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GI > Session 9 > Flashcards

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
Q

Symptoms of large bowel obstruction

A

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
Q

Features of Volvulus

A

Part of the colon twists around its mesentary

Most common in sigmoid colon and caecum

Results in obstruction

27
Q

How can volvulus occur

A

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
Q

Caecal volvulus results in

A

Small and large bowel obstruction

29
Q

Investigations for volvulus

A

CT abdo and pelvis

30
Q

Small vs large bowel obstruction

A
31
Q

What is acute mesenteric ischeamia

A

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
Q

Causes of acute mesenteric ischeamia due to arterial compromise

A

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
Q

Causes of acute mesenteric ischeamia due to venous compromise

A

Mesenteric venous thrombosis, system coagulopathy, malignancy

34
Q

Diagnosis of acute mesenteric ischeamia

A

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
Q

Why is pain with acute mesenteric ischaemia often left sided

A

Blood supply to splenic flexure is most fragile

36
Q

Acute mesenteric ischeamia investigations

A

Blood tests- metabolic acidosis/ increased lactate levels

CT abdo/pelvis, and CT angiography

37
Q

Treatment for mesenteric ischeamia

A

Surgery- resection of ischeamic bowel (bypass graft)

Thrombolysis/angioplasty

Mortality is high- often older patients with co morbidities

38
Q

Peptic ulceration features

A

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
Q

Features of oesophageal varices

A

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
Q

Specifics in oesophageal varices

A

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
Q

causes of portal hypertension

A

Pre-hepatic (portal vein thrombosis)
Hepatic (cirrhosis, schistosomiasis)
Post hepatic (hepatic vein thrombosis, RHF)

42
Q

Treatment of oesophageal varices

A

Banding

TIPS (transjugular intrahepatic portosystemic shunt)

Drug treatment- Terlipressin (reduces portal venous pressure)

43
Q

Explain TIPS

A

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
Q

What is AAA

A

Abdominal aortic aneurysm

Permanent pathological dilation of the aorta with a diameter more than 1.5 times the expected AP diameter

45
Q

More than 90% of AAAs originate below the

A

Renal arteries

46
Q

AAA are usually due to

A

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
Q

Risk factors for AAA

A

Male
Inherited risk
Increasing age
Smoking

48
Q

Most AAAs are

A

Asymptomatic and infrarenal

49
Q

Labelled artery wall

A
50
Q

AAA symptoms

A

Normally asymptotic until acute expansion or rupture

Compress other nearby structures- stomach, bladder, vertebra

Cause nausea, urinary frequency and back pain

51
Q

Usual presentation of AAA rupture

A

Abdominal pain (+/- flank and groin pain)
Back pain
Pulsatile abdominal mass
Transient hypotension
Syncope- retroperitoneum can temporarily tamponade the bleed
Sudden cardiovascular collapse

52
Q

65% of ruptures AAAs

A

Die before hospital due to sudden cardiovascular collapse

53
Q

Diagnosis of AAA

A

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
Q

AAA treatment

A

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
Q

AAA surgery

A

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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