Gastroenterology Flashcards
1
Q
Describe the CAGE questionnaire
A
Do you think you should cut down your drinking?
Do you get annoyed at others commenting on your drinking?
Do you ever feel guilty about drinking?
Do you need a drink in the morning to help your hangover
2
Q
List the complications of alcohol
A
Alcoholic liver disease Cirrhosis and complications including HCC Alcohol dependence and withdrawal Wernicke - Korsakoff syndrome Pancreatitis Alcoholic cardiomyopathy
3
Q
What is the weekly recommended limit of alcohol
A
14 units a week, no more than 5U a day, spread evenly over 3 or more days
4
Q
Describe the AUDIT score
A
10 questions, score >8 indicates harmful drinking
5
Q
List some signs of liver disease
A
Jaundice Hepatomegaly Spider naevi Palmar erythema Gynaecomastia Bruising Ascites Caput medusae Asterixis - flapping tremor
6
Q
What investigations would you do for alcoholic liver disease
A
FBC - raised MCV
LFTs - elevated ALT and AST, low albumin due to reduced synthetic function of the liver, elevated bilirubin in cirrhosis
Clotting - elevated prothrombin time due to reduced synthetic function
U&Es - may be deranged in hepatorenal syndrome
USS - fatty change early on (increased echogenicity)
Fibro scan - used to check the elasticity of the liver by sending high frequency sound waves into the liver - helps to assess the degree of cirrhosis
Endoscopy - to assess and treat varices when portal hypertension is suspected
CT and MRI - look for fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites
Liver biopsy - used to confirm the diagnosis of alcohol related hepatitis or cirrhosis where steroid treatment is being considered
7
Q
Who can be referred for liver transplant in alcoholic liver disease
A
Severe disease if abstained from alcohol for 3 months prior to referral
8
Q
Describe the nutritional support for alcoholic patients
A
High protein diet and B vitamins
9
Q
Describe alcohol withdrawal symptoms
A
6-12hrs - tremor, sweating, headache, craving, anxiety
12-24hrs - hallucinations
24-48hrs - seizures
24-72hrs - delirium tremens
10
Q
Describe the pathophysiology of delirium tremens
A
Medical emergency associated with alcohol withdrawal (35% mortality)
Alcohol stimulates GABA receptors in the brain causing a relaxing effect on the rest of the brain,
Alcohol inhibits glutamate receptors having further inhibitory effect on electrical activity
Chronic alcohol leads to GABA system becoming down regulated and glutamate system being upregulated. When alcohol is removed, GABA under functions and glutamate over functions causing extreme excitability of the brain with excess adrenergic activity
11
Q
List the symptoms of delirium tremens
A
Acute confusion Severe agitation Delusions and hallucinations Tremor Tachycardia Hypertension hyperthermia Ataxia Arrhythmia
12
Q
How is alcohol withdrawal treated?
A
Chlordiazepoxide - benzodiazepine reducing regime titrated to the required dose based on local protocol and continued for up to a week
IV high dose B vitamins - pabrinex
13
Q
What causes Wernicke’s - Korsakoff’s syndrome?
A
Thiamine (B1) deficiency
14
Q
List the features of Wernicke’s encephalopathy
A
Confusion
Oculomotor disturbances
Ataxia
15
Q
List the features of Korsakoff’s syndrome
A
Memory impairment
Behavioural changes
16
Q
How does liver cirrhosis cause portal hypertension
A
Increased resistance in the vessels leading into the liver as a result of fibrosis and scar tissue
17
Q
List some causes of liver cirrhosis
A
Alcoholic liver disease
Non-alcoholic fatty liver disease
Hepatitis B
Hepatitis C
18
Q
List some signs of liver cirrhosis
A
Jaundice Asterixis Caput medusae Spider naevi Hepatomegaly Splenomegaly Gynaecamastia and testicular atrophy Palmar erythema Bruising Ascites
19
Q
List the investigations for cirrhosis
A
LFTs - decreased albumin
Prothrombin time - increased
U&Es - hyponatraemia (fluid retention), Ur and Cr deranged in hepatorenal syndrome
Viral markers and antibodies - see cause
Alpha fetoprotein - hepatocellular carcinoma
Ultrasound
Enhanced lifer fibrosis blood test - 1st line for testing for fibrosis in non-alcohlic fatty liver disease
Liver biopsy - cirrhosis
CT/MRI - vessel and organ changes
Endoscopy - oesophageal varices
20
Q
How often is AFP checked?
