Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Fundamentals of P > Laboratory Investigation of Liver & GI Tract Disease > Flashcards

Laboratory Investigation of Liver & GI Tract Disease Flashcards

1
Q

Describe structure of liver

A

Comprised of large right lobe and smaller left lobe

Has dual blood supply – 2/3 comes from the gut via the portal vein (nutrient rich) and 1/3 from the hepatic artery (oxygen rich)

Blood leaves the liver through the hepatic veins

Substances for excretion from the liver are secreted from hepatocytes into canaliculi.

The bile canaliculi merge and form bile ductules, which subsequently merge to become a bile duct and eventually become the common hepatic duct.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Major functions of the liver

A

Carbohydrate metabolism

Fat metabolism

Protein metabolism

Synthesis of plasma proteins

Hormone metabolism

Metabolism and excretion of drugs and foreign compounds

Storage – glycogen, vitamin A and B12, plus iron and copper

Metabolism and excretion of bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Types of Liver Disease

A

Hepatitis
Cholestasis
Cirrhosis
Tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hepatitis characteristics

A

Damage to hepatocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Cholestasis characteristics

A

Blockage

Intra or extra-hepatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Cirrhosis characteristics

A

Increased fibrosis
Liver shrinkage
Decreased hepatocellular function
Obstruction of bile flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Tumours characteristics

A

Primary cancer

Frequently secondary: colon, stomach, bronchus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Liver Function Test (LFT) - list profile

A 
Liver Function Test (LFT)
Standard LFT profile:
Bilirubin
Albumin
Alanine aminotransferase (ALT) or Aspartate aminotransferase (AST)
Alkaline phosphatase
Gamma glutamyltransferase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

LFTs are not diagnostic but can be used for

A

Differential diagnosis: predominantly hepatic or cholestatic

Screening for the presence of liver disease

Assessing prognosis

Monitoring disease progression

Measuring the efficacy of treatments for liver disease

Assessing severity, especially in patients with cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe LFT for an inflammatory pattern

A

Inflammatory pattern (hepatocellular damage)

Bilirubin
N to ↑

ALT
↑↑↑

ALP
N to ↑

Albumin
N

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe LFT for an cholestatic pattern

A

Bilirubin
↑ to ↑↑↑

ALT
N to ↑

ALP
↑ to ↑↑↑

Albumin
N

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Albumin conc link to liver disease

A

Albumin concentrations only tend to decrease in chronic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is bilirubin

A

Yellow-orange pigment derived from haem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Bilirubin occurs in 2 forms - list

A

Conjugated (direct-reacting bilirubin)

Unconjugated (indirect-reacting bilirubin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe conjugation of bilirubin

A

Binds tightly but reversibly to albumin

Conjugation occurs in the liver → excreted in bile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Jaundice define

A

Jaundice describes the yellow discolouration of tissue due to bilirubin deposition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical jaundice may not be evident until when

A

Clinical jaundice may not be evident until the serum/plasma bilirubin concentration is 2x the upper reference of normal, >50 μmol/L.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

↑ serum/plasma concentrations of bilirubin occur when

A

↑ serum/plasma concentrations of bilirubin occur in imbalance between production & excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe importance to determine if ↑bilirubin is conjugated or unconjugated

A

Unconjugated elevation - production is increased which is beyond capacity of liver conjugation

Conjugated bilirubin elevation – obstruction of bilirubin flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Causes of Jaundice - prehepatic

A

Excessive RBC breakdown:

Haemolysis
Haemolytic anaemia
Crigler-Najjar, Gilbert’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of Jaundice - cholestatic = intrahepatic

A

Dysfunction of hepatic cells:

Viral hepatitis
Drugs
Alcoholic hepatitis
Cirrhosis
Pregnancy
Infiltration
Congenital disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes of Jaundice - cholestatic = extrahepatic

A

Obstruction of biliary drainage:

Common duct stone
Carcinoma
Biliary stricture
Sclerosing cholangitis
Pancreatitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Neonatal Jaundice - define

A

Immaturity of bilirubin conjugation enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Effect of high levels of unconjugated bilirubin to newborn

A

High levels of unconjugated bilirubin - toxic to the newborn

→ due to its hydrophobicity , can cross the blood-brain-barrier & cause kernicterus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Phototherapy for neonatal jaundice

A

Phototherapy with UV light – converts bilirubin to water soluble, non-toxic form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Effect of high levels of conjugated bilirubin to newborn

A

Pathological jaundice if high levels of conjugated bilirubin

E.g. Pale stools in babies with biliary atresia. Urgent surgical treatment is essential.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Gilbert’s Syndrome - define

