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RW Gastroenterology > GI Infections > Flashcards

GI Infections Flashcards

1
Q

What are main issues that are contributed to antibiotic resistance?

A
  • Underdosing or not completing courses
  • Use with livestock
  • Selling them over the counter in some european countries
  • Possibly using the prophylactically before surgery
  • Releasing large quantities of antibiotics into the environment during pharmaceutical manufacturing
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2
Q

What is the definition of antimicrobial resistance (AMR)?

A

Implies that an antimicrobial will not inhibit bacterial growth at clinically achievable concentrations

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3
Q

What is the definition of antimicrobial susceptibility?

A

Implies that an antimicrobial will inhibit bacterial growth at clinically achievable concentrations

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4
Q

What is the laboratory effect of resistance?

A

If resistant in the lab, will more often than not translate into clinical environments

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5
Q

What is MDR?

A

Multidrug resistance: non-susceptibility to at least 1 agent in 3 or more antimicrobial categories

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6
Q

What is XDR?

A

Extensively-Drug resistant: non-susceptibility to at least 1 agent in all but 2 or fewer antimicrobial categories

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7
Q

What is PDR?

A

PanDrug resistance: non-susceptibility to all agents in all antimicrobial categories (no agents can fight the buggers)

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8
Q

What are the 2 types of resistance?

A

Innate or acquired (majority)

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9
Q

What are the 6 main mechanism of resistance?

A

1) Inactivation
2) Impermeability
3) Efflux
4) By-pass
5) Pbps • Penicilan binding proteins which change the structure, so that there isn’t a perfect lock of the antibiotics to the microbe
6) Altered target

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10
Q

What are the 3 mechanisms by which bacteria can transfer the resistant genes?

A
  • Bacterial transformation (direct uptake)
  • Bacterial transduction (via a virus)
  • Bacterial conjugation (through mating)
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11
Q

What are the 4 main solutions to reducing AMR?

A
  • Preventing infections and preventing spread of disease
  • Tracking these resistant bugs
  • Improving antibiotic prescribing and use, aka stewardship
  • Developing new drugs
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12
Q

What is antimicrobial stewardship?

A

The optimal selection, dosage, and duration of antimicrobial treatment that results in the best clinical outcome for the treatment or prevention of infection, with minimal toxicity to the patient and minimal impact on subsequent resistance

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13
Q

What are the 4 D’s of antimicrobial stewardship?

A

Dose, Duration, Drug and De-escalation

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14
Q

In terms of prescribing, what things must be addressed to reduce resistance?

A
  • Broad spectrum antibiotic therapy (choose combination of narrow spectrum instead)
  • Long duration of therapy (give for as short as possible)
  • Low or suboptimal dose of antibiotic
  • Route of therapy makes no difference IV vs Oral)
  • Total amount of antibiotic use
  • Giving antibiotic in the absence of infection
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15
Q

What are host factors that increase risk of GI infections?

A
  • Age (very young & elderly)
  • ↓ gastric acid secretion
  • ↓ gut motility
  • Influence of colonic microflora
  • Altered intestinal immunity
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16
Q

What is the definition of diarrhoea?

A

3 or more loose stools in 24 hours

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17
Q

What kind of bacteria is campylobacter (c. jejuni or c. coli)?

A

Gram negative bacillus

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18
Q

What is the incubation period of campylobacter?

A

3-10 days

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19
Q

What is the commonest cause of bacterial GI infection in the UK?

A

Campylobacter

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20
Q

What is the mechanism of action of campylobacter?

A

Causes inflammation of colon and rectum→bloody diarrhoea

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21
Q

What is the source/vehicle of infection of campylobacter?

A

Farm animals - especially undercooked poultry, but also water and unpasteurised milk

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22
Q

What is the management of unresolved campylobacter with systemic illness?

A

Erythromycin or ciprafloxin for 5 days

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23
Q

What is the incubation period of salmonella enterica?

A

Medium - 12-48hrs

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24
Q

What is the mechanism of action of salmonella enterica?

A

Causes inflammation of ileum and colon – cause mucosal damage, ↓fluid absorption and ↑fluid excretion • Which is what causes the loose stools and diarrhoea

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25
Q

What is the source/vehicle of infection of salmonella enterica?

A

Farm animals, esp. undercooked poultry

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26
Q

What is the management of unresolved salmonella enterica with systemic illness?

A

Ciprafloxin for 5 days

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27
Q

Which is the only shigella species seen in the UK?

A

Shigella sonnei

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28
Q

What is the incubation period for shigella?

