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Y2 Clinical Pathology > Gastrointestinal Infections > Flashcards

Gastrointestinal Infections Flashcards

1
Q

Are infections in the gastrointestinal tract limited to this area?

Give some examples

A

bacteria from within the gastrointestinal tract can cause infections in other body systems

e.g. perforated oesophagus can cause infection in the respiratory system

abdominal infection can result in a fistula into the urinary tract

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2
Q

What are the 2 different types of “sites” in the gastrointestinal tract?

A

there are sites that are normally sterile and sites that are normally not sterile

knowing these sites helps to interpret microbiology culture results from samples

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3
Q

What are the sterile and non-sterile sites in the gastrointestinal tract?

A

sterile sites:

  • peritoneal space
  • pancreas
  • gall bladder
  • liver

non-sterile sites:

  • mouth
  • oesophagus
  • stomach
  • small bowel
  • large bowel
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4
Q

why is it important to know which sites are sterile sites and which are not?

A

it helps to interpret microbiology culture results from samples

e.g. ascitic fluid from the peritoneal cavity should normally be sterile, whilst faeces samples would have bacteria culturable from it

knowing which bacteria are common at certain body sites helps you guess which bacteria cause infections in nearby body sites

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5
Q

What are common causes of urinary tract infections in women?

A

they often result from faecal bacteria present in the nearby rectum

E. coli is a common bacteria in faeces, so a guess that the cause of a UTI is E. coli is reasonable

the same is true of intra-abdominal infections when faeces comtaminate the peritoneal cavity during colorectal surgery

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6
Q

What are the normal flora found in the oral cavity?

A
  • viridans streptococci
  • anaerobic Gram-positive bacilli
    • including Actinomyces spp.
  • anaerobic Gram-negative bacilli
    • Prevotella spp.
    • Fusobacterium spp.
  • Candida spp.
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7
Q

What are the normal flora found on the skin?

A
  • coagulase negative staphylococci
  • Staphylococcus aureus
  • Corynebacterium spp.
  • Propionibacterium spp.
  • Malassezia spp.
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8
Q

What are the normal flora found on the hands?

A

Resident:

  • all the same as the skin flora

Transient:

  • skin flora
    • including methicillin-resistant and other Staph. aureus
  • bowel flora
    • ​including Clostridium difficile, Candida spp. and Enterobacteriaceae
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9
Q

What are the normal flora found in the vagina?

A
  • Lactobacillus spp.
  • Staph. aureus
  • Candida spp.
  • Enterobacteriaceae
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10
Q

What are the normal flora found in the perineum?

A

the same as the skin and large bowel

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11
Q

What are the normal flora found in the nares (nostrils)?

A
  • Staph. aureus
  • Coagulase-negative staphylococci
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12
Q

What are the normal flora found in the pharynx?

A
  • Haemophilus spp.
  • Moraxella catarrhalis
  • Neisseria spp.
    • including N. meningitidis
  • staph. aureus
  • Strep. pneumoniae
  • Strep. pyogenes (group A)
  • viridans streptococci
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13
Q

what are the normal flora found in the small bowel?

A

distally, progressively increasing numbers of large bowel bacteria

Candida spp.

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14
Q

what are the normal flora found in the large bowel?

A
  • enterobacteriaceae
    • Escherichia coli
    • Klebsiella spp.
    • Enterobacter spp.
    • Proteus spp.
  • Enterococci
    • ​E. faecalis
    • E. faecium
  • Milleri group streptococci
    • ​Strep. anginosus
    • Strep. intermedius
    • Strep. constellatus
  • anaerobic gram-positive bacilli
    • ​Clostridium spp.
  • anaerobic gram-negative bacilli
    • ​bacteriodes spp.
    • prevotella spp.
  • candida spp.
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15
Q

What is angular cheilitis and how does it present?

A

an acute or chronic inflammation of the skin and contiguous labial mucosa located at the lateral commisures of the mouth

it typically presents with erythema, maceration, scaling and fissuring at the corners of the mouth

lesions are often bilateral and may be painful

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16
Q

What causes angular cheilitis?

A

it is caused by excessive moisture and maceration from saliva and secondary infection with C. albicans

or less commonly, S. aureus

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17
Q

who is most prone to angular cheilitis?

what are predisposing local factors?