A

Benign liver disorder

Frequency : 10% of population

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Gilbert’s Syndrome - characteristics

A

Characterized by mild, fluctuating increases in unconjugated bilirubin
→ caused by ↓ ability of the liver to conjugate bilirubin

Males more frequently affected than females

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Liver transaminases ALT and AST - used for

A

Most commonly measured markers of hepatocyte injury

Catalyse transfer of amino group
α -amino acid → α-oxo acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ALT Alanine Aminotransferase (ALT) - localisation

A

predominantly localised to liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

AST Aspartate Aminotransferase (AST) distribution:

A

AST Aspartate Aminotransferase (AST) has wide tissue distribution:
heart, skeletal muscle, kidney, brain, erythrocytes, lung & liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

ALT/AST - distribution in cell

A

Both are cytosolic but AST is also present in mitochondria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

ALT use

A

ALT is used to identify liver damage arising from hepatocyte inflammation or necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Diagnosis if AST/ALN 5 * ULN

A 
Modest elevation (5 x ULN):
Fatty liver
Chronic viral hepatitis
Prolonged Cholestatic liver disease
Cirrhosis
 - In compensated cirrhosis values may be normal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Diagnosis if AST/ALN 10-20 * ULN

A

Highest elevation (10-20x ULN):
Acute viral hepatitis
Hepatic necrosis induced by drugs or toxins
Ischaemic hepatitis induced by circulatory shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Alkaline Phosphatase (ALP) - define

A

Enzyme isoforms mainly produced in liver and bone but also placental and intestinal forms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Bile duct obstruction - effect and cause

A

Bile duct obstruction - increased ALP synthesis and thus increase in measured activity

Obstruction may be due to:
extrahepatic (stones, tumour or stricture)
intrahepatic (infiltration or space occupying lesion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

ALP values >3 x ULN found in

A

ALP values >3 x ULN found in intra- & extrahepatic cholestasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

ALP values <3 x ULN found in

A

ALP values <3 x ULN found in hepatocellular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

↑↑ in osteoblastic activity effect

A

↑↑ in osteoblastic activity:
Healing fractures
Vitamin D deficiency
Paget’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

The source of an elevated ALP can be determined by

A

The source of an elevated ALP can be determined by gel electrophoresis. It is possible to separate ALP isoenzymes into liver, bone, and intestinal fractions.

42
Q

Why can the placental ALP be identified

A

The placental isoenzyme of ALP can be identified as it is heat stable at 65oC for 10 minutes, unlike the other isoenzymes.

43
Q

Gamma Glutamyl Transferase (GGT) - define

A

GGT is a membrane bound enzyme that transfers the gamma glutamyl group from peptides such as glutathione to other peptides and to L-amino acids.

44
Q

Gamma Glutamyl Transferase (GGT) - distribution

A

Wide tissue distribution, but liver isoenzyme activity predominates in serum

45
Q

Gamma Glutamyl Transferase (GGT) - used in combination with

A

Used in combination with ALP, ↑ value confirms ALP of hepatic origin

46
Q

Increased GGT due to

A

↑ levels may be due to enzyme induction by alcohol or drugs e.g. anticonvulsants.

47
Q

Increased GGT can occur in

A

↑ levels occur in cholestasis and hepatocellular disease

Can be ↑ in non-hepatic disorders, e.g. pancreatitis, myocardial infarction and diabetes mellitus

48
Q

Interpretation of ALP and GGT results

- ↑ ALP and ↑ GGT

A

↑ ALP and ↑ GGT – suggestive of hepatic cause (cholestasis)

49
Q

Interpretation of ALP and GGT results -

↑ ALP and N GGT

A

↑ ALP and N GGT – suggestive of bone source of ALP

50
Q

Interpretation of ALP and GGT results -

N ALP and ↑ GGT

A

N ALP and ↑ GGT – suggestive of excess alcohol intake

51
Q

Albumin - define + synth where

A

Major circulating plasma protein

Synthesised exclusively in the liver, 12g produced each day

52
Q

Albumin - importance of the concentration value

A

Concentration widely regarded as an index of hepatic synthetic function

Can be normal in early acute hepatitis due to its long half-life (21 days)

Values may be normal in well compensated liver disease

53
Q

Decreased serum albumin in what

A

Acute or chronic destructive liver diseases of moderate severity show decreased serum albumin

54
Q

What can decreased albumin be consistent with

A 
Decreases also consistent with:
Haemodilution
Impaired synthesis e.g. malnutrition
Increased loss e.g. nephrotic syndrome
Inflammatory leak
55
Q