A
Every 6 months along with USS
21
Q
Describe the changes which may be seen on USS in people with cirrhosis
A
Nodularity of surface of the liver
Corkscrew appearance to arteries with increased flow as they compensate for reduced portal flow
Enlarged portal vein with reduced blood flow
Ascites
Splenomegaly
22
Q
Who should fibroscans be done 2 yearly for?
A
Hep C
Heavy alcohol drinkers (>50U men, >35 U women)
Diagnosed alcoholic liver disease
Non alcoholic fatty liver and evidence of fibrosis on ELF blood test
Chronic hep B (yearly)
23
Q
Describe the child-pugh score for liver disease
A
Estimates the severity and prognosis of liver cirrhosis
Min score - 5
Max score - 15
- bilirubin
- Albumin
- INR
- Ascites
- Encephalopathy
24
Q
Describe the MELD score
A
Guides transplant management - estimates the 3 month mortality for compensated cirrhosis
- Bilirubin
- Cr
- INR
- Na
- Dialysis
25
Describe the management of liver cirrhosis
```
USS and AFP every 6 months
Endoscopy ever 3 years
High protein, low Na diet
MELD score every 6 months - see if need referral for transplant
Treat complications
Liver transplant
```
26
List some complications of liver cirrhosis
```
Malnutrition
Portal hypertension
Varices and variceal bleeding
Hepatorenal syndrome
Hepatic encephalopathy
Hepatocellular carcinoma
```
27
How does cirrhosis cause malnutrition and muscle wasting
Increased use of muscle tissue as fuel
Disrupts metabolism of protein in liver
Reduces ability to store glucose as glycogen
28
How do you manage malnutrition in cirrhosis
```
Regular meals (every 2-3hrs)
Low sodium (minimise fluid retention
High protein diet and high calorie
```
29
Describe portal hypertension
Portal vein comes from the superior mesenteric and splenic vein and delivers blood to the liver.
Liver cirrhosis increases the resistance of blood flow in the liver and as a reuslt there is increased back pressure into the portal system
30
Describe the development of varices
Portal hypertension and back pressure causes vessels where portal system anastomoses with systemic venous system to become swollen and tortous
31
Where do varices occur?
Gastro-oesophageal junction
Ileocaecal junction
Rectum
Anterior abdominal wall via umbilical vein - caput medusae
32
Describe the treatment of stable varices
Propranolol - reduce pressure
Elastic band ligation of varices
Injection of sclerosant
Transjugular intrahepatic portosystemic shunt (TIPS)
33
Describe TIPS procedure
IR inserts wire under Xray guidance into jugular, down vena cava and into the liver via the hepatic vein. They make a connection through the liver tissue between the portal and hepatic vein and puts a stent in place to allow blood to flow directly from portal to hepatic vein and relieves pressure on the portal system
34
Describe the management of bleeding oesophageal varices
Vasopressin analogues - terlipressin (cause vasoconstriction and slow bleeding)
Correct coagulopathy - Vit K and FFP
Prophylactic broad spectrum antibiotics
Consider intubation and ICU
Endoscopy - injecting sclerosant to cause inflammatory obliteration of vessel or elastic band ligation.
Sengstaken-blakemore tube - inflatable tube inserted into oesophagus to tamponade the bleeding varices - used when endoscopy fails
35
Describe ascites in cirrhosis
Increased portal system pressure causes fluid to leak out of the capillaries in the bowel and liver into the peritoneal space. The drop of fluid causes a reduced flood flow entering the kidneys. The kidneys sense the lower pressure and release renin which leads to increased aldosterone secretion and reabsorption of fluid and sodium in the kidneys. Cirrhosis causes a transudative ascites (low protein|)
36
Describe the management of ascites
Low sodium diet
Anti-aldosterone diuretics - spironolactone
Paracentesis - ascitic drain/tap
Prophylactic antibiotics - ciprofloxacin for prevention of SBP in patients with <15g/L protein in fluid
TIPS procedure or transplantation
37
How do patients with spontaneous bacterial peritonitis present?