A

it occurs at any age without sex predilection, but is more common in older people wearing dentures

predisposing local factors:

  • wearing orthodontic appliances or ill-fitting dentures
  • sicca symptoms (dry mouth)
  • intraoral fungal infection
  • poor oral hygiene
  • age-related anatomical changes of the mouth
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18
Q

What are the anatomical changes of the mouth that occur in older people?

What are the consequences of these changes?

A

the loss of vertical dimension of the mouth due to recession of the alveolar ridges or edentulous state leads to drooping of the corners of the mouth, drooling and retention of saliva in the creases

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19
Q

What are frequent causes of angular cheilitis in young children?

A

drooling, thumb sucking and lip licking

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20
Q

What are less common causes of angular cheilitis in adults and children?

A
  • nutritional deficiencies
  • type 2 diabetes
  • immunodeficiency
  • irritant or allergic reactions to oral hygiene products or denture materials
  • medications causing dryness and xerostomia
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21
Q

What is the treatment for angular cheilitis?

A

topical antifungals / antibiotics

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22
Q

What is the definition of cheilitis?

A

an acute or chronic inflammation of the lips

usually involves the lip vermillion and vermillion border

the surrounding skin and oral mucosa may also be affected

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23
Q

What type of patients is hairy leucoplakia seen in?

What causes it?

A

it is seen in HIV patients

caused by Epstein Barr virus

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24
Q

How can hairy leucoplakia be recognised?

What is the main treatment?

A

well-demarcated white plaques are visible on the lateral aspects of the tongue

this clears with oral aciclovir

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25
Q

What is shown in this image?

A

oral herpes simplex

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26
Q

What are the 3 main dentoalveolar infections?

A
  • caries
  • pulpitis
  • periapical abscess
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27
Q

What bacteria tend to form caries?

What is this?

A

bacterial plaques form on the tooth surface and form caries

acid produced from the bacteria (Streptococcus mutans and Lacotbacillus spp.) erodes the enamel and bone

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28
Q

What happens in dental infections once acid has eroded the enamel and bone?

A

bacteria can move inside the tooth

they cause an infection when they are within the pulp (pulpal infection)

this results in swelling and acute pain

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29
Q

Which bacteria tend to cause pulpitis and periapical abscess?

A

it is not clear which bacteria are the cause, but it is likely to be oral commensals

e.g. Streptococci and anaerobes

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30
Q

How are caries and pulpitis diagnosed and treated?

A

diagnosed through dental X-rays and examination

caries requires fillings

pulpitis requires a root canal procedure

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31
Q

What is a periodontal infection?

what are the most common ones and what can they progress to?

A

plaque beneath the gingival margin

  • gingivitis
  • periodontitis
  • periodontal abscess
  • acute necrotizing ulcerative gingivitis (Vincent’s angina)

may progress to orofacial space infections

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32
Q

What are periodontal infections associated with?

A

increased detection of anaerobic bacteria

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33
Q

What tends to cause gingivitis?

what can this progress to?

A

inadequate oral hygiene (i.e. no interdental cleaning) results in bacterial infection of the gingival margin (gum-bone interface)

this results in gingivitis

it can progress to periodontitis

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34
Q

What is periodontis?

A

gingival inflammation with accompanying loss of supportive connective tissues including alveolar bone (pockets > 5mm)

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35
Q

What is alveolar bone?

A

the thickened ridge of bone that contains the tooth sockets (dental alveoli) on bones that hold teeth

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36
Q

What can periodontal infection progress to?

A

an acute condition called Vincent’s angina (trench mouth)

or infection can spread within the soft tissue structures in the mouth, which can themselves lead to deep neck space infections

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37
Q

How does gingivitis present?

How is it treated?

A

presents with red, swollen, painful and bleeding gums and halitosis

requires improved oral hygiene

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38
Q

How is periodontitis diagnosed and treated?

A

progression of gingivitis with progressive loss of dental support, structure and function

may require antibiotics in addition to cleaning

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39
Q

What are the 2 different types of periodontal abscess?

How do they present and how are they treated?

