GI Flashcards

1
Q

Describe appendicitis

A
  • Appendix is a small, thin tube of bowel sprouting from the caecum
  • appendicitis is inflammation of the appendix
  • results from obstruction of the appendix and subsequent infection and inflammation of the appendix
  • peak incidence in ages 10-20
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2
Q

What are the symptoms of appendicitis?

A
  • abdominal pain, typically central then settling in the right iliac fossa
  • loss of appetite, N+V
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3
Q

What are the signs of appendicitis?

A
  • tender to McBurney’s point
  • guarding to RIF
  • rebound tenderness and percussion tenderness indicate peritonitis
  • rovsing’s sign positive
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4
Q

Describe the diagnosis of appendicitis

A
  • mostly clinical based on signs and raised inflammatory markers
  • CT can be useful in confirming diagnosis
  • USS can be useful to exclude ovarian and gynae pathology
  • if clinically appendicitis but tests negative, proceed to diagnostic laparoscopy
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5
Q

What are the common differential diagnoses for appedicitis?

A
  • ectopic pregnancy
  • ovarian cysts
  • meckel’s diverticulitis
  • mesenteric adenitis
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6
Q

What are the possible complications fo an appendicectomy?

A
  • bleeding/ infection/ pain/ scars
  • damage to bowel, bladder or other organs
  • removal of normal appendix
  • anaesthetic risk
  • DVT/PE

Laparoscopic is associated with fewer risks and faster recovery

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7
Q

Describe the management of appendicitis

A

Appendicectomy is the definitive management for acute appendicitis.

Laparoscopic surgery is associated with fewer risks and faster recovery compared to laparotomy.

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8
Q

Define haemochromatosis

A

Haemochromatosis is an iron storage disorder that results in excessive total body iron and deposition of iron in tissues.

The human haemochromatosis protein (HFE) gene is located on chromosome 6.

Majority of cases are due to mutation in the HFE gene. Mutation is autosomal recessive.

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9
Q

What are the symptoms of haemochromatosis?

A

Usually presents after the age of 40 when the iron overload becomes symptomatic.

Chronic tiredness
Joint pain
Pigmentation 
Hair loss
Erectile dysfunction
Amenorrhoea
Cognitive symptoms
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10
Q

What is the diagnosis of haemochromatosis?

A

Serum ferritin.
Ferritin is an acute phase reactant meaning that it goes up with inflammatory conditions such as infection.

Transferrin saturation is helpful in distinguishing between iron overload and other causes of high ferritin.

If both are high, do genetic testing to confirm.

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11
Q

What are the complications of haemochromatosis?

A

Type 1 DM

Liver cirrhosis

Iron deposits in the pituitary and gonads lead to endocrine and sexual problems

Cardiomyopathy

Hepatocellular carcinoma

Hypothyroidism

Chrondocalcinosis

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12
Q

What is the management of haemochromatosis?

A
Venesection 
Monitoring serum ferritin
Avoid alcohol
Genetic counselling
Monitoring and treatment of complications
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13
Q

Define acute cholangitis

A

Acute cholangitis is infection and inflammation in the bile ducts.

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14
Q

What are the causes of acute cholangitis?

A
  1. Obstruction int he bile ducts stopping bile flow (i.e. gallstones in the common bile duct)
  2. Infection introduced during an ERCP procedure
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15
Q

What are the most common organisms that cause acute cholangitis?

A
  1. E. coli
  2. Klebsiella species
  3. Enterococcus species
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16
Q

Describe the presentation of acute cholangitis

A

charcot’s triad:

  1. RUQ pain
  2. Jaundice
  3. Fever
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17
Q

What is the management of patients with acute cholangitis?

A

Acute management of sepsis ad acute abdo:

  • Nil by mouth
  • IV fluids
  • Blood culture
  • IV antibiotics

Imaging to diagnose CBD stones and cholanditis:

  • Abdo US
  • CT
  • MRCP

ERCP

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18
Q

Define acute pancreatitis

A

Pancreatitis refers to inflammation of the pancreas. Presents with rapid onset of symptoms

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19
Q

What are the key causes of pancreatitis?

A
  1. Gallstones
  2. Alcohol
  3. Post ERCP
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20
Q

What are the full list of causes of pancreatitis?

A

I GET SMASHED

Idiopathic
Gallstones
Ethanol
Trauma
Steroids
Mumps
Autoimmune
Scorpion sting
Hyperlipidaemia
ERCP
Drugs
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21
Q

Describe the presentation of acute pancreatitis

A
  • Severe epigastric pain
  • Radiating through to the back
  • Associated vomiting
  • Abdominal tenderness
  • Systemically unwell
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22
Q

What are the investigations of acute pancreatitis?