Asymptomatic - low threshold for ascitic fluid culture
Fever
Abdominal pain
Deranged bloods - raised WCC, CRP, Cr, Metabolic acidosis
Ileus
Hypotension
38
Name the common organisms which cause spontaneous bacterial peritonitis
E.coli
Klebsiella pneumoniae
Gram positive cocci - staphylococcus and enterococcus
39
What is spontaneous bacterial peritonitis
Infection develops ion the peritoneal fluid
40
How do you manage spontaneous bacterial peritonitis
Ascitic culture taken prior to Abx
| Give IV cephalosporin - cefotaxime
41
Describe hepatorenal syndrome
Pooling of blood in portal system causes reduction in blood supply to kidneys, vasoconstriction activates RAAS causing renal vasoconstriction and rapidly deterioating kidney function
42
Describe the treatment of hepatorenal syndrome
Liver transplant otherwise fatal within a week
43
Describe the pathophysiology of hepatic encephalopathy
Build up of ammonia which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut
- liver cells prevent the metabolism of ammonia
- collateral vessels mean ammonia bypasses the liver
44
Describe the management of hepatic encephalopathy
Laxatives - lactulose
| Antibiotics - rifaximin - reduce bacteria producing ammonia Nutritional support - NG feed
45
List the precipitating factors for hepatic encephalopathy
```
Constipation#
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications - sedatives
```
46
What can non-alcoholic fatty liver disease progress to
Hepatitis
Fibrosis
Cirrhosis
47
List the stages of non-alcoholic fatty liver disease
1 - NAFLD
2 - Non-alcoholic steatohepatitis
3 - Fibrosis
4 - cirrhosis
48
List the risk factors for NAFLD
```
Obestity
Poor diet and low activity levels
T2DM
High cholesterol
Middle aged
Smoking
High BP
```
49
List the components of a non-invasive liver screen
LFTs
USS liver
Hepatitis B and C serology
Autoantibodies - ANA, SMA, AMA, LKM-1
50
List the investigations in non-alcoholic fatty liver disease
Liver ultrasound
Enhanced liver fibrosis (ELF) blood test - 1st line for fibrosis in NAFLD but not available everywhere, Indicates the severity of fibrosis
NAFLD fibrosis score - 2nd line based on age, BMI< liver enzymes, platelets, albumin and diabetes
Fibroscan - 3rd line, ultrasound that assess the stiffness of liver and gives indication of fibrosis
51
Describe the management of NAFLD
```
Diet
Exercise
Weight loss
Stop smoking
Control DM, HTN, hypercholesterolaemia
Avoid alcohol
Refer to liver specialist if needing Vit E and pioglitazone
```
52
What is the triad in Budd-Chiari syndrome
Sudden onset abdominal pain
| Ascites and tender hepatomegaly
53
What is Budd-Chiari syndrome
Obstruction to hepatic venous outflow
| Occurs in patients in hypercoagulable state but can occur from physical obstruction
54
List the causes of hepatitis
```
Alcoholic
Viral
Autoimmune
NAFLD
Drug induced
```
55
How does hepatitis present
```
Abdo pain
Jaundice
Nausea and vomiting
Pruitis
Muscle aches
Fever
```
56
Describe the LFT picture in hepatitis
High AST and ALT with proportionally high ALP
| High bilirubin
57
Describe Hepatitis A
RNA virus
Faecal oral route
Presents with nausea, vomiting, anorexia and jaundice. May cause cholestasis - pale stools and dark urine
Resolves without treatment in 1-3 months
Manage with basic analgesia
Vaccination before travel
Notifiable disease
58
Describe hepatitis B
DNA virus
Blood borne disease and vertical transmission
Most people recover in 2 months but some become carriers - continue to produce viral proteins as viral DNA integrated into persons DNA
59
What is HBsAg
Hep B surface antigen
| Demonstrates active infection
60
What is HBeAg
E antigen - marker of viral replication and implies high infectivity
61
What is HBcAb
Core antibodies
| Implies past or current infection
62
What is HBsAb
Surface antibody
| Implies past or current infection
63
What is HBV DNA
Hep B virus DNA - direct count of the viral load
64
What do you test for when you screen for hepatitis B
HBcAb - previous infection
HBsAg - active infection - if positive do HBEAg and viral load
HBcAb - IgM version implies acute if high titrre and low titre if chronic and IgG indicates past infection
65
What is given in hep B vaccine?