A

it may be focal or diffuse

presents as a red, fluctuant swelling of the gingiva, which is extremely painful to palpation

abscesses always communicate with a periodontal pocket from which pus can be readily expressed after probing

requires surgical drainage

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40
Q

how does Vincent’s angina present?

What is the treatment?

A

presents with a sudden onset of pain in the gingiva

the tissue appears eroded with superficial grayish pseudomembranes

requires antibiotics

other presentations:

  • halitosis
  • altered taste sensation
  • fever
  • malaise
  • lymphadenopathy
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41
Q

what is halitosis?

A

Bad breath, also known as halitosis, is a symptom in which a noticeably unpleasant breath odour is present

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42
Q

Why is important to identify deep neck space infections?

A

they may have a rapid onset and can progress to life-threatening complications

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43
Q

What are peritonsillar abscesses (quinsy)?

what are they usually caused by and how are they treated?

A

unilateral swellings of the tonsil

normally caused by Streptococcus pyogenes (group A streptococcus)

surgical drainage and antibiotic management are indicated

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44
Q

What are the symptoms and signs of peritonsillar abscesses?

A

symptoms:

  • painful swallowing
  • unilateral sore throat
  • earache

signs:

  • muffled voice
  • trismus (lockjaw)
  • unilateral deviation of the uvula towards the affected side
  • soft palate fullness or oedema
  • the oral airway may be compromised and drooling may occur
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45
Q

What is acute suppurative parotitis?

What is it caused by and in what groups of people is it more common?

A

parotitis (non mumps) occurs in patients with poor oral hygiene and dehydration

it is almost always caused by Staphylococcus aureus

usually only one side is affected

there is a sudden onset of swelling from cheek to angle of the jaw and bacteraemia may result (patient becomes systemically unwell)

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46
Q

What is the treatment for acute supparative parotitis?

A

surgical drainage should be considered and antibiotics administered

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47
Q

What is Ludwig’s angina?

Why does it require careful monitoring?

A

a bilateral infection of the submandibular space

it is an aggressive, rapid-spreading cellulitis without lymphadenopathy

it has potential for airway obstruction so rapid intervention is needed for prevention of asphyxia and aspiration pneumonia

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48
Q

What is the treatment for Ludwig’s angina?

A

antibiotics should be administered

is abscesses form, then surgical drainage is required

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49
Q

How to pretracheal space infections tend to arise?

A

they most commonly arise as a consequence of perforation of the anterior oesophageal wall

occasionally through continguous extension from a retropharyngeal spaced infection

or as a consequence of prolonged tracheostomy

50
Q

what is the clinical presentation of a pretracheal space infection?

A
  • severe dyspnoea, but hoarseness may be the first complaint
  • difficult swallowing
  • fluids may be regurgitated through the nose
51
Q

Why is a pretracheal space infection always serious?

How should it be treated?

A

it is serious due to impending airway obstruction and possible extension into the mediastinum

prompt surgical drainage is critical to prevent such complications

52
Q

How do prevertebral space infections tend to start?

A
  • contiguous spread of a cervical spine infection
    • such as discitis or vertebral osteomyelitis
  • local instrumentation of the trachea or oesophagus
  • haematogenous seeding
53
Q

Why are parapharyngeal space infections potentially life-threatening?

What is the problem with diagnosis?

A
  • possibility of involving carotid sheath and its contents
    • e.g. common carotid artery, internal jugular vein, vagus nerve
  • propensity for airway impingement
  • bacteraemic dissemination

the clinical presentation may be dominated by the symptoms and signs of the primary source of infection, meaning diagnosis of parapharyngeal space involvement is often delayed

54
Q

What is the most common source of parapharyngeal space infection?

A

infection of the parapharyngeal space may arise from different sources throughout the neck

dental infections are the most common underlying cause

55
Q

What are the clinical features of parapharyngeal space infection?

A
  • trismus
  • induration and swelling below the angle of the mandible
  • medial bulging of the pharyngeal wall
  • systemic toxicity with fever and rigors
56
Q

Why is carotid sheath infection such a serious complication of parapharyngeal space infections?

Where can the infection spread from?