A
  • FBC
  • U+E
  • LFT
  • Calcium
  • ABG
  • Amylase if raised more than 3 times upper limit, it is acute pancreatitis
  • CRP
  • USS
  • CT abdo
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23
Q

What is the glasgow score in terms of pancreatitis?

A

Used to determine severity of pancreatitis:
0-1 mild
2 moderate
3 or more severe

PANCREAS
PaO2 <60
Age >55
Neutrophils >15
Calcium <2
uRea >16
Enzymes (LDH>600 or AST/ALT>200)
Albumin <32
Sugar (glucose>10)
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24
Q

What is the management of acute pancreatitis?

A
ABCDE
IV fluids
Nil by mouth
Analgesia
Monitor

Tx of gallstones: ERCP/cholecystectomy

Abs for infection

Tx of complications

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25
Q

What are the complications of acute pancreatitis?

A
Necrosis of the pancreas
Infection in a necrotic area
Abscess formation
Acute peripancreatic fluid collection
Pseudocysts
Chronic pancreatitis
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26
Q

What is the stepwise progression of alcoholic liver diease?

A
  1. Alcohol related fatty liver
    drinking leads to build up of fat in the liver. Can be reversed in 2 weeks with abstinence.
  2. Alcoholic hepatitis
    Drinking over a long period causes inflammation in the liver sites. Mild hepatitis can be reversed,
  3. Cirrhosis
    Liver is made up of scar tissue rather than healthy tissue. Irreversible.
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27
Q

What are the signs of liver disease?

A
Jaundice
Hepatosplenomegaly
Spider Naevi
Palmer erythema
Gynaecomastia
Bruising
Ascites
Caput Medusae
Asterixis
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28
Q

What are the investigations and findings in alcoholic liver disease?

A

Bloods:

  • FBC: raised MCV
  • LFTs: High ALT+AST+GGT. ALP will be raised later. Low albumin and high bilirubin
  • Clotting: elevated PT
  • U+Es: deranged

USS: show early changes and fibroscan to check elasticity of liver to assess degree of cirrhosis.

Endoscopy:
assess for and treat oesophageal varices when portal hypertension is suspected

CT and MRI can look for fatty infiltration of the liver

Liver Biopsy to confirm diagnosis of alcohol related hepatitis or cirrhosis.

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29
Q

What is the general management of alcoholic liver disease?

A

Stop drinking
Consider detoxification
Nutritional support
Steroids improve short term outcomes

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30
Q

What is portal hypertension?

A

Result of resistance in the vessels in the liver due to fibrosis affecting the structure and blood flow

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31
Q

What are the most common causes of liver cirrhosis?

A

Alcoholic liver disease
Non-alcoholic fatty liver disease
Hep B
Hep C

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32
Q

What are the investigations and findings in liver cirrhosis?

A

Liver biochemistry often normal but in decompensated cirrhosis, all markers deranged

Albumin drops and prothrombin time increases

Hyponatramia

Urea and creatinine deranged

USS: nodullarity, corkscrew appearance, enlarged portal vein

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33
Q

What are the markers for synthetic function of the liver?

A

Albumin and prothrombin time

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34
Q

What is the first line investigation for assessing fibrosis in non-alcoholic fatty liver disease?

A

Enhanced liver fibrosis blood test.

Measures HA, PIIINP and TIMP-1

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35
Q

What is a fibroscan?

A

Can be used to check the elasticity of the liver. Retest every 2 years in patients at risk of cirrhosis:

  • Hep C
  • heavy alcoholics
  • diagnosed alcoholic liver disease
  • non-alcoholic liver disease
  • chronic hep B
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36
Q

What is the diagnostic test for liver cirrhosis?

A

Liver biopsy

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37
Q

What score is used to measure severity and prognosis of cirrhosis?

A

Child-pugh score

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38
Q

Which score is used to give estimated 3 month mortality and help guide referral for liver transplant?

A

MELD score

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39
Q

What is the general management of cirrhosis?

A

US and alpha fetoprotein every 6 months for hepatocellular carcinoma

Endoscopy every 3 years in patients with varices

High protein, low sodium diet

MELD score every 6 months

Consideration of a liver transplant

40
Q

What is the treatment of stable varices?

A
  1. propanolol reduces portal hypertension
  2. elastic band ligation of varices
  3. injection of scllerosant
  4. TIPS
41
Q

What are the non-invasive liver screens and what do they look for?