HBsAg - immune system creates response and HBsAb
3 doses at different intervals
Part of routine UK vaccine scale and 6 in 1 vaccine
66
How is Hep B managed?
```
Notify public health
Refer for specialist management
Screen for other blood borne diseases
Advise lifestyle changes
Educate to reduce risk of transmission Test for complications - fibroscan and USS (HCC)
treat complications
liver transplant for end stage disease
Antiviral medication to slow disease
```
67
Describe Hep C
RNA virus
Curable with direct acting medications
1 in 4 full recovery
3 in 4 chronic hep C
68
LIst the complications of Hep C
HCCC and cirrhosis
69
How is Hep C diagnosed
Hepatitic C antibody screening test then if positive do hepatitis C RNA testing to calculate viral load and assess genotype
70
Describe the management of Hep C
```
Low threshold for screening
Notify public health
Screen for other blood borne disease
Refer
Lifestyle changes
Advise on reducing transmission
Test for complications
Antiviral treatment - direct acting antivirals - tailored to genotype - taken for 8-12 weeks
Liver transplant in end stage
```
71
Describe hepatitis D
```
RNA virus
Concurrent hep B infection - requires the hep B antigen
Notify public health
Increased risk of hep B complications
No treatment
```
72
Describe Hepatitis E
```
RNA virus
Faceal oral route, seafood and pork
Mild illness - virus cleared within a month, no treatment
Rarely progresses to liver failure
Notifiable disease
```
73
Describe autoimmune hepatitis
Genetic predisposition and trigger such as viral infection creating T cell response to attack liver cells
Two types - Type 1 occur in adults (woman in late 40s-50s, post menopausal, less acutely with fatigue and features of liver disease), anti-nuclear antibodies (ANA), anti-smooth muscle antibodies (anti-actin), anti soluble liver antigen (anti-SLA/LP)
Type 2 occurs in children (teenage, acute hepatitis with high transaminases and jaundice), Anti-LKM1, anti-LC1
Diagnosis with biopsy
74
How is autoimmune hepatitis treated?
Prednisolone
Azathioprine
Liver transplant if end stage liver disease but autoimmune hepatitis can recur in the transplanted liver.
75
What is the AST:ALT ratio in alcoholic hepatitis
2:1
76
Which hepatitis vaccine should gay men be offered?
Hep A
77
Describe ischaemic hepatitis
Reduced perfusion of liver
| Grossly elevated transaminases with AKI
78
Describe haemachromatosis and its inheritance
Iron storage disorder
Autosomal recessive
Chromosome 6 human haemochromatosis protein (HFE) mutation
79
How does haemachromatosis present?
>40yo or later in females (menstruation)
Chronic tiredness
Joint pain
Bronze discolouration
Hair loss
Sexual problems - amenorrhea and erectile dysfunction
Memory and mood
80
How is haemochromatosis diagnosed
Serum ferritin
Transferrin saturation (high)
Genetic test
Liver biopsy and pearls stain but this replaced by genetics
CT abdomen - increased attenuation of liver - iron overload
MRI - liver iron deposits and heart
81
What is serum ferritin
Acute phase protein - inflammation
82
List some complications of haemochromatosis
```
DM
Liver damage and cirrhosis and HCC
Chrondrocalcinosis - iron in joints
Pituitary gland and gonads - hypogonadism or impotence or amenorrhoea or infertility
Cardiomyopathy - heart failure
Hypothyroidism
```
83
How is haemachromatosis managed
Venesection - weekly
Serum ferritin monitor
Monitor and treat complications
84
Describe Wilsons disease and its inheritance
Accumulation of copper
Autosomal recessive
Mutation in wilsons disease protein on chromosome 13 - ATP7B copper binding protein
85
Describe the symptoms of wilsons disease
Hepatic - hepatitis, cirrhosis
Neurological - concentration, coordination, dystonia, Parkinsonism (symmetrical)
Psychiatric - depression to psychosis
Kayser-Fleischer rings - copper deposition in descements corneal membrane - brown circles surrounding iris
Haemolytic anaemia
Renal tubular acidosis
Osteopenia
86
How is wilsons disease diagnosed
```
Low serum caeruloplasmin
Liver biopsy
24hr urine copper assay
Low serum copper
Kayser fleischer rings
MRI brain showing non specific changes
```
87
How is wilsons disease managed
Copper chelation with penicillamine or trientene
88
What is alpha-1-antitrypsin deficiency
Autosomal recessive defect in gene for alpha-1-antitrypsin which usually prevents the neutrophil elastase enzyme breaking down the connective tissues
Liver cirrhosis >50
Lung bronchiectasis and emphysema >30yo
89
How is alpha-1-antitrypsin diagnosed?