A

1-9 days

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29
Q

True or false: campylobacter and salmonella can enter bloodstream

A

True

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30
Q

True or false: shigella can enter bloodstream

A

False (never seen on blood cultures)

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31
Q

What is the vehicle of infection of shigella?

A

Human only infection - common in children

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32
Q

What is the mechanism of action of Ecoli 0157?

A

The 0157 strain produces a verotoxin (VTEC) which that damages red cells and the kidney, causing haemolytic-uraemic syndrome (HUS)

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33
Q

What is the commonest cause of renal failure in children

A

E coli 0157

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34
Q

What is the source of E Coli 0157?

A

Carried as normal gut flora in cattle - Beef becomes contaminated on the outside at slaughter

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35
Q

What is the vehicle of infection for e coli 0157?

A
  • Contact with cattle, private (untreated) water supplies – run off water from fields and undercooked mince and hamburgers
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36
Q

Is the infectious dose for E coli 0157 low or high?

A

Low

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37
Q

Does management of E coli involve antibiotics?

A

No, as this may increase release of toxin. Supportive and symptomatic treatment only with monitoring for HUS

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38
Q

What is the clinical presentation of HUS?

A
  • Abdo pain,
  • Fever, pallor
  • Petechiae (haemorrhages in skin)
  • Oliguria (↓urine production)
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39
Q

True or False: Most HUS cases are in those under the age of 16

A

True (85%)

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40
Q

When is the peak presentation of HUS (and therefore when should you test for it)?

A

7-10 days after onset of diarrhoea

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41
Q

What would blood tests show with HUS?

A
  • High white cells
  • Low platelets
  • Low HB
  • Red cell fragments
  • Lactate dehydrogenase ↑>1.5 x normal
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42
Q

Which bacteria cause typhoid/paratyphoid fever?

A

Salmonella typhi/paratyphi A & B

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43
Q

Typhoid/paratyphoid fever are examples of febrile illnesses initially, what does this mean?

A

Circulate in bloodstream first causing headache, flu-like symptoms followed by diarrhoea 3 weeks later

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44
Q

What is the incubation period for Typhoid/paratyphoid fever ?

A

Long - 14-21 days

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45
Q

What is the mechanism of action for Typhoid/paratyphoid fever?

A

Organism invades from gut lumen→lymphatic system→ bloodstream→reticuloendothelial system & gallbladder→gut lumen and invades Peyer’s patches.

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46
Q

What is the vehicle of infection of Typhoid/paratyphoid fever?

A

Human only - drinking contaminated water/food, poor sanitation

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47
Q

What are the symptoms of Typhoid/paratyphoid fever?

A

Fever, rash on abdomen (“Rose spots”), headache, dry cough and diarrhoea

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48
Q

What is the management of Typhoid/paratyphoid fever?

A

Antibiotics - depending on sensitivities. IV Ceftriaxone if unstable

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49
Q

Which bacteria causes cholera?

A

Vibrio cholerae

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50
Q

When are outbreaks of cholera common?

A

War or disaster situations

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51
Q

What is the incubation period for cholera?

A

1-9 days

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52
Q

What is the mechanism of action of cholera?

A

Organism produces an exotoxin that causes active outpouring of fluid from cells of small intestine, resulting in severe watery diarrhoea

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53
Q

What is the source/vehicle of infection of cholera?

A

Human only - drinking contaminated water/poor sanitation

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54
Q

Rice water stools

A

Cholera

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55
Q

What is the management of cholera?

A

Fluid and electrolyte replacement. NOT antibiotics (will increase toxin release)

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56
Q

Which infections are associated with pre-formed toxins?

A

Staph aureus, clostridium perfingens, bacileus cereus

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57
Q

What is the classic food associated with staph aureus infection?

A

Cream cake touched by infected baker (aureus apparently soudns like oreo..which has cream in the middle)

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58
Q

What is the mechanism of action of staph aureus?

A

Staph aureus releases entero toxin → Toxin adsorbed quickly→acts directly on vagus nerve & vomiting centre→vomiting within 1-2 hours

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59
Q

What is the source of clostridium perfringens?

A

Part of normal gut flora of humans and animals

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60
Q

What bacteria is meat gravy classically associated with?

A

Clostridium perfringens (because if you dont keep the gravy in the fridge…perFRINGens, get it?)

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61
Q

What is vehicle of transport of clostridium perfringens?

A

Spores survive cooking, then turn into vegetative organisms, some strains of which produce enterotoxin (an exotoxin)

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62
Q

What is the mechanism of action of bacillus cereus?

A

Exotoxin ingested as pre-formed toxin or organism can multiply in intestine. Spores survive cooking, then turn into vegetative organisms, some strains of which produce enterotoxin (an exotoxin)

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63
Q

What bacteria is uncooked rice classically associated with?

