General Surgery GI Flashcards

1
Q

Midgut structures, arterial supply, venous drainage and innervation

A

structures: jejunum, ileum, cecum, large intestine up to left colic flexure

supplied by superior mesenteric artery

drained by superior mesenteric vein to portal system

innervated by lesser (T10-T11) and least (T12) splanchnics from sympathetic system and vagus nerve from parasympathetic system

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2
Q

Hindgut structures, arterial supply, venous drainage and innervation

A

structures: descending colon, sigmoid colon, rectum, anal canal

supplied by inferior mesenteric artery

drained by inferior mesenteric vein to portal system

innervated by lumbar splanchnics (L1-L2) from sympathetic system and pelvic splanchnics (S2-S4) from parasympathetic

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3
Q

Division of the compartment of greater sac

A

greater sac divided by transverse, ascending and descending colon into supra colic compartment, infra colic compartment, right paracolic gutter and left paracolic gutter

the infra colic and supra colic compartment communicate via paracolic gutters

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4
Q

Jejenum vs ileum

A

wall, caliber: jejunum have thicker walls with larger diameter whereas ileum have thinned walls with smaller diameter

location: jejunum located in upper left quadrant whereas ileum is located in lower right quadrant
vascularity: jejunum have greater vascularity so it appears darker and more red whereas ileum have lesser vascularity so it appears lighter and more pink

vasa recta: vasa recta is long in jejunum and short in ileum

mesenteric fat: jejunum have less mesenteric fat and ileum have more mesenteric fat

circular folds: jejunum have tightly packed circular folds whereas ileum have sparse circular folds and absent circular folds distally

intestinal villi: jejunum have more numerous and prominent villi whereas ileum have less numerous and less prominent villi

lymphoïde mode follicules: jejunum have no aggregates (no Peyer’s patches) whereas ileum contain Peyer’s patches

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5
Q

Arterial supply of jejenum vs ileum

A

both jejunal and ileal arteries are branches from superior mesenteric artery (15-18 arteries in total)

jejunum / ileum artery -> arcade -> vasa recta

jejunum have fewer, larger arteries that loops and have longer vasa recta (straight arteries) than ileum

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6
Q

What is the ileoceacal junction

A

ileum terminates by partly invaginating into cecum, forming the ileocecal valve

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7
Q

How to locate the appendix

A

appendix location can vary, it is usually localized by tracing to origin of taenia coli

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8
Q

Blood supply of midgut

A

mid gut supplied by superior mesenteric artery (SMA) at L1 level

superior mesenteric artery have branches to feed small intestines and branches to feed large intestines

all of branches of SMA that course toward the left are jejunal arteries and ileal arteries supply small intestines

branches of SMA that course toward the right include ileocolic artery (with ileal and colic branches), appendicular artery, right colic artery and middle colic artery that supply the large
intestines

the ileocolic artery split into ileal and colic branches that supply ascending colon

appendicular arteries is a branch of ileocolic artery that supply the appendix

the right colic artery is a branch of SMA that supply the ascending colon

middle colic artery is a branch of SMA that supply the transverse colon

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9
Q

Venous drainage of midgut

A

midgut drained by superior mesenteric vein (SMV), which drain to the portal vein (portal system)

SMV branches are paired and travel with arteries with same name (jejunal veins, ileal veins, ileocolic vein, right colic vein, middle colic vein, appendicular vein)

the SMV and its branches are always anterior to its correspondent SMA and its branches

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10
Q

large intestine intraperitoneal and retroperitoneal components

A

large intestines include cecum, appendix, ascending colon, transverse colon, descending colon and sigmoid colon

cecum, appendix, transverse and sigmoid colon are intraperitoneal and covered by mesentery

ascending colon, descending colon and rectum are retroperitoneal

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11
Q

What are the taenia coli

A

taenia coli = 3 strips of longitudinal muscle extending length of large colon

the longitudinal muscle names are taenia libera, taenia omentalis and taenia mesocolica

pulling force of taenia coli result in haustra (sacculated appearance that look like pouches)

taenia coli unite at base of appendix and then splay out to form outer wall of rectum

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12
Q

Locations of longitudinal taenia muscles

A

taenia omentalis is underneath the greater omentum

taenia libera is anterior

taenia mesocolica is posterior

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13
Q

what are epiploic appendages

A

epiploic appendages are small pouches of peritoneum filled with fat along the colon

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14
Q

what are semilunar folds

A

semilunar folds are ridges inside the large intestine between taenia coli that separate the haustra

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15
Q

rectosigmoid junction landmarks

A
  1. located anterior to S3 vertebra
  2. termination of sigmoid mesocolon (mesentery)
  3. colon traits (taenia coli, haustra, appendages) end at rectosigmoid junction
  4. taenia coli stop being distinct bands, flare out and become continuous muscle layer covering the rectum
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16
Q

Rectum, its components and pouches

A

rectum is part of the large intestine that is retroperitoneal and fixed

ampulla of rectum is the inferior dilatation of rectum

lowest extent of peritoneal cavity forms a pouch

rectovesival pouch between rectum and bladder in male

rectouterine pouce between rectum and uterus in female

drainage of excess peritoneal fluid and peritoneal dialysis at these pouches

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17
Q

where is the anorectal junction roughly located

A

pelvic diaphragm

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18
Q

anal canal and its components

A

in anal canal, interior (mucosa) and exterior (skin) surfaces are divided by pectinate line

anal columns are longitudinal ridges that elevate, which is due to superior rectal artery and vein

anal sinuses are grooves between anal columns that secrete mucus

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19
Q

Embryological origin, innervation, arterial supply, venous drainage and lymphatic drainage of tissue above the pectinate line (visceral)

A

Endoderm

Autonomic: distension sensation

Superior Rectal A. (IMA)

Superior Rectal V. (IMV –> Portal drainage)

Visceral pattern (internal iliac lymph nodes –> chyle cistern)

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20
Q

Embryological origin, innervation, arterial supply, venous drainage and lymphatic drainage of tissue below the pectinate line (body wall/somatic)

A

Ectoderm

Somatic: pain sensation (inferior rectal N.)

Inferior Rectal A. (from internal iliac artery)

Middle/inferior rectal V. (int iliac V. –> IVC, caval drainage)

Body wall drainage pattern (superficial inguinal lymph nodes –> body wall)

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21
Q

Branches of inferior mesenteric artery

A

1 = IMA

2 = left colic artery, a branch of IMA, supplies left part of transverse colon and descending colon

3 = sigmoid arteries (usually 2 or 3 arteries), branches of IMA, supply sigmoid colon

4 = superior rectal artery, a continuation of IMA after sigmoidal arteries are given off

blue arrows = marginal artery of Drummond that anastomose between SMA and IMA along length of entire large colon

marginal artery encircles the entire colon

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22
Q

Venous drainage of hindgut

A

hindgut drained by inferior mesenteric vein (IMV), which drain to the portal vein (portal system)

IMV branches are paired and travel with arteries with same name (right colic vein, sigmoidal veins, superior rectal vein)

IMV and its branches are always posterior to the correspondent IMA and its branches

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23
Q

Lymphatic drainage of midgut and hindgut

A

lymph nodes generally associated with arteries (nodes along arteries) to bypass portal venous system

this is unique to GI, where lymph usually follows veins elsewhere in the body

small intestine lymph follows arterial lymph nodes to chyle cistern to thoracic duct

large intestine lymph follows arterial lymph nodes to chyle cistern to thoracic duct

anal canal lymph superior to pectinate line follow arterial lymph node to chyle cistern to thoracic duct (gut drainage pattern)

anal canal lymph inferior to pectinate line drain to superficial inguinal lymph nodes (body wall drainage pattern)

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24
Q

Overall Regulation of GI System

A

3 types of regulation of GI system

1) Nervous system control
autonomic innervation (sympathetic and parasympathetic)
as a rule, sympathetic always inhibit GI function and parasympathetic always stimulate GI function
enteric nervous system

2) Endocrine control
secretion of hormones into bloodstream
e.g. secretin, CCK, somatostatin, VIP, gastrin

3) Paracrine control
secretion of signalling molecule into interstitial for communication between nearby cells

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25
Q

Role of CCK and Secretin

A

CCK and secretin are hormones released by duodenum

fatty chyme stimulate release of CCK

acidic chyme stimulate release of secretin

CCK inhibit gastric emptying, stimulate pancreatic growth, stimulate release of pancreatic enzyme and stimulate release of bile from gallbladder

secretin stimulate release of basic pancreatic fluid and basic bile

CCK and secretion potentiate each other’s effect

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26
Q

Overview of digestion and absorption

A

1) Mouth
mastication
saliva

2) Stomach
pepsin
gastric acid secretion
intrinsic factor

3) Liver
bile acid

4) Pancreas
bicarbonate
amylase
protease
lipase / colipase

5) Duodenum, jejunum
water and electrolyte absorption
nutrient absorption
90% of digestion and absorption occur in duodenum