Low serum alpha-1-antitrypsin
Liver biopsy shows cirrhosis and acid schiff positive staining globules
Genetic testing for A1AT gene
High resolution CT thorax
90
Describe the management of alpha-1-antitrypsin
Stop smoking
Symptom management
Organ transplant
Monitor for complications
91
Describe primary biliary cirrhosis
Autoimmune condition which attacks the small bile ducts in the liver (intralobar ducts)
92
Describe the presentation of primary biliary cirrhosis
```
Middle aged women
Other autoimmune or rheumatoid conditions
Fatigue
Pruitis
GI disturbance and abdominal pain
Jaundice
Pale and greasy stools
Xanthoma and xanthelasma
Signs of cirrhosis and liver failure - ascites, splenomegaly, spider naevi
```
93
How is primary biliary cirrhosis diagnosed?
LFTs - ALP is first liver enzyme to be raised, other liver enzymes and bilirubin are raised in later disease
Auto antibodies - Anti-mitochondrial antibodies, Anti-nuclear antibodies
ESR raised
IgM raised
Liver biopsy - diagnosing and staging disease
94
Describe the treatment of primary biliary cirrhosis
Ursodeoxycholic acid - reduces intestinal absorption of cholesterol
Colestyramine - bile acid sequestrate in that it binds to bile acids and prevents absorption in the gut and can help with pruitis (raised bile acids)
Liver transplant
Immunosuppression
95
Describe the disease progression of primary biliary cirrhosis
```
Advanced liver cirrhosis
Portal hypertension
Symptomatic pruitis
Fatigue
Steatorrhoea
Distal renal tubular acidosis
Hypothyroidism
Osteoporosis
Hepatocellular carcinoma
```
96
Describe primary sclerosing cholangitis
Stricturing and fibrosis of the intrahepatic or extrahepatic ducts causing obstruction to bile
97
Describe the presentation of primary sclerosing cholangitis
```
Jaundice
Chronic right upper quadrant pain
Pruitis
Fatigue
Hepatomegaly
```
98
Describe the diagnosis of primary sclerosisng cholangitis
Deranged ALP and high bilirubin, other liver function off in later disease
Auto antibodies to see if autoimmune component - p-ANCA, ANA, aCL
Gold standard is MRCP
99
Describe the management of primary sclerosing cholangitis
ERCP - stenting of strictures
Colestyramine - prevents pruitis
Monitor for complications
Liver transplant
100
List the complications of primary sclerosisng cholangitis
```
Acute bacterial cholangitis
Cholangiocarcinoma
Colorectal cancer
Liver cirrhosis and failure
Biliary strictures
Fat soluble vitamin deficiency
```
101
Which other GI disease is primary sclerosising cholangitis linked to?
Ulcerative colitis
102
Where does the endoscope travel in ERCP
Through duodenum into the sphincter of oddi and into the ampulla of vater to bile ducts
103
What are the two types of primary liver cancer?
Hepatocellular (80%)
| Cholangiocarcinoma (20%) - bile ducts
104
What are the risk factors for hepatocellular carcinoma
Liver cirrhosis due to viral hep B &C, alcohol, NAFLD
105
What are the risk factors for cholangiocarcinoma
Primary sclerosing cholangitis
106
What is the presentation of liver cancer
```
WEight loss
Abdo pain but no pain in cholangiocarcinoma
Anorexia
Nausea and vomiting
Jaundice
Pruitis
```
107
How is liver cancer diagnosed
```
Alpha fetoprotein - hepatocellular
CA19-9 - cholangiocarcinoma
Liver USS
CT/MRI
ERCP and biopsy
```
108
Describe the treatment of hepatocellular cancer
Resistant to chemo/radiotherapy
Surgical resection or liver transplant if refined to liver
Kinase inhibitors - reduce proliferation - sorafenib, regorafenib, lenvatinib
109
Describe the treatment of cholangiocarcinoma
ERCP and stent
Resistant to chemo and radiotherapy
Surgical resection in very early disease
110
What is a haemangioma
Common benign tumour of liver
| No symptoms and no cancerous potential so no treatment or monitoring
111
What is focal nodular hyperplasia?