A

Bacillus cereus (becuase cereus sounds like rice…apparently)

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64
Q

Which bacteria have short incubation periods (1-6hrs)?

A

staph aureus, bacillus cereus

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65
Q

Which bacteria have medium incubation periods (12-48hrs)?

A

Salmonella/Cl perfringens

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66
Q

Which bacteria have long incubation periods (2-14days)?

A

Campylobacter/E coli 0157)

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67
Q

What kind of infection is cryptosporidium?

A

Protozoal

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68
Q

What is the mechanism of action of cryptosporidium?

A

Infection occurs when cysts are ingested which “hatch” into trophozoites that invade the cells of the small intestine

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69
Q

What is the source of cryptosporidium?

A

Domestic animals, especially calves

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70
Q

What is the vehicle of infection of cryptosporidium?

A

Person-person spread. Outbreaks associated with contaminated water supplies & swimming pools (cysts resistant to chlorine

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71
Q

In which group of patients is cryptosporidium particularly severe?

A

HIV positive

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72
Q

What is the investigation for cryptosporidium?

A

modified Ziehl-Neelson stain

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73
Q

What is the mechanism of action for giardia lamblia?

A

Infection occurs when cysts are ingested which “hatch” into trophozoites that invade the cells of the upper small intestine

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74
Q

What is the vehicle of infection for giardia lamblia?

A

Person to person - associated with contaminated water

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75
Q

What are the symptoms of giardia lamblia?

A

Diarrhoea, malabsorption syndrome, anorexia, abdominal pain, flatulence

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76
Q

What is the management for Giardia lamblia?

A

Oral metronidazole

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77
Q

What are Enterobius vermicularis also known as?

A

Threadworms

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78
Q

What is the pathogenesis for threadworms?

A

Ova (eggs) ingested→hatch in intestine and live in caecum & colon→adult females come out on to perianal skin at night and lay ova→ova cause perianal itch→child scratches bottom→puts fingers in mouth

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79
Q

What is the vehicle of infection of threadworms?

A

Human only - poor hygiene

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80
Q

What are the symptoms of threadworms?

A

Perianal itch, worms seen in stool

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81
Q

What is the management for threadworms?

A

Oral mebendazole. Often have to treat all members of family at once

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82
Q

Who is responsible for monitoring GI infections, potential outbreaks and sending environmental health officers?

A

Health Protection Teams

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83
Q

A patient has diarrhoea whist admitted to hospital - what are you considering.?

A

C. Difficile

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84
Q

In what group of people is C. Difficile rarely seen and why?

A

Rarely see it in children however, as children don’t have receptors in their gut for the toxins, even though they carry it

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85
Q

What is the mechanism of action of C. Difficile?

A

Organism produces 2 toxins:

  • Toxin A (enterotoxin – damages the gut)
  • Toxin B (cytotoxin - damaging cells on the epithelium of gut).

This causes colitis (infection of the colon)

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86
Q

What is the source of C. Difficile?

A

Part of normal gut flora. • Infection occurs when antibiotics are prescribed that kill off normal competitive bowel flora and allows C diff to overgrow.

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87
Q

What is the vehicle of infection of C. Difficile?

A

Human to human/and spore ingestion - Organism produces spores that survive in the environment and are more resistant to disinfectants and the organism CAN be transmitted from one patient to another.

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88
Q

What is C. Difficile fundamentally?

A

A colitis

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89
Q

What can C. Difficile sometimes progress to?

A

Pseudomembranous colitis

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90
Q

What is the management for less severe C. Difficile?

A

Oral metronidazole

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91
Q

What is the management for severe C. Difficile?

A

Oral vancomycin

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92
Q

What are the 4C antibiotics of C Difficile?

A

Clindamycin, cephalosporin, co-amoxiclav and ciprofloxacin

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93
Q

What type of bacteria is C. Difficile?

A

Gram positive spore-bearing bacillus

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94
Q

How would the lab test for C. diff?

A

No one good lab test.

  1. Screening test for presence of the organism (GDH test)
  2. If GDH positive, test for presence of toxin (toxin A&B)
  3. (Culture can be done if strain needs to be typed – not done routinely)
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95
Q

What does it mean if the screening test for C. difficile is positive and the toxin test is negative?

A

Indeterminate result - need to assess patient as send repeat specimen

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96
Q

Which two virus are the main ones for causing diarrhoea?

A

Rotovirus and norovirus

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97
Q

What is the commonest cause of D&V in children

A

Rotovirus

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98
Q

How is rotavirus spread?

