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Clinical Immunology and Biochemistry > GI and Liver Disorders > Flashcards

GI and Liver Disorders Flashcards

1
Q

What nutrients are absorbed in the stomach?

A

H+
Alcohol
H2O

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2
Q

What nutrients are absorbed in the Jejunum?

A 
CHO sugars
Proteins
Lipids
Vitamins
Fe2+
Trace elements
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3
Q

What nutrients are absorbed in the terminal ileum?

A

Vitamin B12

Bile Salts

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4
Q

What are the 11 gut hormones?

A
  • Gastrin
  • Secretin
  • Cholecystokinin
  • Somatostatin
  • Ghrelin
  • Neuropeptide Y
  • Peptide YY3-36
  • Glucagon, GLP, GIP
  • Pancreatic Polypeptide
  • Substance P
  • Serotinin
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5
Q

What is the structure of the gut hormones?

A

All peptides

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6
Q

What is the function of gastrin?

A

Secreted by Gastric antral G cells

Stimulates gastric acid secretion

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7
Q

What is the function of Secretin?

A

Secreted by duodenal cells

Stimulates pancreas to secrete bicarbonate

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8
Q

What is the function of Cholecystokinin?

A

Secreted by duodenal cells

Stimulates Gallbladder contraction, Pancreatic digestive enzyme release

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9
Q

How are carbs broken down?

A

Carbohydrates are broken down by amylase to oligosaccharides: sucrose, isomaltose, lactose

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10
Q

How are lipids broken down?

A

Lipid (TG) are broken down by lipase to monoacylglycerol, FFA and phospholipids, which are broken down by bile salts into Micelles

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11
Q

How are proteins broken down?

A

Proteins are broken down by exo/endo peptidase into amino acids

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12
Q

What are the causes of malnutrition?

A 
Gastric bypass
Thyrotoxicosis
Infective diarrhoea
Pancreatic insufficiency - chronic pancreatitis, CF genetic, pancreatic cancer
Bile salt insufficiency - cholestasis, bacterial overgrowth
Radiation enteritis Lymphoma
Short gut syndrome
Mucosal disorders
- coeliac disease
- infective (inc. tropical sprue)
- Crohn’s disease
- immunodeficiency
Intestinal lymphangiectasia
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13
Q

What are the mechanisms of malnutrition?

A

Intestinal hurry
Impaired secretion of bicarbonate and enzymes
Decreased availability of bile salts
Infiltration and destruction of cells
Decreased absorptive area, lactase deficiency
Lymphatic obstruction

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14
Q

What are the investigations for malabsorption?

A 
Basic Investigations
Biochemistry profile
CRP, ESR
FBC
Haematinics - B12, folate, ferritin
Antibodies
– Anti-endomysial
– Anti-tissue transglutaminase
– Gastric parietal cell/intrinsic factor Abs
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15
Q

What are the consequences of malabsorption?

A

Skin and mucosal lesions (due to vitamin and trace element deficiency)
Muscle weakness (due to reduced muscle mass and Ca2+ and Mg2+ deficiency)
Tetany (due to Ca2+ and Mg2+ deficiency)
Weight loss
Bone pain
Anaemia (due iron, folate and B12 deficiency)
Peripheral neuropathy (due to vitamin deficiency)
Oedema (due to hypoalbuminaemia)
Failure to thrive in neonates
Growth retardation
Diarrhoea

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16
Q

What is Coeliac Disease?

A

Coeliac disease, also spelled celiac disease, is an autoimmune disorder affecting primarily the small intestine that occurs in people who are genetically predisposed against Toxic Factor α-gliadin in gluten

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17
Q

What are the symptoms of Coeliac disease?

A 
Diarrhoea, which may smell particularly unpleasant
abdominal pain
Bloating and flatulence (passing wind)
Indigestion 
Constipation
Fatigue as a result of malnutrition (not getting enough nutrients from food) 
Unexpected weight loss 
An itchy rash (dermatitis herpetiformis)
Problems getting pregnant 
Nerve damage (peripheral neuropathy)
Disorders that affect co-ordination, balance and speech (ataxia)
Growth problems
Delayed puberty
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18
Q

How is Coeliac disease diagnosed?

A

Tests for Tissue Transglutaminase & Anti-endomysial
antibodies
Small Bowel Biopsy: Partial villous atrophy

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19
Q

How is Coeliac Disease treated?

A

Gluten Free diet

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20
Q

What are the causes of Chronic Pancreatitis?

A

Idiopathic
Genetic
Cystic Fibrosis

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21
Q

What are the symptoms of Chronic Pancreatitis?

