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Flashcards in Gastrointestinal Deck (52):
1

A rise in which liver enzymes suggests hepatocellular injury?

Transaminases (ALT and AST)

2

A rise in which liver enzymes suggest a cholestatic picture?

GGT and ALP

3

What liver enzyme profile is seen in a patient with alcoholic hepatitis?

High AST:ALT ratio

4

Where is ALP produced?

Liver, bone, intestine and placenta

5

What is an isolated raised ALP typically due to?

Bone disease (Paget's disease, Vit D deficiency, metastasis)

(Remember: ALP produced by liver, bone, intestine and placenta)

6

What are GGT levels most useful for?

Although isolated raised GGT is associated with alcohol excess, it is most useful in confirming liver origin of ALP.

7

List 7 causes of a 'hepatocellular' LFT profile

Hepatocellular = raised AST and ALT

Infection e.g. hepatitis B,C,A; EBV; CMV

Alcohol

Fatty liver

Drugs e.g. paracetamol

Metal overload e.g. hereditary haemochromatosis, copper overload

Hypoxia (LD usually more than 1.5 times AST)

Autoimmune

8

List 4 causes of a 'cholestatic' liver function test profile.

Cholestatic = raised GGT/ALP

Biliary obstruction

Pregnancy

Drugs e.g. erythromycin, oestrogen

Infiltration e.g. malignancy

9

Which type of bilirubin is usually involved in hyperbilirubinaemia in adults?

Conjugated

10

What does unconjugated hyperbilirubinaemia in adults usually suggest?

Gilbert syndrome or haemolysis

11

Which type of bilirubin is soluble? Insoluble?

Unconjugated = insoluble

Conjugated = soluble

12

Why is there dark urine and pale faeces in biliary obstruction?

In biliary obstruction, below-normal amounts of conjugated bilirubin reach intestine for conversion to urobilinogen

Urobilinogen is normally converted to urobilin which gives urine its yellow colour. It is also converted to stercobilin which gives faeces its brown pigment.

Therefore, small amounts of conjugated bilirubin = small amounts of urobilinogen = small amounts or urobilin and stercobilin = no yellow or brown pigment = dark urine and pale faeces

13

List two congenital conjugated hyperbilirubinaemias

Dubin-Johnson, Rotor's

14

List two congenital unconjugated hyperbilirubinaemia

Gilbert's, Crigler-Najjar

15

What is primary biliary cirrhosis?

Autoimmune liver disease marked by slow progressive destruction of small bile ducts of the liver - more women affected than men.

16

How should PBC be investigated? (4)

LFTs
Antibodies - AMA and ANA
US - to rule out blockage of bile ducts
Can do biopsy

17

What are the more common causes of UGI bleeding?

UVA MED

Ulcers (PUD)
Varices
AVMs
Mallory Weiss Tear
Erosions (Stress gastritis), oesophagitis
Dieulafoy lesion

18

What is suggested with solid food dysphagia?

Solid food more than liquid suggests structural abnormality

19

What is suspected with dysphagia with liquids?

Solids = liquids suggests neuromuscular origin

20

How should acute upper GI bleeding be investigated?

1. FBE - low Hb, low platelets
2. UEC - high urea
3. LFTs - deranged in liver disease
4. Coags - elevated INR
5. Upper GI endoscopy

21

How are bleeding oesophageal varices managed? (5)

1. Variceal ligation OR

2. Sclerotherapy OR

(more severe bleeding)
3. Balloon tamponade with Sengstaken tube OR

4. Transjugular Intrahepatic portosystemic shunt (treats life-threatening oesophageal varices by reducing portal hyprtension) OR

5. Terlipressin or octreotide (reduce portal hypertension)

22

List 4 infectious causes of conjugated hyperbilirubinaemia.

1. Viral Hepatitis A-E
2. CMV
3. EBV
4. Sepsis

23

List 5 inflammatory causes of conjugated hyperbilirubinaemia

1. Drug toxicity

2. Alcoholic hepatitis

3. Iron overload (haemochromatosis)

4. Copper overload (Wilson's disease)

5. Autoimmune hepatitis

24

List 6 metabolic causes of conjugated hyperbilirubinaemia.

1. Ischaemia (shock liver)

2. Acute fatty liver of pregnancy

3. Alpha-1-antitrypsin deficiency

4. Pre-eclampsia

5. Reye syndrome - associated with aspirin consumption by children with viral illness

6. TPN

25

Which serological tests constitute the diagnostic panel for HBV and what do these indicate?

HBsAg - Hep B surface antigen - active infection (Acute or chronic)

Anti-HBc - Hep B core antibody - infection (past or current)

Anti-HBs - Hep B surface antibody - immunity (vaccination or infection)

+/- IgM anti -HBc (positive/high titre indicates ACUTE HBV infection)

26

What are the modes of transmission for HBV?