A

Person-person spread, direct or indirect

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99
Q

True or False: Rotavirus and Norovirus cause bloody diarrhoea

A

False, they dont cause blood

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100
Q

Is the infectious dose of rotoavirus low or high?

A

Low

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101
Q

What is the mechanism of action of rotavirus?

A

↓ absorption of fluids and ↑secretion in bowel, causing dehydration and diarrhoea

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102
Q

How is rotavirus diagnosed?

A

Diagnosis by PCR test on faeces

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103
Q

What is the management of rotavirus?

A

Self-limiting usually within 1 week, so rehydration is key. Vaccine can be preventative

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104
Q

Which virus can affect all ages?

A

Norovirus (rotavirus is mostly children)

105
Q

What is the mode of transmission of noravirus?

A
  • Faecal-oral/droplet routes of spread (spewing in wards = bad) - Person to person (or on contaminated food/water)
106
Q

Why doesnt immunity to norovirus last?

A

Virus also mutates every few years

107
Q

Is the incubation period for norovirus short or long?

A

Short (

108
Q

How long does norovirus normally last for?

A

2-4 days

109
Q

How is norovirus diagnosed?

A

Faeces specimen or vomit swab for PCR test

110
Q

What is the management for norovirus?

A

Rehydration is key, esp. young, elderly. Prevent outbreaks

111
Q

What occurs following cessation of symptoms in norovirus?

A

Asymptomatic shedding occurs for up to 48 hours

112
Q

What is the classic infectious outbreak for cruise ships?

A

Norovirus

113
Q

Which infections require the patient to be in a side room?

A

All diarrhoea patients, but particularly C. Difficile and Norovirus

114
Q

Which infections have particularly low infectious doses?

A

Viruses and E Coli O157

115
Q

By which route are most GI infections transmitted?

A

Faecal-oral route (poor sanitation, kitchen factors)

116
Q

True or False: Salmonella is more common to cause bloody diarrhoea than Campylobacter and E coli

A

False, bloody diarrhoea is more rare in salmonella compared to the other two

117
Q

At which point would you normally notify public health about GI infections (except for E coli)?

A

When you get a positive result from the local lab

118
Q

How is E Coli O157 diagnosed?

A

Culture or toxin testing in the stool

119
Q

What does the O in O157 stand for?

A

The surface antigen on E coli

120
Q

What are the most useful test for HUS?

A

FBC and blood film, and U&Es

121
Q

Which kind of bacteria are staphylococci?

A

Gram positive cocci in clusters

122
Q

Which kind of bacteria are E Coli (and other coliform)?

A

Gram negative bacilli

123
Q

Where do penicillins and cephalosporins act on bacteria and how?

A

Act on the bacterial cell wall by preventing cross-linking of peptidoglycan which weakens the wall and causes them to rupture under pressure

124
Q

What is gastroenteritis?

A

Inflammation of the stomach and small intestine (Gastritis is jus the stomach and enteritis is just the small intestine)

125
Q

What is the pathophysiology of gastroenteritis?

A

Inflammation of stomach or intestines inhibits nutrient absorption and excessive H2O and electrolyte loss

126
Q

What kind of infections causes the majority of gastroenteritis?

A

Viruses

127
Q

True or False: Food poisoning is a subtype pf gastroenteritis

A

True, it is gastroenteritis resulting from ingestion of contaminated food

128
Q

What is the general onset of food poisoning?

A

1-6hrs (pre-made toxin so doesnt need time to replicate etc)

129
Q

How long does it normally take food poisoning to resolve?

A

6-10hrs

130
Q

What actually is food poisoning?

A

Food poisoning is illness caused by ingestion of food or water contaminated with bacteria and/or their toxins, viruses, parasites, or chemicals. Contamination usually arises from improper handling, preparation, or storage of food or drinks

131
Q

Why is food poisoning rapidly emerging in industrialised countries?

A
  • Poor sanitation & hygiene
  • Commercialisation of food production and food service (poor hygiene); big change in eating habits
  • Importation of food from developing countries
  • Increase in day-care centre attendance
  • Increase in institutions that care for the elderly
  • International travel, contact with animals/reptiles
  • Role of acid suppression, age and immunosuppressive drugs
  • People have more weird pets
132
Q

What are the 3 presenting clinical syndromes of food poisoning?

A
  1. Acute enteritis (e.g. salmonella): fever. D&V, abdominal pain
  2. Acute colitis (e.g. campylobacter): fever, pain, bloody diarrhoea
  3. Enteric fever like illness (e.g. typhoid): fever, rigors, pain but little diarrhoea
133
Q

How long does camplybacter infection generally last?