A

US liver

Hep B and C serology

Autoantibodies (autoimmune hep, primary biliary cirrhosis and primary sclerosing cholangitis)

Immunoglobulins (autoimmune hep and primary biliary cirrhosis)

Caerulopllasmin (wilsons disease)

Alpha 1 anti-trypsin levels (alpha 1 anti-trypsin deficiency)

Ferritin and transferrin saturation (hereditary haemochromatosis)

42
Q

What are the investigations in non-alcoholic fatty liver disease?

A

Liver US

Enhanced liver firbosis blood test (first line)

NAFLD fibrosis score (2nd line)

Fibroscan (3rd line)

43
Q

What is the management of non-alcoholic fatty liver disease?

A
Weight loss
Exercise
Stop smoking
Control of diabetes, BP and cholesterol
Avoid alcohol
44
Q

What are the causes of hepatitis?

A
Alcoholic hep
Non-alcoholic fatty liver disease
Viral hep
Autoimmune hep
Drug induced hep
45
Q

What is the presentation of hepatitis?

A
Abdo pain
Fatigue
Puritis
Muscle and joint aches
Nausea and vomiting
Jaundice
Fever (viral hep)
46
Q

What is hep A and how is it transmitted?

A

It is an RNA virus. Transmitted via faecal-oral route

47
Q

How does hep A present?

A
Nausea
Vomiting
Anorexia 
Jaundice
Cholestasis - dark urine and pale stools 
Hepatomegaly
48
Q

What is the management for hep A?

A

Resolves without treatment in 1-3 months

49
Q

What is hep B and how is it transmitted?

A

DNA virus. Transmitted by direct contact with blood or bodily fluids

50
Q

What percentage of people go onto get chronic hep B?

A

Most people recover within 2 months but 10% go onto become chronic hep B carriers

51
Q

What are the viral markers and their meaning for hep B?

A

Surface antigen (HBsAg) - active infection

E antigen (HBeAg) - high infectivitiy

Core antibodies (HBcAb) - past or current infection

Surface antibody (HBsAb) - vaccination or past or current infection

Hep B virus DNA (HBV DNA) - direct count of viral load

52
Q

What is hep c and give the transmission?

A

RNA virus

Spread by blood and bodily fluids

53
Q

What is the disease course of hep c?

A

25% full recovery

75% becomes chronic

54
Q

What are the complications of hep c?

A

Liver cirrhosis and hepatocellular carcinoma

55
Q

What is the test for hep c?

A

Hep C antibody is the screening test

Hep C RNA testing is used to confirm diagnosis of hep C

56
Q

What is the management of hep c?

A

direct acting antivirals are tailored and successfully cure the infection in over 90% of patients

57
Q

What is hep D and E?

A

can only get hep d if you have hep b as well

Hep e is faecal oral route and v rare in the UK

58
Q

Who does type 1 autoimmune hepatitis affect and what are the associated anitbodies?

A

Occurs in adults

Women
Around or after menopause
Less acute than type 2

Anti-nuclear antibodies
Anti-smooth muscle antibodies
Anti-soluble liver antigen

59
Q

Who does type 2 autoimmune hepatitis affect and what are the associated anitbodies?

A

Teenagers or early twenties with acute hep with high transaminases and jaundice

Anti-liver kidney microsome-1 (anti-LKM1)
Anti-livre cytosol antigen type 1 (anti-LC1)

60
Q

What are the treatments for autoimmune hepatitis?

A

High dose steroids (prednisolone) tapered over with other immunosuppressants

61
Q

What is wilson’s disease?

A

Excessive accumulation of copper in the body caused by a mutation in the wilsons disease protein on chromosome 13

62
Q

Describe the presentation of Wilson’s disease?

A
Hepatic problems (cirrhosis)
Neurological problems
Psychiatric problems 
Kayser-Fleischer rings
Haemolytic anaemia
Renal tubular acidosis
Osteopenia
63
Q

What is the diagnosis of Wilson’s disease?

A

Initial investigation: Serum caeruloplasmin low = Wilson’s

Diagnostic investigation: liver biopsy

Other:
24hr urine copper
Low serum copper
Kayser-Fleischer rings

64
Q

What is the management of Wilson’s disease?

A

Copper chelation with:
Penicillamine
Trientene

65
Q

What is primary biliary cirrhosis?

A

Where the immune system attacks the small bile ducts. This causes obstruction of the outflow of bile (cholestasis) leading to bile acids, billilrubin and cholesterol building up in the body

66
Q

Describe the presentation of primary biliary cirrhosis

A
Fatigue
Pruritus
GI disturbance and abdo pain
Jaundice
Pale stools
Xanthoma and xanthelasma
Signs of cirrhosis and failure
67
Q

What is primary biliary cirrhosis associated with?

