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Gastrointestinal infections Flashcards

1
Q

What are the sterile sites of the GI tract?

A

Peritoneal space
Pancreas
Gallbladder
Liver

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2
Q

Non sterile sites of the GI tract

A 
Mouth
Oesophagus
Stomach
Small bowel
Large bowel
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3
Q

Angular chelitis - what is it and how does it present?

A

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

erythema
maceration
scaling
fissuring

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4
Q

What causes angular chelitis?

A

excessive moisture and maceration from saliva and secondary infection with C. albicans or S. aureus

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5
Q

Oral herpes simplex

A

cold sore on lip

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6
Q

Hairy leucoplakia

A

Seen in HIV patients

Caused by Epstein Barr virus

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7
Q

What causes dental infections?

A

Bacterial plaques form on the tooth surface
e.g. Streptococcus mutans and Lactobacillus spp

They produce acid that then erodes the enamel and bone

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8
Q

Types of dental infections

A

Caries
Pulpitis
Periapical abscess

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9
Q

When bacteria is inside the tooth:

A

when within the pulp cause inflammation which results in swelling and acute pain

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10
Q

Types of periodontal infections

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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11
Q

What bacteria are periodontal infections associated with?

A

anaerobic bacteria

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12
Q

How does gingivitis present?

A

Presents with red swollen painful and bleeding gums, and halitosis. Clinical diagnosis. Requires improved oral hygiene.

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13
Q

How does periodontitis present?

A

Progression of gingivitis with progressive loss of dental support structure function. May require antibiotics in addition to cleaning.

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14
Q

What causes a periodontal abscess?

A

may be focal or diffuse and presents as a red, fluctuant swelling of the gingiva, which is extremely tender to palpation.

The abscesses always communicate with a periodontal pocket from which pus can be readily expressed after probing. Requires surgical drainage.

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15
Q

How does Vincent’s angina present?

A

Presents with a sudden onset of pain in the gingiva, and the tissue appears eroded with superficial grayish pseudomembranes. Other manifestations include halitosis, altered taste sensation, fever, malaise, and lymphadenopathy. Requires antibiotics.

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16
Q

Examples of deep neck space infections

A

Peritonsillar abscess (quinsy)

Acute suppurative parotitis

Submandibular space infections (Ludwig’s angina)

Pretracheal space infections

Prevertebral space infections

Parapharyngeal space infections

Retropharyngeal and danger space infections

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17
Q

Nature of deep neck space infections

A

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

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18
Q

How do peritonsillar abscesses present and their tx?

A

Unilateral swelling of tonsil and presents as:
painful swallowing, unilateral sore throat and ear ache. Signs include muffled voice, trismus (lock jaw), unilateral deviation of the uvula towards the unaffected side, and soft palate fullness or oedema

tx:
Surgical drainage and antibiotic management are normally indicated.

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19
Q

Parotitis presents as

A

Normally one side is affected. There is a sudden onset of swelling from cheek to angle of the jaw and bacteraemia may resu

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20
Q

Parotitis is caused by

A

Staphylococcus aureus

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21
Q

Ludwig’s angina presents as

A

bilateral infection of the submandibular space.

It is an aggressive, rapidly spreading cellulitis without lymphadenopathy with

requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia

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22
Q

What are pretracheal space infections?

A

The clinical presentation is characterized by severe dyspnoea, but hoarseness may be the first complaint.

Swallowing may be difficult, and fluids may be regurgitated through the nose.

A pretracheal space infection is always serious because of impending airway obstruction and possible extension into the mediastinum.

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23
Q

Prevertebral space infections originate from and spread to…

A

from contiguous spread of a cervical spine infection (such as discitis or vertebral osteomyelitis), by local instrumentation of the trachea or oesophagus, or by haematogenous seeding.

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24
Q

Why are parapharyngeal space infections life threatening?