A

potential for carotid artery erosion and suppurative jugular thrombophlebitis

the carotid sheath abuts all three layers of deep cervical fascia, so infection can spread from:

  • parapharyngeal space
  • submandibular space (Ludwig’s angina)
  • suppuration of the deep cervical lymph nodes
57
Q

What are the signs and symptoms of a carotid sheath infection?

A

there are no characteristic symptoms or signs of carotid sheath infection

a history of sore throat is usually, but not always, present

this may be mild or unilateral

58
Q

How do patients tend to present with obvious manifestations of a deep neck space infection?

A

there may be a latent period of up to 3 weeks before symptoms arise

patient presents in a toxic condition or insidiously with a fever of undetermined origin

trismus is absent and signs of local suppuration may be subtle initially due to tight connective tissue around and within the carotid sheath

in some patients there is diffuse swelling along the sternocleidomastoid muscle with marked tenderness and torticollis to the opposite side

59
Q

What is torticollis?

A

Torticollis, also known as wry neck, is a dystonic condition defined by an abnormal, asymmetrical head or neck position, which may be due to a variety of causes

60
Q

What can happen if there is erosion of the carotid artery?

A

carotid artery mycotic aneurysms

this arises from arteritis due to contiguous inflammation, resulting in the formation of a false aneurysm which may rupture

61
Q

What may happen before the carotid artery aneurysm haemorrhages?

What happens after this?

A

erosion and rupture of the carotid artery may be heralded by recurrent small haemorrhagtes from the nose, mouth or ear

these are “herald bleeds”

this is followed by haematoma formation in surrounding tissues and eventual onset of shock due to exsanguination

62
Q

what is the treatment for carotid artery mycotic aneurysm?

A

ligation of the carotid artery may be necessary in case of major haemorrhage

the mortality rate remains high and the risk of stroke is significant

63
Q

What causes suppurative jugular thromboplebitis (Lemierre’s syndrome)?

In what patients should it be expected?

A

expected in patients with:

  • antecedent pharyngitis
  • septic pulmonary embol
  • persistent fever despite antimicrobial therapy

it is caused by:

  • Fusobacterium necrophorum, which is often present in the bloodstream
64
Q

Why are retropharyngeal and danger space infections the most serious of deep neck space infections?

A

retropharyngeal abscesses can extent directly into the anterior or posterior regions of the superior mediastinum

or into the entire length of the posterior mediastnum via the danger space

65
Q

What are the clinical features and diagnosis of a retropharyngeal space infection?

A

infection may reach the retropharyngeal space from either local or distant sites

local spread:

  • usually due to penetrating trauma
  • sore throat / difficulty breathing is first sign of infection

distant spread:

  • from odontogenic sepsis & peritonsillar abscess
66
Q

Why is a retropharyngeal space infection from distant sites harder to diagnose?

A

infection from distant sources often obscures a diagnosis of a retropharyngeal abscess due to associated trismus

this makes a direct examination of the posterior pharyngeal wall difficult

67
Q

What is the most severe complication of a retropharyngeal space infection?

A

acute necrotising mediastinitis

infection in the “danger space” between the alar and prevertebral fasciae may drain by gravity into the posterior mediastinum

this results in mediastinitis and empyema

68
Q

why is mediastinal extension (through the danger space) now more uncommon?

A

due to the introduction of antibiotics

most cases of acute mediastinitis result from oesophageal perforation

69
Q

What is the onset of acute necrotising mediastinitis like?

What features is it classifed by?

A

it has a rapid onset and is characterised by:

  • widespread necrotising process extending the length of the posterior mediastinum, occasionally into the retroperitoneal space
  • rupture of mediastinal abscess into the pleural cavity with empyema or development of loculations
  • pleural / pericardial effusions, frequently with tamponade

mortality is high, even when antibiotics are administered

70
Q

What is mucositis?

What tends to induced it and when does it occur?

A

inflammation of the mucous membranes of the GI tract

it is chemotherapy induced and occurs about 2 weeks after stopping chemotherapy

71
Q

what are the risk factors for mucositis?

A
  • caries
  • periodontal diseases

a dental review is carried out before chemotherapy

72
Q

What are the different types of mucositis?

What are patients with mucositis at increased risk of and how is this avoided?