```
Benign liver tumour made of fibrotic tissue
Found incidentally
No symptoms and no malignant potential
More common in women taking COCP
No treatment or monitoring required
```
112
Name the two types of incision in liver transplant
Roof top
| Mercedes benz
113
List some contraindications of liver transplant
```
Significant co morbidity - severe kidney or heart disease
Excessive weight loss and malnutrition
Active hepB and C or other infection
End stage HIV
Active alcohol use
```
114
What is the lining to the oesophagus
Squamous epithelial lining
115
What is the lining to the stomach
Columnar epithelial lining
116
Describe the symptoms of GORD
```
Heart burn
Acid regurgitation
Pain in retrosternal area or epigastrium
Bloating
Bowels
Nocturnal cough
Hoarse voice
```
117
When would you refer a GORD patient for endoscopy
Bleed (malaena and coffee ground vomit) - urgent admission and endoscopy
```
2 week wait -
Dysphagia
Age >55
Weight loss
Upper abdominal pain/reflux
Treatment resistant dyspepsia
Low Hb
Raised platelet count
```
118
Describe the treatment of GORD
Lifestyle - reduce tea, coffee, alcohol, weight loss, avoid smoking, avoid heavy meals, stay upright after eating
Gaviscon and rennie
PPI - lansoprazole and omeprazole
Ranitidine - H2 receptor antagonist (antihistamine), reduce acid secretion
Surgery - laparoscopic fundoplication - tie fundus around the lower oesophageal sphincter to narrow it
119
What tyype of bacteria is Helicobacter pylori
Gram negative aerobic bacteria
120
Describe H pylori
Lives in stomach
Causes damage to the epithelial lining resulting in gastritis, ulcers and increases risk of stomach cancer
Evades the stomach acid by forcing its way into the gastric mucosa and creating breaks in the mucosa to expose the epithelial cells under the acid
Produces ammonia to neutralise the acid - this directly damages the epithelial lining
121
How is H.pylori tested for?
Urea breath test - radiolabelled carbon 13
Stool antigen test
Rapid urease test (CLO) test - performed during endoscopy and involves taking biopsy of stomach mucosa, adding urea. If H.pylori is present then this produces urase enzymes that convert the urea to ammonia - ammonia makes the solution more alkali giving a positive result when pH is tested
122
How is H.pylori eradicated?
Triple therapy - PPI and 2 antibiotics (amoxicillin and clarithromycin) for 7 days
Urea breath test after treatment to test for eradication
123
What is Barrett's oesophagus
Pre-malignant condition for development of adenocarcinoma of the oesophagus
Changing of the squamous epithelium to columnar epithelium (metaplasia) this is then at risk of dysplasia
124
How is Barrett's oesophagus treated?
PPI
| Ablation treatment - photo-dynamic therapy, laser therapy and cyrotherapy in dysplasia
125
Which ulcer is worsened by eating food?
Peptic ulcer
126
Which ulcer is improved by eating food?
Duodenal ulcer
127
How are peptic/duodenal ulcers treated?
High dose PPI
128
List some complications of duodenal/peptic ulcers
Bleeding
Perforation
Scarring/strictures
129
List some causes of Upper GI bleed
Oeosphageal varices
Mallory weiss tear - tear of oesophagus mucous membrane
Ulcers
Cancer
130
How do peopl with upper GI bleeds present
Haematemeiss
Coffee ground comit
malaena
Haemodynamic instability - hypotension, tachycardia, sign of shocj (young people compensate)
131
Name the scoring system used in predicting upper GI bleeds
```
Glasgow blatchford score
Score >0 indicates high risk of GI bleed
- Drop in Hb
- Raised ur - breakdown of blood by acid and digestive enzyme
- BP
- HR
-Melaena
Syncope
```
132
Name the scoring system used to predict mortality and risk of re bleeding after endoscopy
```
Rockall score
- age
- comorbidity
- shock
cause of bleed
- endoscopic stigmata of recent haemorrhage - visible bleeding vessels and clots
```
133
Describe the management of upper GI bleed
ABCDE approach
Access - 2 large bore cannulae
Bloods - FBC (Hb, plts), U&Es (Ur), coagulation (INR), LFTs (liver disease), cross match 2 Units.