A

5-14 days

134
Q

What is a rare but important complication of Campylobacter?

A

Guillian-Bare Syndrome

135
Q

What is Guillian-Bare Syndrome?

A

Tingling of the feet leads to progressive paralysis of the legs, arms and rest of the body

136
Q

What is the key to diagnosis of typhoid fever?

A

Blood cultures

137
Q

Which risk factors put patients at particular risk of recurrent infections and c. difficile?

A
  • Administration of antibiotics after initial treatment of CDI
  • Prolonged hospitalization or stay in long-term care facility (LTCF)
  • Defective immune response to toxin A
  • Gastric acid suppression
138
Q

With diarrhoea pts, what should you ask about in particular with medication history?

A

Recent antibiotics and PPIs

139
Q

What are the drivers for C. difficile infection?

A

A. Broad spectrum antbiotic therapy

B. Specific antibiotic types e.g 4C’s

C. Long duration of therapy

D. Vulenrable population e.g elderly, nursing home, co-morbidities, hospitalised

F. Total amount of antibiotic use – number of exposures

G. Giving antibiotic in the absence of infection

140
Q

Which 3 organisms are particularly associated with traveller’s diarrhoea?

A
  • Amoebiasis - Giardiasis - Cryptosporidiosis
141
Q

What is the average duration of traveller’s diarrhoea?

A

4 days

142
Q

What is amoebiasis and its route of infection?

A

Protozoal infection spread by faeco-oral route or by an ill or asymptomatic carrier

143
Q

How is amoebiasis diagnosed?

A

By examination of hot stool for ova and cysts (I dont think so pal)

144
Q

What is the treatment of amoebiasis?

A

Metronidazole, and remove from lumen with diloxanide furoate or paromomycin

145
Q

How are giardiasis and cryptosporidiosis diagnosed?

A

Duodenal aspiration

146
Q

Which part of the bowel does amoebiasis mostly affect?

A

Large bowel

147
Q

Which part of the bowel does giardiasis mostly affect?

A

Small bowel

148
Q

Which part of the bowel does cryptosproidosis mostly affect?

A

Small bowel

149
Q

What are the 6 main ways that infections can be transmitted during sex?

A

1) Direct inoculation (eg. Herpe simplex)
2) Trauma (eg. HCV)
3) IVDU (eg. HIV)
4) Fomites- inanimate objects (eg. gonorrhoea)
5) Ingestion (eg. shigella)
6) Sexual/genital secretions

150
Q

Which bacteria causes rectal gonorrhea?

A

Neisseria gonorrhoea

151
Q

How is gonorrhea and chlamydia transmitted?

A

Direct contact of mucosal surfaces. So for proctitis: sex, transmucosal spread, fomite

152
Q

Is the incubation period for gonorrhea short or long?

A

Short (5-10 days)

153
Q

What are the symptoms for rectal gonorrhea?

A

Asymptomatic or Low abdo pain, diarrhoea, rectal bleeding, anal discharge, tenesmus

154
Q

What would be seen on proctoscopy with rectal gonnorhea?

A

Inflamed mucosal and purulent exudate

155
Q

Which bacteria causes chlamydia?

A

Chlamydia trachomatis

156
Q

What are the symptoms of chlamydia?

A

Majority are asymptomatic - if symptomatic, milder than gonorrhoea: Anal discomfort/itch, discharge

157
Q

What is the management of chlamydia?

A

Azithromycin or Doxycycline (7/7 course)

158
Q

Which STI can present like Crohn’s?

A

Syphilis

159
Q

What are the symptoms of primary syphilis?

A

Solitary painless ulcer

160
Q

What are the symptoms of secondary syphilis?

A

• Mucosal patches and ulcers • Eye conditions • Mouth, anogenital, rectal • Condylomata lata • Systemic inflammation (rash on trunk, lymphadenopathy) • Hepatitis

161
Q

How is herpes simplex virus transmitted?

A

Ano-genital or oro-anal

162
Q

Which area of the lower GI tract is most affected by herpes simplex virus?

A

peri-anal mucosa but may extend into rectum

163
Q

What are the symptoms of HSV?

A

Pain, ulcers, painful defaecation, bleeding, mucus, viraemic symptoms (in primary infection)

164
Q

How is human papillomavirus transmitted?

A

ano-genital, oro-anal

165
Q

Which HSV virus is usually associated with HSC proctitis?

A

HSV 2

166
Q

Which HPV virus is usually associated with HPC proctitis?

A

HPV 6, 11, 16, 18

167
Q

What is Lymphogranuloma venereum?

