week 3

Question 1

coeliac disease

Answer 1

a gluten-sensitive enteropathy. Small intestinal atrophy which resolves when gluten is removed from the diet

Question 2

where is iron primarily absorbed

Answer 2

duodenum and upper jejunum

Question 3

z line

Answer 3

the line of transition from the oesophageal mucosa to gastric mucosa

Question 4

location of pancreas

Answer 4

retroperitoneal. Epigastric and left hypochondrium

Question 5

blood supply of the pancreas

Answer 5

pancreatic branches of the splenic artery. Head supplied by branches of the coeliac trunk and mesenteric arteries.

Question 6

drainage of pancreas

Answer 6

head drained into superior mesenteric branches of hepatic portal vein.
Pancreatic veins drain rest of pancreas into splenic vein

Question 7

how much iron is in the body

Answer 7

4g

Question 8

how much iron is contained within the rbcs and bone marrow?

Answer 8

3g

Question 9

would ferritin be increasedor decreased in IDA?

Answer 9

decreased

Question 10

what is the effect of hepcidin

Answer 10

reduces level of iron in the plasma by binding ferroportin and degrading it

Question 11

defects in hepcidin (its loss) cause

Answer 11

increased iron absorption in the gut, increased iron release and increased Transferrin saturation which leads to parenchymal iron overload

Question 12

Hep a

Answer 12

Rna virus, self-limiting, 30 days incubation period, only acute illness, IgM + or RNA in serum if acute illness. No treatment
Vaccine exists

Question 13

Hep a vaccine

Answer 13

inactivated virus vaccine, 95% efficacy, given pre-exposure to at risk groups. Generally given for travel-related reasons

Question 14

Hep e

Answer 14

RNA virus, similar to hep a but has rare neuro effects. No vaccine, faeco orla and pork but not really person-person
4 genotypes

Question 15

Hep B

Answer 15

DNA virus, infected bodily fluids, acute and chronic, age factor in whether it will progress to chronic,
Chronic - can leads to HHC and CLD. Patients in two groups, eAg+ or eAG-.
To treat chronic either give IFN or anti-viral drugs to suppress viral replication.

Question 16

Hep d

Answer 16

ss RNA virus, have to have hep B. Either co-infect with Hep b Or acquire at a later date. Can only treat with ifn alpha

Question 17

hep c

Answer 17

6-7 week incubation after which 25% of people will be asymptomatic. Of thoss infectefd 30% will clear and 70% will develop chronic. Of these 25% will develop cirrhosis and 1-5% HCC
Treated with either IFN alpha + riabavarin or DAAs

Question 18

reducing sugars

Answer 18

those that contain an aldelhyde group

Question 19

reducing power

Answer 19

the smaller the chain the greater the reducing power. Greater power = greater sweetness

Question 20

unconjugated hyperbilirubinaemia

Answer 20

indirect bilirubin wil be >85% of total bili.

Increased bili production, defects in hepatic uptake or conjugation

Question 21

conjugated hyperbilirubinaemia

Answer 21

direct bilirubin >50%. Occurs where defects in hepatic excretion are seen

Question 22

Gilbert’s syndrome

Answer 22

benign autosomal dominant condition. Caused by deficiency of enzymes that conjugate bilirubin. High levels of uncojugated bilirubin with normal LFTs is what you would see

Question 23

which bacteria produce a toxin prior to infection?

Answer 23

S. aureau and B. cereus.

patients become unwell rapidly

Question 24

which bacteria produce a toxin after consumption?

Answer 24

C.diff and E.coli 157

Question 25

which bacteria invade across the epithelial cell barrier

Answer 25

salmonella

Question 26

3 elements of a syndromic approach to enteric infection

Answer 26

vomiting, diarrhoea, non-intestinal manifestations

Question 27

campylobacter

Answer 27

from chicken normally. 9000 infecting dose which is high. Normal incubation of 3 days but can vary depending on infecting dose. Vomiting is rare. Sensitive to stomach acid. Normally 7 day course. Can become resitant to anti-biotics during treatment. Guillan barré and reactive arthritis

Question 28

Salmonella

Answer 28

typhoidal and non-typhoidal serotypes. Spreads person to person. Infectious dose of 10,000 organisms. Treat if worried about bacteraemia. Risk increased if reduced stomach acidity or diminished intestinal flora fall ill within 72 hours.