A

1) the possibility of involving the carotid sheath and its vital contents (e.g., common carotid artery, internal jugular vein, vagus nerve),
2) propensity for airway impingement
3) bacteraemic dissemination

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25
Clinical features and presentation of parapharyngeal space infections
Trismus, Induration and swelling below the angle of the mandible, Medial bulging of the pharyngeal wall Systemic toxicity with fever and rigors.
26
Retropharyngeal and danger space infections
Retropharyngeal abscesses are among the most serious of deep space infections, since infection can extend directly into the anterior or posterior regions of the superior mediastinum
27
Clinical features of Retropharyngeal and danger space infections - what causes it and then what happens?
Penetrating trauma (eg, from chicken bones or following instrumentation) is the usual source of local spread; in such cases, a sore throat or difficulty in swallowing or breathing may be the first indication of infection. More distant sources of infection include odontogenic sepsis and peritonsillar abscess
28
What is mucositis?
inflammation of the mucous membranes of the GI tracy
29
What causes mucositis?
Chemotherapy induced Duration: About 2 weeks after stopping chemotherapy Risk factor-caries, periodontal diseases. Dental review before chemotherapy.
30
Clinical presentation and increased risks of mucositis
Increased risk of bacteraemia, principally viridans streptococci Oral mucositis and intestinal mucositis (with diarrhoea) occur, they may present individually or separately.
31
What is oesophageal rupture?
Effort rupture of the esophagus, or Boerhaave syndrome, is a spontaneous perforation of the esophagus that results from a sudden increase in intraesophageal pressure combined with negative intrathoracic pressure (e.g., severe straining or vomiting).
32
What happens to the mediastinal cavity upon rupture of the intathoracic oesphagus?
contamination of the mediastinal cavity with gastric contents. 1 chemical mediastinitis with mediastinal emphysema and inflammation, 2. subsequently bacterial infection and mediastinal necrosis
33
How is oesophageal rupture managed?
Avoidance of all oral intake, Nutritional support, typically parenteral, antibiotics, Intravenous proton pump inhibitor, drainage of fluid collections/debridement of infected and necrotic tissue
34
Signs of oesophageal rupture
signs require at least an hour to develop after an oesophageal perforation odynophagia (painful swallowing) dyspnoea, sepsis fever, tachypnoea, (RR of 20+ per min) tachycardia, cyanosis, hypotension on physical examination. A pleural effusion may also be detected .
35
Heliobacter pylori infection - why is it able to penetrate the gastric mucous layer?
Bacterial urease hydrolyzes gastric luminal urea to form ammonia that helps neutralize gastric acid enabling it to penetrate the gastric mucus layer
36
Transmission of H.pylori
Person-to-person transmission of H. pylori through either fecal/oral or oral/oral exposure seems most likely
37
10-15% patients with H. pylori infection develop what?
Ulcer disease Pain Bleeding Perforation
38
How is H. pylori detected and then treated?
``` Diagnosis: Urease breath test Faecal antigen test Serology (IgG) Culture and sensitivity ``` Treatment: Triple antibiotic therapy plus a proton pump inhibitor (PPI) for 7-14 days.
39
Biliary tract infection: Choliangitis
The classic presentation is fever, abdominal pain, and jaundice (Charcot's triad),
40
Biliary tract infections cause: Cholestatic pattern of liver test abnormalities, with elevations in...
serum alkaline phosphatase (ALP) gamma-glutamyl transpeptidase (GGT) bilirubin (predominantly conjugated)
41
What bacteria cause biliary tract infections
Enterobacteriaceae principally, and Enterococcus spp)
42
Cholecystitis
Abdominal pain, fever, history of fatty food ingestion one hour or more before the initial onset of pain. Elevation in the serum total bilirubin and alkaline phosphatase concentrations are not common in uncomplicated acute cholecystitis Murphy's sign +ve Normally associated with gall stones
43
Bacterial overgrowth in the GI Tract
on the small bowel is believed to be associated with malabsorption or chronic diarrhoea. may result from achlorhydria (e.g. after gastric surgery), impaired motility, blind loops of bowel, surgery and radiation damage. Bacteria may bind vitamins e.g. B12, to produce fatty acids
