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Phase 2- GI > Week 3 > Flashcards

Week 3 Flashcards

1
Q

What part of the intestine can an endoscopy not visualise well?

A

Ileum

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2
Q

What is fluoroscopy useful for visualising?

A

Perforation in upper GI tract

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3
Q

What can fluoroscopy be used to test for?

A

Blockages in swallowing

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4
Q

What radiological scan is used to image the colon?

A

CT

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5
Q

What structures is ultrasound useful for imaging?

A

Liver, pancreas and gall bladder

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6
Q

What is the best test to detect gall stones?

A

Ultrasound

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7
Q

Describe some disadvantages of MRI in GI radiology

A

Very slow, and small space can make claustrophobic patients uncomfortable. Also cannot be used on patients with pacemakers.

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8
Q

What are the main uses of CT in GI radiology?

A

Diagnose disease, staging of malignancy, assess response to treatment and percutaneous biopsy

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9
Q

What is PET-CT?

A

Functional imaging of metabolic activity fused with anatomical information from CT

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10
Q

What is PET-CT useful for?

A

Staging, and finding the extent of cancer

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11
Q

What are the roles of MRI in GI imaging?

A

Non-invasive imaging of biliary tree and small bowel, local staging of rectal cancer and diagnosing liver lesions

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12
Q

What are right upper quadrant pain, jaundice and pale stools indicative of?

A

Gall stones

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13
Q

What imaging modality could be used in the investigation of appendicitis?

A

Ultrasound (maybe CT)

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14
Q

What does pneumoperitoneum indicate?

A

Perforation, usually from a gastric or duodenal ulcer

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15
Q

What can CT angiography be used for in patients with gastric/duodenal ulcers?

A

Identification and treatment of acute bleeding

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16
Q

How can CT angiography be used to treat acute bleeding from a perforated gastric or duodenal ulcer?

A

Coli embolisation:

  • intimal damage leads to thrombogenic factors
  • fibres provide thrombogenic surface
  • continue to inject dye until no leakage out of blood vessel
  • mechanical occlusion
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17
Q

What is always assumed to be a sign of colon cancer in men and post-menopausal women?

A

Microcytic anaemia

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18
Q

What is the total body iron content?

A

4 grams

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19
Q

What is iron stored as in cells?

A

Ferritin and haemosiderin

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20
Q

How is iron transported in plasma, and what is the transporters iron saturation?

A

Transferrin (a glycoprotein synthesised in hepatocytes). 30% saturated with iron

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21
Q

How much iron is absorbed from an average western diet?

A

15 mg

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22
Q

Where does iron absorption take place?

A

Predominantly in the duodenum (duodenal enterocytes)

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23
Q

Is haem iron or non-haem more readily absorbed?

A

Haem iron (non-haem released from foodstuffs by acid digestion proteolytic enzymes in stomach)

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24
Q

How is Fe2+ taken into the enterocyte?

A

By the divalent metal transport 1 (DMT1), an electrogenic pump

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25
Q

What is ferroportin?

A

A transmembrane protein, essential in the export of iron from the enterocyte

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26
Q

What hormone interacts with ferroportin to regulate GI iron absorption, and RES iron release?

A

Hepcidin

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27
Q

How much iron does the RES store?

A

500 mg

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28
Q

After being released by the RES, what cells take up iron from the plasma?

A

Erythroblasts and hepatocytes, via the Tf receptors

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29
Q

Where is transferrin synthesised?

A

The liver

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30
Q

How many iron atoms can each transferrin bind?

A

2

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31
Q

Does the bulk of iron in plasma come from the diet or from stored iron in the RES?

A

The RES

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32
Q

How is iron delivered to tissues?

A

Iron is delivered to tissues by binding of the transferrin-iron complex to transferrin receptors found on the cell surface

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33
Q

Where is the highest concentration of transferrin receptors found?