Sexual contact - most common

Other modes include: percutaneous exposure (IVDU, tattoos and transfusion of blood products), organ transplantation and perinatal transmission

27

What percentage of HBV-infected individuals develop chronic infection?

Approx 2-6% of immunocompetent adults

28

How is the diagnosis of acute HBV infection confirmed?

The presence of HBsAg and anti-HBc IgM in serum suggests recent infection

29

What is the treatment for acute HBV infection?

Most cases resolve spontaneously. Interferon not indicated in acute setting.

30

What are major sequelae of chronic HBV infection?

Cirrhosis with portal HTN and HCC

31

What is the mode of transmission for Hep A?

Faecal-oral, person-to-person contact (e.g. in day-care centres or with high-risk sexual practices) and contaminated food or water. Endemic in underdeveloped countries

32

What is the usual clinical presentation of Hep A infection?

Incubation period is 2-6 weeks. Most adults experience a benign, short-lived episode of acute hepatitis. Cholestatic and relapsing hepatitis can occur. Fulminant hepatic failure is rare and occurs more commonly in patients with underlying comorbidities such as chronic HBV or HCV.

33

What does Hep A IgM signify and what is its time course?

Present with the development of symptoms and confirms diagnosis of acute Hep A infection

34

What does Hep A IgG signify and what is its time course?

Denotes previous infection and recovery or vaccination with Hep A vaccine. Present in nearly all patients after 3 weeks of disease and persists indefinitely

35

What complication, other than fulminant hepatic failure, can rarely be seen in acute Hep A infection?

Aplastic anaemia

36

What is the treatment for acute Hep A infection?

Primarily supportive (good nutrition, avoidance of alcohol and hepatotoxic agents, and precautions to prevent spread). Transplantation may be needed if fulminant hepatitis occurs

37

What is primary sclerosing cholangitis?

PSC - progressive fibrosing inflammation of the intrahepatic and extrahepatic bile ducts, resulting in cholestasis, bile duct obliteration and cirrhosis of the liver

38

What are usual laboratory findings at the time of diagnosis of PSC? (3)

Elevated ALP, transaminases and fluctuating bilirubin evels

Elevated serum IgM in 50-50% of cases

p-ANCA in 65% of cases

39

How is the diagnosis of PSC made? (3)

ERCP - multifocal structures and dilated areas (string-of-beads appearance) of extrahepatic and intrahepatic bile ducts

Liver biopsy - nondiagnostic, but helpful in excluding other processes and for staging degree of PSC

As PSC can precede UC symptoms by several years, colonoscopy should be performed despite absence of bowel symptoms

40

What diseases have been seen in association with PSC?

70% have UC

41

What is the most important clinical manifestation of acute liver failure?

Neurological compromise

42

Which infectious agents are common causes of bloody stool?

CHESS

Campylobacter
Haemorrhagic E.coli
Entamoeba histolytica
Salmonella
Shigella

43

What dermatologic manifestation is associated with coeliac disease?

Dermatitis herpetiformis

44

What serologic markers should be checked in suspected coeliac disease? (2)

IgA anti-endomysial antibodies or ELISa for tissue transglutaminase

Antigliadin antibodies

45

What investigations confirm coeliac disease?

Small bowel biopsy, shows blunt flattened villi and an inflammatory infiltrate in the lamina propria

Should be repeated after 4-6 months of a gluten-free diet - if no histologic improvement is seen, diagnosis should be questioned

46

What key symptoms are virtually diagnostic for IBS? (3)

1. Diarrhoea does not awaken patient from sleep
2. Patient denies weight loss
3. Symptoms related to stress

47

What are the modified Rome criteria?

Presence of 12 weeks in the preceding 12 months (not necessarily consecutive) of abdominal discomfort or pain, without an objective explanation, along with two or more of the following:
1. Relief of pain with deaecation
2. Change in frequency of bowel movements
3. Change in form of stool

48

What are the non medication treatments of IBS?

1. Emotional support and reassurance, as well as stress reduction
2. Diet and fibre therapy - avoidance of foods that cause symptoms and addition of 20-30g per day of fibre

49

What are the subgroups of IBS?

Constipation-predominant, diarrhoea-predominant, alternating diarrhoea/constipation

50

What medications can be used to treat IBS?

Tegaserod (constipation and bloat predominant) and alosetron (diarrhoea-predominant) - specific

Otherwise symptomatic
Antispasmodics

Antidepressants

Antidiarrhoeals (loperamide) when diarrhoea predominates, laxatives when constipation predominates

51

What major arteries supply blood to the small intestines and colon?

Coeliac axis, superior mesenteric artery, inferior mesenteric artery

52

What are the signs and symptoms of ischaemic colitis?

Sudden crampy mild left-sided abdominal pain, urge to defaecate, passage of red or maroon blood mixed with stool