S9: GI emergencies & infections Flashcards

1
Q

What is peritonitis?

A

Inflammation of the serosal membrane that lines the abdominal cavity
Can be primary or secondary

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2
Q

Describe primary peritonitis

A

Spontaneous bacterial peritonitis – infection of ascitic fluid that cannot be attributed to any intra-abdominal, ongoing inflammatory or surgically correctable condition
Most common in patients with end stage liver disease (cirrhosis):
1) Portal hypertension – increased hydrostatic pressure in the veins
2) Decreased liver function resulting in less albumin production
3) Result = net movement of fluid into the peritoneal cavity
Symptoms: abdominal pain, fever & vomiting (normally mild symptoms, diagnosed by aspirating ascitic fluid)

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3
Q

Describe secondary peritonitis

A

A result of an inflammatory process in the peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal/retroperitoneal structure
Common causes: peptic ulcer disease (perforated), appendicitis (perforated), diverticulitis (perforated) & post surgery
Non bacterial causes: tubal pregnancy that bleeds & ovarian cyst

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4
Q

Describe the clinical presentation and treatment of peritonitis

A

Abdominal pain – may come on gradually/acutely
-diffuse abdominal pain is common in perforated viscera
Patients often lie very still – any movement makes the pain worse (often have knees flexed & shallow breathing)
Treatment: control the infectious source (surgery), eliminate bacteria and toxins (antibiotics) & maintain organ system function

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5
Q

Describe bowel obstruction

A

Mechanical or functional problem that inhibits the normal movement of gut contents
Can affect the large and small intestine
Common causes in children: intussusception & intestinal atresia
Common causes in adults: adhesions & incarcerated hernias

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6
Q

Describe intussusception

A

One part of the gut tube telescopes into an adjacent section
Cause is not well known
Can extend quite far (can prolapse out of rectum); as soon as the lymphatic and venous drainage is impaired you get oedema
Symptoms: abdominal pain, vomiting & haematochezia
Treatment: air enema & surgery

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7
Q

Describe small bowel obstruction

A

Nausea and vomiting (bilious) – most common symptoms, can have abdominal distension & abdominal constipation (late)
Caused by:
1) Intra-abdominal adhesions – arise after abdominal surgeries, damage to mesothelium
2) Hernias can narrow lumen enough to cause obstruction
3) Crohn’s – repeated episodes of inflammation/healing causes narrowing
Diagnosis: history – abdominal pain is crampy & intermittent, physical examination & imaging

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8
Q

Describe large bowel obstruction

A

Typically affects older age groups
Common causes: colon cancer, diverticular disease & volvulus
Symptoms often appear gradually if caused by cancer but are abrupt with volvulus: change in bowel habit, abdominal distension, crampy abdominal pain & nausea/vomiting (late)

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9
Q

What is a volvulus?

A

Part of the colon twists around its mesentery
Most common in sigmoid colon and caecum – results in obstruction
Can result from overloaded sigmoid colon – extra mass predisposes & elongates the sigmoid
Caecal volvulus results in small and large bowel obstruction

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10
Q

Compare small and large bowel obstruction

A
Small bowel:
1) Younger age group
2) Abdominal pain – colicky (3-4 mins)
3) Vomiting – relatively early 
4) Constipation – relatively late
5) Imaging – bowel > 3cm, central position & plica circularis 
Large bowel:
1) Older age group
2) Abdominal pain – colicky (10-15 mins)
3) Vomiting – relatively late 
4) Constipation – relatively early 
5) Imaging – peripheral, bowel > 6cm, haustra don’t go all the way across
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11
Q

Describe acute mesenteric ischaemia

A

Symptomatic reduction in blood supply to the GI tract
Risk factors: females, history of peripheral vascular disease
Causes: acute occlusion, non-occlusive mesenteric ischaemia & mesenteric venous thrombosis
Symptoms: abdominal pain disproportionate to clinical findings (comes on 30 mins after eating), nausea, vomiting, left-sided pain

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12
Q

Describe investigations and treatment for acute mesenteric ischaemia

A

Investigations: blood tests, erect chest x-ray & CT angiography
Treatment: surgery – resection of ischaemic bowel, thrombolysis/angioplasty
Mortality is high – often older patients with comorbidities

