GI Flashcards

1
Q

What are the main causes Of liver cirrhosis

A

Alcohol related liver disease
NAFLD
Hep B
Hep C
Autoimmune hep
Wilsons/ haemochromatosis
Primary Hillary cirrhosis

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2
Q

What is in a non invasive liver screen

A

USS liver
Hep B/C serology
Autoanitbodies (ANA, SMA, AMA)
Immunoglobulins
Caeruloplasmin
Alpha-1 antitrypsin def
Ferritin and transferritin

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3
Q

What investigations are used to diagnose liver cirrhosis

A

USS - NAFLD- fatty changes= increased echo

Fibroscan- transient elastrography

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4
Q

What is the scoring system for cirrhosis

A

Child Pugh Score
Minimum score 5 max is 15
ABCDE
Albumin, bilirubin, clotting INR, dilation (ascites), encephalopathy

Do MELD score every 6 months for end stage liver disease in compensated liver cirrhosis

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5
Q

What is the management of bleeding oesophageal varices

A

Prevention- non selective bet a blockers or variecal band ligation

Bleeding varices- blood transfusion (major Haemoglobin protocol), FFP,vasopressin, somatostatin, broad spectrum abx, urgent endoscopy with vatical band ligation

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6
Q

What infection can occur in patients with ascites and how is it managed

A

Spontaneous bacterial peritonitis
Caused by E.Coli or Klebsiella pneumonia

Sample ascitic fluid for culture before giving abx
IV broad spectrum abx0 piperacillin with tazobactam

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7
Q

What are the stages of alcoholic liver disease

A
  1. Alcoholic fatty liver- hepatic steatosis - reversible with abstinence

2.Alcoholic hepatitis

  1. Cirrhosis
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8
Q

What is the main issue with alcohol withdrawal

A

Delerium tremens- under functioning GABA and over functioning glutamate - extreme brain excitability

Management: Chlorodiazepoxide- bento with dose reduced over 5-7 days
High dose B vitamins IM or IV and long term thiamine

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9
Q

What is Kernicke Korsakoff Syndrome

A

Thiamine deficiency causes confusion, ataxia etc

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10
Q

How do you diagnose NAFLD

A

1ST LINE- enhanced liver fibrosis (ELF) blood test - 10.51 or < = advanced fibrosis

ALT:AST <0.8

liver biopsy = gold standard but painful

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11
Q

How do you get Hep A

A

RNA- faecal oral route- contaminated water etc
Vaccine available

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12
Q

How do you get Hep b

A

DNA
Blood contact/ body fluids
Most recover, some will be chronic carriers

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13
Q

what are the different Hep B antibodies and what do they mean

A

HBsAG- surface antigen- active infection

HBeAg- infectivity

HBcAb- core antibodies- previous infection

IgM= active infection
IgG= past infection

HBsAb= antibody= vaccination

HBV DNA- direct viral load count

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14
Q

How do you get Hep C and what is it associated with

A

RNA, spread blood and body fluids
Curable with antiviral meds but no vaccine
Associated with liver cirrhosis and hepatic cellular carcinoma

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15
Q

What are the two types of autoimmune hepatitis and how is it diagnosed ?

A

Type 1- women in later 40s/50s around menopause- fatigue and liver disease

Type 2- children and young people

Investigations
Liver biopsy will show interface hepatitis and plasma cell infiltration
High ALT and AST no change in ALP
Raised IgG
ANA, anti-smooth muscle ab and anti-soluble liver antigen

Treat with steroids and immunosuppressants

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16
Q

What is haemochromatosis and how is it treated

A

Autosomal recessive -Chr 6

Diagnosed
Serum ferritin and transferrin saturation

Genetic testing
Liver biopsy with perls stain

Management
Venesection
Monitoring serum ferritin and complications

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17
Q

What is Wilson’s disease ?

A

Autosomal recessive - Chr 13
Teens/ young adults- liver neuro, psych, anaemia

Diagnosis
Serum caeuloplasmin screening test (if low Wilson’s)
24 hr urine copper assay- high urinary copper
Liver biopsy
Genetic testing

Management
Copper chelation
Penicillamine
Trientine

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18
Q

What is alpha-1 antitrypsin deficiency

A

Affects lungs- COPD and liver fibrosis
-Autosomal codominant Chr 14
-Alpha-1 antitrypsin made in liver - builds up in hepatocytes when mutated - fibrosis , lack of it also causes neutrophils to attack elastin in lungs

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19
Q

Describe the pathology of primary biliary cholangitis

A

Autoimmune system attacks small bile ducts in liver- obstructive jaundice and liver disease (intrahepatic)

Blocked flow of bile acids (itching), bilirubin (jaundice) and cholesterol (xanthelasma)

Women 40-60

Auto-antibodies - anti-mitochondrial antibodies most specific

20
Q

What is the treatment for primary biliary cholangitis

A

Ursodeoxycholic acid (a bile acid)
Colestyramine (bile acid sequestrate to stop itching)
Replace fat soluble vitamins
Immunosuppression
Liver transplant

21
Q

Describe the pathophysiology of Primary Sclerosing Cholangitis

A

Intra and extra hepatic bile ducts become inflamed and blocked and obstruct bile flow

