1. Jack’s Jaundice
Glands of the GI Tract
1.Name the glands1
2.What is the difference
between merocrine,
apocrine, holocrine?2
3.Name the 3 salivary
glands3
4. What is the difference between serous (dark staining) and pale staining glands?4
5. What can you tell about an acinar gland that has a serous demilune?5
6. What is the mucuous/serous makeup of the 3 salivary glands?6
7. What is a myoepithelial cell?7
8. What are the 3 ducts in acinar glands?8
9. What are striated ducts?9
10.Which antibody is particularly present in saliva?10
1 Left to right: simple tubular, simple acinar, simple branched acinar
2 Merocrine = exocytosis, Apocrine = membrane bound vesicles released, Holocrine = where whole cells are
released, sebaceous glands
3 Parotid, sublingual and submandibular glands
4 Serous = thin watery secretion, Pale staining (Mucous) = thick mucosal secretion
5 It contains both serous and mucous secreting cells
6 Parotid = serous, sublingual = mucous, submandibular = mixed cells
7 Found in acinar glands, secretions exit firstly into intercalated duct, then into striated duct (which decreases
tonicity, like sweat glands)
8 Secretions firstly into intercalated duct, then striated duct (reabsorbtion), then into excretory duct (large)
9 The site of Na+ pumps which reabsorb Na+ and Cl- and replace them with K+ and HCO3- so the saliva
becomes hypotonic
10 IgA, secreted by plasma cells in supporting connective tissue

2. 11.Which part of the pancreas is endocrine?11
12.Other than insulin and glucagon, what other hormones are produced by Islets12
13.Approximately how many lobules are there in the adult liver?13
14.What is the histological structure of a hepatic lobule/portal triad?14
15.What is a sinusoid?15
16.What are Kupffer cells?16
17.What is the function of bile salts?17
18.What are bile pigments?18
19.Describe the oxygenation of the blood closest the triad vs the central vein?19
20.How much paracetomol relative to the recommended dose is toxic and why?20
21.How much bile can the gallbladder store?21
22.What type of pumps are active in the gallbladder?22
23.What does cholecystokinin do?
11 The Islets of Langerhans, which secrete insulin and glucagon
12 Pancretic polypeptide, somatostatin
13 1 million
14 Each are connected to a central vein in the middle of the aciuns, surrounded by ʻtriadsʼ of bile duct, portal
vein, hepatic artery
15 A space where blood drains past a row of hepatocytes
16 Specialised phagocytic cells only present in the liver
17 Synthesised from cholesterol - function to emulsify fats in the duodenum
18 Biliruben and biliverdin, breakdown products of haemoglobin
19 Blood most oxygenated and nutrient rich nearest the triad, most depleted of oxygen and nutrients nearest
the central vein
20 4x recommended dose, normally metabolised by P450s which can become depleted if overused. If
depleted, quinone binds covalently to cell proteins and kills cells. Induction of liver enzymes and alcohol
potentiates toxicity. Death slowly occurs 5 days from liver failure.
21 50ml
22 Na+, K+ ATPase which act to absorb water from the bile the same way as in the kidney

3. Epidemiology of Viral Hepatitis
1. What is the difference between a virion and a nucleocapsid?23
2. IgG and IgA antibodies are indicative of what stages of immunity?24
3. What is the main pathology caused by viral hepatitis?25
4. What is the virus that causes hepatitis?26
5. What are the routes of transmission of hepatitis A and B?27
6. Which types of hepatitis do not cause chronic infection?28
7. What are the symptoms of viral hepatitis?29
8. What is the incubation period for hepatitis A?30
9. How do you diagnose Hep A?31
10.What is an enteric virus?32
11.What are the structural components of a hepatitis B virus?33
12.What are the modes of transmission for Hep B, given that it is parenteral?34
23 Virion = complete particle, Nucleocapsid = protein coat and nucleic acid
24 IgM is a sign of acute or recent infection. IgG is a sign of past infection, immunisation or presence of
passively acquired antibody.
25 Inflammation of the liver
26 Adenovirus hepatitis
27 A = faecal-oral, B = parenteral (other than mouth, e.g. IV)
28 A and E. Whilst B, C, and D do cause chronic infection.
29 Malaise, fever, headache, jaundice, dark urine and clay coloured faeces, anorexia, vomiting.
30 3-5 weeks
31 Detection of Hep A virus IgM in blood samples. IgG shows past exposure and antibody.
32 One which inhabits the intestinal tract
33 Inner protein core around DNA and DNA polymerase, outer lipid envelope containing surface antigens
34 Sexual intercourse, blood and blood products, injecting drugs, tattoos and piercings, accupuncture