A

Tropical STI found in Africa

168
Q

What is the treatment for Lymphogranuloma venereum?

A

Doxycycline

169
Q

What is Lymphogranuloma venereum associated with?

A
  • MSM
  • HIV+
  • Group sex
  • Drug use
  • Syphilis
  • Hepatitis C
170
Q

How does Lymphogranuloma venereum present?

A
  • Primary (3-30 days):
    • Ulcer
  • Secondary (3-6/12):
    • Inguinal syndrome
    • Ano-rectal syndrome
  • Tertiary:
    • Strictures
    • Fistulae
    • Genital elephantiasis
171
Q

Why is Gut-Associated Lymphoid Tissue (GALT) particularly susceptible to HIV infection and then replication?

A
  • Often the first point of contact
  • Compared with circulating lymphocytes, a greater percentage of these mucosal CD4+ lymphocytes express the CCR5 chemokine co-receptor
    • These are the preferred targets for HIV-1
  • GI tract in constant state of “physiological inflammation” due to proximity to external environment
  • Dense clustering of lymphocytes facilitating cell-cell transmission
172
Q

What are important features to look for in returning travellers with fever?

A
  • Rash
  • Hepatosplenomegaly
  • Lymphadenopathy
  • Insect bites
  • Wounds
173
Q

What is acute traveller’s diarrhoea?

A

At least 3 loose stools in 24h, often with self reported fever of multiple possible causes

174
Q

What are 6 main organisms associated with acute travellers diarrhoea?

A
  • Enterotoxigenic E. coli
  • Campylobacter
  • Salmonella
  • Shigella
  • Norovirus
  • Rotavirus
175
Q

What is the primary investigation for acute traveller’s diarrhoea?

A

Stool culture

176
Q

What medicine can travellers take to stop worsening?

A

Fluoroquinolone (ciprafloxacin)

177
Q

What are the main forms of enteric fever?

A

Typhoid/parathyroid fever

178
Q

Which countries are Enteric fevers most associated with?

A

India and SE Asia

179
Q

Which tropical infections can cause prehepatic jaundice?

A
  • Malaria
  • HUS as a complication of E coli
  • Sickle cell crisis triggered by infection
180
Q

Which tropical infections can cause hepatic jaundice?

A
  • Hepatitis A and E – acute (occasionally Hepatitis B)
  • Leptospirosis
  • Malaria
  • Enteric fever
  • Typhus
  • Viral haemorrhagic fever
181
Q

Which tropical infections can cause post-hepatic jaundice?

A

Ascending cholangitis and helminths

182
Q

Which investigations would you do for fever and jaundice in a traveller?

A
  • Malaria blood film and rapid antigen
  • Blood film for red cell fragmentation (HUS)
  • FBC/UE/LFT/coagulation
  • Blood cultures
  • USS abdomen
  • Serological testing for viruses
183
Q

What is the incubation period for amoebic liver abscess?

A

8-20 weeks

184
Q

What are the symptoms of amoebic liver abscesses?

A

Fever, cough, aching abdominal pain, hepatomegaly, sometimes a history of GI upset (dysentery) – usually male

185
Q

What would you see on CXR with amoebic liver abscess?

A

Raised right semi-diaphram

186
Q

What is the management for amoebic liver abscesses?

A

Metronidazole and Paramomycin/diloxanide to clear the lumen of parasites

187
Q

What are helminth infections?

A

Parasitic worms

188
Q

Which immune cells are helminths associated with?

A

Eosinophils

189
Q

What are nematodes?

A

Roundworms

190
Q

What are trematodes and their infection?

A

Flukes - schistosomiasis

191
Q

What are cestodes?

A

Tapeworms

192
Q

What is the most common helminthic infection?

A

Ascariasis - Roundworms

193
Q

What is the life cycle of ascariasis?

A
  1. Egg ingested
  2. hatch in small intestine
  3. invade gut wall into venous system and via liver and heart reach lungs
  4. break into alveoli
  5. ascend tracheobroncial tree
  6. swallowed and in the gut
  7. develop into adult worm where they start to produce eggs.
194
Q

What is the pathophysiology of schistosomiasis?

A

Adult worms located in portal venules which can lead to hepatolmegaly and liver fibrosis and portal hypertension

195
Q

What kind of exposure can cause schistosomiasis?

A

Fresh water exposure

196
Q

What organisms cause Chagas’ Disease?

A

Trypanasoma cruzi

197
Q

Aerobes

A

Organisms that grow better with oxygen, but can also grow without it

198
Q

What are examples of aerobes?

A

• Staphylococci • Streptococci • Enterococci • Coliforms

199
Q

What are strict aerobes?