6) Terminal ileum
bile salt transport
vitamin B12 absorption
absorption of fat soluble vitamins

7) Colon
water absorption
bacterial fermentation of disaccharide into short chain fatty acids and acids (CO2, methane)
short chain fatty acids are used by colonic epithelium or metabolized by liver

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27
Q

Digestion and absorption of proteins

A

1) Digestion in stomach
proteins denatured in gastric acid

pepsinogen (secreted by chief cells in stomach) is activated in gastric acid to pepsin, which cleave protein into peptides

2) Digestion in duodenum
pancreatic proteases cleave peptides into oligopeptides (2-6 amino acids) and amino acids
trypsin, chymotypsin, elastase and carboxypeptidase
duodenum mucosal enzyme enterokinase cleave and activate trypsin, which then cleave and activate chymotrypsin

brush border enzymes cleave oligopeptides into tri-peptides, dipeptides and amino acids
aminopeptidase, carboxypeptidase, dipeptidase

3) Absorption in small intestine
amino acids are absorbed into enterocytes by co-transport with Na

dipeptides and tripeptides are absorbed into enterocytes by co-transport with H+ and hydrolyzed into amino acids inside the cell

4) Absorption into blood
amino acids leave epithelial cell by facilitated diffusion, which then enter capillary blood in villi to hepatic portal vein to liver

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28
Q

Digestion and absorption of carbohydrates

A
1) Digestion in mouth
salivary amylase (secreted by salivary glands) break starch (amylose and amylopectin) into oligosaccharides
disaccharide (lactose and sucrose) and monosaccharides (glucose and fructose) go through mouth, esophagus and stomach without any digestion

2) Digestion in duodenum
pancreatic amylase further break starch into oligosaccharides (maltose, maltotriose, dextrin)

3) Digestion in small intestine
brush border enzyme (lactase, maltase and sucrase) break disaccharide (lactose, maltose and sucrose) into monosaccharides (glucose, fructose, galactose)

4) Absorption in small intestine
monosaccharide absorbed into enterocytes
glucose and galatose are absorbed into enterocytes via co-transport with Na
fructose enter enterocytes by facilitated diffusion
all monosaccharides leave epithelial cells via facilitated diffusion, which then enter capillary blood in villi to hepatic portal vein to liver

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29
Q

Digestion and absorption of fat

A

1) Mixing in mouth and stomach
fat (triglyceride, phospholipid and cholesterol) are crushed and mixed in mastication within the mouth and stomach
small amount of fat broken by gastric lipase

2) Emulsification to fat droplets in duodenum
bile salts (secreted by liver into gallbladder) that emulsify (surround) fat, to break it down into fat droplets and make it soluble in water

3) Digestion in duodenum
pancreatic lipase cleave triglyceride into fatty acids and a monoglyceride
pancreatic phosphlipase break phospholipids into fatty acids and lysophosphatidylcholine
pancreatic cholesterol esterase break cholesterol into sterol

4) Emulsification to micelle in duodenum
cleaved fatty acids, monoclygeride, choline and sterol are emulsified by bile salt into micelles

5) Absorption of micelle in small intestine (mainly duodenum and jejunum)
fatty acids leave micelle and diffuse into enterocytes
in enterocytes, fatty acids and monoglycerides are reformed into triglycerides, which are packaged with triglycerides, cholesterol, phospholipids and protein to form chylomicron (a
lipoprotein particle)
chylomicron exit enterocyte by exocytosis and enter lacteals in villi, where they enter the lymphatics
short chain fatty acids and glycerol are absorbed directly into blood stream and do not enter the lymph system
bile salts are absorbed in ileum

6) Transport from lymph into blood
lymphatics carry chylomicron to thoracic duct, where it enters the blood stream to the liver

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30
Q

Hernia epidemiology

A

affects more commonly males than females, males have 25% lifetime risk of hernia whereas females have 2% lifetime risk of hernia

50% hernias are indirect inguinal hernia; 25% hernias are direct inguinal hernia; 5% hernias are femoral hernias

most common hernias in male and female are indirect inguinal hernia, but male are more predisposed to indirect hernia due to opening of inguinal canal

females are more pre-disposed to femoral hernias

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31
Q

Hernia risk factors

A

increased intra-abdominal pressure

body habitus that increase intra-abdominal pressure: obesity, pregnancy, ascites

activities that increased intra-abdominal pressure: chronic cough, constipation, straining on urination / defecation, heavy lifting

congenital abnormality (patent processus vaginalis)

previous history of hernia and hernia repair

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32
Q

Hernia anatomical classification

A

A) Internal hernia

B) External hernia
1) groin hernia

a) indirect inguinal hernia: herniation originating from deep inguinal ring lateral to inferior epigastric artery descending into scrotal sac or labia majora
b) direct inguinal hernia: herniation through Hesselbach’s triangle, medial to inferior epigastric artery usually does not descent into scrotal sac

“MD don’t LIe” = Medial to inferior epigastric artery is the Direct hernia; Lateral to inferior epigastric artery is the Indirect hernia

c) pantaloon hernia: combined direct and indirect groin hernia with peritoneum draped over inferior epigastric vessels

d) femoral hernia: herniation into femoral canal below inguinal ligament medial to femoral vein within femoral canal
femoral hernia have highest risk of incarceration and strangulation

2) epigastric hernia
epigastric hernia: defect in linea alba above umbilicus causing hernia

3) incisional hernia
incisional hernia: ventral hernia at site of wound closure

4) other types of hernia
Littre’s: hernia involving Meckel’s

Amyand’s: hernia containing ruptured appendix

lumbar hernia

obturator hernia

parastomal hernia

umbilical hernia

Spigelian hernia: ventral hernia through linea semilunaris

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33
Q

Hernia complications

A

incarceration, where hernia cannot be reduced

strangulation, where an irreducible hernia have ischemia
strangulation of hernia can cause intestinal obstruction, necrotic bowel, sepsis

strangulated hernia is a surgical emergency

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34
Q

Hernia clinical presentation

A

History:

swelling or fullness at hernia site, mass of variable size, hernia enlarges with coughing / lifting / straining and disappears in supine position

aching sensation radiating into area of hernia, tender at end of day relieved with supine position or with reduction

abdominal fullness, burning / gurgling / aching sensation

no pain or tenderness on palpation of hernia

incarcerated hernia: painful enlargement of previous hernia, irreducible either spontaneously or manually through defect, may have symptoms of bowel obstruction (nausea &
vomiting, distended abdomen, constipation, obstipation)

strangulated hernia: irreducible hernia with increasing pain and tenderness, symptoms of bowel obstruction (nausea & vomiting, distended abdomen, constipation, obstipation), fever,
chills

Physical Exam (of Groin Hernia):

on inspection, bulges at femoral or inguinal areas with patient standing while straining down

in male, palpation by invaginating loose skin of scrotum with index finger up into inguinal canal to feel for any palpable herniation descending onto finger while patient strains down or
coughs

in female, palpation with open hand over groin area to detect impulse of hernia descending during straining or coughing

incarcerated hernia: irreducible hernia

strangulated hernia: fever, distended abdomen, peritonitis

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35
Q

Hernia diagnosis

A

usually physical exam sufficient for diagnosis of hernia
may use ultrasound or CT to aid in diagnosis of hernia

CT useful for diagnosis of obturator hernia, internal abdominal hernia, Spigelian femoral hernia in obese patients

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36
Q

Hernia management for non-incarcerated non-strangulated hernias

A

a) small, minimally symptomatic, first occurrence hernia
surgical repair is not necessary and patients can be followed expectantly

if no surgical repair, then patients counselled on symptoms of incarceration and strangulation, so that they can seek prompt healthcare evaluation

b) all other hernia
surgical repair (herniorrhaphy) for all other hernias
symptomatic, large or recurrent hernia should have surgical repair within 1 month of detection

surgical repair of hernia to prevent incarceration and strangulation; or to treat symptoms; or for cosmesis

surgical repair can be open or laparoscopic, depending on surgeon preference, usually uses mesh for tension-free closure

repair can be done with plug in hernia defect with patch over it or patch alone

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37
Q

Post-surgical complications of hernia surgery

A

recurrence (15-20% risk), which is less common with mesh / tension-free surgical repair

scrotal hematoma (3% risk) from compromised venous return of testes

nerve (ilioinguinal or genital branch of genitofemoral) entrapment

stenosis or occlusion of femoral vein, causing acute leg swelling

ischemic colitis

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38
Q

Hernia management for acutely incarcerated or strangulated hernia

A

acutely incarcerated hernia have risk of subsequent strangulation, so patients should undergo attempts at reduction followed by surgical repair

strangulated hernia should undergo emergent surgical repair

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39
Q

hernia definition

A

hernia = fascial defect resulting in protrusion of a viscus into an area in which it is not normally contained

