39
Describe lithogenic bile
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
40
Describe acute cholecystitis
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
41
Describe chronic cholecystitis
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
42
How does acute pancreatitis present?
severe RUQ pain fever leukocytosis raised serum amylase
43
Describe pancreatic abscess
potential complication of acute pancreatitis infected pancreatic necrosis avascular haemorrhagic pancreas good culture medium drainage or necrosectomy plus antibiotics
44
Describe a pancreatic pseudocyst
``` 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 ```
45
What are the differentials of pancreatic pseuodocysts
mucinous cystic neoplasm - ovarian type intraductal papillary mucinuos neoplasm serous cystadenoma
46
What are the risk factors for pancreatic cancer?
``` gremlin mutations (BRCA) account for small proportion smoking is by far the biggest risk factor ```
47
What are the signs and symptoms of pancreatic cancer?
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
48
Describe pancreatic endocrine tumours
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
49
Describe cholagniocarcinoma
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
Describe carcinoma of the gallbladder
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
Describe the exocrine function of the pancreas
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
describe cholelithasis
gallstones most common cause of RUQ pain abdominal ultrasound /EUS, MRCP
53
Describe acute cholecystitis
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
Describe biliary sepsis
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
Describe the presentation of acute pancreatitis
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
What are the two signs of AP?
Cullen's | Grey Turner
57
Describe the diagnosis of AP
``` 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
What is the aetiology of AP?
``` I GET SMASHED idiopathic gallstones ethanol trauma steroids mumps / malignancy autoimmune scorpion sting hyperlipidaemia, hypercalcaemia ERCP / EUS drugs (azathioprine) ```
59
How can AP be classified?
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
What is the management of acute pancreatitis?
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
Describe chronic pancreatis
``` inflammatory condition parenchyma replaced with fibrous tissue pain malnutrition diabetes increased risk of pancreatic cancer ```
62
What are the the risk factors for CP?
TIGAR - O Toxic/metabolic - alcohol tobacco, hyperlipidaemia, CKD Idiopathic genetic Autoimune RAP/SAP associated - post necrotic, vascular, post -irradiation obstructive
63
Describe the diagnosis of CP
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
What is the treatment of CP?
``` potent analgesia duct drainage address exocrine and endocrine needs smoking cessation alcohol cessation surgery - ```
65
What are the mechanisms of exocrine pancreas insufficiency?
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
What are the causes of PEI?
``` acute pancreatitis chronic pancreatitis cystic fibrosis pancreatic cancer diabetes myelitis pancreatectomy gastrectomy coeliac disease IBD Zollinger-Ellision syndromw ```
67
What are the clinical consequences of PEI?
malnutrition is main clinical consequence - more pain episodes, more hospitalisation, cardiovascular events, fracture risk, infection risk
68
How is PEI diagnosed?
confirmation with tests not always essential direct, indirect, faecal consider a trial off PERT in suspected PEI patients
69
What are the aims of PEI theraoy
to avoid steatorrhoea weight loss maldigestion related symptoms to ensure a normal nutritional status
70
What are the layers of the oesophagus?
``` mucosa (non-keratinised stratified squamous) muscularis mucosae submucosa muscularis proproa adventitia ```
71
What is the appearance of reflux oesophagitis?
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
What can cause infections of the oesophagus?
``` candida albicans (fungus) herpes simplex virus ```
73
What chemicals can cause oesophagitis?
reflux of acid, bile caustics - cleaning products (NaOH) Pills: iron, bisphosphonates, tetracyclines
74
What are other causes of oesophagitis?
diverticula, achalasia, schatzki ring, systemic sclerosis, hiatus hernia
75
Describe eosinophilic oesophagitis
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
Describe oesophageal cancre
late presentation - high lethality squamous carcinoma - associated with smoking and drinking adenocarcinoma- associated with gastro-oesophageal reflux disease and obesity
77
Describe Barrett's oesophagus
metaplastic response to mucosal injury - squamous becomes glandular usually intestinal with goblet cells associated with benign strictures but also with adenocarcinomas
78
Describe dysplasia
architecturally and cytologically abnormal low grade - cells polarised, nuclei stratified high grade - polarity lost, nuclei rounder, vesicular, prominent nucleoli, abnormal mitoses, necrosis
79
What are the causes of acute gastritis?
alcohol, NSAIDs, severe trauma
80
What are the causes of chronic gastritis?
