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MBChB - year 2 > Week 3 GI lectures > Flashcards

Week 3 GI lectures Flashcards

1
Q

What are the symptoms of an enteric infection?

A
  • vomiting
  • diarrhoea
  • Non intestinal symptoms
    Botulism
    Guillain Barre (campylobacter)
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2
Q

What is indicated when vomiting is a predominant symptom?

A
  • Ingestion of a preformed toxin

- viral aetiology (norovirus)

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3
Q

What is the definition of diarrhoea?

A

3 or more loose or watery stools per day

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4
Q

What are the different pathological mechanisms that cause diarrhoea?

A
  • toxin mediated
  • damage to the intestinal epithelial surface
  • invasion across intestinal epithelial barrier (enterocytes infected)
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5
Q

What are the three main things when assessing a patient with GI symptoms?

A
  • History
  • stool examination / culture
  • endoscopy
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6
Q

What information should be gathered when taking a history from a patient relating to enteric infection?

A
  • Food history
  • Onset and nature of symptoms
  • Residence
  • Occupation
  • Travel
  • Pets/hobbies
  • Recent hospitalisation/antibiotics
  • Co-morbidity
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7
Q

What are treatment options for enteric infection?

A
  • Oral rehydration solution
  • Fluid IV replacement may be required if there’s a lot of vomiting
  • Antibiotics
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8
Q

Who should get antibiotics for diarrhoea?

A
  • Very ill patients
    Sepsis or evidence bacteraemia
  • Consider if significant co morbidity
    Reduction in duration diarrhoea clinically meaningful
  • Certain causes
    C.difficile associated diarrhoea (metronidazole/vancomycin)
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9
Q

What are the symptoms of campylobacter gastroenteritis?

A 
- Diarrhoea 
Frequent and can be high volume 
Blood in stool common
- Abdominal pain
Often severe
- Nausea common / vomiting rare
- Fever
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10
Q

What is the clinical course of campylobacter gastroenteritis?

A

Self limiting - 7 days

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11
Q

What are potential complications of campylobacter gastroenteritis?

A
  • Reactive arthritis

- Guillain barre

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12
Q

What are the symptoms of salmonella?

A

Nausea, diarrhoea, abdominal cramps, fever

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13
Q

What is the pathogenesis of E. coli?

A

Attachment –>Shiga toxin production –> Enterocyte death –> Enters systemic circulation

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14
Q

What are the symptoms of E.coli?

A

Bloody diarrhoea and abdominal tenderness

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15
Q

What is Haemolytic uraemic syndrome?

A

A systemic effect of shigatoxin that results in a triad of:

  • Microangiopathic haemolytic anaemia
  • Acute renal failure
  • Thrombocytopenia
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16
Q

What is the pathogenesis of C. diff?

A

Decreased colonisation resistance –> colonic colonisation –> toxin production

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17
Q

What are the risk factors for C. Diff?

A
  • Antibiotic exposure
  • older age (>65 years)
  • hospitalisation
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18
Q

What are the symptoms of C. diff?

A
  • Loose stool and colic
  • Fever
  • Leucocytosis
  • Protein losing enteropathy
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19
Q

What is the treatment of C. Diff?

A
  • Stop causative antibiotics if possible (narrow spectrum)
  • Metronidazole/ Vancomycin
  • Recolonise with normal flora
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20
Q

How is norovirus transmitted?

A

Faecal oral route

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21
Q

What are the clinical features of norovirus?

A
  • Acute diarrhoea and vomiting
  • Lasts 24-48 hours
  • No lasting immunity
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22
Q

What shape are red blood cells?

A

Biconcave discs

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23
Q

What is the total body content of iron?

A

4g

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24
Q

How is the total body content of iron distributed?

A
  • Bone marrow and RBCs – 3g
  • RES – 200-500mg
  • Myoglobin – 200-300mg
  • Enzymes – 100mg
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25
Q

What are the two ways iron can be stored?

A

Ferritin and hemosiderin

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26
Q

How is ferritin as a storage facility for iron?

A
  • Soluble
  • Iron safe and readily available from RES
    Serum Ferritin
  • Tiny amount in serum- directly related to RES iron stores
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27
Q

How is hemosiderin as a storage facility for iron?

A
  • Insoluble conglomerates of ferritin

- Iron only slowly available

28
Q

What are serum ferritin levels like in IDA?

