Week 2 Flashcards
(154 cards)
1
Q
What is the function of the pancreas?
A
Secretion of NaHCO3 and a range of enzymes for digestion of protein, carbohydrate and fat
2
Q
Give examples of reducing sugars and their importance
A
Glucose, galactose, lactose, maltose, glyceraldehyde, maltotriose; reducing power determines sweetness
3
Q
Describe Benedict’s test
A
Detects presence of reducing sugars -
blue solution to insoluble yellow/red cuprous oxide precipitate
4
Q
Describe Barfoed’s test
A
Detects presence of monosaccharides -
blue solution to red precipitate in presence of acid
5
Q
What colour changes are observed when iodine is added to starch, dextrin and glycogen?
A
Starch - blue
Dextrin - red/purple
Glycogen - red/brown
6
Q
What is acute pancreatitis?
A
Disease of the pancreas in which pancreatic enzymes auto-digest the gland due to activation of trypsin; can be mild or fatal
7
Q
What does pancreatic amylase digest?
A
α-1,4 glucose-glucose bonds only (starch and glycogen → maltose, maltotriose, dextrins)
8
Q
What is starch broken down to by α-amylase?
A
Maltose, maltotriose and α-limit dextrins
9
Q
What are maltose, maltotriose and α-limit dextrins broken down to by brush border enzymes?
A
Glucose
10
Q
What brush border enzymes break down carbohydrates?
A
Sucrase, glucoamylase and α-dextrinase
11
Q
What pancreatic enzymes break down protein?
A
Trypsin, chymotrypsin, carboxypeptidase and elastase
12
Q
Which proteolytic pancreatic enzymes are activated by trypsin?
A
Chymotrypsinogen, procarboxypeptidase, proelastase, prophospholipase, procolipase
13
Q
What non-proteolytic enzymes are released by the pancreas?
A
Amylase, lipase, ribonuclease, deoxyribonuclease
14
Q
Outline the enzymes/mechanisms involved in the 4 stages of protein digestion
A
- Pepsin in the stomach
- Trypsin, chymotrypsin and carboxypeptidase in the small intestine
- Amino peptidase at the brush border
- Sodium linked carriers
15
Q
What is the pathogenesis of acute pancreatitis?
A
Uncertain mechanism Pancreatic insult (duct obstruction or acinar cell injury) → activation of inactive enzyme precursors → inflammatory cytokines
16
Q
What are the symptoms of acute pancreatitis?
A
Sudden onset abdominal pain, nausea and vomiting, fever, hypotension, shock, multi-organ failure
17
Q
What are the biochemical features of acute pancreatitis?
A
Increased amylase, lipase, urea and triglycerides
Decreased albumin and calcium
18
Q
What are the main causes of acute pancreatitis?
A
Gallstones or alcohol (80%), infection (mumps), tumour, drugs (furosemide, oestrogen, opiates, steroids), post-surgical, duct obstruction, genetic, hyperlipidaemia, hypercalcaemia
19
Q
What is chronic pancreatitis?
A
Irreversible pancreatic damage causing destruction of endocrine and exocrine functions; often secondary to repeat acute attacks or alcohol abuse
20
Q
What are the symptoms of chronic pancreatitis?
A
Recurrent abdominal pain radiating to the back, diabetes mellitus, weight loss, steatorrhoea, malabsorption (90% of acinar cell death)
21
Q
What are the causes of chronic pancreatitis?
A
Alcohol, genetic, trauma, hypercalcaemia, tropical, idiopathic
22
Q
What are the benefits and limitations to measuring
α-amylase to assess pancreatic function?
A
Benefits - small enough to pass through glomerulus and into urine, blood level is low and constant in absence of acute pancreatitis
Limitations - isoenzymes present elsewhere in the body (e.g. testes, fallopian tubes, lungs)
23
Q
What pattern does serum amylase follow in acute pancreatitis?
A
Rises within 5-8 hours of symptoms
Appears 4-6 times normal
Normalises by day 4
24
Q
What are the limitations of using serum amylase as a test for pancreatic function?
A
Low specificity; can be raised by many causes - abdominal disease, ruptured ectopic pregnancy, salivary gland lesion, renal insufficiency, diabetic ketoacidosis, tumours, drugs, macroamylase
25
What is macroamylase and how might its presence skew test results?