4. 13.What is the incubation period for Hep B?35
14.What are icteric and anicteric?36
15.What is immune dependent cytotoxicity?37
16.What is the difference between active and passive immunisation?38
17.How can Hep B be prevented, treated and controlled?39
18.Name two antivirals used to treat Hep B40
19.What percentage of Hep C carriers will experience chronic liver damage?41
Bile and the Biliary System
1. What stimulates bile production by the liver?42
2. What is cholecystokinin?43
3. What series of events causes the release of bile from the gallbladder?44
4. What is the relationship between liver blood flow and bile flow?45
35 6 weeks to 6 months (mean 2.5 months)
36 Icteric is where the infection is resolved without causing symptoms, anicteric is the carrier state 6 weeks to
6 months which results in cirrhosis of the liver and carcinoma ultimately. It is possible to be an asymptomatic
carrier and this is more likely the younger you are (80% infected before 1yrs become carrier rather than
resolve infection).
37 Where an effector cell of the immune system lyses a target cell whose membrane surface antigens have
been bound by specific antibodies
38 Active immunity is development of immunity following exposure to the pathogen, passive immunity is
inherited antibodies. Vaccination is active immunity because you have been exposed to the pathogen and
developed your own antibodies to it (albeit it a non-harmful strain of the pathogen).
39 Passive and active immunization, antiviral therapy, immunomodulators
40 Lamivudine and Adefovir
41 40-50%
42 Parasympathetic impulses across the vagus nerve stimulates production in the liver
43 A hormone secreted by the small intestine which signals for the release of bile from the gallbladder
44 Acidic chyme entering the duodenum stimulates secretion of secretin into blood which causes flow of bile
from liver to gallbladder. Fatty acids stimulate release of CCK which causes contraction of gallbladder
45 Bile flow tends to increase with greater blood flow to liver but is not a consequence of greater blood flow

5. 5. What are the sphincter of Oddi and ampulla ofVater?46
6. What co-transporters are used in the gallbladder to concentrate bile?47
7. What are the key differences between hepatic bile and gallbladder bile?48
8. What is the major component of bile and where does it come from?49
9. What is the relationship between bile and cholesterol?50
10.Under what circumstances might you develop ‘painless jaundice’?51
11.Describe the process of fatty acid absorbtion by the lumenal cells of the
intestine52
12.Where doVLDLS, Chylomicrons, LDLs and HDLs carry fats from and to?53
13.Explain the passage of bilirubin from the blood to conjugated bilirubin in the bile
canaliculus54
Alcohol - Ethanol Content of Drinks, Metabolism and Acute Effects
on the Liver and CNS, and Teratogenic Effects on the Developing
Fetus
46 Ampulla of Vater = where the bile duct enters the duodenum, Sphincter of Oddi = the sphincter that
controls this
47 Na+/Cl- co-transporters are used to draw fluid and salts out of the bile and concentrate it
48 hepatic bile = less acidic, lower concentration of sodium, potassium, chloride, calcium, bilirubin,
phospholipids, cholesterol,
49 bilirubin, 85% from breakdown of red blood cells
50 Bile allows cholesterol to become soluble in water
51 May occur in the case of malignant obstruction of the bile duct. May be associated with anorexia, weight
loss or loose stools because bile not reaching intestine. Instead it is being forced back into blood and
causing yellow tinge. However non-biliary causes should be considered, such as increased bilirubin prod.
52 Micelle formed by bile salts and glycerides, long chain fatty acids taken up into cell, converted back into
triglycerides etc. in the SER, fat droplets then formed, packaged into apoproteins in the Golgi, chylomicrons
and VLDLs bud off and exit the cell as vesicles via exocytosis from the basal membrane, passing into the
capillaries.
53 VLDLs = from liver to adopicytes and muscle, Chylomicrons = gut to liver, LDLs = tissues to liver, HDLs =
from tissues to liver to be broken down/excreted
54 Bilirubin bound to albumin in the blood, separates off and enters the hepatocyte where it is reacted with
UDP glucuronic acid (product of UTP and glucose) in the presence of glucronyl transferase into conjugated
bilirubin