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40
Q

complete hernia definition

A

complete hernia = hernia sac and contents protrude through defect

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41
Q

incomplete hernia definition

A

incomplete hernia = partial protrusion through defect

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42
Q

internal hernia definition

A

internal hernia = sac herniating into or involving intra-abdominal structure

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43
Q

external hernia definition

A

external hernia = sac protruding completely through abdominal wall

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44
Q

sliding hernia definition

A

sliding hernia = part of wall of hernia formed by protruding viscus

ex. sliding hernia where cecum forms part of hernia wall

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45
Q

Richter’s hernia definition

A

Richter’s hernia = only part of circumference of bowel (usually anti-mesenteric border) is incarcerated or strangulated, so may not cause bowel obstruction

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46
Q

What is Hesselbach’s triangle

A

Anatomical triangle formed by 3 borders:

medial border = lateral margin of rectus abdominis

lateral border =
inferior epigastric artery

inferior = inguinal ligament

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47
Q

Most common complication of hernia repair

A

most common complication of hernia repair include hematoma, penile ecchymosis, scrotal ecchymosis, wound infection, chronic pain

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48
Q

Types of IBD

A

many types of inflammatory bowel disease including
Crohn’s disease (CD): relapsing transmural inflammation and ulceration of GI tract anywhere from mouth to anus

Ulcerative colitis (UC): inflammation and ulceration of rectum extending proximally to large bowel

other IBD include microscopic colitis, diversion colitis, radiation colitis, drug induced colitis, indeterminate colitis

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49
Q

Epidemiology of IBD

A

highest incidence and prevalence of IBD in Europe and North America

bimodal age distribution, with 1st peak at age 20-30 and 2nd peak at age 60

highest prevalence in Caucasian and African American

lowest prevalence in Asians and Hispanics

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50
Q

Pathophysiology of IBD

A

aetiology of IBD unknown, but hypothesized to be a multifactorial disease

genetic predisposition, dysregulation in mucosal immune system and environmental trigger cause chronic inflammation in GI tract, resulting in IBD

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51
Q

UC vs CD overall severity

A

overall, CD is worse than UC, because CD has many complications (e.g. peri-anal disease, obstructions) and it can affect any part of the GI tract

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52
Q

Crohn’s location

rectal bleeding

diarrhea

abdominal pain

fever

palpable mass

recurrence after surgery

endoscopic features

Histologic features

Radiologic features

Complications

Colon cancer risk

A

Location- any part of GI tract
Small bowel + colon 50%
Small bowel only 30%
Colon only 20%

rectal bleeding uncommon

diarrhea less prevalent

abdominal pain post-prandial/colicky

fever common

palpable mass frequent (25%) RLQ

recurrence after surgery common

endoscopic features
Discrete aphthous ulcers
Patchy lesions
Pseudopolyps

Histologic features 
Transmural distribution with skip lesions 
Focal inflammation 
Sometimes non caseating granulomas 
Deep fissuring + aphthous ulcerations 
Strictures 
Glands intact 

Radiologic features
cobblestone mucosa
frequent strictures and fistulae
AXR: bowel wall thickening “string sign”

Complications
Strictures
Fistulae
Perianal disease

Colon cancer risk increased if >30% of colon involved

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53
Q

UC location

rectal bleeding

diarrhea

abdominal pain

fever

palpable mass

recurrence after surgery

endoscopic features

Histologic features

Radiologic features

Complications

Colon canc

A

Locationisolated to large bowel
always involves rectum, may progress proximally

rectal bleeding very common (90%)

diarrhea frequent small stools

abdominal pain pre-defecatory urgency

fever uncommon

palpable mass rare (if present, likely cecum full of stool)

recurrence after surgery none-post colectomy

endoscopic features
Continuous diffuse inflammation 
Erythema 
Friability 
Loss of normal vascular pattern 
Pseudopolyps 
Histologic features 
Mucosal distribution 
Continuous disease (no skip lesions) 
Granulomas absent 
Gland destruction, crypt abscess 

Radiologic features
Lack of haustra
Strictures rare and suggests complicating cancer

Complications
Toxic megacolon

Colon cancer risk increased except in proctitis

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54
Q

Common presentation of IBD

A
Symptoms
abdominal pain, frequent bowel movement, diarrhea
bloody stools
urgency
failure to thrive or weight loss

Extraintestinal manifestations of IBD

Derm- erythema nodosum, pyoderma grangenosum, perianal skin tags, oral mucosal lesions, psoriasis

Rheum
Peripheral arthritis, ank spondylitis, sacroiliitis

Ocular
Uveitis (vision threatening), episcleritis (benign)

Hepatobiliary
Cholelithiasis, PSC, fatty liver

Urologic
Calculi, ureteric obstruction, fistulae

Others 
VTE 
vasculitis 
osteoporosis 
vitamin deficiencies (B12, ADEK) 
Cardiopulmonary disorders 
Pancreatitis (rare) 

Most of these are more common in CD except sacroiliitis (equal)

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55
Q

Complications of IBD, their pathophysiology, clinical presentation, diagnosis and treatment

A
  1. Toxic Megacolon:

most commonly in UC

pathophysiology: inflammation result in colonic paralysis and obstruction with high risk of perforation

clinical presentation: fever, tachycardia, leukocytosis, peritoneal signs on abdominal exam

treatment: fluid resuscitation, NG tube, IV Solumedrol, immediate surgical colectomy
2. Bowel Perforation
pathophysiology: perforation of intestinal content into abdominal cavity, resulting in bacterial infection and peritonitis

clinical presentation: fever, chills, nausea & vomiting, severe abdominal distention, peritoneal signs on abdominal exam

diagnosis: free gas / air under diaphragm on X-ray
treatment: fluid resuscitation, IV antibiotics, surgery
3. Dysplasia
pathophysiology: IBD leads to dysplasia, which increase risk of colorectal carcinoma

clinical presentation: dysplasia associated lesion or mass (DALM) on endoscopy

treatment: surveillance colonoscopy, prophylactic colectomy in high risk patients

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56
Q

Crohn’s disease epidemiology

A

incidence 1-6/100,000, prevalence 10-100/100,000

common in Caucasian and Ashkenazi Jews

M=F

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57
Q

Crohn’s disease clinical presentation

A

recurrent abdominal cramps, diarrhea and weight loss

most commonly affect terminal ileum and ascending colon

ileitis: vomiting, post-prandial pain, RLQ mass

fistula, fissure, abscess

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58
Q

Crohn’s disease investigations

A

colonoscopy with biopsy

CT enterography for involvement of small bowel

elevated ESR and CRP

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59
Q

Crohn’s disease management

A

non-pharmacological: smoking cessation

anti-diarrheal: Loperamide (Imodium), Diphenoxylate (Lomotil)

mild CD: 1) antibiotics (Metronidazole or Ciprofloxacin); and 2) 5-ASA (5-Aminosalicyclic acid)

moderate CD: 1) steroid Prednisone or Budesonide; and 2) immune-modulator Azathioprine (AZA; Imuran), 6-Mercaptopurine (6-MP) or Methotrexate (MTX)

severe CD: surgery and / or biologics Infliximab (Remicade) or Adalimumab

surgery indicated in complications of fistula, obstruction, abscess, perforation, bleeding and medically refractory disease

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60
Q

Ulcerative colitis epidemiology

A

incidence 2-10/100,000, prevalence 35-100/100,000 (more common than Crohn’s)

M=F

inflammation to rectum or left colon more common

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61
Q

Ulcerative colitis clinical presentation

A

chronic abdominal cramps / pain with defecation, diarrhea and rectal bleeding

may have tenses, urgency, incontinence

systemic symptoms include fever, anorexia, weight loss and fatigue in severe cases

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62
Q

Ulcerative colitis clinical classification

A

mild UC: <4 stools / day and nothing else

moderate UC: >4 stools / day with minimal signs of toxicity (fever, tachycardia, anemia, high ESR)

severe UC: >6 stools / day and signs of systemic toxicity (fever, tachycardia, anemia, high ESR)

fulminant UC: >10 stools / day; continuous bleeding requiring blood transfusion; systemic toxicity (fever, tachycardia, anemia, high ESR); abdominal tenderness and distension; and
colonic dilation on abdominal plain film

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63
Q

Ulcerative colitis investigation

A

sigmoidoscopy with mucosal biopsy for diagnosis, which can be substituted with CT colonography