Complex of IgG/IgA and amylase; cannot be filtered through the kidney, causing a 2-8 fold increase in serum amylase levels
26
What is a normal serum amylase concentration?
<100 U/L
27
What is a normal urine amylase concentration?
30-600 U/L
28
What are the benefits of measuring urine amylase for pancreatic function?
Can be used to identify macroamylase presence (increased in serum but reduced in urine) and to differentiate between salivary and pancreatic amylase
29
What pattern does serum lipase follow in acute pancreatitis?
Rises within 4-8 hours of symptoms
Peaks at 24 hours
Appears 5-10 times normal
Normalises by 8-14 days
30
What is a normal serum lipase concentration?
30-210 U/L
31
What direct function tests are there for the pancreas?
Secretin-pancreozymin test - measures trypsin in the duodenum
Lundh test - measures amylase/trypin/bicarbonate concentration after a meal
32
What indirect function tests are there for the pancreas?
Enzyme concentration measurement in blood, urine and faeces
33
What is the NBT-PABA test for pancreatic function?
P-aminobenzoic acid is cleaved from N-benzoyl-I-tyrosyl-p-aminobenzoic acid by pancreatic enzymes
Limited, not used
34
What is the pancreaolauryl test for pancreatic function?
Fluorescein is cleaved from fluorescein dilaurate by pancreatic enzymes
Limited, not used
35
What is the faecal chymotrypsin test for pancreatic function?
Tests for proteolytic enzymes; low value indicates pancreatic insufficiency but there is a lack of standardisation
Severe disease 77% sensitivity, 85% specificity
36
What is the faecal elastase test for pancreatic function?
Endopeptidase and sterol binding protein;
<200 μg/g stool indicates pancreatic insufficiency; useful in determining amount of enzyme replacement needed in cystic fibrosis and chronic pancreatitis
Severe disease 100% sensitivity, 96% specificity
37
What is a normal faecal elastase concentration?
200-1000 μg/g
38
What are the components of bile?
Bicarbonate, cholesterol, phospholipids, bile pigments, bile salts/acids
39
Where does bile pigment/bilirubin come from?
Breakdown of haem group (porphyrin ring) of haemoglobin by macrophages in the reticulo-endothelial system of the spleen/liver/bone marrow
40
Which enzyme breaks down haem to biliverdin?
Haem oxygenase
41
Which enzyme breaks down biliverdin to unconjugated bilirubin?
Biliverdin reductase
42
What is unconjugated bilirubin bound to and why?
Albumin; U-bilirubin is insoluble and cannot be transported in blood otherwise
43
What is bilirubin?
Yellow/orange pigment present in bile
44
How does U-bilirubin bound to albumin enter the liver?
Via sinusoidal bilirubin transporters
45
What happens to U-bilirubin in the liver?
UDP glucuronyl transferase adds glucuronic acid which conjugates the bilirubin (mono and diglucuronide) which is then transported into bile canaliculi for accumulation in bile
46
What happens to C-bilirubin in the small intestine?
C-bilirubin is converted to U-bilirubin by β-glucoronidase and is then fermented by microflora to produce meso, sterco and urobilinogen
47
What do the microflora of the large intestine do to meso, sterco and urobilinogen?
Mesobilinogen - converted to mesobilin
Stercobilinogen - stercobilin (faeces)
Urobilinogen - transported to liver and excreted by kidneys; urobilin (urine)
48
What are bile salts/acids?
Biological emulsifiers with hydrophilic and hydrophobic faces; glycine and taurine derivatives of cholic acid (e.g. glycholic and taurocholic acid); OH groups point downwards
49
Outline the breakdown of lipids
1. Bile salts breakdown large lipid globules (1000nm) into emulsion droplets for digestion by lipases into free fatty acids in the intestinal lumen
2. Bile salts form micelles (4-7nm) with FFAs/phospholipids/cholesterol/fat soluble vitamins which enter intestinal cells which continously breakdown and reform to allow contents to cross into epithelium
3. Triglycerides are packaged into chylomicrons which enter the blood via lymphatics
50
What is the sphincter of Oddi?
Muscular valve which controls the flow of bile and pancreatic fluid into the duodenum; contracted at rest, causing bile to collect in the gallbladder due to back pressure
51
What happens to bile in the gallbladder?
Stored and concentrated by epithelial cell reabsorption of water and electrolytes
52
What causes bile to be released from the gallbladder?