A

On RBC precursors (approx 80%)

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34
Q

What is hereditary haemochromatosis?

A

An autosomal recessive disorder of iron metabolism, causing iron overload

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35
Q

Abnormalities with which gene are responsible for the majority if HH cases?

A

HFE gene, which is essential in hepcidin synthesis

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36
Q

What is the role of hepcidin?

A

Hepcidin reduces the levels of iron in plasma

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37
Q

What are some symptoms/complications of HH?

A

Bronze pigmentation in the skin, diabetes, restrictive cardiomyopathy and cirrhosis

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38
Q

How is HH treated?

A

Weekly venesection to remove excess iron by removing 500 mls of blood

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39
Q

What period of time does the hepatitis virus have to be present for to become chronic hepatitis?

A

6 months

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40
Q

How are hepatitis A and E transmitted?

A

Faeco-oral, contaminated food and water, person-person

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41
Q

What is the main determinant of severity of hepatitis A infection?

A

Age, mostly asymptomatic in children under 5 years old

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42
Q

Are there any treatments for hepatitis A?

A

No (prophylaxis is available with vaccine)

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43
Q

Who is offered the hepatitis A vaccine?

A

People travelling to at risk areas, homosexual men, intravenous drug users and chronic liver disease patients

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44
Q

How many genotypes of hepatitis E are there?

A

4

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45
Q

What is a unique clinical feature of hepatitis E, and which genotype is it associated with?

A

Neurological symptoms (Guillaine Barre, encephalitis, ataxia and myopathy), GT 3

46
Q

What are three differences between hepatitis A and E?

A

Hep E has a higer mortality rate (especially in pregnancy with GT 1), hep E has neurological symptoms, and hep E can be carried chronically

47
Q

How are hepatitis B,C and D transmitted?

A

Bodily fluids (blood, semen), transfusion, organs and tissue transplantation, mother to baby (most common cause globally), contaminated needles and syringes and child to child (children playing together)

48
Q

How is hepatitis B transmitted in the UK?

A

95% of new diagnoses in the UK are immigrants infected elsewhere, many picked up on antenatal screening. New sexual infections in UK are rare

49
Q

What determines the severity of acute illness, and the risk of chronic HBV infection?

A

Age at the time of infection: infection at birth- asymptomatic, but leads to chronic infection; infection as an adult is usually symptomatic but cleared

50
Q

How is HBV infection diagnosed?

A

If sAg (surface antigen), or HBV DNA are detectable

51
Q

What does HBV cAb + only indicate?

A

Past infection, that has now cleared

52
Q

How are acute and chronic HBV treated?

A

There is no treatment for acute HBV. Only patients with liver inflammation due to chronic HBV are treated, with pegylated interferon alpha (enhances anti-viral immune components), or antiviral drugs to suppress viral replication (treatment for life)

53
Q

What are the three interventions to prevent HBV transmission during pregnancy?

A
  1. HBV vaccination to all newborns
  2. HBV immunoglobulin if eAg + or high viral load (VL)
  3. Tenofovir during the last trimester if high VL
54
Q

How does hep D compare to hep B?

A

Requires HBV to replicated; transmission is same as hep B, though vertical transmission is rare. Treatment is with peg interferon only

55
Q

How is HCV transmitted?

A

Injecting drugs, transfusion and transplantation (sexual/vertical transmission rare)

56
Q

Describe the natural history of HCV

A

Acute infection -> 70% develop chronic HCV, 30% clear infection. Of the 70% with chronic infection 25% develop cirrhosis, and 1-5% develop hepatocellular carcinoma

57
Q

How is HCV diagnosed?

A

Mostly diagnosed by screening of high risk groups (drug users, immigrants from high prevalence countries)

58
Q

How is HCV treated (pre-2012)?

A

Pegylated interferon alpha and ribavirin (overall cure rate around 40-60% after 24-48 weeks of difficult treatment)

59
Q

How is HCV treated (post-2012)?