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64
Q

Ulcerative colitis management

A

total colectomy for refractory & severe UC, colonic stricture, life-threatening UC complications (severe bleeding, toxic megacolon, impending perforation), dysplasia or carcinoma

mild UC: 1) 5-ASA

moderate UC: 1) 5-ASA; and 2) steroid Prednisone or Budesonide

severe UC: 1) surgery; and 2) Cyclosporine

consider adding immunomodulator AZA or 6-MP; or biologics Infliximab for moderate to severe UC

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65
Q

General indications for surgery in IBD

A

severe disease: intractable symptoms and failure to respond to medical therapy, extra-intestinal manifestations, chronic disability, failure to thrive in children, poor quality of life

GI emergencies: toxic megacolon, bowel perforation, uncontrolled hemorrhage, bowel obstruction

structural abnormalities: fistula, stricture

infectious: abscess
malignancy: pre-cancerous lesions, colorectal cancer

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66
Q

General principles of surgery in IBD

A

surgeries can alleviate symptoms, address complications and improve quality of life

principle of to conserve as much bowel as possible (i.e. resect as little as possible to avoid short gut syndrome)

perioperative management:
a) optimize medical status with bowel rest, which may require TPN if >7 days of NPO

b) hold immune suppressive therapy pre-op, provide pre-op stress dose of corticosteroid if patient had recent steroid therapy, taper steroids post-op
c) DVT prophylaxis

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67
Q

Surgery in Crohn’s Disease specific indications

A

structural lesions (stricture, fistula): bowel resection and anastomosis (or stoma if active inflammation, perforation, fistula)

small bowel obstruction due to stricture or inflammation: bowel resection and anastomosis

stricture: stricturoplasty (widening of lumen in bowel stricture)
abscess: surgical incision and drainage

peri-anal disease: appropriate surgical treatment for types of peri-anal disease

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68
Q

Surgery in Crohn’s Disease complications

A

small bowel resection -> short bowel syndrome
short bowel syndrome if functional small intestine <50% or <200cm
short bowel syndrome = malabsorption disorder due to surgical removal of small intestine resulting in diarrhea, steatorrhea, malnutrition
symptoms: abdominal pain, diarrhea, steatorrhea, weight loss, malnutrition, fatigue
vitamin A, D, E, K, folic acid, B12, Ca, Mg, iron, zinc deficiency
hypo calcium increases risk of kidney stones

ileal resection -> watery diarrhea, steatorrhea, gall stones
<100cm resection cause watery diarrhea due to impaired bile salt absorption treated with cholestyramine or anti-diarrheal (Loperamide)
>100cm resection cause steatorrhea due to reduced mucosal surface area for fat absorption and bile salt deficiency treated with fat restriction and medium chain triglycerides
decreased bile absorption -> increased risk of gallstone

any abdominal surgery -> fistula, adhesions

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69
Q

Surgery in Crohn’s Disease prognosis

A

post surgical removal, 10 year recurrence rate: 25-50% in ileocolic region, 50% in small bowels, 50% in large bowels

proportion requiring re-operation due to recurrence: primary resection have 20% re-operation, bypass have 50% re-operation, stricturoplasty have 10% re-operation

80-85% of patients who require surgery will lead normal lives

post surgery, 15% mortality risk at 30 years

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70
Q

Surgery for UC indications

A

severe to fulminant UC: total colectomy with ileal pouch - anal anastomosis
can resect only portion of colon that is pathologic (e.g. proctocolectomy, rectal mucosectomy)

decrease colorectal cancer: total proctocolectomy

in surgical emergencies: total colectomy and ileostomy with Hartmann closure of rectum, rectal preservation

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71
Q

Complications of surgery in UC

A

early: anastomotic leak, dehydration from high stoma output, bowel obstruction, transient urinary dysfunction
late: stricture, anal fistula / abscess, pouchitis, poor anorectal function, infertility

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72
Q

Surgery for UC prognosis

A

post surgery, 5% mortality risk at 10 years

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73
Q

IBS epidemiology

A

prevalence of 20% in North America

females > males

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74
Q

IBS pathophysiology

A

likely due to visceral hypersensitivity with possible psychological or environmental trigger

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75
Q

IBS clinical presentation

A

GI symptoms: chronic abdominal pain or discomfort; chaotic defecation (period of normal bowel movement punctuated by episodes of constipation and / or diarrhea)

abdomen exam: unremarkable

80% IBS cases improve over time and have normal life expectancy

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76
Q

IBS diagnosis

A

diagnosis based on symptoms alone (Rome criteria) see Tony’s page 118

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77
Q

IBS subtypes

A

subtype of IBS based on consistency of stool and percentage of time

IBS-C = IBS with mainly constipation

IBS-D = IBS with mainly diarrhea

IBS-M = mixed IBS with some constipation or diarrhea

IBS-U = untyped IBS

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78
Q

IBS investigations

A

if benign history and physical exam, diagnosis clinically on Rome 3 criteria and no investigations required

additional investigations to be considered:

blood work: CBC, TSH, albumin, CRP, tTG

stool C & S O & P, fat excretion

sigmoidoscopy

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79
Q

Management of IBS

A

1) make positive diagnosis of IBS
comfort / reassure patient, address patient concerns and establish patient-doctor relationship to enhance placebo effect (most effective treatment)
explain, support, aim for realistic goals

2) diet and lifestyle advice
balanced and healthy diet
exercise
dietary fiber or fiber supplement for constipation
if lactose intolerance, restrict diary
if food intolerance, eliminate food from diet
reduce sorbitol, reduce fructose
avoid caffeine and alcohol

3) if suspected psychological trigger (anxiety, depression or phobia)
behavioural therapy
drugs
consider relaxation therapy, biofeedback, hypnosis, stress reduction

4) if severe symptoms, drugs to address the symptoms
pain: anti-spasmodic before meals (Hyoscine, Pinaverium, Trimebutine), tricyclic antidepressants (TCA), selective serotonin re-uptake inhibitor (SSRI)
diarrhea: Loperamide, Diphenoxylate, cholestyramine
constipation: osmotic or other laxatives

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80
Q

What is a peptic ulcer

A

defect (erosion, ulceration) of inner mucosal lining that penetrate muscularis mucosal layers of the stomach (gastric ulcer) or duodenum (duodenal ulcer)

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81
Q

Etiology of peptic ulcer

A

gastric acid is necessary for ulcer to form, but it does not cause peptic ulcer

1) H. pylori infection
H. pylori infection cause 60% gastric ulcer and 90% duodenal ulcer

2) NSAID
NSAID cause 35% gastric ulcer and 7% duodenal ulcer

3) gastric cancer
other: physiologic stress induced in severely ill patients, Zollinger-Ellison syndrome, chemotherapy or radiation ulcer, alcohol, CMV infection, ischemia, idiopathic

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82
Q

Peptic ulcer clinical presentation

A

GI symptoms: asymptomatic (70% cases), nausea, dyspepsia (classically worse with food in gastric ulcer and better with food in duodenal ulcer)

abdominal exam: usually benign exam, may have epigastric tenderness

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83
Q

Complications of peptic ulcers pathophysiology, symptoms, presentation, treatment

A

1) Upper GI Bleed (10-15% cases)
pathophysiology: erosion of ulcer into blood vessel (classically gastroduodenal artery by duodenal ulcer), causing upper GI bleeding
symptoms: hemetemesis, melena

treatment: ABC, fluid resuscitation, IV PPI, endoscope injection of epinephrine / cauterization / hemoclip, interventional radiology angiography with embolization / coiling, surgery if
severe or recurrent bleeding

2) Perforation (2% cases)
pathophysiology: erosion through entire lining, resulting in perforation through stomach or duodenum

symptoms: acute onset severe abdominal pain
abdominal exam: peritoneal signs

imaging: free air on X-ray (70% cases) or abdominal CT
treatment: surgery

3) Obstruction (2% cases)
pathophysiology: ulcer can cause inflammation & swelling or can heal & scar, which obstruct the GI tract, classically at gastric outlet by duodenal ulcer

symptoms: nausea & vomiting, abdominal pain, obstipation, constipation
abdominal exam: distended abdomen, succussion splash on auscultation, may have peritoneal signs if ischemia or perforation

treatment: NG decompression, correct fluid & electrolyte imbalance, high dose PPI therapy, surgery
4) Fistula / Penetration (<1% cases)

pathophysiology: ulcer can penetrate to adjacent organs, forming a fistula connecting the 2 organs
ulcer in duodenum can penetrate into pancreas, causing pancreatitis
gastric ulcer can penetrate into liver or colon, causing perforation

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84
Q

General indications for gastric and duodenal ulcer surgery

A

unresponsive to medical treatment (including endoscopy)

hemorrhage

perforation

obstruction

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85
Q

Peptic ulcer surgery procedures

A

gastrectomy = removal of portion of stomach usually with reconstruction (Billroth 1, Billroth 2, Roux-en-Y)