Autoimmune Bacterial (H. pylori) Chemical
81
Describe the absorption of B12
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
Describe autoimmune gastritis
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
Describe Zollinger-Ellison syndrome
Hypersecretion of gastrin by an endocrine tumour (gastrinoma) in pancreas or duodenum leads to increased gastric acid output and severe peptic ulceration
84
Describe H.Pylori gastritis
potentially lifelong. colonises gastric mucosa and leads to chronic inflammation: IL8 attracts neutrophils
85
Describe antral-predominant gastritits
hypergastrinaemia and duodenal ulceration
86
Describe pangastriits
hypochlorhydria, multifocal atrophic gastritis, IM, cancer (intestinal type)
87
What are the causes of chemical gastritis?
bile reflux, NSAIDs, ethanol, oral iron
88
Describe gastric cancer
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
Describe diffuse gastric cancer
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
Describe familial gastric cancer
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
Describe giardiasis
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
Describe cytomegalovirus infection in the GI tract
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
Describe Whipple's disease
``` very rare affects middle aged men weight loss, arthralgia, diarrhoea, abdominal pain Diagnosed by biopsy tropheryma whipplei ```
94
Describe a tropical sprue
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
What are the intestinal diseases of entamoeba histolytica infection?
asymptomatic dysentery acute necrotising colitis with perforation toxic megacolon ameboma perianal ulceration with fistula formation
96
Describe the histopathology of coeliac disease
villous atrophy crypt hyperplasia increased number of intraepithelial lymphocytes increased number of plasma cells in lamina propria
97
What should prompt serological testing for coeliac disease?
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
What can malabsorption lead to?
iron deficiency anaemia fatty diarrhoea, bulky, pale, greasy, offensive weight loss reduced bone density with increased risk of fracture
99
What are the complications of acute appendicitis?
transmural gangrene leading to perforation generalised peritonitis right iliac fossa abscess
100
Describe the pathology of UC
``` chronic inflammation usually confined to large intestine rectum always involved inflammation confined to mucosa and submucosa no granulomas ```
101
Describe the pathology of Crohn's disease
mouth - anus commonly affects terminal ileum inflammation commonly transmural granulomas are diagnostic
102
What are the causes of ischaemic gut?
``` mesenteric artery or vein thrombosis mesenteric artery embolus hypotension stragulated hernia volvulus ```
103
Describe the history for IBD
stool frequency, constancy, urgency, blood abdo pain, malaise, fever weight loss extra intestinal symptoms (joint, eyes, skin) Travel family history smoking
104
Describe the examination for IBD
``` weight pulse temperature anaemia abdominal tenderness perineal examination ```
105
Describe erythema nodosum
perniculitis usually on shins exquisitely tender- associated with strep, sarcoid and IBD
106
Describe pyoderma gangrenosum
``` central ulceration surrounded by purple not painful does tend to heal without much scarring will respond to immunomodilatory therapy sometimes topical steroids ```
107
Describe the investigations for IBD
``` FBC, ESR U&E, LFTS CRP stool cultures + C.dif toxin faecal calprotectin AXR rigid sigmoidoscopy colonoscopy small bowel radiology labelled WCC scanning ```
108
Describe the categories of treatment for IBD
``` corticosteroids thiopurines biologics UC - 5ASAs Crohns - methotrexate, immune modulating diets ```
109
Describe the main roles of aminosalicylates
induction of remission in mild-moderate ulcerative colitis maintenance of remission in UC maintenance therapy may reduce cancer risk renal impairment
110
Describe thiopurines
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
What are the side effects of thiopurines
``` leucopenia nausea, vomiting arthralgia pancreatitis hepatitis squamous skin cancres haematological malignancy ```
112
What are the side effects of methotrexate?
``` GI upset hepatotoxicity immunosuppression sepsis pulmonary fibrosis ```
113
What is the treatment for acute severe colitis?
prophylactic LMW heparin IV hydrocortisone 100mg QDS or methylprednisalone 30mg BD treat for 72 hours if no improvement - reduce therapy
114
What is the rescue therapy for acute severe colitis?
ciclosporin infliximab surgery
115
How does upper GI bleeding present?
haematemesis | coffee ground vomiting or malaena
116
What are the causes of upper GI bleeding?
``` peptic ulcer oesophagitis gastritis duodenitis varices malignancy mallory-weiss tear other ```
117
Describe the management of upper GI bleeding
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
Describe endoscopic therapy of upper GI bleed
adrenaline injection heater probe endoscopic clips
119
Describe the use of blood products in upper GI bleedss
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
Describe the management of acute variceal bleeding
``` resucitation - diagnosis - endoscopy therapy - antibiotics early vasopressors early endoscopic banding treatment ```
121
What is used to prevent rebreeding of varices?
beta blockers and banding

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