A

Organisms that require oxygen for growth

200
Q

What is an example of strict aerobes?

A

Pseudomonas sp

201
Q

Which antibiotic are strict aerobes sensitive to?

A

Gentamycin

202
Q

What are anaerobes?

A

Organisms that will not grow in the presence of oxygen

203
Q

What are examples of anaerobes?

A

• Clostridium sp • Bacteroides sp • Anaerobic cocci

204
Q

Which antibiotic are anaerobes sensitive to?

A

Metronidazole

205
Q

What are coliforms?

A

Organisms that inhabit the large bowel

206
Q

What are examples of coliforms?

A

• E coli • Klebsiella sp • Proteus sp • Enterobacter • Serratia sp

207
Q

Which antibiotic are coliform sensitive to?

A

Gentamycin

208
Q

Which features of the mouth inhibits colonisation?

A

Mucosal shedding

209
Q

What are the main locations for colonisation in the mouth?

A

Teeth (Dental plaque → dense biofilms → polymicrobial)

210
Q

Why aren’t there commensal bacteria of the stomach and duodenum?

A

Low pH

211
Q

What are the commensal bacteria of the remaining small intestine?

A

Coliforms and anaerobes (small numbers due to proximity to stomach)

212
Q

What are commensal bacteria groups of the large intestine?

A

Anaerobes, coliforms and enterococci

213
Q

What is peritonitis?

A

Breakdown in the mucosa of GI tract etc can cause leakage of contents which can result in colonisation

214
Q

What is the management for abscesses and why?

A

Drainage; antibiotics can’t be used as large abscesses have poor blood supply so poor antibiotics penetration

215
Q

In general, which antibiotics are for abdominal infections?

A

AmoxGenMet (if in doubt)

216
Q

Colonisation

A

The presence of a microbe in the human body that does not cause infection due to a specific inflammatory response

217
Q

sWhat is the pathway of sepsis?

A

1) Colonisation
2) Infection
3) SIRS
4) Sepsis
5) Severe sepsis
6) Septic shock

218
Q

What is SIRS?

A

Systemic inflammatory response syndrome.

A non-specific clinical response including at least 2 of the following:

  • Temperature >38oC
  • 90 beats/min
  • Respiratory rate >20/min
  • White blood cell count >12,000/mm3 or 10% immature neutrophils
219
Q

Sepsis

A

The systemic inflammatory response to infection (different from bacteraemia)

Defined as the presence of systemic inflammatory response syndrome (SIRS) with the addition of a confirmed or presumed microbiological infection

220
Q

Severe sepsis

A
  • Defined as sepsis with signs of at least one acute organ dysfunction e.g. renal dysfunction, hypotension
221
Q

Septic shock

A

Sepsis-induced refractory hypotension that persists despite adequate fluid resuscitation, along with the presence of hypoperfusion abnormalities or organ dysfunction

222
Q

Which areas of the GI tract are usually sterile?

A

Stomach, duodenum and bile ducts

223
Q

What are the 6 vital steps with sepsis?

A

O2 FLUID:

Oxygen

Fluids IV

Lactate measurement

Urine output measurement (catheterisation)

Infection screen inc. blood cultures, FBC, CRP +/- urine dip/culture

Drugs – antibiotics as appropriate

224
Q

Which source of infection are you thinking of with contaminated eggs, poultry, meat, unpasteurised milk or juice, cheese?

A

Salmonella

225
Q

What is the time frame of symptoms with bacillus cereus?

A

30 mins-6 hrs (vomiting), 6-15hrs (diarrhoea)

226
Q

Which source of infection are you thinking of with dairy products, uncooked and handmade food, e.g. salads and sandwiches?

A

Staph aureus

227
Q

Which antibiotics is used to treat staph aureus?

A

Flucloxacillin

228
Q

Which source of infection are you thinking of with beef, poultry, gravy?

A

Clostridium perfringens

229
Q

Which source of infection are you thinking of with Produce, shellfish, contaminated ready-to-eat food, cruise ship?

A

Norovirus

230
Q

Which source of infection are you thinking of with children in winter?

A

Rotavirus

231
Q

Which source of infection are you thinking of with contaminated food or water or contact with animals, travel related ?

A

Cryptosporidium

232
Q

Which source of infection are you thinking of with trip to SE Asia and change in bowel habit/dry cough?

A

Enteric fever

233
Q

Which source of infection are you thinking of with o Ova and cysts in hot stool, acute bloody diarrhoea, can cause abscess?