Billroth 1 = removal of pylorus and anastomosis of proximal stomach to duodenum

Billroth 2 = (removal of antrum and pylorus of stomach with) anastomosis of greater curvature of stomach to jejunum

Roux-en-Y = proximal segment of stomach anastomosis with jejunum, distal stomach to duodenum anastomosis with jejunum

vagotomy = transection or removal of portion of vagus nerve to decrease gastric secretion

pyloroplasty = widening of pylorus to facilitate gastric emptying

gastrojejunostomy = anastomosis between dependent portion of stomach to jejunum to facilitate gastric emptying

suture ligation = oversew of an vessel to stop bleeding

Pauchet procedure = distal gastrectomy extending along lesser curvature to include ulcer

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86
Q

Complications of peptic ulcer surgery

A

fistula, commonly gastrocolic, gastrojejunal fistulas

dumping syndrome

post-vagotomy diarrhea

afferent loop syndrome

87
Q

Specific indications for surgery for gastric ulcer

A

unresponsive to medical treatment (including endoscopy)

perforation

gastric dysplasia or carcinoma, usually based on endoscopic biopsy

failure to heal completely after medical treatment (due to risk of malignancy)

any hemorrhage (due to high risk of hemorrhage for gastric ulcer compared to duodenal ulcer)

88
Q

Types of gastric ulcers

A

type 1 gastric ulcer (most common) = along lesser curvature near function of fundus and antrum

type 2 gastric ulcer = combined gastric and duodenal ulcer

type 3 gastric ulcer = prepyloric ulcer

type 4 gastric ulcer = high along lesser curvature close to gastroesophageal junction

89
Q

Gastric ulcer surgery procedures

A

removal of ulcer:

type 1 ulcer requires distal gastrectomy with (Billroth 1 or 2) reconstruction

type 2 or 3 ulcer requires antrectomy and vagotomy with (Billroth 1 or 2) reconstruction

type 4 ulcer requires subtotal gastric resection or Pauchet procedure with Roux-en-y reconstruction

perforation: partial gastrectomy to include ulcer
hemorrhage: partial gastrectomy with (Billroth 1 or 2) reconstruction; or ulcer excision with trundle vagotomy and pyloroplasty

90
Q

Surgery for duodenal ulcer specific indications

A

unresponsive to medical treatment (including endoscopy)

perforation

failure to heal completely after medical treatment (due to risk of malignancy)

hemorrhage (large amount of blood loss >8 units, rate of bleeding, hemodynamic instability)

91
Q

Duodenal ulcer surgery procedures

A

perforation: oversew ulcer (plication) and omental (Graham) patch
hemorrhage: oversewing of ulcer and pyloroplasty
obstruction: antrectomy / distal gastrectomy; or vagotomy with drainage

elective surgery to reduce acid secretion: vagotomy, gastrectomy

92
Q

Treatment for peptic ulcer

A

no dietary recommendation

acid suppression: proton pump inhibitor (PPI) or histamine 2 receptor antagonist (H2RA)

if test positive for H. Pylori, eradication regimen:

1st line = triple therapy (PPI + Amoxicillin + Clarithromycin)

2nd line = quadruple therapy (PPI + bismuth + Tetracycline +
Metronidazole)

discontinue NSAID if possible

for gastric ulcer, repeat endoscopy after resolution to confirm that gastric ulcer healed (unhealing gastric ulcer suggests malignancy)

93
Q

What structure separates upper from lower GI bleed

A

Mouth to ligament of Treitz to anus

94
Q

Upper GI bleed epidemiology

A

upper GI bleed constitute majority (75%) of GI bleed

commonly affects males more than females

incidence increase with age

associated with mortality rate of ~10% (higher than lower GI bleed)

usually majority (80%) of upper GI bleed are self limited

95
Q

Upper GI bleed causes

A

from most common to less common causes:

1) peptic ulcer in 50% of cases

2) varices (esophageal or gastric) in 15% of cases
due to liver disease: portal hypertension, cirrhosis

3) arterial venous malformation (angiodysplasia) in 5% of cases
4) Mallory Weiss tears (tears at gastroesophageal junction from severe vomiting, retching or coughing) in 5% of cases
5) tumours in 5% of cases
6) erosions in 5% of cases

96
Q

Upper GI bleed clinical presentation

A

generally, upper GI bleed is more likely to present with hemodynamic instability due to rich blood supply of upper GI tract

Symptoms
hematemesis (bright red blood worse than coffee grounds)

melena from digested blood

increased bowel movement
blood is a laxative
increased frequency is indicator of rapidity of bleeding

hemodynamic symptoms
pre-syncope or syncope
orthostatic dizziness, lightheadedness
chest pain or dyspnea due to hypo perfusion of heart

hematochezia (red blood per rectum) i.e. massive rectal bleeding
hematochezia usually a sign of lower GI bleed, but can occur with brisk upper GI bleed
patient with upper GI bleed and hematochezia usually are hemodynamically unstable
if rectal bleeding, use NG tube lavage to rule out a brisk upper GI bleed, frank blood aspirated from NG lavage suggest brisk upper GI bleed and should be followed by EGD

other symptoms depend on cause: nausea, vomiting, dysphagia, heart burn, abdominal pain

97
Q

Lower GI bleed epidemiology

A

lower GI bleed constitute minority (25%) of GI bleed

associated with mortality rate of 2% (lower than upper GI bleed)

98
Q

Lower GI bleed causes

A

from most common to less common:

1) diverticular bleed in 33% of cases
2) colon cancer in 20% of cases
3) angiodysplasia in 10% of cases
4) ischemic colitis
5) brisk upper GI bleed

6) other inflammatory or ulcer causes
inflammatory bowel disease, ischemic bowel, vasculitis, infectious, radiation induced, NSAID induced

7) anorectal bleeding in 5% of cases
fissures, hemorrhoids
usually very small amount of blood (e.g. on toilet paper)

99
Q

Lower GI bleed clinical presentation

A

hematochezia (red blood per rectum)
blood can be bright red blood or dark / maroon
bright red blood suggest left colon as source
dark or maroon suggest distal small bowel or right colon as source
blood can be mixed inside stool or covering outside of stool
blood covering outside of stool suggest perianal source
blood mixed inside stool suggest right colonic source

change in bowel movement
increased frequency due to cathartic effect of blood
decreased form / consistency (diarrhea)

melena
melena usually a sign of upper GI bleed, but can occur in lower GI bleed if the source is the distal small bowel, cecum or right colon
patient with lower GI bleed and melena usually are hemodynamically stable with very slow bleeding
other symptoms depend on cause: fever, chills, weight loss, abdominal pain or cramps, fecal urgency, tenesmus, fecal incontinence
angiodysplasia and diverticular bleeding usually not painful
ischemic colitis very painful

100
Q

What can mimic melena

A

iron pills and bismuth (Peptol Bismol) can mimic melena

101
Q

Upper GI bleed symptoms, signs and labs

A

Symptoms - hematemesis, melena, usually acute

Signs - tend to be hemodynamically unstable, NG lavage of blood from suction

Labs - High [BUN x 10] : Cr ratio (>1.5)

102
Q

Lower GI bleed symptoms, signs and labs

A

Symptoms - hematochezia, usually chronic

Signs - tend to be hemodynamically stable, no NG lavage findings

Labs - Equal [BUN x 10] : Cr ratio (~1)

103
Q

Empiric upper GI bleeding management

A

if upper GI bleeding, then empiric IV PPI, IV somatostatin and pro kinetics

a) empiric IV PPI to treat possible peptic ulcer until EGD performed
PPI stabilize ulcer and promote clotting, shown to decrease need for endoscopic therapy and decrease risk
e.g. Esomeprazole 50mg IV bolus BID or Pantoprazole 40mg IV bolus BID

b) empiric IV somatostatin (Octreotide) to treat possible variceal bleed
somatostain vasoconstricts splanchnic arteries to decrease portal hypertension and thus decrease bleeding
e.g. Octreotide 50mcg bolus followed by 50mcg / hr infusion

c) prophylactic antibiotic therapy for patients with cirrhosis
prophylactic antibiotic can be any of the following
Ciprofloxacin 400-1000mg mg IV for 7 days
Ceftriaxone 1g IV daily for 7 days

d) pro kinetics (metoclopramide (Maxeran) or IV erythromycin) to prepare for EGD
pro kinetics clear UGI tract of blood for better visualization with scope
e.g. Erythromycin 3mg/kg IV over 20-30 minutes done 30-90 minutes prior to endoscopy

104
Q

Indications for urgent EGD

A

EGD urgent if any of the following

a) hemodynamically unstable
shock (systolic <100, heart rate >100, orthostatic hypotension)
hemoglobin <80
requires >2 packs of RBC transfusion
hematemesis

b) hematochezia in suspected upper GI bleed
c) suspected varices
d) serious comorbidity (malignancy or cirrhosis)