A

oral mucositis and intestinal mucositis (with diarrhoea) occur, and they may present individually or together

there is increased risk of bacteraemia, mainly viridans streptococci

patients are given specific prophylaxis for mucositis (antibiotics)

73
Q

What is Boerhaave syndrome?

A

also known as “effort rupture of the oesophagus”

it is a spontaneous perforation of the oesophagus that results from a sudden increase in intraoesophageal pressure combined with negative intrathoracic pressure

(e.g. severe straining or vomiting)

74
Q

how do patients with Boerhaave syndrome present?

What do most of them have a history of?

A

present with excruciating retrosternal chest pain due to intrathoracic oesophageal perforation

usually a history of severe retching and vomiting preceding the onset of pain (25-45% do not have this)

75
Q

Why might patients with Boerhaave syndrome have crepitus on palpation of the chest wall?

What is the problem with using this to make a diagnosis?

A

this is due to subcutaneous emphysema

in patients with mediastinal emphysema, mediastinal crackling with each heartbeat may be heard on auscultation

(especially if the patient is in the left lateral decubitus position / Hamman’s sign)

these signs require at least an hour to develop after oesophageal perforation and are only present in a small proportion of patients

76
Q

What symptoms do patients develop within hours of an oesophageal perforation (Boerhaave syndrome)?

A
  • odynophagia
  • dyspnoea
  • sepsis
  • fever
  • tachypnoea
  • tachycardia
  • cyanosis
  • hypotension
  • pleural effusion may be detected
77
Q

What does rupture of the intrathoracic oesophagus result in?

A

contamination of the mediastinal cavity with gastric contents

this leads to chemical mediastinitis with mediastinal emphysema and inflammation

this leads to bacterial infection and mediastinal necrosis

78
Q

How do patients with cervical oesophageal perforations present?

A

present with neck pain, dysphagia or dysphonia

patients may have tenderness to palpation of the sternocleidomastoid muscle and crepitation due to the presence of cervical subcutaneous emphysema

79
Q

How do patients with an intra-abdominal oesophageal presentation tend to present?

A
  • epigastric pain that may radiate to the shoulder
  • back pain
  • inability to lie supine or present with an acute (surgical) abdomen
  • sepsis may rapidly develop within hours of presentation
80
Q

What is involved in the management of oesophageal rupture?

A
  • avoidance of all oral intake
  • nutritional support - typically parenteral
  • antibiotics
  • intravenous proton pump inhibitor
  • drainage of fluid collections / debridement of infected necrotic tissue if present
  • surgical consultation should be obtained for all patients
81
Q
A
82
Q

what happens in a Helicobacter pylori infection?

How is this organism able to cause infection?

A

bacterial urease hydrolyses gastric luminal urea to form ammonia

this neutralises gastric acid and forms a protective cloud around the organism

this enables it to penetrate the gastric mucus layer

83
Q

How is H. pylori transmitted?

What other animals is it seen in?

A

person-to-person transmission is either faecal/oral or oral/oral

humans are the major reservoir of infection, but it has been seen in primates in captivity and domestic cats

84
Q

What % of patients with H. pylori infection develop ulcer disease?

what are the symptoms?

A

10-15% of patients with H. pylori infection develop ulcer disease

this causes pain, bleeding and perforation

85
Q

How is H. pylori infection diagnosed and treated?

A

diagnosis:

  • urease breath test
  • faecal antigen test
  • serology (IgG)
  • culture and sensitivity

treatment:

  • triple antibiotic therapy plus a PPI for 7-14 days
86
Q

What is cholangitis?

What is the classic presentation?

A

it is a biliary tract infection

the classic presentation is fever, abdominal pain and jaundice

this is Charcot’s triad and 75% of patients have all 3 findings

87
Q

What tends to cause cholangitis?

A

it is caused by colonic bacteria:

mainly Enterobacteriaceae and also Enterococcus spp.

this is secondary to:

stones, stenosis, stents, surgery and cancer

88
Q

What is meant by the cholestatic pattern of liver test abnormalities?

A

there are elevations in:

  • serum alkaline phosphatase (ALP)
  • gamma-glutamyl transpeptidase (GGT)
  • bilirubin (predominantly conjugated)
89
Q

What is cholecystis?