A

Direct acting antiviral (DAAs) have substantially increased the chance of curing HCV- delivered with methadone at pharmacy for IVDUs

60
Q

What must patients with hepatitis B,C and D also be screened for?

A

HIV

61
Q

What is the definition of diarrhoea?

A

3 or more loose or watery stools per day

62
Q

What are some pathogenic mechanisms of diarrhoea?

A

Toxin mediated (produced prior to consumption (S aureus), or after consumption (c.diff)), damage to intestinal epithelial surface, or invasion across intestinal epithelial barrier

63
Q

Describe small intestinal diarrhoea

A

Large volume of watery diarrhoea. Cramps, bloating, wind, weight loss. Fever and blood in stool are rare

64
Q

Describe large intestinal diarrhoea

A

Frequent small volume diarrhoea, painful stool. Fever and blood common

65
Q

What are some bacterial causes of diarrhoea?

A

Campylobacter, salmonella, shigella, E.coli (0157;H7), clostridium difficile

66
Q

What are some viral causes of diarrhoea?

A

Norovirus, sapovirus, rotavirus, adenoviruses

67
Q

What are some parasitic causes of diarrhoea?

A

Cryptosporidium, giardia, entamoeba histolytica, cyclospora, isopora

68
Q

How is diarrhoeal aetiology diagnosed?

A

History (best guide to potential pathogen), faecal leukocytes and occult blood, stool examination/culture or endoscopy

69
Q

What should you ask about to establish cause of diarrhoea?

A

Food history, onset and nature of symptoms, residence, occupation, travel, pets/hobbies, recent hospitalisation/antibiotics, co-morbities

70
Q

How is diarrhoea treated?

A

Oral rehydration solution (ORS), may require IV fluid replacement

71
Q

When should antibiotics be used to treat diarrhoea?

A

When patients are severely ill (sepsis or bacteraemia), when reduction in diarrhoea duration is clinically meaningful, or c.diff associated diarrhoea

72
Q

Describe campylobacter infection

A

Diarrhoea is frequent and can be high volume, blood in stool. common. Often severe abdominal pain. Nausea common/vomiting rare> Fever. Self limiting (7 days). Antibiotics rarely indicated

73
Q

Describe salmonella infection

A

Numerous serotypes ((non)typhoidal), infectious dose roughly 10,000 organisms. Increased risk with decreased stomach acid, and diminished gut flora. Invasion of enterocytes with subsequent inflammatory response. Illness within 72hrs of ingestions (higher innocuous = more rapid onset). Nausea, diarrhoea, abdominal cramps, fever. Invasive disease: bacteraemia in <5%, secondary infection (endocarditis, osteomyelitis, mycotic aneurysm). Self limiting, antibiotics indicated in severe disease.

74
Q

Describe E.Coli 0157: H7 infection

A

Shiga toxin production, enterocyte death, enters systemic circulation. Infection load as low as 10 organisms. Sporadic outbreaks. Incubation period 3-4 days. Bloody diarrhoea and abdominal tenderness. Fever is rare. Management is supportive. Strict infection control for healthcare workers to prevent spread

75
Q

Describe complications of E.Coli 0157:H7 infection

A

Haemolytic Uraemic Syndrome: systemic effect of Shiga toxin. Microangiopathic haemolytic anaemia, acute renal failure, thrombocytopenia. Up to 9% of patients. 5-10 days after onset of diarrhoea. 50% require dialysis. Mortality 3-5%. Association with antibiotics

76
Q

What are some risk factors of C.Diff infection?

A

Antibiotic exposure, older age (>65 years), PPI use(?), hospitalisation

77
Q

Describe the pathogenesis of C.Diff infection?