EGD is non-urgent in young and healthy patient with minimal bleeding

105
Q

Upper GI bleed EGD should be done when

A

within 24h

106
Q

Management if unclear if upper or lower GI bleed

A

treat empirically with medication (IV PPI, IV somatostatin, pro kinetics) as upper GI bleed

do EGD first, then colonoscopy

107
Q

Lower GI bleed colonoscopy should be done when

A

if lower GI bleeding, wait for bleeding to stop and then do colonoscopy

generally lower GI bleed less severe, so colonoscopy is not urgent

colonoscopy mainly diagnostic and not therapeutic, because it is difficult to identify source

108
Q

Alternatives to scope to find and stop bleeding

A

endoscopy always 1st line treatment for bleed

if endoscopy fails to identify source or failed to stop bleeding, then angiography (by interventional radiology) or RBC scan

Surgery
intra-operative enteroscopy by surgery
surgery = oversewing bleeding vessel and resection of bleeding segments within GI tract (e.g. vagotomy with pyloroplasty, partial gastrectomy)

109
Q

EGD endoscopic therapy for GI bleeding

A

endoscopy is diagnostic and therapeutic
endoscopy is definitive bleeding management for GI bleed

many methods for hemostasis by EGD
1) injection
injection of vasoconstrictor (epinephrine), saline, sclerosants or tissue adhesives

2) thermal therapy
electrocoagulation
laser photocoagulation

3) mechanical therapy
hemoclips, rubber bands
closure of vessel

110
Q

What is angiography and sensitivity and specificity

A

angiography is diagnostic and therapeutic done by IR

catheter through femoral artery to abdominal aorta and its branches

can inject dyes to find bleeding site

lower sensitivity, but higher specificity (can rule in)

can perform therapy by embolization

111
Q

What is RBC scan and sensitivity and specificity

A

RBC is diagnostic but not therapeutic

patient infused with radioactive tagged RBC

high sensitivity, but lower specificity (can rule out)

112
Q

Indications for surgery to stop upper or lower GI bleeding

A

hemodynamic instability including hypovolemic shock despite vigorous resuscitation

prolonged bleeding with transfusion requirement >3 units

failure of medical management

recurrent hemorrhage after initial stabilization procedure with >2 attempts of endoscopic hemostasis

peritonitis, suggestive of perforation

113
Q

Causes of acute abdomen

A

causes of bowel obstruction

small bowel obstruction: adhesion post abdominal surgery, hernia, malignancy (metastasis to small bowel)

large bowel obstruction: malignancy (colorectal cancer and metastasis), diverticular stricture, colonic volvulus

causes of peritonitis

inflammation / infection: pancreatitis, appendicitis, diverticulitis, pelvic inflammatory disease, large intra-abdominal abscess
bowel perforation
bowel obstruction
vascular: intra-abdominal hemorrhage (e.g. aortic aneurysm rupture, trauma, surgery, ectopic pregnancy), ischemic colitis

114
Q

Bowel obstruction pathophysiology

A

1) disruption of normal flow of intestinal contents cause upstream proximal intestinal dilatation and downstream distal decompression
proximal intestinal dilatation may cause bowel perforation

2) obstruction and dilatation may interrupt blood supply causing bowel ischemia via strangulation of blood supply or bowel wall inflammation
3) bowel wall edema from venous congestion and disruption of normal bowel absorption function from interruption of intestinal contents cause increased intra-luminal fluid and fluid loss into peritoneal cavity as well as electrolyte disturbance

115
Q

Complications of bowel obstruction

A

strangulating obstruction (10% of bowel obstruction), which is a surgical emergency

bowel perforation -> sepsis

hypovolemia from third spacing of fluids

116
Q

Clinical presentation of strangulating bowel obstruction

A

cramping pain -> continuous ache

GI bleed (hematemesis, melena)

fever

tachycardia

hypotensive shock

peritoneal signs

leukocytosis

117
Q

Types of bowel obstruction

A

small bowel obstruction = obstruction at small bowel

large bowel obstruction = obstruction at large bowel

pseudo-obstruction / ileus = obstruction due to dysfunctional peristalsis

118
Q
Clinical presentation of SBO: 
N/V
abdo pain
abdo distension
constipation
other 
bowel sounds 
AXR findings
A

N/V early, may be bilious

abdo pain colicky

abdo distension + (prox)< ++ (distal)

constipation +

other sometimes visible peristalsis

bowel sounds normal, increased or absent if secondary ileus

AXR findings air fluid levels, 'ladder' pattern (plicae circularis) 
proximal distension (>3 cm) + no colonic gas
119
Q
Clinical presentation of LBO: 
N/V
abdo pain
abdo distension
constipation
other 
bowel sounds 
AXR findings
A

N/V late, may be feculent

abdo pain colicky

abdo distension ++

constipation +

other sometimes visible peristalsis

bowel sounds normal, increased (borborygmi), absent if secondary ileus

AXR findings
air fluid levels
‘picture frame’ appearance
proximal distension + distal decompression
no small bowel air if competent ileocecal valve
coffee bean sign

120
Q
Clinical presentation of paralytic ileus: 
N/V
abdo pain
abdo distension
constipation
other 
bowel sounds 
AXR findings
A

N/V present

abdo pain minimal or absent

abdo distension +

constipation +

other

bowel sounds decreased, absent

AXR findings
air throughout small bowel and colon

121
Q

What is borborygmi

A

a rumbling or gurgling noise made by the movement of fluid and gas in the intestines.

122
Q

Bowel obstruction investigations

A

Labs:
if emesis, venous blood gas, which may show metabolic alkalosis

if suspected strangulation, lactate and LDH, which may be elevated in ischemia

Imaging:
Upright chest X-ray for free air under diaphragm, suggestive of bowel perforation

abdominal X-ray (3 views, AP, lateral decubitus, upright) may show dilated bowel loops, air fluid levels

abdominal CT can confirm obstruction and determine structural cause for obstruction

upper GI series / small bowel series for small bowel obstruction if no apparent cause

rectal water soluble Gastrografin enema

123
Q

Small vs large bowel obstruction on abdominal xray

A

abdominal series enough to diagnose small bowel obstruction 60% of time

obstructed small bowel:

  1. plicae circularis that go the whole way across the intestine
  2. have a thicker wall (white line border)
  3. located in middle of abdomen
  4. smaller in diameter
  5. supine abdomen X-ray: distended loop of small bowel and collapsed colon
    increased risk of perforation if small bowel diameter >3cm
  6. normal (unobstructed) small bowel is not clearly visible on X-ray, because it is white and loops around one another

obstructed large bowel
1. striae that do not go all the way across the intestine

  1. have thinner wall (no white line border)
  2. located around the abdomen
  3. larger in diameter
124
Q

bowel obstruction diagnosis

A

diagnosis confirmed by abdominal series X-ray (supine, upright, left lateral decubitus) and CT (if still unclear on abdominal X-ray)

125
Q

bowel obstruction general management

A
  1. stabilize patient
  2. NPO, suck (NG tube) and drip (IV fluids)
    NG tube to relieve vomiting, prevent aspirations and decompress small bowel
    IV fluid resuscitation due to fluid loss in intestine and peritoneal cavity
  3. correct electrolyte abnormalities
  4. Foley catheter to monitor fluid output
  5. surgery for correctable cause or non-resolving cases
126
Q

Small bowel obstruction top 3 causes

A

top 3 causes = ABCs

1) A = adhesion (from previous abdominal surgery)
2) B = bulge i.e. hernia (incarcerated / strangulated)
3) C = cancer, commonly metastasis to small bowel (e.g. melanoma)

127
Q

Intraluminal causes of SBO

A

Intussusception

Gallstones

128
Q

Intramural causes of SBO

A

Crohn’s

Radiation stricture

Adenocarcinoma

129
Q

Extramural causes of SBO

A

Adhesions

Incarcerated hernia

Peritoneal carcinomatosis

130
Q

Clinical presentation of small bowel obstruction

A

symptoms: nausea & vomiting, bloating, diffuse cramp abdominal pain, constipation, obstipation (not passing gas)

abdominal exam: distended abdomen, high pitched bowel sound, hyper-resonant / tympanic abdomen, no localized tenderness, no peritoneal signs

131
Q

Mortality in small bowel obstruction

A

mortality: <1% in uncomplicated small bowel obstruction; 10% with strangulation; 50% with ischemia

132
Q

Small bowel obstruction labs

A

CBC: normal or slightly high WBC

electrolytes: low Cl, low K, metabolic alkalosis due to vomiting

133
Q

Indications for surgery in SBO

A

small bowel obstruction with history of abdominal / pelvic surgery with no resolution in 2-3 days

small bowel obstruction with no previous surgery and no evidence of carcinomatosis

complete bowel obstruction

complications: strangulation, perforation

134
Q

Indications for conservative management in SBO

A

small bowel obstruction with history of abdominal / pelvic surgery for the first 2-3 days (70% chance of spontaneous resolution)