44
Treatment of bacterial overgrowth:
dietary changes, surgical, motility, non-absorbable antibiotics.
45
What is Whipple's disease clinical presentation?
Classic Whipple’s disease is a multi-systemic process characterized by joint symptoms, chronic diarrhoea, malabsorption, and weight loss. Pathology in didtal duodenum. White plaques representing engorged lymph vessels
46
What causes Whipple's disease?
Tropheryma whipplei
47
Liver abscess pathogenesis
Ascending biliary tract infection (Coliforms, Streptococci, anaerobes) Portal vein after peritonitis or colonic perforation (Coliforms, Streptococcus, anaerobes) Haematogenous e.g. endocarditis (Staphylococcus aureus)
48
Effects of liver abscess
Increased risk of colonic malignancy
49
What causes liver abscess
Entamoeba histolytica
50
Clinical indicators of liver abscess
Serum alkaline phosphatase is elevated in 67 to 90 percent of cases aspartate aminotransferase concentrations are elevated in 50% cases
51
What is Entamoeba histolytica
The parasite exists in two forms, a cyst stage (the infective form) and a trophozoite stage (the form that causes invasive disease High rates of infection in mexico, india, africa and south america
52
How does TB affect the GI tract?
May affect any bit of the GI tract with local symptoms e.g. non healing oral ulcers, gastric ulcers giving gastric outflow obstruction, enterocutaneous fistulas
53
How can pancreatitis have complications on the GI tract?
Necrotising pancreatitis (15%) Peripancreatic fluid collection Pancreatic pseudocyst Acute necrotic collection Walled-off necrosis
54
What is diverticulosis - | Treatment and presentation
Tx: managed with antibiotics and surgery e.g. abscess drainage, resection of the affected bowel. Presents as most common cause of LIF pain
55
How is appendicitis treated?
Complicated appendicitis: Surgical management plus antibiotics Uncomplicated appendicitis: Surgical management plus single dose antibiotic prophylaxis
56
Why is uncomplicated appendicitis hard to diagnose?
CT often misses it
57
What percentage of patients with app. undergo an appendicectomy?
20% immediate 25-30% in the next year
58
What are intra-peritoneal abscesses?
Localised area of peritonitis with build-up of pus | Subphrenic, subhepatic, paracolic, pelvic etc.
59
Pre-disposing factors of intra-peritoneal abscesses
``` Perforation Peptic ulcer Perforated appendix Perforated diverticulum Mesenteric ischemia/bowel infarction Pancreatitis/pancreatic necrosis Penetrating trauma Postoperative anastomotic leak ```
60
Treatment of intra-peritoneal abscess
Drainage: Surgical or radiological | Combined with antimicrobial therapy
61
Presentation of intra - peritoneal abscesses
Nonspecific presentation Sweating, anorexia, wasting Swinging pyrexia Localising features Subphrenic abscess: Pain in shoulder on affected side, persistent hiccup, intercostal tenderness, apparent hepatomegaly (liver displaced downwards, ipsilateral lung collapse with pleural effusion Pelvic abscess: Urinary frequency, Tenesmus
62
Post operative infection - what are the 3 types?
Superficial Surgical Site Infection: SSI-S Deep Surgical Site Infection: SSI-D Organ space SSI: SSI-O
63
When does POI occur?
Within 30 days of surgery or 1 year if prosthetic infection
64
What is Spontaneous bacterial peritonitis (SBP)
Spontaneous bacterial peritonitis (SBP) is defined as an ascitic fluid infection without an evident intra-abdominal surgically treatable source.
65
Aetiology of SBP
Bacteria within the gut lumen cross the intestinal wall into mesenteric lymph nodes (translocation, a normal process). Lymphatics carrying the contaminated lymph ruptures because of the high flow and high pressure associated with portal hypertension. Seeding of ascitic fluid via the blood also occurs.
66
Complications and treatment of SBP
The vast majority of patients with SBP have advanced cirrhosis with ascities Treatment is based upon antibiotics Antibiotic prophylaxis may be indicated.
67
What is colonic malignancy & infection association?
Patients with bowel cancer can present with a bacteraemia caused by Streptococcus bovis (now re-named S. gallolyticus).

CLINICAL PATHOLOGY (56 decks)

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