Large Bowel Flashcards

1
Q

pathophysiology of appendicitis

A

typically caused by luminal obstruction via a faecolith, impacted stool and rarely an appendiceal/caecal tumour

lumen is blocked, commensal bacteria colonise and cause acute inflammation, this results in swelling of the appendix

this swelling interrupts venous and lymph drainage and increases the pressure which eventually can turn into ischaemia

ischaemia can then become necrosis of the appendiceal wall and then finally perforation

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2
Q

risk factors for appendicitis

A

genetic factors - 30% of risk

ethnicity - more common in caucasians

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3
Q

describe the pain in appendicitis

A

pain initially starts peri-umbilical and is dull and poorly localised - this is due to inflammation of the visceral peritoneum

the pain then progresses to become sharp and well localised in the RIF region - this is due to inflammation of the parietal peritoneum

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4
Q

clinical features of appendicitis

A

pain - initially peri-umbilical but then progression to RIF region

nausea and vomiting

rebound tenderness, percussion pain and guarding

+ve Rovsing and Psoas sign

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5
Q

what is Rovsing and Psoas sign - and what do they indicate

A

Rovsing = pain in RIF when palpating the LIF

Psoas sign = pain on extension of the right hip (inflamed appendix abutting the psoas muscle in the retrocaecal position)

indicate appendicitis

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6
Q

investigations into suspected acute appendicitis

A

urinalysis - exclude renal or urological cause

pregnancy test - exclude pregnancy in women of reproductive age

routine bloods - especially CRP and other inflammatory markers

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7
Q

imaging into suspected appendicitis

A

clinical diagnosis mainly but USS and CT can be used

with USS being first line - minimal radiation exposure

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8
Q

management of appendicitis

A

mainstay of treatment is via laparoscopic appendectomy

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9
Q

what is the most common type of colorectal cancer

A

adenocarcinoma

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10
Q

risk factors for colorectal cancer

A

increasing age

family history - strong genetic component especially in the instance of FAP

IBD

low fibre, high fat intake diet

smoking and excess alcohol intake

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11
Q

what are the common clinical features of colorectal cancer

A

change in bowel habit

weight loss

abdominal pain

rectal bleeding

symptoms of iron deficiency anaemia

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12
Q

how do the presenting sings change in left colorectal vs right sided colorectal cancer

A

left sided = present earlier, tenesmus, rectal bleeding, change in bowel habit, palpable mass in the LIF.

right sided = present late, abdo pain, iron deficiency anaemia, palpable mass in RIF (present late as it takes longer for bowel changes to occur - further away from rectum)

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13
Q

what tumour marker is linked with colorectal cancer

A

Carcinoembryonic antigen

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14
Q

Lab tests and imaging in suspected colorectal cancer

A

FBC - routine and check for anaemia

CEA - tumour marker

gold standard imaging = colonoscopy with biopsy

CT + MRI - check invasion and mets

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15
Q

what is the gold standard imaging technique for a suspected colorectal cancer

A

colonoscopy with biopsy

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16
Q

management of colorectal cancers

A

only definitive treatment is via surgery

chemo and radiotherapy are used as adjuvant therapy

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17
Q

what types of surgery are there for colorectal cancers

A

right sided hemicolectomy - caecal or ascending colon tumours

left hemicolectomy - descending colon tumours

sigmoidcolectomy - sigmoid colon tumours

Hartmann’s procedure - complete resection of the recto-sigmoid colon

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18
Q

what is a diverticulum and where are they most commonly found

A

its an outpouching of the bowel wall

most commonly found in the sigmoid colon

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19
Q

describe diverticulosis vs diverticular disease vs diverticulitis vs diverticular bleed

A

diverticulosis = presence of diverticula (asymptomatic)

diverticular disease = symptoms arising from the diverticula

diverticulitis = inflammation of the diverticula

diverticula bleed = where the diverticula erodes into a vessel and causes a large volume painless bleed

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20
Q

pathophysiology of diverticulosis

A

aging bowel is already weakened

movement of stool in the lumen causes in increase in luminal pressure

this results in outpouchings of the mucosa in the weaker areas of the bowel wall

diverticulitis then occurs when bacteria overgrow within the outpouchings resulting in inflammation

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21
Q

risk factors for diverticulosis

A

age

low dietary fibre

obesity

smoking

family history

NSAID use

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22
Q

clinical features of acute diverticulitis

A

acute abdo pain

sharp in nature and localised to the LIF

localised tenderness

decreased appetite, pyrexia and nausea

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23
Q

imaging of choice in suspected diverticulitis

A

CT abdo pelvis

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24
Q

why should a colonoscopy never be performed on a patient with suspected acute diverticulitis

A

increased risk of perforation

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25
Q

management of diverticulum and associated conditions

A

mostly conservative; analgesia, abx, IV fluids, increased fluid intake

surgical; only in cases of perforation or sepsis - usually involves a Hartmann’s procedure