Crohn’s disease

recurrent small bowel obstructions

carcinomatosis

majority of small bowel obstruction will resolve in 12-24 hours with conservative treatment

135
Q

LBO top 3 causes

A

top 3 causes

1) colorectal cancer
2) diverticular stricture
3) colonic volvulus (5-10% of large bowel obstruction)

136
Q

LBO intraluminal causes

A

Constipation

137
Q

LBO intramural causes

A

Adenocarcinoma

Diverticulitis

IBD stricture

Radiation stricture

138
Q

LBO extramural causes

A

Volvulus

Adhesions

139
Q

LBO clinical presentation

A

history: history or presentation of colorectal cancer (melena, blood per rectum, change in bowel habit, decreased caliber of stool, incomplete emptying, soiling underwear)

same presentation as small bowel obstruction

140
Q

LBO mortality

A

mortality: 10% in uncomplicated large bowel obstruction; 20% with perforation and feculent peritonitis

141
Q

LBO investigations

A

1) Abdominal X-ray

dilated colon
increased risk of perforation if distal colon >6cm; proximal colon >9cm; cecum >12cm

distinguish between closed loop vs. open loop
closed loop (80-90% cases) = competent ileocecal valve blocking air in colon from entering small bowel
small bowel is not dilated in closed loop
closed loop has a high risk of ischemia -> necrosis -> perforation and is a surgical emergency

open loop (10% cases) = incompetent ileocecal valve allowing air in colon from entering small bowel
small bowel dilated in open loop

2) Abdominal CT
abdominal CT can differentiate between causes of large bowel obstruction by visualization of site and structural cause for obstruction

3) Colonoscopy
colonoscopy can assess for cancer

142
Q

LBO management

A

if closed loop obstruction, then urgent surgery to correct underlying cause

if sigmoid volvulus, then colonoscopy decompression followed by delayed surgical sigmoid resection, or surgical reduction if colonoscopic decompression
unsuccessful

143
Q

What is the pathophysiology of a contained perforation

A

full thickness perforation of well wall but free spillage of intestinal contents and air is prevented because a nearby organ walled off the perforated area

144
Q

What is the pathophysiology of a free perforation

A

perforation of bowel wall resulting in leakage of intestinal contents and air into the peritoneal space, which cause infection and inflammation of the peritoneal cavity
(peritonitis)

145
Q

Bowel perforation management

A

1) stabilize patient, ensuring ABC
aggressive fluid resuscitation (boluses 2L NS or RL IV) to maintain blood pressure and hydration status
correct any electrolyte abnormalities
monitor fluid status

2) empiric antibiotic coverage
broad IV antibiotic coverage for intestinal flora (gram negatives and anaerobes), which can be any of the following
Ceftriaxone + Metronidazole OR
Piperacillin-Tazobactam

3) surgery as definitive treatment to correct perforation and underlying cause
exploratory laparotomy, closure of perforation (e.g. resection of perforated bowel segment and anastomosis), peritoneal wash

146
Q

Toxic megacolon causes

A

inflammatory: ulcerative colitis, Crohn’s disease
infectious: bacterial colitis (C. difficile, Salmonella, Shigella, Campylobacter), vital colitis (cytomegalovirus), parasite (E. histolytica)
mechanical: volvulus, diverticulitis, ischemic colitis, obstructing colon cancer

147
Q

Toxic megacolon pathophysiology

A

extension of inflammation into smooth muscle layer of colon bowel wall causing paralysis of peristalsis, resulting in dilatation of colon increasing risk of bowel perforation

148
Q

Toxic megacolon clinical presentation

A

symptoms: abdominal distention, abdominal tenderness, diarrhea, hematochezia
vitals: may be septic (fever, tachycardia, hypotension, tachypnea)

abdominal exam: distended abdomen, peritoneal signs (rigidity, guarding, rebound tenderness) if perforation

149
Q

Toxic megacolon mortality

A

mortality: 25-30% mortality rate

150
Q

Toxic megacolon imaging

A

abdominal X-ray: dilated colon (>12cm in right colon, >6cm in transverse colon, >9cm in left colon), loss of haustra, thumb printing sign

abdominal CT with IV contrast: visualization of underlying cause of toxic megacolon

151
Q

Toxic megacolon diagnosis

A

patient diagnosed with toxic megacolon if patient has all of the following criteria

  1. some systemic manifestations: fever, tachycardia, hypotension, altered level of consciousness, leukocytosis, anemia, fluid and electrolyte imbalance
  2. radiologic evidence of dilated colon
152
Q

Toxic megacolon management

A

1) stabilize patient

2) prevent worsening of colon dilatation
NPO, NG tube
stop constipation agents

3) empiric antibiotic coverage
broad IV antibiotic coverage for intestinal flora (gram negatives and anaerobes), which can be any of the following:
Ceftriaxone + Metronidazole or
Piperacillin-Tazobactam

4) treat underlying cause
aggressive treatment of underlying disease
e.g. systemic steroids in inflammatory bowel disease
e.g. antibiotic therapy for infectious colitis

5) monitoring
monitor with serial abdominal X-rays

6) surgery if indicated
surgery = subtotal colectomy and end ileostomy (may have 2nd operation for re-anastomosis later)

153
Q

Indications for surgery in toxic megacolon

A

worsening or persistent systemic toxicity or colon dilation after 48 to 72 hours

severe hemorrhage

bowel perforation

high lactate and WBC

154
Q

Volvulus definition

A

volvulus = rotation of a bowel segment about its mesenteric axis

155
Q

Volvulus most common type

A

sigmoid (65%) > Cecum (30%) > transverse colon (3%) > splenic flexure (2% case)

156
Q

Volvulus risk factors

A
elderly, where age predisposes to stretching and elongation of bowel
high fibre diet
chronic constipation
laxative abuse
pregnancy
bedridden
institutionalization
congenital hypermobile cecum
157
Q

Volvulus clinical presentation

A

symptoms: nausea & vomiting, colicky abdominal pain, obstipation, constipation

abdominal exam: distended abdomen, may have peritoneal signs

158
Q

Volvulus imaging

A

abdominal X-ray: signs of large bowel obstruction

sigmoid volvulus = coffee bean with central cleft pointing to LLQ

cecal volvulus = coffee bean with central cleft pointing to RLQ

omega sign, bent inner tube sign

abdominal CT: can diagnose volvulus not visualized on abdominal X-ray

barium enema: ace of spades or birds beak sign

159
Q

Volvulus management

A

a) sigmoid volvulus
non-surgical: flexible sigmoidoscopy decompression and insertion of rectal tube past obstruction, followed by subsequent elective surgery due to 50-70% recurrence if no surgery
surgical: left hemi-colectomy + ileotransverse colonic anastomosis

b) cecal volvulus
non-surgical: colonoscopy detorsion and decompression
surgical: right hemi-colectomy and ileotransverse colonic anastomosis

160
Q

What is tenesmus

A

sense of incomplete emptying in rectum

161
Q

Physical exam for peri-anal disease should include

A

inspection of peri-anal area

DRE

proctoscope (anoscope) for examination of inner anal canal

rigid sigmoidoscope for examination of rectum

162
Q

Visualization characteristics of hemorrhoids

A

pain, lump, painless bleeding

163
Q

Visualization characteristics of anal/colorectal cancer

A

lump, bleeding mixed with faeces

164
Q

Visualization characteristics of anal fissure

A

pain with bowel movement, bleeding on toilet paper

165
Q

Visualization characteristics of peri-anal abscess

A

lump, pain, signs of infection (skin swelling, erythema, tenderness, warmth, fluctuance), drainage

166
Q

Peri-anal disease differential diagnosis

A

mechanical: anal fissure
infection: peri-anal / ischiorectal abscess, pilonidal sinus, anal herpes, peri-anal warts
neoplastic: anal cancer, colorectal cancer, colorectal polyps
vascular: peri-anal hematoma, hemorrhoids

167
Q

Hemorrhoids epidemiology

A

5-30% prevalence in general population

168
Q

Hemorrhoids risk factor

A

pregnancy

spinal injured population

169
Q

Hemorrhoids anatomy

A

hemorrhoids are part of the normal human anatomy
in normal anatomy, hemorrhoids are cluster of cushion

made of vascular tissue, smooth muscle and connective tissue lined by epithelium of anal canal
hemorrhoids contain many arterio-venous channels

hemorrhoid cushions located an right anterior, right posterior and left lateral, acting as conformable plug that contribute to resting anal pressure and continence
cushions at 3, 7, 11 o’clock position when examining patient in lithotomy position

there are external and internal hemorrhoids

external hemorrhoids
arise from external hemorrhoidal plexus
below the pectinate line
covered by squamous epithelium
somatic innervation, so can feel pain
drain by inferior rectal vein to IVC

internal hemorrhoids
arise from superior and middle hemorrhoidal plexus
above the pectinate line
covered by columnar epithelium
sympathetic innervation, so cannot feel pain
drain through superior rectal vein to portal system