A

Decrease in colonisation resistance, colonic colonisation, toxin production

78
Q

Describe C.Diff infection

A

Loose stool and colic, fever, leukocytosis, protein losing enteropathy

79
Q

Describe the treatment of C.Diff associated diarrhoea

A

Stop causative antibiotics is possible, metronidazole/vancomycin, recolonise with normal flora

80
Q

Describe norovirus infection

A

Faecal oral transmission, infections dose 10-100 viruses, occurs in all months with peak in winter. Acute explosive diarrhoea and vomiting, lasts 24-48 hours with no lasting immunity

81
Q

What is coeliac disease?

A

Gluten-sensitive enteropathy, characterised by small intestinal villous atrophy that resolves when gluten is withdrawn from the diet, inappropriate T cell-mediated immune response in genetically susceptible individuals (alpha-gliadin is most toxic moiety)

82
Q

What is the common genetic profile of individuals with coeliac disease?

A

95% are HLA-DQ2 (rest are HLA-DQ8)

83
Q

What is the prevalence of coeliac disease?

A

1% in the UK, with more females being affected than males. 20% are over 60 at diagnosis

84
Q

What is the infectious hypothesis in coeliac disease?

A

Infection with adenovirus 12 in genetically susceptible individuals, peptide on alpha-gliadin similar to that within E1b portion of the virus, leads to cords reactivity with alpha-gliadin and development of coeliac disease

85
Q

What happens in the digestion of alpha-gliadin?

A

Digestion of alpha-gliadin produces stable peptide, which is absorbed into the lamina propria. Exposure to tTG (from damaged epithelium) leads to deamination of glutamine residues, and enables bonding to HLA-DQ2 and activation of pro-inflammatory T-cell response

86
Q

How does coeliac disease present in infants?

A

Presents aged 4-24 months (after cereals have been introduced) with impaired growth, diarrhoea, vomiting and abdominal distension

87
Q

How does coeliac disease present in older children?

A

Anaemia, short stature, pubertal delay, recurrent abdominal pain or behavioural disturbance

88
Q

How does coeliac disease present in adults?

A
  1. Symptomatic:
    - diarrhoea, bloating, flatulence, abdominal discomfort
    - 50% have no history of diarrhoea, may be constipated
    - symptomatic disease may be provoked by infection, pregnancy or surgery
  2. Chronic or Recurrent iron deficiency anaemia (IDA
    - 50% of presentations with coeliac
    - 3-12% of all IDA
89
Q

How else does coeliac present in adults?

A
  1. Nutritional deficiency
  2. Reduced fertility/amenorrhoea
  3. Osteoporosis
  4. Unexplained increased AST/ALT
    - 10% with isolated transaminitis
  5. Neurological/psychiatric symptoms
    - e.g. peripheral neuropathy (anti-ganglioside abs); epilepsy
90
Q

What are the pathological changes in coeliac disease?

A

Mucosal inflammation can vary in severity and extend- mild proximal disease typically occurs; mucosal damage may be patchy; loss of villous height; villi may be completely flat or short and broad (sub-total villous atrophy); no change in total mucosal thickness as crypts become elongated (hypertrophy); increased plasma cells and intraepithelial lymphocytes (IELs)

91
Q

What are the histological changes in coeliac disease?

A

Loss of villous height
Reduced surface area
Reduced absorptive capacity

92
Q

What bowel changes happening coeliac disease?

A

Diarrhoea (watery and high volume, rarely bloody), steatorrhoea, malabsorption (fats/vitamins/carbs/protein), weight loss, abdominal pain and vomiting

93
Q

What are the indicators of small bowel disease?

A

Malabsorption and electrolyte imbalances: folate, Ca/Vit D, Vit K/coagulopahty, Mg, Vit B12, and chronic or recurrent IDA

94
Q

What proportion of total body iron is incorporated into red cell haemoglobin?

A

80%

95
Q

What is the recommended daily intake of iron?

A

8-18 mg (27 mg in pregnant women)

96
Q

How much iron is lost each day, and how is it lost?