Presence of amino and fatty acids in the duodenum stimulates CCK secretion which causes contraction of the gallbladder and relaxation of the sphincter of Oddi to release bile
53
What causes bile production in the liver?
Acidic chyme in the duodenum stimulates secretin secretion which causes duct cells in the liver to produce bile and add more bicarbonate to it
54
Why and how are bile salts reabsorbed?
There are not enough bile salts in the body to process fats in a typical meal; 95% recycled
Bile salts are moved from digestive tract to intestinal capillaries and then to the liver via the hepatic portal vein where they are taken up by hepatocytes and secreted into canaliculi
55
What is hyperbilirubinaemia?
Excess of bilirubin in the blood
56
What is a normal value for total blood bilirubin?
<21 μmol/L
57
What is a normal value for blood conjugated bilirubin?
< 7 μmol/L
58
At what levels of total bilirubin is jaundice visible in the sclera and skin?
Sclera - >30 μmol/L
| Skin - >100 μmol/L
59
What are the 3 types of jaundice (with possible causes)?
1. Pre-hepatic (elevated haemolysis)
2. Hepatic (liver damage)
3. Post-hepatic (blockage of bile ducts)
60
Describe pre-hepatic jaundice
```
Increased breakdown of RBCs leads to increased unconjugated bilirubin
Tropical disease (malaria), drugs (anti-malarials), genetics (sickle cell anaemia)
```
61
Describe 2 types of neonatal jaundice
Physiological - common, usually harmless; foetal Hb needs to be replaced by adult Hb but underdeveloped liver lacks glucoronyl transferase (impaired conjugation); bilirubin peaks at 3-5 days and lasts <14 days; phototherapy treatment
Haemolytic disease - Rh incompatibility; very high bilirubin concentration; at risk of kernicterus (brain damage); treated with phototherapy and blood transfusion
62
How does phototherapy treatment work to reverse jaundice?
Blue light converts U-bilirubin to water soluble form which can be excreted
63
Describe hepatic jaundice
Problems can occur at several points, leading to different presentations
E.g. Gilbert's - reduced glucuronyl transferase activity; primary biliary cholangitis - autoimmune destruction of bile ducts; cirrhosis, hepatotoxic drugs, viral hepatitis
64
Describe post-hepatic jaundice
Obstruction of hepatic/cystic/bile duct leading to cholestasis
E.g. gallstones, pancreatitis, head of pancreas tumour
65
What are gallstones and how are they treated?
Small cholesterol pebbles formed when the capacity of bile salts/phospholipids to solubilise cholesterol is exceeded
Surgical removal, oral ursodeoxycholic acid, lithotripsy ultrasonic shockwaves
66
What are the consequences of gallstone obstruction in the cystic duct?
Joins gallbladder to common bile duct
| Painful contractions
67
What are the consequences of gallstone obstruction in the common bile duct?
Joins hepatic and cystic duct to duodenum
| No bile secretion, steatorrhoea, grey faeces, post-hepatic jaundice
68
What are the consequences of gallstone obstruction in the duodenal papilla?
No bile or pancreatic secretions into duodenum
| Malnutrition, acute pancreatitis
69
What are the implications of post-hepatic jaundice on surgery?
Bile salts needed for absorption of lipid-soluble vitamins (A, D, E, K); vitamin K needed for coagulation factors and so must be administered before surgery to prevent haemorrhage
70
How are bile pigments measured in serum?
Direct conjugated bilirubin - diazo reagent at low pH added to sample which converts C-bilirubin to C-azobilirubin (blue/purple), absorbance measured at 530-545nm, values compared
Total bilirubin - diazo reagent at low pH plus caffeine which displaces U-bilirubin from albumin, U and C azobilirubin formed and measured
71
What bile pigment analysis can be carried out using MultiStix urinalysis?
Urobilinogen (p-aldehyde used, pink) and bilirubin (conjugated, diazide used, tan)
U and C bilirubin should not be detectable
72
Why are bile pigments not normally measured in faeces?
Visual inspection is easy, free and obvious
73
What bedside methods can be used to measure bilirubin?
Blood gas analyser - early detection, severity monitoring, compare with labs
Bilirubinometer - thermometer-like, measures yellowness of skin, forehead/sternum best
74
What sphincters of the digestive tract are under voluntary control?
Upper oesophageal sphincter and external anal sphincter
75
What is the function of interstitial cells of Cajal?