6. 1. How much alcohol is there in 1 unit in ml?55
2. How many units in a pint of beer?56
3. and cider...?57
4. How many units in a (i) small 175ml and (ii) large 250ml glass of wine?58
5. How many units in a single measure of spirits (40% alcohol) or a WKD bottle?59
6. What is the recommended daily allowance for men and women in units?60
7. Describe the chemical stages of metabolizing ethanol into carbon dioxide and
water61
8. What is the rate in units/hour that alcohol is eliminated by the body?62
9. What is the Km range in mM for the variants of class 1 alcohol dehydrogenase
found in the liver?63
10.What types of alcohol dehydrogenase vary between ethnicities?64
11.What does having a low Km for something mean in terms of affinity?65
12.What is associated with increased risk of colon cancer in heavy drinkers of
Japanese ethnic origin?66
55 10ml of pure alcohol (which equates to 8g)
56 2-3 units (2 units if weak e.g. 3%, 3 if stronger e.g. 5%)
57 Roughly the same, 2-3 units/pint depending on strength
58 Wine is around 15% alcohol, 2.5 units or 3.5 units in these volumes repectively
59 1-1.5 units
60 Men should not regularly exceed 3-4 units and women 2-3
61 Ethanol broken down into acetaldehyde by Cytochrome P450 (CYP2E1), alcohol dehydrogenase and
catalase; this is converted into acetate by acetaldehyde dehydrogenase. Acetate is finally broken down into
CO2 and H20
62 1 unit per hour
63 0.05-34mM
64 ADH2 and 3
65 Low Km = high affinity, high Km = low affinity
66 ALDH2 polymorphism which occurs in 40% of people with east Asian ethnicity allows acetaldehyde to
reach high concentrations in blood, this is associated with increased rates of colon cancer.

7. 13.Which drug has been given to alcoholics to deliberately cause a negative reaction
if they drink excessively whilst taking it and what is its mechanism?67
14.What is the mechanism of methanol poisoning?68
15.Why can you get methanol poisoning in the case of alcohol consumption if
alcohol doesn’t contain methanol?69
16.What would you use to treat this?70
17.Describe the mechanism by which ethanol metabolism disturbs liver function71
18.What are the toxic effects of acetaldehyde (enzyme used in ethanol metabolism)?
72
19.What is the legal blood alcohol concentration limit for driving in the UK?73
20.What what blood alcohol concentration does the consumer experience gross
motor impairment and lack of physical control?74
21.At what blood alcohol concentration is the gag reflex impaired making it possible
to choke on your own vomit?75
22.What BAC is associated with the onset of coma, and possible death due to
respiratory arrest?76
23.Which four neuronal channels does ethanol have an intoxicating effect?77
67 Antabuse (“anti-abuse”) aka disulfiram, Inhibits aldehyde dehydrogenase so alcohol metabolised slower
68 causes CNS toxicity due to formation of formic acid which disturbs neuronal mitochondrial function and
causes acidosis
69 Ethanol extends the half life of methanol from 3 hours to 52 hours so it builds up in the system
70 Fomepizole - a potent-long acting inhibitor of ADH
71 metabolism of ethanol increases NADH/NAD+ ratio so less Acetyl CoA can enter citric acid cycle, fatty
acids cannot be oxidised and accumulate, so they are be converted into triglycerides
72 Interferes with proteins to produce a neoantigen (antigen within tumor cells) which leads to influx of
inflammatory cells.
73 0.08 BAC = 80mg/100ml
74 0.13-0.15
75 0.20 BAC
76 0.40 BAC
77 specific GABa channels, glutamate NMDA receptor channels, enhancement of slo-1 large conductance BK
potassium channels, thalamic T-type calcium channels

8. 24.What is gamma-aminobutyric acid?78
25.What are the most common mechanisms for alcohol dependence?79
26.What are the signs of foetal alcohol syndrome?80
The Liver and Protein Synthesis
1. Name the two most clinically important liver synthesised proteins?81
2. What is ascites?82
3. What are the three main pathologies caused by liver disease (cirrhosis) and liver
failure?83
4. What is the half-life of albumin?84
5. What is the main cause of portal hypertension?85
6. Why does fluid specifically accumulate in the peritoneal space in ascites?86
7. What are porto systemic shunts?87
8. What is the most common pharmacological treatment for ascites?88
78 a.k.a. GABA - the chief inhibitory neurotransmitter. Inhibited by ethanol.
79 Adaptation to one of the four channel effects. Enhanced dopamine (nucleus accumbens), like in other
addictive behaviours.
80 One or more dysmorphic facial features, growth deficiency and CNS impairment which affects learning
and behaviour, reduction in size of corpus callosum, reduction in brain size in pre-frontal and parietal cortex
81 Prothrombin (precursor of thrombin, which catalyses the production of soluble fibrin blood clots) and
albumin (the main blood protein, contributing to the 22mmHg plasma colloid oncotic pressure)
82 Accumulation of fluid in the peritoneal cavity causing bloated abdominal region and often ʻmedusaʼs headʼ
83 Jaundice, Ascites (fluid accumulation), Encephalopathy (brain damage)
84 14 days
85 Reduced blood flow through the liver because of liver fibrosis
86 Because the liver is fibrosed - portal hypertension causes a backlog of fluid in the abdomen which
preferentially diffuses out into the tissues.
87 New channels developed from portal circulation to systemic circulation in the presence of portal
hypertension.
88 Spironolactone - aldosterone antagonist