A
  • Abdominal Pain
  • Malabsorption -Steatorrhoea (excess fat in faeces)
  • Diabetes Mellitus
  • Pancreatic Calcification
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22
Q

How is chronic pancreatitis diagnosed?

A
  • Faecal Elastase - low values indicative of pancreatic exocrine insufficiency
  • Amylase - acute pancreatitis- 3-4x ULN, chronic pancreatitis may not elevate plasma amylase
  • Lipase - greater specificity
  • Others - Para-aminobenzoic acid (PABA) Test, Pancreolauryl Test
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23
Q

How is Chronic Pancreatitis treated?

A

Lifestyle changes:

  • Avoiding alcohol
  • Stopping smoking
  • Dietary changes (A low-fat, high-protein, high-calorie diet with fat-soluble vitamin supplements is usually recommended)

Enzyme supplements

Steroid medication

Pain relief

Surgery (endoscopic to remove stones, pancreatic resection, total pancreatectomy)

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24
Q

What are the causes of peptic ulcer disease?

A
  • Helicobacter Pylori
  • Hyperacidity
  • Non-Steroidal Anti-inflammatory Drugs (NSAIDs)
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25
Q

How is peptic ulcer disease diagnosed?

A 
Testing for H. pylori infection
 - urea breath test
 - stool antigen test
 - blood test
Gastroscopy (may include biopsy)
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26
Q

What is the mechanism for Urea Breath test?

A

H Pylori contains urease

14C-Urea -Urease–> NH3 + 14CO2

Infection indicated by increase breath 14CO2

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27
Q

If a biopsy is performed in a Gastroscopy, how is H. Pylori infection detected?

A

• CLO Test:
Biopsy tissue is placed in a medium containing urea & phenol red. If H Pylori is present the NH3 liberated increases pH and solution goes from yellow to red.

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28
Q

How is Peptic Ulcer disease treated?

A

Treatment depends on the cause of the ulcer:

  • If ulcer is due to H. Pylori infection, a course of antibiotics and PPI is prescribed
  • If caused by NSAIDs, PPI’s are prescribed, and NSAID use is reviewed
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29
Q

What is IBS?

A

IBS is a functional bowel abnormality: altered motility and increased sensitivity ‘hyper vigilance’

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30
Q

How is IBS diagnosed?

A

Using Rome III criteria:

At least 3 months recurrent abdominal pain associated with 2 or more of the following:

  • improvement with defecation
  • onset associated with a change in frequency of stool
  • onset associated with a change in form (appearance) of stool
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31
Q

What are the different types of Inflammatory Bowel Disease?

A

Ulcerative Colitis

Crohn’s disease

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32
Q

What is Ulcerative Colitis?

A

Diffuse mucosal ulceration presenting with bloody diarrhoea and abdominal pain, with increased risk of colorectal cancer

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33
Q

What is Crohn’s disease?

A

Transmural patchy inflammation any part of GI tract, usually the terminal ileum.

Symptoms include diarrhoea, pain, weight loss
Complications are strictures, fistulae, malabsorption

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34
Q

How is IBD diagnosed?

A

Physical examination – nutrition, anaemia, fluid status, abdomen (?mass), rectal, perineum

Laboratory:

  • FBC, CRP, U+E, LFTs
  • pANCA (Perinuclear Anti-Neutrophil Cytoplasmic Antibodies) - 40-80% UC, 5-20% Crohn’s
  • anti-Saccharomyces cerevisiae Abs(ASCA) – 60-70% Crohn’s, 10-15% UC
  • Microbiology: stool MC&S test, parasites, C. difficile toxin
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35
Q

How is IBD treated?

A

There is currently no cure for ulcerative colitis or Crohn’s disease. Treatment aims to relieve symptoms and prevent them from returning.

Aminosalicylates, or in more severe cases, corticosteroids – to reduce inflammation
Immunosuppressants – to reduce the activity of the immune system

In very severe cases, where inflammation does not respond to medication, the inflamed section of the digestive system may be surgically removed

36
Q

What is faecal calprotectin?

A

Faecal Calprotectin is a protein that accounts for 60% of neutrophil cytoplasmic protein

It is a calcium binding protein

37
Q

When is faecal calprotectin released?

A

It is released into faeces when neutrophils gather at the site of GI tract inflammation

38
Q

How is faecal calprotectin measured?

A

It is measured in faeces as it is stable in faeces with next to no degradation
- Good correlation with Indium labelled WBC

39
Q

What are the functions of the liver?

A

Metabolism
Excretion and Detoxification
Storage

40
Q

How is the liver involved in the metabolism of carbohydrates?