A

1 mg of iron is lost each day through sloughing of cells from skin and mucosal surfaces, including the lining of the GI tract. Menstruation increased the average daily iron loss to about 2 mg per day in premenopausal female adults

97
Q

Where does iron absorption occur?

A

Primarily in the duodenum and upper jejunum

98
Q

How does iron absorption occur?

A

At physiological pH, ferrous iron (Fe2+) is rapidly oxidised to the insoluble ferric (Fe3+) form. Gastric acid lowers the pH in the proximal duodenum, enhancing the solubility and uptake of ferric iron. Absorption is enhanced by Vit C, citric acid and inhibited by phytates and tannins (tea)

99
Q

How is coeliac diagnosed on an endoscopy?

A

Distinct changes are seen:

  • scalloping of the folds
  • paucity of folds
  • mosaic pattern (‘cracked mud’)
  • prominent submucosal blood vessels
  • nodular pattern to the mucosa
100
Q

How is coeliac diagnosed with a SB biopsy?

A

Must be on a gluten rich diet. Biopsy of distal duodenum, minimum 4 biopsies (patchy changes), biopsies from duodenal bulb may improve diagnosis

101
Q

What can cause villous atrophy, but have a negative coeliac serology?

A

Selective IgA deficiency, giardiasis, CVID, radiation enteritis, Crohn’s disease, lymphoma, Whipple’s disease, tropical sprue, HIV enteropathy, chronic ischaemia, NSAIDs

102
Q

What diseases are associated with coeliac?

A 
Dermatitis herpetiformis:
 - itchy rash on extensor surfaces
 - gluten sensitive/Dapsone
 - 90% villous atrophy
Other autoimmune diseases:
 - T1DM
   - 3-8% NICE advise screening all patients
 - Thyrotoxicosis
 - Addison's disease
103
Q

What are the complications of coeliac disease?

A

Infection, osteoporosis, refractory coeliac disease and malignancy

104
Q

How does infection occur in coeliac disease?

A 
Functional hyposplenism.
Risk of infection:
- encapsulated organisms
- pneumococcal
- haemophilus influenzae
- meningococcus
- vaccination
105
Q

How does osteoporosis occur in coeliac disease?

A

25% of coeliac patients develop osteoporosis (calcium/Vit D deficient). Consider DEXA at diagnosis- adequate calcium/Vit D intake/supplementation

106
Q

What is refractory coeliac disease?

A

RCD 1: persistent villous atrophy but normal immunophenotype
RCD 2: persistent villous atrophy with abnormal immunophenotype (CD3/Cd8 -ve) (associated with ulcerative jejunitis; ulceration in jejunum/ileum; 60-80% progression to enteropathy associated t-cell lymphoma)

107
Q

What malignancies are related to coeliac disease?

A

Enteropathy-associated T-cell lymphoma:
- weight loss, night sweats, itch, overt/occult GI bleeding, venous thromboembolism
- 1.2% of Non-Hodgkin’s lymphoma
- Often advanced and incurable
- Chemotherapy and autologous stem cell treatment
- Poor response; 5-year survival 8-20%
Small Bowel Adenocarcinoma:
- Rare
- Only 50% survival at 30 months
Oesophageal and colonic adenocarcinoma
Risk of coeliac related malignancy is reduced by adherence to gluten free diet

108
Q

A hepatitis B patient is considered highly infectious if his/her blood test shows positive for which antigen?

A

eAg (e antigen)

109
Q

Deficiency of pancreatic protease enzymes can lead to what?

A

Increased risk of intestinal infections

110
Q

With which ion are di- and tripeptides co-transported into the enterocyte?

A

H+

111
Q

Gall bladder relaxation and closure of sphincter of Oddi is regulated by which peptide?

A

Vasoactive intestinal polypeptide (VIP)

112
Q

With which ion are amino acids co-transported into the enterocyte?

A

Na+

Phase 2- GI (5 decks)

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