Mediate enteric neurotransmission; serve as a pacemaker to allow smooth muscle contraction
76
What types of muscle are present in the upper half and lower half of the oesophagus?
Upper - striated, circular
| Lower - smooth, longitudinal
77
What is manometry used for?
Measures function of the oesophagus by recording pressure changes along the length of the upper GI tract
78
How is achalasia treated?
Balloon dilatation of LOS, laproscopic Heller's myotomy, endoscopic myotomy
79
How often does the MMC occur?
Every 90 minutes
80
What are the 4 phases of the MMC?
1. Prolonged quiescence
2. Increased frequency of contractility
3. Peak electrical and mechanical activity
4. Declining activity
81
What is motilin and what is its importance?
Polypeptide hormone which regulates the MMC; produced by M cells in the small intestine; housekeeper of the gut; enhances gastric emptying
82
How long does it take liquids and solids to leave the stomach?
Liquids - 20 minutes
| Solids - 3-4 hours
83
What can be caused by accelerated gastric emptying?
Diarrhoea, dumping syndrome
84
What are the symptoms of delayed gastric emptying (gastroparesis)?
Abdominal pain, vomiting, GORD, malnutrition, weight loss
85
How is gastroparesis managed?
Dietary - small frequent meals, liquids, nutritional support, post-pyloric feeding
Underlying cause - opiates, diabetes, virus
Medication - serotonin/motilin agonists, dopamine antagonists
Endoscopic - botox injection
Gastric electrical stimulation device - high frequency low amplitude contractions
86
How does food move through the small intestine?
Intermittently in boluses via prolonged propagated contraction
87
What motility disorders can arise in the small intestine?
Chronic intestinal pseudo-obstruction - signs of obstruction without occlusion causing abdominal pain, constipation and weight loss; neuropatic (Parkinson's)/myopathic (scleroderma), endocrine (diabetes), drugs (anti-Parkinson's)
Acute post-operative ileus - constipation and oral intolerance without obstruction after surgery; 0-2 hours SI, 24-48 hours stomach, 48-72 hours colon
88
What motility disorders can arise in the large intestine?
Acute colonic pseudo-obstruction (Ogilvie's syndrome) - parasympathetic dysfunction commonest after spinal/cardiothoracic surgery; risk of caecal perforation; gut rest, decompression, neostigmine (acetylcholinesterase inhibitor)
89
Describe the motility of the colon
No pacemaker activity
Mixture of short and long contractions
Movement through colon takes 1-2 days
90
What drugs decrease colonic motility?
Opiates, anticholinergics, loperamide
91
What drugs increase colonic motility?
Laxatives, serotonin receptor agonists (chronic constipation), gualylate C receptor agonist (IBS)
92
What problems can occur with anal sphincter dysfunction?
Incontinence, anorectal constipation, obstructive defecation, rectocoele, anal fissure
93
What problems can arise with the colon in SCI patients?
Flaccid bowel, slow stool propulsion through colon, flaccid anal sphincter causing incontinence
94
What are the main liver function tests?
Bilirubin, albumin, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase, gamma glutamyl transferase (γ-GT), total protein
95
Why might LFTs be ordered?
Screening healthy people, investigating symptoms, pre-operative assessment, monitoring established liver disease
96
Define U-hyperbilirubinaemia
Indirect bilirubin >85% of total bilirubin
97
Define C-hyperbilirubinaemia
Direct bilirubin >50% of total bilirubin
98
What do aminotransferases do?
Participate in gluconeogenesis
Catalyse transfer of amino groups from aspartic/alanine to ketoglutaric acid to produce oxaloacetic/pyruvic acid respectively
Markers of hepatocellular injury
99
Describe AST as a marker of liver function
Cytosolic and mitochondrial isoenzymes
Found in liver, cardiac/skeletal muscle, kidneys, brain, pancreas, lungs, WBC/RBCs
Less specific for the liver than ALT
Half-life 48 hours
100
Describe ALT as a marker of liver function
Cytosolic
Similar distribution to AST but extra-hepatic tissue activity is much lower
More specific for liver than AST
Half-life 18 hours
101
What is γ-glutamyl transferase?
Microsomal enzyme
Transfers glutamyl groups from γ-glutamyl peptides to other peptides/amino acids
Found in liver, hepatobiliary tree, heart, kidneys, lungs, pancreas, seminal vesicles
Plasma activity most related to liver isoenzyme
Poor specificity but useful for linking with ALP and identifying chronic alcohol consumption
102
How can raised γ-GT be used as an indicator of chronic alcohol consumption?