A

Involved in glycogen synthesis and metabolism

41
Q

How is the liver involved in the metabolism of fats?

A

Cholesterol, bile acid, and lipoprotein synthesis

42
Q

How is the liver involved in the metabolism of proteins?

A

Protein and urea synthesis

43
Q

How is the liver involved in the metabolism of hormones?

A

Vitamin D, regardless of origin, is an inactive prohormone and must first be metabolized to its hormonal form before it can function.

Once vitamin D enters the circulation from the skin or from the lymph, it is cleared by the liver or storage tissues within a few hours.

44
Q

What are the current liver function tests?

A 
Serum aminotransferases e.g. AST, ALT
 – For parenchymal injury
Serum bilirubin
 – For cholestasis
Serum alkaline phosphatase,γ glutamyltranspeptidase
 – For biliary epithelial damage and biliary obstruction (alcohol), cholestasis
Serum albumin
 – For synthetic function
Prothrombin time (INR)
 – For clotting (dynamic indicator)
45
Q

What is AST?

A

Aspartate aminotransferase

46
Q

What is ALT?

A

Alanine aminotransferase

47
Q

Where is AST found?

A 
Liver
Heart
Skeletal Muscle
Erythrocytes
Kidney
48
Q

What causes high AST in the liver?

A

Mitochondrial and cytoplasmic injury

49
Q

Where is ALT found?

A

Mainly Liver

Lesser extent Heart, Skeletal Muscle, Kidney

50
Q

What is causes high ALT in the liver?

A

Cytoplasmic injury

51
Q

What causes ALT>AST?

A

Cytoplasmic disease
- Necrotic liver disease (eg viral hepatitis)
- NAFLD
Obstructive liver disease

52
Q

What causes AST>ALT?

A

Cytoplasmic & mitochondrial disease

  • chronic liver damage (cirrhosis),
  • infiltrative disease (eg alcohol, neoplasms
  • Metabolic
53
Q

What causes a minor (<100iu/l) increase in ALT and AST?

A

Chronic Hepatitis B
Chronic Hepatitis C
Haemochromotosis
Fatty Liver

54
Q

What causes a moderate (100-300 iu/l) increase in ALT and AST?

A 
Chronic Hepatitis B
Chronic Hepatitis C
Haemochromotosis
Fatty Liver
Alcoholic hepatitis
Non-alcoholic steatohepatitis 
Autoimmune hepatitis
Wilson's Disease
55
Q

What causes a major (>1000 iu/l) increase in ALT and AST?

A

Drug toxicity, particularly paracetamol
Acute viral hepatitis
Autoimmune hepatitis
Ischaemic liver

56
Q

Where is ALP found?

A

Mainly liver and bone, but also intestinal, placental (pregnancy) and biliary isoenzymes.

57
Q

What causes increased hepatic ALP?

A

Hepatobiliary obstruction causes increased sinusoidal hepatocyte synthesis of ALP

58
Q

Where is γGT found?

A

Mainly Liver but also kidney, pancreas and prostate

59
Q

What is γGT?

A

Most sensitive but non-specific marker of liver disease

Sited in endoplasmic reticulum and increased in;

  • ER damage: hepatocellular damage and obstruction
  • ER proliferation: Enzyme induction eg alcohol & drugs
60
Q

What is albumin a marker of?

A

Reduced hepatic functioning mass

But also occurs in:

  • Negative acute phase protein
  • Malnutrition including malabsorption
  • Protein loss: e.g. nephrotic syndrome
61
Q

What is jaundice?

A
  • Elevation of bilirubin in the serum (normal <20umol/L)

* May be unconjugated and/or conjugated bilirubin.

62
Q

What is normal bilirubin level?

A

20μmol/L

63
Q

What causes jaundice to be visible in the sclera?

A

Serum bilirubin >50μmol/L may be visible in sclera as

jaundice

64
Q

What causes jaundice to be visible in the skin?

A 
Serum bilirubin >100μmol/L the patient's skin may
appear yellow (“jaundiced”)
65
Q

Describe bilirubin metabolism

A

Haem is catabolized to unconjugated bilirubin in the reticuloendothelial system.
Unconjugated bilirubin is bound to albumin in the plasma and transported bound to albumin to the liver and is conjugated with glucuronic acid in the hepatocytes; the conjugation is catalyzed by glucuronyl transferase.
Conjugated bilirubin is secreted into the bile and enters the duodenum. In the small bowel, some of the bilirubin is hydrolyzed to yield unconjugated bilirubin and glucuronic acid.
Most unconjugated bilirubin is excreted in the stool, but some is reabsorbed and returned to the liver for reconjugation (enterohepatic circulation).