A

Amoebiasis or giardiasis

234
Q

Mucosa

A

Aka mucous membrane, membrane that lines various cavities in the body and surrounds internal organs, most of which secrete mucous which stop pathogens and dirt from entering the body and to prevent bodily tissues from becoming dehydrated.

235
Q

True or False: Lymph nodes are concentrationa around sites of mucosal tissue

A

Tue

236
Q

Which 3 tracts in particular have mucosal tissues?

A

Respiratory trcat, GI tract and genito-urinary tract

237
Q

Which immune cell predominate in the gut lymphoid tissue?

A

Memory T cell

238
Q

What are the 2 compartments of the adaptive immune system?

A

That containing the peripheral lymph nodes and spleen, and then the Mucosal Associated Lymhpoid Tissue (MALT)

239
Q

What are the main components of the GALT for the induction of immune response?

A

1) Waldeyer’s ring (ring of tonsils)
2) Peyers patches of the small intestine
3) Solitary lympohid follicles of large intesitne and rectum

240
Q

What are the important features of the anatomy of the peyers patches?

A

Dome-like structures extending into the lumen.The overlying layer of follicle-associated epithelium contains microfolds on their surface (instead of microvilli) known as microfold cells or M cells, interspersed between enterocytes. Adapted to direcftly interact with molecules and particules in the gut lumen

241
Q

What happens when the antigens in the lumen meet the M cells?

A

M cells transport the anigen into the cell by transcytosis and deliver it to antigen presenting cells and lymphocytes (dendtires) of the mucosal immune system. These then release cytokines chemokines which initiate an inflamamtory response

242
Q

What is the function of the solitary lymphoids scattered in the gut wall?

A

Act as the effector cells

243
Q

What happens when these solitary lymphoid tissues meet antigens?

A

They activate and move via the lymphatics from the intestines, through mesenteric lymph nodes to thoracic duct to enter blood system and reenter all mucosal lymphoid tissue from there. Therefore the response to the antigen is spread throughout the body.

244
Q

What is MAdCAM-1?

A

Ligand bound homing receptor (addressin) for gut mucosal tissue

245
Q

What is the dominant antibody isotype for the mucosal immune system?

A

IgA

246
Q

What are the two distinct compartments of the mucosal immune system?

A

Epitheliuma and lamina propria

247
Q

Which kind of immune response occurs in the epithelial and lamina propria compartments of the mucosal immune system?

A

Adaptive and innate response in the lamina propria, and adaptive response in the epithelium

248
Q

What are addressins e.g. MAdCAM-1?

A

Homing receptors which direct lymphocytes to particular comparments

249
Q

What is oral tolerance?

A

The feeding of foreign antigens typically leads to a state of specific and active unresponsiveness - tolerance. Although this wouldnt be the case if the same antigens were injected subcutaneosly. Helps maintain the balance between protective immunity and homeostasise

250
Q

What is involved in the innate response of thr mucosal immune system?

A
  • IgA
  • Commensal bacteria compete (and win) for nutrients etc)
  • Various barriers (mechanical - cilia, tight junctions; chemical - low pH, fatty acids and microbiological- commensals)
251
Q

What are the main mucosal disorders associated with primary immunodeficiency?

A
  • Selective IgA deficiency
  • Common Variable Immune Deficiency (CVID)
  • X-Linked Agammaglobulinaemia (XLA)
  • Chronic Granulomatous Disease (CGD)
  • Severe Combined Immune Deficiency (SCID)
252
Q

What organisms are always invovled in Chronic Granulomatous Disease (CGD)?

A

Staph aureus and asbergillus

253
Q

What kind of reactions are food allergies and what is the pathophysiology?

A

Type I hypersensitivity reaction initiated by crosslinking of allergen specific IgE on the surface of mast cells with the specific allergen causing degranulation of mast cells in the mucosa

254
Q

Which cells are actually causing the underlying damage in coelic disease?

A

Immunopathology causing the actual damage is T cell/IEL mediated and their reaction to gluten. Enzyme tissue transglutaminase alters the gluten so that the immune system reacts to it

255
Q

What is the pathophysiology of coeliac disease?

A

Gamma interferon from Gluten specific T cell activate epithelial cells which produce IL-15 which induces proliferation and activation of IEL. Both T cells and IEL can then kill epithelial cells

256
Q

How do you diagnose coeliac disease?

A

Serology screening test IgA anti-tissue transglutaminase autoantibodies

257
Q

Which infectious organism would you think of with hazelnut yoghurt?

A

Clostridium botulinum (bot/pot of yoghurt)

258
Q

Which infectious organism would you think of with soft cheese/coleslaw?

A

Lesteria monocytgenen (Leicester cheese)

RW Gastroenterology (13 decks)

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