Question 29

E.coli 0157

Answer 29

person to person, Very lowinfectious dose of 10. Attaches to the large bowel and secretes shiga toxin. Kills enterocytes and enters systemic circulation. CAn cause haemolytic uremia syndrome- microangiopathic uraemic syndrome- deposition of fibrin clots, renal failure and thrombocytopenia. Bloody diarrhoea and abdominal tenderness, fever is rare. Supportive treatment.

Question 30

C. diff

Answer 30

Less diverse gut flora. Have a loose stool and colic, and fever. If bad can develop into pseudomembranous colitis. Toxin is important. Lab tests - tissue culture assay (takes ages). C. diff antigen and then C.diff toxin. Treating - change to narrow spectrum anti-biotic e.g. metronidazole. Faecal transplant.

Question 31

Norovirus

Answer 31

faecal-oral, 10-100 infectious dose. very stable. 24-28 hours acute explosive diarrhoea and vomiting. No lasting immunity

Question 32

pancreatic enzymes secreted as zymogens

Answer 32

trypsin (proteins), chymotrypsin (proteins), carboxypeptidase (proteins),. elastase (proteins), phospholipase (phospholipids), co-lipase

Question 33

pancreatic enzymes secreted in their active form

Answer 33

amylase (starches), lipase (triglycerides), ribonuclease (ribonucleic acids), deoxyribonuclease (deoxyribonucleic acids)

Question 34

MMC

Answer 34

Migrating motor complex - 90-120 minutes between meals. Causes weak repetitive peristaltic waves

Question 35

chronic pancreatitis

Answer 35

chronic inflammation of the pancreas, leading to destruction of the exocrine and endocrine components

Question 36

surface marking of the liver

Answer 36

same level as costal margin

Question 37

location of gall bladder (surface anatomy)

Answer 37

where the right edge of rectus abdominus reaches the costal margin

Question 38

how saturated is transferrin generally?

Answer 38

30%

Question 39

Where does GI absorption of iron mainly take place?

Answer 39

duodenum

Question 40

gastro-ileal reflex

Answer 40

segmentation in the ileum begins due to gastrin secreted in response to the presence of chyme in the stomach

Question 41

major form of propulsion in the small intestine

Answer 41

peristalsis

Question 42

hepcidin

Answer 42

hormone that binds ferroportin and degrades it. It reduces the level of iron in the plasma, reduces GI iron absorption and reduces macrophages iron release from the RES system. produced by the liver. Loss results in haemacromatosis

Question 43

hereditary haemachromatosis

Answer 43

autosomal recessive disorder or iron metabolism causing iron overload. Abnormalities of the HFE gene are responsible for most cases. Thought to work mainly through reducing hepcidin production. Can see transferrin concentrations of 100%

Question 44

Normal transferrin saturation

Answer 44

30% | IDA - <15%

Question 45

refractory coeliac disease

Answer 45

recurrent malabsorptive symptoms and villous atrophy despite strict adherence to GF diet for at least 6-12 months and i absence of any other causes or malignancy Type I: villous atrophy with negative immuno-phenotype Type Ii: villous atrophy with abnormal immunio-phenotype

Question 46

length of the duodenum

Answer 46

25-38cm

Question 47

blood supply of duodenum

Answer 47

proximal to major dueodenal papilla - gastroduodenal artery (coeliac trunk) Distal to major duodenal papilla supplied by superior mesenteric artery

Question 48

length of the jejunum

Answer 48

2.5m

Question 49

what marks the division between the duodenum and jejunum?

Answer 49

suspensory muscle of duodenum

Question 50

lenght of the ileum

Answer 50

about 3 m long

Question 51

characteristic pathology in coeliac

Answer 51

loss of villous height due to atrophy and inflammatory infiltrate

Question 52

dermatitis herpetiformis

Answer 52

intensely itchy rash on extensor surfaces, associated with coeliac disease

Question 53

what would suggest a chronic hep B carrier had a low chance of progression to HCC and cirrhosis

Answer 53

eAg negative - suggestive of low viral load and that they are less infectious

Question 54

treatment of chronic Hep B sufferers with liver inflmmtion (LFT and biopsy)

Answer 54

immunological - pegylated IFN-alpha. Year long treatment but with lots of side effects anti-viral drugs - tenofovir. Need to be taken life long. Fewer side effects

Question 55

treatment of hep D

Answer 55

requires Hep B to be there. Increases likelihood of progression to chronic liver disease Can only be treated with pegylated IFN-alpha

Question 56

treatment of Hep C

Answer 56

pegylated IFN-alpha and ribavrin - cure rate of 40-60% after 24-48 weeks of treatment which is hard to maintain. Direct-acting anti-virals: attack viral replication cycle with a cure rate of 95%. 8-12 week tablet course.