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GGGGGGII > week 3 > Flashcards

week 3 Flashcards

1
Q

coeliac disease

A

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

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2
Q

where is iron primarily absorbed

A

duodenum and upper jejunum

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3
Q

z line

A

the line of transition from the oesophageal mucosa to gastric mucosa

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4
Q

location of pancreas

A

retroperitoneal. Epigastric and left hypochondrium

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5
Q

blood supply of the pancreas

A

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

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6
Q

drainage of pancreas

A

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

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7
Q

how much iron is in the body

A

4g

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8
Q

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

A

3g

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9
Q

would ferritin be increasedor decreased in IDA?

A

decreased

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10
Q

what is the effect of hepcidin

A

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

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11
Q

defects in hepcidin (its loss) cause

A

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

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12
Q

Hep a

A

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

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13
Q

Hep a vaccine

A

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

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14
Q

Hep e

A

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

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15
Q

Hep B

A

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.

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16
Q

Hep d

A

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

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17
Q

hep c

A

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

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18
Q

reducing sugars

A

those that contain an aldelhyde group

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19
Q

reducing power

A

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

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20
Q

unconjugated hyperbilirubinaemia

A

indirect bilirubin wil be >85% of total bili.

Increased bili production, defects in hepatic uptake or conjugation

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21
Q

conjugated hyperbilirubinaemia

A

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

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22
Q

Gilbert’s syndrome

A

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

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23
Q

which bacteria produce a toxin prior to infection?

A

S. aureau and B. cereus.

patients become unwell rapidly

24
Q

which bacteria produce a toxin after consumption?

A

C.diff and E.coli 157

25
Q

which bacteria invade across the epithelial cell barrier

A

salmonella

26
Q

3 elements of a syndromic approach to enteric infection

A

vomiting, diarrhoea, non-intestinal manifestations

27
Q

campylobacter

A

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

28
Q

Salmonella

A

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.

29
Q

E.coli 0157

A

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.

30
Q

C. diff

A

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.

31
Q

Norovirus

A

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

32
Q

pancreatic enzymes secreted as zymogens

A

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

33
Q

pancreatic enzymes secreted in their active form

A

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

34
Q

MMC

A

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

35
Q

chronic pancreatitis

A

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

36
Q

surface marking of the liver

A

same level as costal margin

37
Q

location of gall bladder (surface anatomy)

A

where the right edge of rectus abdominus reaches the costal margin

38
Q

how saturated is transferrin generally?

A

30%

39
Q

Where does GI absorption of iron mainly take place?

A

duodenum

40
Q

gastro-ileal reflex

A

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

41
Q

major form of propulsion in the small intestine

A

peristalsis

42
Q

hepcidin

A

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

43
Q

hereditary haemachromatosis

A

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%

44
Q

Normal transferrin saturation

A

30%

IDA - <15%

45
Q

refractory coeliac disease

A

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

46
Q

length of the duodenum

A

25-38cm

47
Q

blood supply of duodenum

A

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

48
Q

length of the jejunum

A

2.5m

49
Q

what marks the division between the duodenum and jejunum?

A

suspensory muscle of duodenum

50
Q

lenght of the ileum

A

about 3 m long

51
Q

characteristic pathology in coeliac

A

loss of villous height due to atrophy and inflammatory infiltrate

52
Q

dermatitis herpetiformis

A

intensely itchy rash on extensor surfaces, associated with coeliac disease

53
Q

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

A

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

54
Q

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

A

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

55
Q

treatment of hep D

A

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

56
Q

treatment of Hep C

A

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.

GGGGGGII (9 decks)

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