26
Q

what are some complications of diverticulitis

A

stricture formation and fistula formation;

colovesical fistula - bowel and bladder

colovaginal fistula - bowel and vagina

27
Q

what is the microscopic appearance of Crohn’s disease

A

non-caseating granulomatous inflammation

28
Q

what is the difference in inflammation depth between UC and Crohn’s

A

UC = mucosal inflammation only

Crohn’s = transmural inflammation

29
Q

what is the difference in location between UC and Crohn’s

A

Crohn’s = affects anywhere in the GI tract, mouth to anus

UC = large bowel only

30
Q

what are the characteristic macroscopic changes seen in Crohn’s

A

fistula formation

cobblestone appearance (fissures and deep ulcers)

skip lesions

31
Q

what are the characteristic features of UC

A

continuous inflammation - no skip lesions

crypt abscesses

32
Q

clinical features of crohn’s

A

episodic abdo pain - colicky in nature

chronic diarrhoea - mucus and blood

general malaise

oral aphthous ulcers and perianal disease (if entire GI tract is affected)

33
Q

extra-intestinal features of crohn’s disease

A

MSK - arthritis, nail clubbing, bone disease

skin - erythema nodosum, pyoderma gangrenosum

eyes - iritis, uveitis

HPB - gallstones

renal - renal stones

34
Q

investigations into suspected Crohn’s disease

A

routine bloods

faecal calprotectin

stool culture - infective cause

gold standard = colonoscopy + biopsy

35
Q

what is the gold standard investigation into supsected Crohn’s

A

colonoscopy + biopsy

36
Q

management of Crohn’s

A

inducing remission = corticosteroid and immunosuppression therapy

maintaining remission = azathioprine + smoking cessation

surgical = usually some sort of resection

37
Q

what histological changes are seen in ulcerative colitis

A

non-granulomatous inflammation

crypt abscesses

reduced goblet cells (goblet cell hypoplasia)

38
Q

clinical features of ulcerative colitis

A

bloody diarrhoea

PR bleeding

mucus discharge

increased frequency and urgency

tenesmus

39
Q

extra-intestinal features of UC

A

MSK - arthritis and nail clubbing

skin - erythema nodosum

eyes - iritis, uveitis

HPB - primary sclerosing cholangitis

40
Q

investigations into UC

A

routine bloods - baseline + inflammatory markers

faecal calprotectin

stool sample - infective cause

41
Q

imaging for UC

A

colonoscopy + biopsy

AXR + CT can be used to check for toxic megacolon

42
Q

what causes toxic megacolon

A

Toxic megacolon occurs when inflammatory bowel diseases cause the colon to expand, dilate, and distend. When this happens, the colon is unable to remove gas or feces from the body. If gas and feces build up in the colon, your large intestine may eventually rupture.

43
Q

what is a characteristic radiological sign of chronic UC

A

lead pipe colon

44
Q

what is the main complication to be worried about in UC

A

toxic megacolon

45
Q

what drugs are used to treat UC

A

corticosteroid, immunosuppressors, biological agents = induce remission

(5-ASAs) mesalazine, sulfasalazine or azathioprine = maintain remission

46
Q

what is rigler’s sign and what does it suggest

A

bowel wall visualised on both sides due to intra and extraluminal air

air in the peritoneum

characteristic of bowel perforation

47
Q

what radiological sign do you expect to see in bowel perforation

A

riglers sign

48
Q

what is pseudo-obstruction of the bowel

A

dilatation of the colon due to an adynamic bowel, in the absence of mechanical obstruction

49
Q

pathophysiology of pseudo-obstruction

A

interruption of the autonomous nervous supply to the colon resulting in the absence of smooth muscle contraction in the bowel wall

50
Q

causes of pseudo-obstruction

A

electrolyte imbalance

medication; opioids, CCBs, anti-depressants

recent surgery, illness, trauma

neurological disease; parkinson’s, multiple sclerosis

51
Q

clinical features of pseudo-obstruction

A
same as bowel obstruction;
abdo pain 
vomiting 
constipation 
abdo distension
52
Q

investigations into suspected pseudo-obstruction

A

blood tests - biochemical causes

AXR

CT abdo-pelvis with IV contrast

53
Q

management of pseudo obstruction

A

endoscopic decompression and selective use of neostigmine (acetylcholinesterase inhibitor)

or surgical resection - for those failing medical management

54
Q

what drug classes are associated with pseudo-obstruction

A

anti-depressants

CCBs

opioids

55
Q

what is a volvulus

A

twisting loop of intestine around its mesenteric attachment, resulting in a closed loop bowel obstruction

56
Q

where is the most common place a volvulus occurs

A

sigmoid colon

57
Q

risk factors for volvulus

A

increasing age

chronic constipation or laxative use

male gender

previous abdo surgeries

58
Q

what are the noteworthy clinical features of a sigmoid volvulus

A

degree of abdo distension

rapidity of onset

59
Q

what are the characteristic radiological signs of sigmoid volvulus

A

whirl sign on CT

coffee bean sign arising from LIF on AXR

60
Q

management of volvulus

A

decompression by sigmoidoscope via rectum

surgery in cases of perforation, failed decompression and necrotic bowel

61
Q

what is the 2nd most common place of volvulus

A

caecal volvulus

62
Q

how can you tell the difference on AXR between caecal and sigmoid volvulus

A

sigmoid starts from LIF

caecal starts from RIF