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13
Q

Describe peptic ulceration

A

20-50% of acute upper GI bleeding
Disruption in the gastric/duodenal mucosa
Duodenal ulcers most common, then gastric ulcers

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14
Q

Describe oesophageal varices

A

Example of porto-systemic anastomosis
Portal drainage – oesophageal veins drain into left gastric vein, drains into portal vein
Systemic drainage – oesophageal veins drain into azygous vein, drains into superior vena cava
Endoscopy & band ligation
If bleeding not controlled by banding – transjugular intrahepatic portosystemic shunt (TIPS), drug treatment (terlipressin)

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15
Q

Describe an abdominal aortic aneurysm

A

Permanent pathological dilation of the aorta > 1.5 times the expected AP diameter of that segment
Usually due to the degeneration of the media layer of the artery
Risk factors: male, inherited risk, increasing age & smoking
Most AAAs are infrarenal

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16
Q

Describe the clinical presentation of an AAA

A

Normally asymptomatic until acute expansion or rupture
Usual presentation: abdominal pain, back pain, pulsatile abdominal mass, transient hypotension & sudden cardiovascular collapse

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17
Q

Describe the diagnosis of an AAA

A

1) Physical examination – presence of a pulsatile abdominal mass
2) Ultrasonography – non-invasive
3) CT – can detect a lot of surrounding anatomy that may be relevant
4) Plain x-rays – calcified aneurysms

18
Q

Describe treatments for an AAA

A

Non-surgical: smoking cessation & hypertension control
Surveillance of AAA: > 5.5cm refer to vascular surgeons
Surgery
-endovascular repair: relining the aorta using an endograft (inserted through the femoral artery)
-open surgical repair: clamp aorta, open the aneurysm & suture in a synthetic graft to replace the diseased segment

19
Q

Describe the importance of the gut microbiome

A

Benefits: harmful bacteria cannot compete for nutrients, microbiome produces antimicrobial substances, helps to develop newborn’s immune system & produce certain nutrients
Bacteria in colon produce SCFAs
High fibre diets influence the composition of gut microbiota (increase in health)

20
Q

Describe faecal microbiota transplant

A

Stool is a biologically active complex mixture of living organisms with therapeutic potential
Pseudomembranous colitis has been treated by faecal enemas since 1985
Get faeces from 10-25 year olds
Fresh to transplantation or storage (1 hour) – stool is centrifuged, filtered & diluted

21
Q

List bacterial infections of the gut

A

Gram negative rods – salmonella, campylobacter, shigella & enterotoxigenic E-coli
Gram positive – clostridium difficile

22
Q

Describe salmonella

A

Symptoms: nausea, vomiting, diarrhoea (mostly non-bloody), fever & abdominal cramping
Spread by ingesting infected food or water
Healthy individuals = self-limiting

23
Q

Describe the pathophysiology of salmonella infection

A

Salmonella gain access to enterocytes
Move to submucosa where encounter macrophages
Macrophages transfer salmonella to RES where they multiply inside cells
Cause lymphoid hyperplasia
Re-enter gut from the liver

24
Q

Describe campylobacter

A

Spiral shaped organism, mainly microaerophilic
Spread to humans via faecal-oral route
Needs to multiply within host before symptoms appear (incubation period 1-7 days)
Symptoms: fever, abdominal cramping & diarrhoea (can be bloody)
Releases a cytotoxin & can last days to weeks (generally self-limiting)
Treatment: fluid/electrolyte replacement, consider abx if bloody diarrhoea

25
Q

Describe shigella

A

Causes shigellosis which commonly affects young children
Spread from infected stools, person to person – only needs a small dose to cause infection
Invades large intestine colonocytes, multiplies in cells & invades neighbouring cells -> kills colonocytes and forms abscesses in the mucosa
Symptoms: abdominal cramping and bloody diarrhoea with mucus
Usually resolves in a week

26
Q

Describe enterotoxigenic E-coli

A

Commensal of the colon but can also be a pathogen
Spread by faecal oral route by contaminated water
Common cause of travellers’ diarrhoea:
1) Invade enterocytes (produces enterotoxins)
2) These cause hypersecretion of chloride ions
3) Water leaves cells into the gut lumen

27
Q

Describe clostridium difficile

A

Gram positive, anaerobic, spore-forming bacillus
Can be transferred via faecal-oral route
Spores are very difficult to get off from an environment
Following antibiotic therapy, C-diff can colonise gut and release toxins:
-toxin A: enterotoxin that results in excessive secretion
-toxin B: cytotoxin

28
Q

Describe treatment of clostridium difficile

A

Most abx can precipitate C-diff proliferation
Resulting in: asymptomatic, varying degrees of diarrhoea & abdominal cramping
In few cases: pseudomembranous colitis & toxic megacolon
Treatment: remove offending antibiotic, fluid resus, metronidazole/vancomycin & probiotics

29
Q

What is pseudomembranous colitis?

A

Inflammatory condition

Elevated yellow plaques join to form a pseudomembrane

30
Q

Describe rotavirus

A

<5 years old
Double stranded RNA virus spread by faecal-oral route
Vomiting with a fever are first symptoms, diarrhoea follows
Treatment: managing dehydration

31
Q

Describe pathophysiology of rotavirus

A

1) Chloride secretion – creates a gradient for the movement of Na into lumen, water moves by osmosis -> diarrhoea
2) SGLT1 disruption – reduced movement of Na/glucose into enterocyte, higher osmotic load in gut & water movement by osmosis
3) Brush border dysfunction – general malabsorption

32
Q

Describe norovirus

A

Can affect any age, only requires a small dose so highly contagious
Virus resistant to cleansing
Incubation is 1-2 days and symptoms last 1-3 days
Symptoms: vomiting, watery diarrhoea & fever
Treatment: oral rehydration therapy

33
Q

List causes of parasitic gastroenteritis

A

Cryptosporidium – sporozoan
Giardia lamblia – flagellate
Entamoeba – amoeba

34
Q

Describe cryptosporidium

A

Transmitted by the faecal-oral route but can also survive and spread via bodies of water
Disease caused by ingestion of an oocyst – reproduces inside the epithelial cells of the distal SI & oocysts are excreted in faeces to continue cycle
Produces watery diarrhoea that is normally self-limiting
Treatment is supportive (fluids)

35
Q

Describe giardia

A

Protozoal infection that causes diarrhoea
Symptoms are more common in children, spread via faecal-oral route with water supplies often affected (developing countries)
If symptomatic (after 10+ days incubation): diarrhoea & abdominal cramping
Common cause of persistent diarrhoea

36
Q

Describe the life cycle and treatment of giardia

A

Life cycle:
1) Cyst is ingested – stomach acid/pancreatic enzymes release parasite from cyst which multiplies in SI, damages proximal SI causing symptoms & villous atrophy occurs
2) Parasite then goes back into cyst stage in colon – excreted to repeat the cycle
Treatment: antibiotics and fluid replacement therapy
(NB: post infection, lactase deficiency is common)

37
Q

Describe entamoeba histolytica

A

Higher prevalence in developing countries
Most cases are asymptomatic, but if symptomatic, diarrhoea & liver abscesses (rare)
Transmitted by faecal-oral route from contaminated food or water
Affects:
1) People who have travelled to tropical places that have poor sanitary conditions
2) People who live in institutions that have poor sanitary conditions
3) Men who have sex with men

38
Q

Describe pathophysiology and treatment of entamoeba histolytica

A

Infection follows the ingestion of cysts
Excystation occurs in colon where trophozoites invade mucosa
Infection can also spread to liver (abscesses form)
Cysts then pass out with faeces – infect others
Treatment: anti-protozoals/metronidazole, surgery for complications

39
Q

Describe travellers’ diarrhoea

A

ETEC most common cause
Passing 3 or more loose/watery stools +/- fever, abdominal pain (> 14 days symptoms make it less likely to be bacteria)
Abx are only recommended for vulnerable patients

40
Q

Describe prevention and treatment for travellers’ diarrhoea

A

Prevention: good hand hygiene, food & water precautions
Treatment: mild/moderate (less than 6 stools/24 hours) – hydration & antidiarrheal agents; severe (> 6 stools/24 hours) – IV fluids & antibiotics

41
Q

Explain the pathophysiology of oesophageal varices

A

1) Hepatic portal hypertension due to liver cirrhosis
2) Causes a shunt of blood from the portal system to the systemic venous system
3) Via anastomosis at the oesophagus which are not normally used
4) Leads to distension in the veins at the site of the anastomosis - varices