Transfuse - depending on individual presentation, blood, platelets and clotting factors (FFP) to patients with massive haemorrhage, prothrombin complex in someone taking warfarin
Endoscopy - urgent if unstable, within 24hrs if stable - OGD - provide interventions to stop bleeding (banding and cauterisation)
Drugs - stop NSAIDs and anticoagulants, some senior doctors give PPI
If oesophageal varices - give terlipressin and prophylactic broad spectrum antibiotics
134
Describe the features of crohns disease
```
No blood or mucus
Entire GI tract
Skip lesions
Terminal ileum and Transmural thickness inflammation
Smoking is a RF
Weight loss, strictures and fistula
```
135
Describe the features of ulcerative colitis
```
Continuous inflammation
Limited to Rectum and colon
Only the superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use of aminosalicylates
Primary sclerosisng cholangitis
```
136
List the tests for IBD
Bloods - FBC, U&E, LFT, CRP
Faecal calprotectin
Endoscopy - OGD and colonoscopy
Imaging - USS, CT, MRI - fistulas, abscesses and strictures
137
How do you induce remission in crohns
Oral prednisolone or IV hydrocortisone
138
How do you maintain remission in crohns
```
Azathioprine
Mercaptopurine
Methotrexate
Infliximab
Adalinumab
```
Surgery when affecting distal ileum
139
How do you induce remission in mild/moderate UC
Aminosalicylate - mesalazine PO/PR or corticosteroids (prednisolone)
140
How do you induce remission in severe disease
```
IV corticosteroids (hydrocortisone)
IV ciclosporin
```
141
How do you maintain remission in UC
Aminosalciylates - mesalazine PO/PR
Azathioprine
Mercaptopurine
Panproctocolectomy (remove the colon and rectum), ileostomy or J-pouch (ileo-anal anastomosis where the ileum is folded back into itself and fashioned into a larger pouch that functions like a rectum)
142
Which scoring system is used for the severity of IBD flare
Truelove and Witts criteria
143
List some symptoms which are suggestive of IBD
Abdominal pain relieved on opening bowels or associated with a change in bowel habit, abnormal stool passage, bloating, worse symptoms after eating and PR mucus
144
Describe the management of IBD
Adequate fluid intake
Regular small meals
Reduced processed food
Limit caffeine and alcohol
Low FODMAP diet
Trial of probiotic supplement 4 weeks
Loperamide for diarrhoea and laxatives (not lactulose for constipation as causes bloating)
Antispasmodics - hyoscine butylbromide (buscopan)
Tricyclic antidepressants (amitriptyline) or SSRI antidepressants and CBT
145
Describe coeliac disease
Autoantibodies produced in response to exposure to gluten
| Lead to inflammation of the epithelial cells in intestine
146
How is coeliac diagnosed
Total immunoglobulin A levels - exclude IgA deficiency
Raised anti-TTG (tissue transglutaminase antibodies) antibodies
Raised anti-EMA (endomysial antibodies) antibodies
Deaminated gliadin peptide antibodies (anti-DGPs)
Endoscopy and intestinal biopsy - crypt hypertrophy and villous atrophy
147
Which genes are implicated in coeliac disease
HLA-DQ2 and HLA-DQ8
148
Describe the presentation of coeliac disease
```
Failure to thrive
Diarrhoea
Fatigue
Weight loss
Mouth ulcers
Anaemia secondary to B12 and folate deficiency
Dermatitis herpetiformis
Peripheral neuropathy
Cerebellar ataxia
Epilepsy
```
149
List the associations of coeliac disease
```
T1DM
Thyroid disease
Autoimmune hepatitis
Primary biliary cirrhosis
Primary sclerosing cholangitis
```
150
List the complications of untreated coeliac disease
```
Vitamin deficiency
Anaemia
Osteoporosis
Ulcerative jejunitis
Enteropathy associated T cell lymphoma
Non-Hodgkin lymphoma
Small bowel adenocarcinoma
```
151
What is the treatment for coeliac disease
Life long gluten free diet
| Pneumococcal vaccine every 5 yrs
152
Which anti-emetic should be avoided in bowel obstruction
Metoclopramide - increases the peristalsis and can precipitate perforation
153
What is the treatment of C.difficle
Oral vancomycin
154
What is Plummer Vinson syndrome
Oesophageal web associated with iron deficiency anaemia