A

Middle aged women
Other autoimmune diseases
Rheumatoid conditions

68
Q

What is the diagnosis of primary biliary cirrhosis/

A

ALP raised first
Bilirubin and others raised later

Diagnostic: Anti-mitochondrial antibodies
Anti-nuclear antibodies

ESR raised
IgM raised

Livery biopsy

69
Q

What is the treatment for primary biliary cirrhosis?

A

Ursodeoxycholic acid
Colestyramine
Liver transplant
immunosuppression

70
Q

What is primary sclerosing cholangitis?

A

Where the intrahepatic and extrahepatic ducts become strictured and fibrotic. Causes an obstruction to the flow of bile out of the liver

71
Q

What are the risk factors for primary sclerosing cholangitis

A

Male
Aged 30-40
UC
Family history

72
Q

What is the presentation of primary sclerosing cholangitis?

A
Jaundice
Chronic RUQ pain
Pruritus
Fatigue
Hepatomegaly
73
Q

What is the diagnosis of primary sclerosing cholangitis?

A

Gold standard: MRCP

High ALP
p-ANCA
ANA
aCL

74
Q

What is the management of primary sclerosing cholangitis?

A

Liver transplant can be curative

ERCP
Ursodeoxycholic acid
Colestyramine

75
Q

What is the test for H. pylori

A

Need to not use PPI for 2 weeks before

Urea breath test
Stool antigen test
Rapid urease test

76
Q

What is the eradication regime for H. pylori?

A

Triple therapy with PPI + 2 antibiotics for 7 days

77
Q

What is the presentation of peptic ulcers?

A
Epigastric discomfort or pain
N+V
Dyspepsia
Bleeding "coffee ground" vomit and melaena
Iron deficiency anaemia

Eating worsens pain = gastric ulcers

Eating improves pain = duodenal ulcers

78
Q

What are the features of crohns?

A

Crows NESTS

No blood or mucus
Entire GI tract
Skip lesions on endoscopy
Terminal ileum most affected
Transmural inflammation 
Smoking is a risk factor
79
Q

What are the features of ulcerative colitis?

A

U-C- CLOSEUP

Continuous inflammation
Limited to colon and rectum
Only superficial mucosa affected
Smoking is protective
Excrete blood and mucus
Use aminosalicylates
Primary sclerosing cholangitis
80
Q

What is the test for inflammatory bowel disease?

A

1st line: Stool microscopy

Faecal calprotectin is a useful screening test

Endoscopy with biopsy is diagnostic

81
Q

What is the management of crohns?

A

First line: steroids
± immunosuppressant

Maintaining:
First line: Azathiprine or mercaptopurine

Surgery if it only affects the distal ileum

82
Q

What is the management of UC?

A

Inducing remission mild to moderate:
First line: aminosalicylate e.g. mesalazine
Second line: corticosteroids

Inducing remission severe:
First line: IV corticosteroids
Second line: IV ciclosporin

Maintaining remission:
aminosalicylate, azathioprine or mercaptopurine

Surgery

83
Q

What is the diagnosis of coeliac disease?

A

Must be carried out when they are still on gluten diet.

Raised anti-TTG
Raised EMAs

Endoscopy and intestinal biopsy shows:
crypt hypertrophy
villous atrophy

84
Q

What is necrotising enterocolitis?

A

Disorder affecting premature neonates where part of the bowel becomes necrotic.

85
Q

What is the presentation of necrotising enterocolitis?

A
Intolerance to feeds
Vomiting with green bile
Generally unwell
Distended, tender abdomen
Absent bowel sounds
Blood in stools
86
Q

What is the diagnosis of necrotising enterocolitis?

A

Abdominal xray: diagnostic

  • dilated loops of bowel
  • bowel wall oedema
  • pneumatosis intestinalis
  • Pneumoperitoneum
  • gas in portal veins
87
Q

What is Budd-Chiari syndrome?

A

Obstruction of the hepatic venous outflow

88
Q

What is the presentation of Budd-Chiari syndrome?

A

Sudden onset abdominal pain
Ascites
Tender hepatomegaly

89
Q

What condition increases plasma urea levels?

A

Gastric ulcer

90
Q

Relapsing coeliac disease that initially settled with gluten free diet could mean which condition?

A

T-cell lymphoma

91
Q

ABG of obstructive sleep apnoea

A

Compensated respiratory acidosis

92
Q

Which is the most sensitive blood test for acute pancreatitis?

93
Q

What is the triad for acute liver failure presentation?

A

Encephalitis
Coagulopathy
Jaundice

94
Q

History of PSC and painless jaundice = which cancer?

A

Cholangiocarcinoma

95
Q

Which dermatological condition is linked with IBD?

A

Erythema nodosum