Non-Alcoholic Fatty Liver Disease (NAFLD) - stages

A

Stages:

Hepatic steatosis (fat >5% liver volume)
Greater risk of progressing to fibrosis, cirrhosis, HCC
56
Q

Non-Alcoholic Fatty Liver Disease (NAFLD) - major risk factors

A

Major risk factors:

Obesity
Diabetes/insulin resistance
Hypertension

57
Q

Overview of the GI Tract

A

Oesophagus

=

Ingestion, release enzymes

Stomach = digestion, lower pH + release enzymes

SI =

Duodenum = digestion, Increase pH + add pancreatic enzymes + bile

Jejunum + ileum + colon (LI)

=

Absorption

stabilise pH, signal to brain and body to handle incoming nutrients, modify hunger

58
Q

Gastric Ulcers - causes

A

Gastric ulcers are caused by a break in the protective stomach mucosal lining

Helicobacter pylori infection (80% of cases)

Use of aspirin and NSAIDs – non-steroidal anti-inflammatory drugs (20% of cases)

59
Q

Signs and symptoms of gastric ulcers include:

A

Signs and symptoms of gastric ulcers include:
Pain in the abdomen that may come and go (may be eased with antacid)
Waking up with a feeling of pain in the abdomen
Bloating, retching and feeling sick
Feeling particularly ‘full’ after a normal size meal

60
Q

Helicobacter Pylori - define

A

H. pylori - helix-shaped gram-negative bacteria, survives in gastric acid by secreting urease

61
Q

Urea breath test - function

A

The urea breath test is rapid and non-invasive procedure used to identify active infection by H. pylori.

62
Q

Urea breath test - process + result

A

Patient drinks a solution containing urea labelled with an uncommon isotope (non-radioactive carbon-13).

The detection of isotope-labelled carbon dioxide in exhaled breath indicates that the urea was split by urease -secreting H. pylori, present in the stomach.

63
Q

Vitamin B12 - define

A

Vitamin B12 (cobalamin) is a water soluble vitamin that has an essential role in the nervous system and the formation of red blood cells as a co-factor for DNA synthesis.

64
Q

Vitamin B12 absorption

A

When dietary B12 enters the stomach it is bound by intrinsic factor (IF), a 45 kDa glycoprotein by the parietal cells of the stomach

The B12-IF complex enters the intestine where it binds to receptors on the mucosal cells of the ileum and is absorbed into the blood stream.

65
Q

Effect of pernicious anaemia

A

Pernicious anaemia, an autoimmune attack on the gastric mucosa, causes severe Vitamin B12 deficiency. This leads to the atrophy of the stomach wall and the IF secretion is absent or severely depleted.

66
Q

Signs and symptoms of vitamin B12 deficiency include:

A

Macrocytic anaemia (increased MCV, decreased haemoglobin)
Weakness and tiredness
Pale skin
Glossitis – inflammation of the tongue
Nerve problems such as numbness or tingling (severe deficiency)

67
Q

Testing for Vitamin B12 deficiency - Serum vitamin B12 level:

A

Serum vitamin B12 level: <150 pmol/L indicates probably B12 deficiency

68
Q

Testing for Vitamin B12 deficiency - Methylmalonic acid:

A

Methylmalonic acid: elevated in tissue B12 deficiency (may also be elevated in renal disease)

69
Q

Testing for Vitamin B12 deficiency - Homocysteine:

A

Homocysteine: elevated in B12 deficiency as not converted to methionine. Less specific than MMA as it is also elevated in folate deficiency and hypothyroidism, but test is more readily available

70
Q

Testing for Vitamin B12 deficiency - Holotranscobalamin (active B12):

A

Holotranscobalamin (active B12): measurement of B12 bound to transcobalamin and may be the first detectable marker of B12 deficiency

71
Q

Intrinsic factor and antiparietal cell antibodies in pernicious anaemia

A

Intrinsic factor and antiparietal cell antibodies are positive in pernicious anaemia

72
Q

Coeliac Disease - define

A

Coeliac disease is an autoimmune disorder, primarily affecting the small intestine.

73
Q

Coeliac Disease - cause

A

The disease results from immunological hypersensitivity to ingested to gliadin (gluten protein), found in wheat and other grains such as barley and rye.

Upon exposure to gluten in the small intestine there is an inflammatory reaction leading to the shortening of the villi lining and villous atrophy.

74
Q

Coeliac Disease - symptoms

A

Classic symptoms of coeliac disease include anaemia, weight loss, and GI problems e.g. diarrhoea, abdominal distention, malabsorption and loss of appetite.