29
Q

What are serum ferritin levels like in iron overload?

30
Q

What happens to serum ferritin levels in tissue inflammation?

A

Increased - Can rise to inappropriately high levels

31
Q

What protein transports iron in the blood?

A

Transferrin

32
Q

Where is transferrin synthesised?

A

Hepatocytes

33
Q

How does transferrin transport iron?

A

It has 2 iron binding domains and is normally 30% saturated with Fe

34
Q

What is the daily iron need?

35
Q

What are the two types of dietary iron?

A

Haem and non-haem iron

36
Q

What foods is haem iron found in?

37
Q

What foods is non- haem iron found in?

A

white meat, green veg, cereals

38
Q

What is the only mechanism that regulates iron balance?

A

Regulation of dietary iron absorption (there is no excretory mechanism for excess iron)

39
Q

What is mostly responsible for absorbing iron?

A

Duodenal enterocytes

40
Q

Is haem or non-haem iron absorbed more easily?

41
Q

How is non-haem iron released from food?

A

Acid digestion and proteolytic enzymes in the stomach

42
Q

What extra step must non- haem undergo that haem iron does not?

A

It must be reduced from the ferric to the ferrous form by duodenal cytochrome b1(dCytb1)

43
Q

What is iron taken into the enterocyte by?

A

divalent metal transporter 1 (DMT1)

44
Q

What exports iron from the enterocyte to the blood?

A

ferroportin and hepcidin

45
Q

What is ferroportin?

A

A transmembrane protein that is present on duodenal enterocytes and macrophages of the RES

46
Q

How is iron taken up from storage when needed?

A

The RES releases iron to transferrin in the plasma and then the iron on transferring is taken up via transferrin receptors on erythroblasts, hepatocytes etc.

47
Q

How many atoms of iron can transferrin bind?

48
Q

What is an erythroblast?

A

A developing RBC in bone marrow

49
Q

where does the Bulk of iron in the plasma comes from?

A

macrophages

50
Q

How is oxygen transported throughout the body?

A

By haemoglobin which can reversibly bind to O2 without undergoing oxidation or reduction

51
Q

What different disorders of iron metabolism are there?

A

Not enough iron

too much iron

52
Q

How are red blood cells described in IDA?

A

Microcytic and hypochromic

53
Q

In males and post-menopausal females what is IDA caused by (until proven otherwise)?

A

GI blood loss

54
Q

What types of haematinic deficiencies are possible?

A
  • folate deficiency
  • Iron deficiency
  • vitamin B12 deficiency
55
Q

What is the function of hepcidin?

A

The most important influence on iron metabolism. It is the ‘low iron’ hormone and reduces the levels of iron in the plasma

56
Q

How does hepcidin reduce the levels of iron in plasma?

A

hepcidin binds to ferroportin and degrades it which reduces GI iron absorption and reduces macrophage release from the RES

57
Q

Where is hepcidin synthesised?

58
Q

What does loss of hepcidin cause?

A

Increased GI iron absorption, increased RES iron release, increased Tf% saturation parenchymal iron overload (HH)

59
Q

What is hereditary haemochromatosis?

A

autosomal recessive disorder of iron metabolism causing iron overload

60
Q

What causes Hereditary haemochromatosis?

A

Abnormalities of the HFE gene are responsible for most cases.
Mutations in HFE are thought to cause HH principally by reducing hepcidin production

61
Q

What sex is more affected by hereditary haemochromatosis?

A

Males

Females are protected by menstruation and child birth

62
Q

What are transferrin levels like in hereditary hemochromatosis?

A

Transferrin less produced highly saturated with iron meaning free iron – iron is very metabolically active

63
Q

What are some complications of hereditary haemochromatosis?

A
  • Restrictive cardiomyopathy
  • skin pigmentation
  • arthritis
  • diabetes
  • Cirrhosis
64
Q

What is restrictive cardiomyopathy?

A

The walls of the ventricles become stiff (but not necessarily thickened)

65
Q

What is the treatment for hereditary haemochromatosis?

A
  • venesection (take blood) – initially up to weekly. 500mls whole blood - 250mg iron
  • Monitor ferritin and transferrin saturation
  • prevent or limit organ damage

MBChB - year 2 (25 decks)

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