Chronic liver disease = higher γ-GT activity
May indicate damage or excessive alcohol consumption
False positives and false negatives possible
103
What is alkaline phosphatase?
Group of enzymes which hydrolyse phosphate esters in alkaline solutions
Types - tissue non-specific ALP (osteoblasts, hepatocytes); intestinal, placental, germ cell
Liver isoenzyme on the exterior surface of the bile canalicular membrane
Rises in bile duct obstruction
104
What proteins are synthesised in the liver?
All plasma proteins except immunoglobulins
| Albumin, CRP, fibrinogen, transferrin, vitamin D BP, α1-antitrypsin
105
How are LFTs used in diagnosis?
Used as an aid with caution
Patients with normal LFTs may have advanced disease
Clinical history must also be used
Abnormal cut-offs may be skewed towards pathological levels due to undiagnosed patients
106
How should patients with abnormal LFTs be evaluated?
1. Clinical history (symptoms, hepatotoxin exposure, family history, virus exposure)
2. Physical examination (BMI, nutrition, jaundice, stigmata, ascites)
3. Interpretation of initial screening (LTFs, patterns, FBC)
107
What do raised ALT/AST, GGT/ALP, bilirubin indicate?
ALT/AST - hepatocellular injury
GGT/ALP - cholestasis
Bilirubin - both
108
If AST is increased 3x and ALP is decreased 2x normal, what type of liver disease does this indicate?
Hepatocellular disease
Normal albumin - acute hepatitis
Decreased albumin - chronic hepatitis
109
If AST is decreased 3x and ALP is increased 2x normal, what type of liver disease does this indicate?
Cholestatic disease
Normal albumin - acute
Decreased albumin - chronic
110
What does increased ALP in the absence of increased GGT indicate?
Bone disease
111
What does increased ALP in the presence of increased GGT indicate?
Cholangitis (if US/CT indicates dilated ducts)
| Primary biliary cirrhosis (if US/CT indicates non-dilated ducts and positive for anti-mitochondrial antibodies)
112
If hepatocellular disease is suspected by AST/ALT and ALP, what is the next stage of investigation?
Serology and liver biopsy
113
What pattern of AST/ALT and ALP results indicate hepatocellular disease?
ALT or AST > 150 U/L
| ALP < 200 U/L
114
What pattern of AST/ALT, ALP, GGT and bilirubin results indicate cholestatic disease?
ALP > 180 U/L
ALT < 150 U/L
GGT > 100 U/L
Bilirubin < 50 umol/L
115
If cholestatic disease is suspected by AST/ALT and ALP, what is the next stage of investigation?
Ultrasound abdomen for dilated ducts
116
Define screening
The detection of pre-symptomatic disease
117
Outline Wilson's criteria for screening programmes
```
Important health problem
Easy test to perform and interpret which is accurate, acceptable, reliable, sensitive and specific
Accepted treatment recognised
Cost-effective diagnosis and treatment
Natural history understood
Latent/early symptomatic stage
Early treatment more effective
Policy on who should be treated
Continuous case-finding
```
118
What screening programmes are available currently?
```
Bowel
Breast
Cervical
AAA
Glaucoma
```
119
Outline some details about Down's syndrome
Trisomy 13 (extra copy of chromosome 21)
Risk depends on maternal age
Physical/mental features - learning difficulties, congenital heart problems, thyroid problems, reduced muscle tone, single palmar crease, small nose, flat nasal bridge
Ultrasound and biochemistry
120
Define paternalistic
Restriction of freedom and responsibilities of subordinates/dependants in their supposed interest
121
Outline the screening for Down's syndrome
Screening test - ultrasound and biochemistry in first trimester, maternal age taken into account
Categorised into high and low risk
Diagnostic test for high risk - amniocentesis/chorionic villus sampling
Positive test - termination offered
122
What is the Harmony Prenatal Test?
Commercial blood test to screen at 10 weeks for Down, Patau and Edward syndromes
123
In terms of reproductive health, how does the law in Northern Ireland differ from the rest of the UK?
Termination of pregnancy is against the law, unless under exceptional circumstances
Pregnant women are not screened but are offered a foetal anomaly scan in the second trimester
124
What is the difference between a screening test and a diagnostic test?