75
Q

Severe coeliac disease can lead

A

Severe coeliac disease can lead

to anaemia and osteoporosis

76
Q

Tissue transglutaminase (TTG) - define

A

Tissue transglutaminase (TTG) is a enzyme that deaminates glutamine residues to glutamic acid on the gliadin fragment.

77
Q

Tissue transglutaminase (TTG) - target for what

A

The enzyme can be a target autoantigen in the immune response, leading to destruction of intestinal epithelial cells and the production of anti-TTG antibodies.

78
Q

TTG in coeliac disease testing

A

Anti-TTG antibodies belong to the IgA subclass of immunoglobulins.

A proportion of the healthy population are deficient in IgA

this test would produce a false negative result in IgA deficient patients with coeliac disease.

79
Q

Endomysial antibodies (EMA) use

A

Testing for Coeliac disease

Endomysial antibodies (EMA): these become elevated as part of ongoing damage to the intestine

80
Q

A duodenal biopsy use

A

Testing for Coeliac disease

A duodenal biopsy is the gold standard diagnosis of coeliac disease.

81
Q

Gluten challenge use

A

Testing for Coeliac disease

Gluten challenge: patients already on a gluten-free diet cannot be diagnosed as serology and histology tests will be normal until gluten is ingested.

82
Q

Inflammatory bowel disease - includes what

A

Inflammatory bowel disease(IBD) encompasses two distinct autoimmune conditions of the GI tract: ulcerative colitis and Crohn’s disease.

83
Q

Ulcerative colitis - define

A

Diffuse inflammation affecting the mucosa of the colon only.

84
Q

Crohn’s disease - define

A

Patchy ulceration affecting any part of the GI tract and may extend through the full thickness of the bowel.

85
Q

Crohn’s disease - complications

A

Complications include fistulae, abscess formation and stricturing.

86
Q

IBD test

A

Colonoscopy is the definitive test for diagnosis of IBD.

87
Q

Crohn’s disease and Ulcerative colitis have common signs and symptoms: list them

A 
Abdominal pain
Prolonged diarrhoea with bowel urgency
Blood and/or mucus in stools
Fatigue
Weight loss and malnutrition
88
Q

Crohn’s disease may present with:

A

Perianal lesions

Bowel obstruction i.e. abdominal bloating, distension, vomiting or constipation

89
Q

IBD vs IBS - define

A

IBD = inflammation of intestinal system

IBS = not a disease, functional disorder w/vague GI symptoms

90
Q

IBD vs IBS - features

A

IBD = extra intestinal manifestations in addition to GI symptoms

IBS = only in intestine area

91
Q

IBD vs IBS - treatment

A

IBD = anti-inflammatory meds + might need surgery

IBS = not with A-I meds + don’t need surgery

92
Q

Common signs and symptoms for IBD and Irritable bowel syndrome (IBS):

A

Common signs and symptoms for IBD and Irritable bowel syndrome (IBS): abdominal pain or discomfort with diarrhoea or constipation.

93
Q

IBD vs IBS - what is needed for differential diagnosis

A

Need biochemical markers for differential diagnosis.

94
Q

Leakage of neutrophils and calprotectin due to

A

Any disturbance in the mucosal architecture due to the inflammatory process results in leakage of neutrophils and calprotectin

95
Q

Calprotectin - define + function

A

Calprotectin is a protein released by neutrophil

When there is inflammation in GI tract, calprotectin released, resulting in an increased amount released into the stool

96
Q

What do neutrophils release in inflammation

A

Zinc and calcium binding protein released by neutrophils in inflammation

97
Q

Colorectal cancer - from where

A

It arises predominantly from adenomatous polyps

98
Q

Colorectal cancer - signs

A

Colorectal cancer is often asymptomatic until late-stage disease (poor prognosis)

99
Q

Colorectal cancer - testing

A

Tests must detect the small amounts of blood in faeces that may be present in asymptomatic individuals with bowel lesions

Guaiac faecal occult blood (FOB) method widely used in screening.

100
Q

Faecal Immunochemical Test (FIT) - define and compare with FOB

A

‘Dipstick’ test for blood in stool
Quantitative measurement of Hb in faeces

Higher sensitivity than guaic FOB method

101
Q

Colorectal testing in symptomatic patients meeting the following criteria

A

Over 50y with unexplained abdominal pain or weight loss
50 to 60y with changes in bowel habit or iron-deficiency anaemia
60y or over with anaemia without iron deficiency

102
Q

OC-Sensor FIT kit - use

A

OC-Sensor FIT kit (made by MAST) -immunoassay test which can be used with an automatic analyser.

Fundamentals of P (62 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions