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Session 9 Flashcards

1
Q

What is peritonitis

A

Inflammation of the serosal membrane that lines the abdominal cavity

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2
Q

What type of environment is the peritoneal cavity

A

Sterile

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3
Q

Types of peritonitis

A

Primary- spontaneously
Secondary- breakdown of the peritoneal membranes leading to foreign substances entering cavity

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4
Q

What is the peritoneal cavity

A

Space between the visceral and parietal layers of the peritoneum

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5
Q

Components of the peritoneal cavity

A

Visceral and parietal = continuous

Visceral = not lining abdominal wall
Parietal = lines abdominal wall

Cavity (yellow) contains no viscera, only a small amount of fluid

greater and lesser sac connected by Foramen of Winslow

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6
Q

Usual cause of 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 with patients with end stage liver disease (cirrhosis)

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7
Q

What is ascites

A

A pathological collection of fluid within the peritoneal cavity

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8
Q

Why does cirrhosis cause ascites:

A

Portal hypertension- increased hydrostatic pressure in veins draining gut

Decreased liver function- less albumin production and decreased intravascular oncotic pressure

Net movement of fluid into peritoneal cavity

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9
Q

Symptoms and diagnosis of primary peritonitis

A

Abdo pain, fever, vomiting

Can be mild

Aspirate ascitic fluid- neutrophil count over 250cells/mm3

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10
Q

What is secondary peritonitis

A

Secondary/surgical peritonitis

Inflammatory process in peritoneal cavity secondary to inflammation, perforation, or gangrene of an intra-abdominal or retroperitoneal structure

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11
Q

Common causes of secondary bacterial peritonitis

A

Peptic ulcer disease (perforated)
Appendicitis (perforated)
Diverticulitis (perforated)
Post surgery

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12
Q

Common non bacterial causes

A

Tubal pregnancy that bleeds (peritoneal cavity is not enclosed in females)

Ovarian cyst

Blood is highly irritant to the peritoneal cavity

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13
Q

Clinical presentation of peritonitis

A

Abdo pain - gradual or acute

Diffuse in perforated viscera

Patients lie still- knees flexed, shallow breathing

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14
Q

Treatment approaches to peritonitis

A

Control infectious source- surgery

Eliminate bacteria and toxins - antibacterial therapy

Maintain organ system function- intensive care

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15
Q

What is bowel obstruction

A

A mechanical or functional problem that inhibits the normal movement of gut contents

Can affect LI or SI

All ages

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16
Q

Common causes of bowel obstruction

A

Children - Intussusception or intestinal atresia

Adults- adhesions or incarcerated hernias

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17
Q

What is intussusception

A

When one part of the gut tube telescopes into an adjacent section

Potential motility issues, lead point (mass that precipitates e.g. Meckel’s diverticulum or enlarged lymph node)

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18
Q

Consequences of intussuscpetion

A

Can extend far even prolapse out of rectum

Lymphatic and venous drainage is impaired = oedema (enough oedema can impede arterial supply/infarction)

Abdo pain, vomiting, haematochezia

Treatment- air enema, surgery

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19
Q

Signs and symptoms of small bowel obstruction

A

Nausea and vomiting (bilious)

Abdo distension, absolute constipation (late)

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20
Q

Small bowel obstruction can be caused by

A

Intra-abdominal adhesions

  • abdominal surgery, greater omentum or bowel involved
  • mesothelium (direct trauma, post op infection, capillary bleeding leads to exudation of fibrinogen)
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21
Q

Consequences of adhesions

A

Small bowel obstruction, abdo pain, secondary infertility

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22
Q

Other causes of small bowel obstruction

A

Hernias - can narrow lumen enough to cause obstruction, incarcerated groin hernias most common

IBD- Crohns (repeated episodes of inflammation/healing causes narrowing)

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23
Q

Diagnosis of small bowel obstruction

A

History- abdominal pain is crampy, intermittent

Physical examination- abdominal distension, increased/absent bowel sounds, presence of hernia

Imaging- CT abdo and pelvis

24
Q

Common causes of large bowel obstruction

A

Older generation typically

Colon cancer, Diverticular disease causing strictures, volvulus- sigmoid (older) caecal (younger)

25
Symptoms of large bowel obstruction
Often gradually if caused by cancer but abrupt with volvulus (twisting of mesentary) Change in bowel habit (cancer) Abdominal distension Crampy abdominal pain Nausea/vomiting (later)
26
Features of Volvulus
Part of the colon twists around its mesentary Most common in sigmoid colon and caecum Results in obstruction
27
How can volvulus occur
Can result from overloaded sigmoid colon (constipation) Extra mass predisposes elongation of sigmoid (relatively smaller mesenteric attachment) High fibre diets can also lead to sigmoid overload and twisting
28
Caecal volvulus results in
Small and large bowel obstruction
29
Investigations for volvulus
CT abdo and pelvis
30
Small vs large bowel obstruction
31
What is acute mesenteric ischeamia
Symptomatic reduction in blood supply to the GI tract Arterial or venous compromise More common in females and if you have a history of peripheral vascular disease
32
Causes of acute mesenteric ischeamia due to arterial compromise
Occlusion (70% of cases)- arterial embolism/thrombosis usually affecting SMA, vasculitis narrowing artery (not acute) Non occlusive mesenteric ischeamia- low cardiac output, splenic flexure and recto-sigmoid junction are two watershed areas where collateral is action of blood flow may be limited
33
Causes of acute mesenteric ischeamia due to venous compromise
Mesenteric venous thrombosis, system coagulopathy, malignancy
34
Diagnosis of acute mesenteric ischeamia
Most cases are more elderly patients with Cardiovascular risk factors Symptoms can be non-specific Abdo pain is disproportionate to clinical findings- 30 mins after eating and lasts 4 hours Nausea and vomiting, pain left sided usually
35
Why is pain with acute mesenteric ischaemia often left sided
Blood supply to splenic flexure is most fragile
36
Acute mesenteric ischeamia investigations
Blood tests- metabolic acidosis/ increased lactate levels CT abdo/pelvis, and CT angiography
37
Treatment for mesenteric ischeamia
Surgery- resection of ischeamic bowel (bypass graft) Thrombolysis/angioplasty Mortality is high- often older patients with co morbidities
38
Peptic ulceration features
Disruption in the gastric/duodenal mucosa - greater than 5mm, going through to submucosa through muscularis mucosa Duodenal ulcers most common- first part, gastro-duodenal artery lies behind Gastric ulcers- lesser curve and antrum common sites
39
Features of oesophageal varices
Porto-systemic anastomosis Portal hypertension (pre hepatic, hepatic, post hepatic), normal pressure in portal vein (5-10mmHg), sites of Porto-systemic anastomosis are areas that have venous ages through portal vein and systemic veins
40
Specifics in oesophageal varices
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
41
causes of portal hypertension
Pre-hepatic (portal vein thrombosis) Hepatic (cirrhosis, schistosomiasis) Post hepatic (hepatic vein thrombosis, RHF)
42
Treatment of oesophageal varices
Banding TIPS (transjugular intrahepatic portosystemic shunt) Drug treatment- Terlipressin (reduces portal venous pressure)
43
Explain TIPS
Transjugular intrahepatic portosystemic shunt - An expandable metal is placed within the liver - Bridges the portal vein into a hepatic vein - Decompresses the portal vein pressure - Reduction in variceal pressure - Reduction in ascites
44
What is AAA
Abdominal aortic aneurysm Permanent pathological dilation of the aorta with a diameter more than 1.5 times the expected AP diameter
45
More than 90% of AAAs originate below the
Renal arteries
46
AAA are usually due to
Degeneration of the media layer of the arterial wall Media- smooth muscle cells with elastin and collagen, AAAs form due to degradation of elastin and collagen Lumen gradually starts to dialte
47
Risk factors for AAA
Male Inherited risk Increasing age Smoking
48
Most AAAs are
Asymptomatic and infrarenal
49
Labelled artery wall
50
AAA symptoms
Normally asymptotic until acute expansion or rupture Compress other nearby structures- stomach, bladder, vertebra Cause nausea, urinary frequency and back pain
51
Usual presentation of AAA rupture
Abdominal pain (+/- flank and groin pain) Back pain Pulsatile abdominal mass Transient hypotension Syncope- retroperitoneum can temporarily tamponade the bleed Sudden cardiovascular collapse
52
65% of ruptures AAAs
Die before hospital due to sudden cardiovascular collapse
53
Diagnosis of AAA
Physical examination- Pulsatile abdo mass less Than 50% of cases Ultrasound- non invasive, can be sensitive and specific, can detect free peritoneal blood Computed Tomography (CT)- can detect a lot of surrounding anatomy, planning for elective surgery
54
AAA treatment
Non surgical- smoking cessation, hypertension control Surveillance of AAA- less than 5.5cm (most grow slowly enough not to need treatment), more than 5.5cm = refer to vascular surgeons
55
AAA surgery
Endo vascular repair- re-lining the aorta using an endo graft (an exoskeleton of metallic stents over a fabric lining) Inserted through the femoral artery (seals below renal arteries and above common iliacs) Open surgical repair- clamp aorta, open the aneurysm (remove thrombus and debris), suture in a synthetic graft to replace diseased segment

GI (22 decks)

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