9. 9. What is INR and why is it an indicator of acute liver failure?89
10.How is aldosterone affected by failure of detoxification/breakdown?90
11.What is the cause of gynecomastia in liver damage?91
12.What is the main cause of hepatic encephalopathy?92
13.Why is hypoglycaemia a symptom of liver damage?93
14.What are the reasons liver damage can result in malnutrition?94
15.What is the consequence of the loss of Kupffer cell function?95
16.What is the normal range for total bilirubin?96
17.What is the median length of survival time from onset of ascites?97
Oral Administration and Absorbtion of Drugs
1. What is the difference between ‘pharmacokinetics’ and ‘pharmacodynamics’?98
2. What is bioavailablilty?99
89 International Normalised Ratio - measure of blood coagulability and indicative of liver failure because if
liver stops producing prothrombin, INR changes rapidly (prothrombin half life is only 6 hours)
90 A number of hormones including aldosterone buildup because they cannot be cleared by the failing liver, in
this case leads to salt and water retention contributing to ascites.
91 inability to breakdown oestrogen
92 Accumulation of ammonia and nitrogenous compounds resulting from inability to synthesise urea.
93 Again - it is hormone dependent, because insulin cannot be broken down by liver.
94 Glucose intolerance, alterations in amino acid metabolism, reduced bile acid synthesis so cannot absorb
fats, ascites causes decreased appetite, hypermetabolism occurs from hormone imbalance, increased
resting energy expenditure, presence of pro-inflammatory cytokines,
95 Bacterial challenge from the gut, frequent gram-negative infections with gut related organisms.
96 3-17umol/l
97 2 years
98 PK = drug movement, absorbtion, distribution and metabolism, PD = site and mechanism of action
99 The proportion of drug absorbed which reaches the systemic circulation. Bioavailability for an oral drug is
the ʻarea under the curveʼ as a % of what it would be compared with IV administration.

10. 3. How might drugs cross physiological barriers in the body?100
4. Why do drug plasma concentrations decline after reaching the systemic
circulation?101
5. What chemical property prevents drugs from being immediately metabolised?102
6. What characteristic of chemicals in portal blood makes them diffuse from blood
into hepatocytes?103
7. Which stage of drug metabolism are P450 enzymes involved in?104
8. What is meant by ‘conjugation’ in relation to drug metabolism?105
9. Describe the two pathways used for paracetomol metabolism under normal
conditions?106
10.What changes occur in paracetomol overdose and what would you give to treat
an overdose? 107
100 Lipid soluble or water soluble (via transporters), small molecules between cells ʻtightʼ epithelia, larger
molecules ʻleakyʼ epithelia.
101 Distribution - into fluid compartments and tissues in relation to its physiolochemical properties and
existence of specialised tissue barriers and transporters. Clearance - metabolism and excretion by the liver
and kidneys.
102 Lipid solubility, metabolism aims to make drugs water soluble so they can be excreted.
103 If they are lipophilic, otherwise they require the involvement of transporter proteins in the hepatocyte
membrane.
104 P450 enzymes are involved in the first stage (oxidation) which takes place on the SER of hepatocytes,
where the drug encounters many lipophilic surfaces
105 Coupling of the drug to a substrate via an enzyme reaction (such as glucuronate, acetate or sulphate)
106 1/ Conjugation with glucuronide sulphate into non-toxic metabolites (over 90%, but can become
saturated), 2/ Metabolism by CYP450 isoforms to N-acetyl-p benzuquinone-imine (NABQI) which is toxic in
large doses, under normal conjugation is detoxified with gluthathione.
107 Glucuronide pathway becomes saturated and glutathione levels depleted so NABQI pathway becomes
depleted. So N-acetyl cysteine can be given to detoxify NABQI.