Screening - simple, non-invasive test applied to asymptomatic individuals
Diagnostic - definitive test for whether the condition is present or not
125
What is the prevalence of a disease and how is it found?
Total number of cases of the disease in the population
| Total number of cases divided by total population
126
What is the sensitivity of a test and how is it found?
Proportion of actual positives which are correctly identified as such
Ability to detect the disease if present - true positive
Number of test +ve who are disease +ve/ total number of disease +ve
127
What is the specificity of a test and how is it found?
Proportion of negatives which are correctly identified
Ability to detect if disease not present - true negative
Number of test –ve, who are disease –ve / total number of disease –ve
128
What is the positive predictive value of a test and how is it found?
Probability of the person having the disease when the test is positive - proportion of screening tests that are correct
Number of test +ve, who are disease +ve/total number of test +ve
129
What is the negative predictive value of a test and how is it found?
Probability of the person not having the disease when the test is negative
Number of test –ve, who are disease –ve/total number of test -ve
130
What is the reciprocal of the PPV and what can it be used for?
100/PPV
| Tells us how many tests need to be performed for 1 case to be detected
131
What are the disadvantages of screening for Down's syndrome?
Further devaluation of the condition being screened for
Screening for an untreatable condition
Potential influence on choice of whether to continue a pregnancy said to be at high risk
132
What are the advantages of screening for Down's syndrome?
Increased choice for parents
Ability to prepare in advance
Decreased costs to parents/insurance/NHS (if terminated)
133
Where does the lesser omentum attach to the liver?
Groove on the posterior surface
134
In relation to the lesser omentum, where is the bile duct located?
At the free edge
135
What type of epithelium is the gallbladder composed of?
Simple columnar (absorptive)
136
Where does the head of the pancreas sit anatomically?
In the duodenal curvature
137
Where is the greater duodenal papilla located?
2/3rds down the descending duodenum on the posteriomedial side
138
What is the anatomical name for the sphincter of Oddi?
The sphincter of the hepato-pancreatic ampulla
139
Which lobe of the liver is only visible posteriorly?
Caudate lobe
140
What areas of the liver are drained by the left hepatic duct?
Left, caudate and quadrate lobes
141
How many hepatic veins open into the inferior vena cava?
3
142
What is the bare area of the liver?
Area without peritoneum lying directly against the diaphragm
143
What artery supplies the gallbladder?
Cystic artery (usually branches from the right hepatic artery)
144
What is the hepatorenal recess?
The space which separates the liver from the right kidney
145
What is Gilbert's syndrome?
Benign autosomal dominant condition which affects up to 7% of the population and is asymptomatic
Unconjugated bilirubin test required
146
What are the 3 main types of alcoholic liver disease?
Fatty liver
Alcoholic hepatitis
Cirrhosis
147
Outline hepatic alcohol metabolism
2 main metabolic pathways (cytoplasmic alcohol dehydrogenase and microsomal ethanol oxidising system; 3:1) which oxidise alcohol to acetaldehyde → acetate → acetyl CoA → TCA cycle → fatty acid formation
Reduced capacity to oxidise other molecules
148
Which of the hepatic alcohol metabolism pathways are inducible?
Microsomal ethanol oxidising system
149
How does alcohol increase hepatic lipids, leading to fatty liver?
Altered hepatocyte fat metabolism
Increased peripheral fat mobilisation
Reduces lipoprotein synthesis
150
Besides alcohol, what other causes of fatty liver disease are there?
Obesity, type 2 diabetes, nutritional imbalance (coeliac), drugs (methotrexate)
151
What is steatosis?
Fatty liver
Lipid droplets in hepatocytes which are microvesicular initially before coalescing and becoming macrovesicular
Seen after only 2 days of alcohol excess, rapid reversal on abstinence
152
What are the main features of alcoholic hepatitis?
Related to volume and duration of alcohol excess
Only occurs in 1/3 alcoholics
Females at greater risk
Genetic component
Fatty liver, fibrosis, hepatocyte ballooning/mallory bodies/necrosis, neutrophil inflammation
153
What are the main features of alcoholic cirrhosis?
10% of chronic alcoholics
| Complications - portal hypertension (shunts, varices, ascites, splenomegaly), liver failure, cancer
154
What are the main features of hepatocellular cancer?
Geographical age variation
80% occur in males
80% from cirrhosis