66
Q

What is hyperbilirubinaemia?

A

Hyperbilirubinaemia is a condition in which there is too much bilirubin in the blood.

67
Q

What are the types of bilirubinaemia?

A

Pre-hepatic (eg Haemolysis)
- Unconjugated hyperbiliribinaemia
Hepatic
- Unconjugated hyperbilirubinaemia e.g. Gilberts
- Usually unconjugated & conjugated hyperbilrubinaemia
Post-hepatic (Extrinsic Obstruction of biliary drainage)
- Conjugated Hyperbilirubinaemia

68
Q

What causes prehepatic jaundice?

A

Haemolysis

  • Unconjugated hyperbilirubinaemia - Fat soluble, crosses blood brain barrier if protein carrying capacity is exceeded.
  • Increased urine urobilinogen
  • Anaemia
  • Reticulocytosis: Increased red cell production
69
Q

What are the features of hepatocellular jaundice?

A
  • Unconjugated & conjugated hyperbilirubinaemia
  • Increased liver transaminases (AST/ALT)
  • Increased ALP and γGT)
  • Reduced synthetic activity.
70
Q

What is Gilbert’s Syndrome?

A

Gilbert’s syndrome is a common autosomal dominant
benign condition producing a mild unconjugated
hyperbilirubinaemia with an estimated prevalence of
3-8% in the general population

71
Q

What defect causes Gilbert’s Syndrome?

A

Defect is a TA insertion in the TATA repeat box of the
gene promoter region. Homozygosity reduces the
capacity for gene expression

72
Q

How is bilirubin conjugation mediated?

A

Bilirubin conjugation is mediated by UDPglucoronosyl

transferase 1A

73
Q

When does plasma bilirubin increase in patients with Gilbert’s syndrome?

A

In situations of increased demand e.g. illness, infections, fasting a marked rise in plasma bilirubin (40-80 umol/L) can occur

74
Q

What are the various types of hepatitis?

A

Viral hepatitis A, B and C
Alcoholic hepatitis
Autoimmune hepatitis

75
Q

What are the diagnostic features of alcoholic hepatitis?

A

Transaminases not usually so raised

Often high GGT, urate, triglycerides and macrocytosis

76
Q

What are the diagnostic features of autoimmune hepatitis?

A

F:M ratio - 4:1

Hepatic pattern-↑ALT, ↑Bilirubin, ALP normal, ↑gammaglobulins, autoantibodies - antinuclear and antismooth muscle antibodies

77
Q

What is NAFLD?

A

Non-alcoholic fatty liver disease

78
Q

What is NASH?

A

Non-alcoholic steatohepatitis

79
Q

What are the features of NAFLD and NASH?

A

Fatty infiltration not due to excessive alcohol
Associated with insulin resistance and metabolic syndrome
NAFLD is benign and reversible
NASH which is a severe form of NAFLD there is cellular damage, elevated liver enzymes, 28% of patients with NASH may progress to cirrhosis

80
Q

How can NAFLD and NASH be detected?

A

Definitive test : liver biopsy

  • Liver enzymes : differences in AST and AST/ALT ratio in patients with fatty liver alone and those with NASH (AST, AST/ALT ratio higher in NASH)
  • Markers of liver fibrosis : type IV collagen, hyaluronic acid (higher in patients with NASH)
81
Q

How many patients with NASH progress to cirrhosis?

A

28%

82
Q

What is cirrhosis?

A

End result of almost any liver disease, fibrous scar tissue distorts architecture leading to increased pressure in portal vein

83
Q

What are the biochemical test results for cirrhosis?

A

LFTs often completely normal
Slight rise in transaminases
Low albumin – impaired synthesis
Rise in bilirubin is late feature

84
Q

What is obstructive jaundice?

A

Obstructive jaundice is a particular type of jaundice and occurs when the essential flow of bile to the intestine is blocked and remains in the bloodstream.

85
Q

What features are characteristic of obstructive jaundice?

A

Impaired biliary excretion of conjugated bilirubin & increased synthesis of alkaline phosphatase.

86
Q

How does obstructive jaundice present?

A

Conjugated hyperbilirubinaemia
Increased hepatic Alkaline Phosphatase
Increased Urine Bilirubin (Dark Urine)
{Pale stools –reduced faecal stercobilin}

May be intrahepatic or extrahepatic

  • Intrahepatic: e.g. Primary Biliary Cirrhosis
  • Extrahepatic: e.g. Cancer head of pancreas, gall stones

Clinical Immunology and Biochemistry (14 decks)

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