What are the symptoms and signs?

A

it is a biliary tract infection

  • abdominal pain
  • fever
  • history of fatty food ingestion one hour or more before the initial onset of pain
  • murphy’s sign is positive
  • normally associated with gall stones
90
Q

What is meant by Murphy’s sign?

A

there is a “catch” in the breath elicited by gently pressing on the right upper quadranrt and asking the patient to take a deep breath

91
Q

what changes in LFTs would be associated with cholecystitis?

A

elevation in the serum total bilirubin and alkaline phosphatase concentrations are not common in uncomplicated acute cholecystitis

92
Q

What is involved in diagnosis of a biliary tract infection?

A
  • clinical examination and LFTs
  • radiological
  • endoscopic
  • surgical
93
Q

what causes bacterial overgrowth?

A
  • achlorhydria (e.g. after gastric surgery)
  • impaired mobility
  • blind loops of bowel
  • surgery and radiation damage

bacteria may bind vitamins (e.g. B12), use nutrients, produce metabolites (e.g. fatty acids)

94
Q

What is overgrowth of bacteria on the small bowel associated with?

How is it treated?

A

it is associated with malabsorption or chronic diarrhoea

treatment:

  • dietary changes
  • surgical
  • motility
  • non-absorbable antibiotics
95
Q

What causes Whipple’s disease?

Where is this organism found?

A

Tropheryma whipplei

it is ubiquitous in the environment

the bacteria has been detected in sewage and is more prevalent in the faecal samples of sewage workers than the general population

96
Q

What is Whipple’s disease?

How do the symptoms present?

A

it is a multi-systemic process characterised by joint symptoms, chronic diarrhoea, malabsorption and weight loss

the disease presents over time, with joint symptoms preceding the others by many years

not all symptoms may be present at the time of presentation in affected individuals

97
Q

In what patients should whipple’s disease be considered?

A

in all patients with the four cardinal manifestations

(arthralgias, diarrhoea, abdominal pain, weight loss)

after more common conditions have been excluded

98
Q

Who is more commonly affected by Whipple’s disease?

How is it diagnosed?

A

it involves white plaques representing engorged vessels in the distal duodenum

it mainly affects white males of European ancestry

upper gastrointestinal endoscopy with biopsies of the small intestine is the diagnostic test with PCR for the organism

99
Q

What is involved in the pathogenesis of liver abscess?

A
  • ascending biliary tract infection
    • coliforms, streptococci, anaerobes
  • portal vein after peritonitis or colonic perforation
    • ​coliforms, streptococci, anaerobes
  • haematogenous
    • ​e.g. endocarditis (Staphylococcus aureus)
  • increased risk of colonic malignancy
  • Entamoeba histolytica
100
Q

What is involved in the laboratory investigations for a liver abscess?

A
  • elevated serum alkaline phosphatase elevated in 67-90% cases
  • elevated serum bilirubin & aspartate aminotransferase in 50% cases
101
Q

what are the 2 forms of Entamoeba histolytica?

How does infection occur?

A

it exists as a cyst stage (infective form) and trophozoite stage (form that causes infective disease)

infection occurs following ingestion of amoebic cysts

this is usually via contaminated food or water but can be associated with venereal transmission through faecal-oral contact

102
Q

What are areas with high rates of amoebic infection?

How does this affect travellers?

A
  • India
  • Africa
  • Mexico
  • parts of Central and South America

it is relatively common among short-term travellers, but amoebic liver abscesses can occur after travel exposures as short as 4 days

103
Q

What is shown here?

A

hydatid liver cyst

this is present in echinococcosis, a parasitic disease of tape worms

104
Q

Where along the GI tract is susceptible to Mycobacterium tuberculosis?

What symptoms does this present?

A

it can affect any bit of the GI tract with local symptoms

e.g. non-healing oral ulcers, gastric ulcers giving gastric outflow obstruction, enterocutaneous fistulas

ileo-caecal tuberculosis is the most common GI site, and may be confused with colonic malignancy

105
Q

What are the complications of pancreatitis?

A
  • necrotising pancreatitis (15%)
  • peripancreatic fluid collection
  • pancreatic pseudocyst
  • acute necrotic collection
  • walled-off necrosis

all can be infected with enteric bacteria

106
Q

What is the treatment for pancreatitis?

