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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
What are the two ways iron can be stored?
Ferritin and hemosiderin
26
How is ferritin as a storage facility for iron?
- Soluble - Iron safe and readily available from RES Serum Ferritin - Tiny amount in serum- directly related to RES iron stores
27
How is hemosiderin as a storage facility for iron?
- Insoluble conglomerates of ferritin | - Iron only slowly available
28
What are serum ferritin levels like in IDA?
Decreased
29
What are serum ferritin levels like in iron overload?
Increased
30
What happens to serum ferritin levels in tissue inflammation?
Increased - Can rise to inappropriately high levels
31
What protein transports iron in the blood?
Transferrin
32
Where is transferrin synthesised?
Hepatocytes
33
How does transferrin transport iron?
It has 2 iron binding domains and is normally 30% saturated with Fe
34
What is the daily iron need?
1-2mg/d
35
What are the two types of dietary iron?
Haem and non-haem iron
36
What foods is haem iron found in?
red meat
37
What foods is non- haem iron found in?
white meat, green veg, cereals
38
What is the only mechanism that regulates iron balance?
Regulation of dietary iron absorption (there is no excretory mechanism for excess iron)
39
What is mostly responsible for absorbing iron?
Duodenal enterocytes
40
Is haem or non-haem iron absorbed more easily?
Haem iron
41
How is non-haem iron released from food?
Acid digestion and proteolytic enzymes in the stomach
42
What extra step must non- haem undergo that haem iron does not?
It must be reduced from the ferric to the ferrous form by duodenal cytochrome b1(dCytb1)
43
What is iron taken into the enterocyte by?
divalent metal transporter 1 (DMT1)
44
What exports iron from the enterocyte to the blood?
ferroportin and hepcidin
45
What is ferroportin?
A transmembrane protein that is present on duodenal enterocytes and macrophages of the RES
46
How is iron taken up from storage when needed?
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
How many atoms of iron can transferrin bind?
2
48
What is an erythroblast?
A developing RBC in bone marrow
49
where does the Bulk of iron in the plasma comes from?
macrophages
50
How is oxygen transported throughout the body?
By haemoglobin which can reversibly bind to O2 without undergoing oxidation or reduction
51
What different disorders of iron metabolism are there?
Not enough iron | too much iron
52
How are red blood cells described in IDA?
Microcytic and hypochromic
53
In males and post-menopausal females what is IDA caused by (until proven otherwise)?
GI blood loss
54
What types of haematinic deficiencies are possible?
- folate deficiency - Iron deficiency - vitamin B12 deficiency
55
What is the function of hepcidin?
The most important influence on iron metabolism. It is the 'low iron' hormone and reduces the levels of iron in the plasma
56
How does hepcidin reduce the levels of iron in plasma?
hepcidin binds to ferroportin and degrades it which reduces GI iron absorption and reduces macrophage release from the RES
57
Where is hepcidin synthesised?
the liver
58
What does loss of hepcidin cause?
Increased GI iron absorption, increased RES iron release, increased Tf% saturation parenchymal iron overload (HH)
59
What is hereditary haemochromatosis?
autosomal recessive disorder of iron metabolism causing iron overload
60
What causes Hereditary haemochromatosis?
Abnormalities of the HFE gene are responsible for most cases. Mutations in HFE are thought to cause HH principally by reducing hepcidin production
61
What sex is more affected by hereditary haemochromatosis?
Males | Females are protected by menstruation and child birth
62
What are transferrin levels like in hereditary hemochromatosis?
Transferrin less produced highly saturated with iron meaning free iron – iron is very metabolically active
63
What are some complications of hereditary haemochromatosis?
- Restrictive cardiomyopathy - skin pigmentation - arthritis - diabetes - Cirrhosis
64
What is restrictive cardiomyopathy?
The walls of the ventricles become stiff (but not necessarily thickened)
65
What is the treatment for hereditary haemochromatosis?
- 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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