Risk factors- male., aged 30-40, ULCERATIVE COLITIS, family history

Antibodies not as helpful in diagnosis but p-ANCA antibody may help

Need an MRCP to show bile duct strictures
Colonoscopy if UC suspected

22
Q

What is the management of primary sclerosis cholangitis

A

ERCP for big strictures
Cholesytamine for itching
liver transplant if needed

23
Q

What are the risk factors for hepatocellular carcinoma

A

Alcohol related liver disease, NAFLD, Hep B/C, Primary sclerosis cholangitis

24
Q

What are the investigations in liver cancer

A

Liver USS- first line imagine
Alpha-fetoprotein
CT and MRI
Biopsy

25
Q

What are the main features of a cholangiocarcinoma

A

Cancer of the bile ducts
Mainly adenocarcinoma
Perihilar region most commonly affected- where ducts meet to become common hepatic duct

Associated with primary sclerosing cholangitis
Obstructive jaundice is a key feature, CA19-9 tumour marker

26
Q

What are the features of GORD and what are it’s main causes

A

Acid from stomach flows through lower sphincter into oesophagus

Greasy/spicy foods,
tea/ coffee
alcohol/NSAIDs, stress, smoking, obesity, hiatus hernia

27
Q

What are the main red flag features related to GORD

A

Dysphagia at any age
Over 55
Weight loss
Upper abdo pain
Reflux
Treatment resistant dyspepsia
N&V
Upper abdo mass on palp
Low Hb
Raised plt count

Urgent 2 week wait endoscopy

28
Q

What are the main investigations for H.Pylori

A

H.Pylori test given to anyone with dyspepsia - need 2 weeks without a PPI before testing

Stool antigen test
Urea breath test
H.Pylori antibody test
Rapid urease test- small stomach biopsy during endoscopy

29
Q

What is the treatment for H.Pylori and a peptic ulcer

A

Triple therapy with a PPI- Omeprazole and 2 abx- amoxicillin and clarithromycin for 7 days

Ulcer treatment
Stop NSAIDs, treat H.Pylori, PPIS and repeat endoscopy in 4-8 weeks

30
Q

What is the procedure for barrels oesophagus monitoring

A

Metaplasia- lower oesophageal epithelium changes from squamous to columnar epithelium - pre malignant and high risk for oesophageal adenocarcinoma

Endoscopic monitoring for progression
PPI
Endoscopic ablation to destroy columnar epithelial cells

31
Q

What is Zollinger Ellison syndrome

A

Duodenal or pancreatic tumour secretes excessive gastrin that stimulates excessive acid secretion

Associated with MEN1

32
Q

What are the risk factors for peptic ulcers and risk of bleeding ulcers

A

H.Pylori
NSAIDs

Bleeding
NSAID’s
Aspirin
DOACS
Steroids
SSRIs

33
Q

How to tell the difference between a gastric and peptic ulcer

A

Eating will worsen a gastric ulcer -more associated with weight loss

Eating will improve a duodenal ulcer

34
Q

What are the main causes of an upper GI bleed

A

Peptic ulcers
Mallory Weiss tear
Oesophageal varices
Stomach cancers

35
Q

What scores are taken into account in an upper GI bleed

A

Glasgow-Blatchford bleeding score - anything over 0 is high risk

Rockall Score - after endoscopy assesses risk of re-bleed

36
Q

What is the management of an upper GI bleed

A

ABATED

ABCDE
Bloods- FBC, U&E, Coag, LFTs, crossmatch
2 large bore cannula
Tranfusions
Endoscopy
Drugs- Stop NSAIDs and Anticoags

Transfusion
In massive bleed - blood, plus and FFP (clotting factors)

In active bleeding -Plt

In active bleeding and taking warfarin - prothrombin complex

37
Q

What are specific steps to manage oesophageal varices

A

Terlipressin and broad spectrum abx

OGD needed to treat source of bleeding and vatical band ligation

38
Q

What are the main features of Crohn’s

A

NESTS
No blood or mucus
Entire GI tract affected
Skip lesions
Terminal ileum most affected
Smoking is a risk factor

Fistulas and strictures associated

39
Q

What are the main features of Ulcerative Colitis

A

CLOSEUP
Continuous inflammation
Limited to colon and rectum
Only superficial mucosa
Smoking protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosis cholangitis

Also associated with eye issues

40
Q

What investigations are needed for iBD diagnosis

A

Stool microscopy to exclude infection
Faecal calprotectin 90% sensitive and specific for IBD before endoscopy
Colonoscopy with multiple intestinal biopsies

41
Q

What is the management plan of Ulcerative colitis

A

1st line Aminosalicylates (mesalazine)
2nd line steroids (pred)

IV steroids if severe (IV hydro)

Maintaining remission
Aminosalicylate
Azathioprine (Immunosurpressant)
Mercaptopurine

42
Q

What are the management steps for Crohn’s

A

Induce remission
1.Steroids
Nutrition if needed

Can also use
Inflicimab and adalimumab - biologics

Maintaining remission
Azathioprine
Mercaptopurine

Methotrexate can also be used

Surgical options
Resect distal ileum
Treat strictures
Treat fistulas

43
Q

What is the criteria for an IBS diagnosis

A

6 months of abdo pain/ discomfort and 1 of
1. Pain relieved by posing
2. Bowel habit abnormalities
3. Stool abnormalities

And 2 of
Straining, urgent need to open bowels or incomplete emptying
Bloating
Worse after eating
Passing mucus

44
Q

What is the management for IBS

A

Lifestyle management
FODMAP diet

Medications
Loperamide for diarrhoea
Bulk forming laxatives (avoid lactulose causes bloating)
Antispasmodics for cramps

CBT, SRRIs if needed

45
Q

What are the main antibodies in coeliac disease

A

Anti-TTG - main one
Anti-EMA
Anti-DGP

For features * think malabsorption*

46
Q

What will endoscopy show in coeliac

A

Jejunum particularly affected
Crypt hyperplasia
Villous atrophy