A

debridement and antibiotics

107
Q

What is a complicated intra-abdominal infection?

A

infection that extends beyond the hollow viscus of origin into the peritoneal space

it is associated with either abscess formation or peritonitis

108
Q

What are the main complicated intra-abdominal infections?

A
  • perforated cholecystitis
  • perforated diverticulitis
  • perforated appendicitis
  • perforated gastric / duodenal ulcer
  • post-operative anastomotic leak / iatrogenic
  • colonic perforation after Clostridium difficile infection
  • ischaemic colon or malignancy with perforation of bowel
  • colonic fistula communicating with the peritoneal space
  • abscess in solid organ communicating with the peritoneal space e.g. liver abscess
109
Q

What is the treatment for complicated diverticulitis?

A

it is managed with antibiotics and surgery

e.g. abscess drainage, resection of the affected bowel

antibiotics have no proven efficacy for uncomplicated diverticulitis

110
Q

What is diverticulitis?

A

inflammation of abnormal pouches (diverticula) which can develop in the wall of the large intestine

111
Q

What is the treatment for complicated and uncomplicated appendicitis?

A

complicated:

  • surgical management and antibiotics

uncomplicated:

  • surgical management and a single dose of antibiotic prophylaxis
112
Q

What is involved in the expectant and antibiotic management of uncomplicated appendicitis?

A

expectant management:

  • 20% of all appendixes removed are normal

antibiotic management:

  • 25-30% of patients undergo appendicectomy in the next year
  • antibiotics have no efficacy if the pathology is similar to diverticulitis
113
Q

What is a intra-peritoneal abscess?

What are the predisposing factors?

A

localised area of peritonitis with build-up of pus

(subphrenic, subhepatic, paracolic, pelvic, etc.)

predisposing factors:

  • perforation - peptic ulcer, perforated appendix, perforated diverticulum
  • mesenteric ischaemia / bowel infarction
  • pancreatitis / pancreatic necrosis
  • penetrating trauma
  • postoperative anastomic leak
114
Q

What is the treatment for intra-peritoneal abscess?

A

it can be a late complication several months after the predisposing factor

it is trated through surgical or radiological drainage combined with antimicrobial therapy

115
Q

How does an intra-peritoneal abscess present?

A

it has a nonspecific presentation

  • sweating, anorexia, wasting
  • swinging pyrexia
  • localising features
116
Q

What are the features of a subphrenic and pelvic abscess?

A

subphrenic abscess:

  • pain in shoulder on affected side
  • persistent hiccup
  • intercostal tenderness
  • apparent hepatomegaly
  • ipsilateral lung collapse with pleural effusion

pelvic abscess:

  • urinary frequency
  • tenesmus
117
Q

What are the different types of post-operative infection?

A
  • superficial surgical site infection SSI-S
  • deep surgical site infection - SSI-D
  • organ space surgical site infection - SSI-O

occurs within 30 days of surgery or 1 year if it is a prosthetic infection

118
Q

What is spontaneous bacterial peritonitis (SBP)?

How is it diagnosed?

A

it is an ascitic fluid infection without an evident intra-abdomnal surgically treatable source

diagnosis is based on a positive ascitic fluid bacterial culture and an elevated ascitic fluid absolute polymorphonuclear leukocyte (PMN) count (>/= 250 cells / mm3)

119
Q

What is the cause of spontaneous bacterial peritonitis?

A

bacteria within the gut lumen cross the intestinal wall into mesenteric lymph nodes (translocation)

lymphatics carrying contaminated lymph ruptures due to high flow and high pressure associated with portal hypertension

seeding of ascitic fluid via the blood also occurs

120
Q

What do most patients with SBP have?

How is it treated?

A

the vast majority of patients with SBP have advanced cirrhosis with ascites

treatment is based upon antibiotics

antibiotic prophylaxis may be indicated

121
Q

How may patients with a colonic malignancy present?

A

bacteraemia caused by Streptococcus bovis (now called S. gallolyticus)

S. bovis bacteraemia is also associated with endocarditis

Y2 Clinical Pathology (76 decks)

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