170
Q

Hemorrhoids pathophysiology

A

hemorrhoids only cause symptoms when they swell and prolapse

1) swelling of hemorrhoid cushions
increased anal resting pressure (from straining, prolonged toilet time or inadequate fiber) may cause hemorrhoid swelling

2) swelling dilate and engorge the arteriovenous plexus inside hemorrhoid
long term blood engorgement can cause thrombosis of hemorrhoids

3) engorged arteriovenous plexus stretch suspensory muscle and may lead to prolapse of hemorrhoid through anal canal or bleeding through erosion

171
Q

Hemorrhoids clinical presentation

A

symptoms mainly from stretched suspensory muscle and engorged arteriovenous plexus

internal hemorrhoids: swelling, rectal fullness, pruritus, prolapse, painless rectal bleeding (bright red coating stool at end of defecation or drip into toilet)

prolapsed internal hemorrhoids: mild fecal incontinence, mucus discharge, wetness, sensation of fullness in peri-anal area

external hemorrhoids: swelling, pain after bowel movement, itchiness, peri-anal mass

thromboses external hemorrhoids: acute pain, hard lump that cannot be pushed back inside, may leave pari-anal skin tag after resolution within 2 weeks
DRE: tender palpable hemorrhoids if thrombosed

172
Q

Internal hemorrhoids classification

A

management depend on grading of internal hemorrhoid

grade 1: cushion protrude into lumen of anal canal, which is only visualized on anoscope

grade 2: prolapse beyond external sphincter, but spontaneously reduce

grade 3: prolapse beyond sphincter and require manual reduction

grade 4: irreducible prolapse

173
Q

Hemorrhoids diagnosis

A

hemorrhoids are a diagnosis of exclusion

all suspected hemorrhoids should be scoped (anoscopy) to rule out fissure, fistula, abscess, anal cancer, colorectal cancer, rectal varices

174
Q

Hemorrhoids management

A

1) conservative treatment (for all hemorrhoids)
lifestyle modification: Sitz bath, improved anal hygiene, avoid constipation & diarrhea, increased fibre & fluid intake

topical treatment: topical treatment to alleviate pain, which include local anesthetics Parmoxine (Anusol), corticosteroids, vasoconstrictor, antiseptics, protectants

2) non-surgical treatment (grade 2 internal hemorrhoids)
rubber band ligation
sclerotherapy (injection of agent to form scar)

3) surgical treatment (grade 3-4 internal hemorrhoids)
surgery is most effective and have lowest recurrence but have the highest complication rate
surgery = hemorrhoidectomy or stapled hemorrhoidectomy or Doppler guided hemorrhoidal artery ligation

175
Q

Hemorrhoid surgery indications

A

refractory to non-surgical treatment

large external hemorrhoids or mixed internal-external hemorrhoids with significant prolapse

grade 3 or 4 hemorrhoids

176
Q

Hemorrhoid surgery complications

A

fecal incontinence

177
Q

Treatment of thrombosed hemorrhoids

A

if within first 2 days of thrombosis, then surgical decompression, otherwise medical treatment as above

178
Q

Perianal abscess risk factors

A
smoking
diabetes type 2
obesity
male
previous episode of peri-anal abscess
179
Q

Perianal abscess causes

A

moss commonly crypto glandular abscess

other causes: Crohn’s disease, tuberculosis, actinomycosis, lymphogranuloma venereum, radiation, leukemia

180
Q

Perianal abscess pathophysiology

A

1) anal crypts at pectinate line become obstructed
the anal glands drained by crypts are also obstructed

2) glandular secretion become static, resulting in infection
usually bacterial infection by e. coli, proteus, streptococcus, staphylococcus, bacteroides, anaerobes

3) infection lead to formation of pus and abscess
over time, abscess may drain pus through spontaneously formed sinus tracts from abscess to epithelium layer of skin or anal canal

181
Q

Perianal abscess common comorbid entity

A

over time, 50% abscess will have fistula

182
Q

Location of anal duct infection

A

from most common to least common location: perianal (60% cases), ischiorectal (20% cases), inter-sphincteric (5% cases), supra-levator (5% cases)

ischiorectal abscess = abscess in ischiorectal fossa

inter-sphincteric abscess = abscess in inter-sphincteric groove between internal and external sphincter

supra-levator abscess = abscess above levator ani muscle

horseshoe abscess = ischiorectal abscess around anal canal

183
Q

Perianal abscess clinical presentation

A

symptoms: dull peri-anal discomfort or pain out of proportion, pruritus, pain with defecation / sitting, purulent discharge, constitutional symptoms (fever, chills)
signs: rectal exam may show signs of infection (skin erythema, swelling, tenderness, warmth), fluctuate and tender mass, may have drainage through sinus

DRE: palpable inter-sphincteric abscess or sinus tracts

184
Q

Perianal abscess investigation

A

CT or MRI if suspected non-palpable abscess or deep abscess (i.e. not peri-anal) to differentiate ischio-rectal abscess vs. inter-sphincteric abscess vs. supra-levator abscess

185
Q

Perianal abscess diagnosis

A

peri-anal abscess diagnosed based on clinical history and physical exam

186
Q

Perianal abscess management

A

incision and drainage of abscess, which is more effective in OR than ER

consider fistulotomy in horseshoe abscess

antibiotics Cephalexin PO indicated if diabetic, immunocompromised, valvular heart disease or important cellulitis

187
Q

Fistula-in-Ano (Anal Fistula) definition

A

fistula = abnormal connection (tract) connecting 2 epithelial surfaces

fistula in ano is a hollow tract connecting an internal opening inside the anal canal to an external opening in peri-anal skin

188
Q

Fistula-in-Ano (Anal Fistula) causes

A

anal fistula almost always caused by previous anorectal abscess that drained to the peri-anal skin

other causes include: post-operative incision & drainage of abscess, trauma, malignancy, radiation proctitis

189
Q

Fistula-in-Ano (Anal Fistula) location

A

based on Parks classification

Intersphincteric fistula (Parks Type 1)

Transphincteric fistula (Parks Type 2)

Suprasphincteric fistula (Parks Type 3)

Extrasphincteric fistula (Parks Type 4)

190
Q

Fistula-in-Ano (Anal Fistula) clinical presentation

A

previous history of painful and swollen abscess that drained spontaneously or surgically

symptoms: peri-anal discharge, pain, swelling, may have rectal bleeding, diarrhea, skin excoriation

inspection of entire perineum: external opening in perianal skin

DRE: induration, palpable fibrous sinus tract

191
Q

Fistula-in-Ano (Anal Fistula) investigations

A

no investigations needed for diagnosis

ultrasound, CT or MRI indicated only if complex peri-anal inflammation (e.g. Crohn’s disease)

192
Q

Fistula-in-Ano (Anal Fistula) diagnosis

A

diagnosis based on inspection of tract opening on peri-anal skin with history of previous abscess drainage

193
Q

What is Goodsall’s Rule

A

For anorectal fistulas

fistula with anterior external opening (on skin) follow straight tracts

fistula with posterior external opening (on skin) follow curved path to internal opening at midline (primary opening in crypt)

194
Q

Fistula-in-Ano (Anal Fistula) management

A

surgical intervention under anesthesia sealing the fistula (any of the options below)

fistulotomy, which is surgical unroofing of fistula tract from external to internal opening, allowing drainage and healing by secondary intention

fibrin sealant

insertion of Seton (string threaded through fistula)

fistula plug

mucosal advancement flap (flap of muscle covering external fistula tract opening)

195
Q

Anal fistula surgical complications

A

recurrence

fecal incontinence

196
Q

Anal fistula post-op care following surgery

A

Sitz baths

Irrigation and packing to ensure healing proceeding from inside to outside

197
Q

Anal fissure definition

A

tear in the anoderm distal to the pectinate line

198
Q

Anal fissure epidemiology

A

risk factors include local trauma (passage of hard stool, prolonged diarrhea, vaginal delivery, anal sex)

199
Q

Anal fissure causes

A

midline fissure: trauma that stretch anal mucosa

non-midline fissure: Crohn’s disease, neoplasm, infection (tuberculosis, syphilis, HIV)

200
Q

Anal fissure midline pathophysiology

A

1) stretching of anal mucosa beyond its normal capacity
2) stretching tears the anal mucosa, exposing the internal sphincter and forming the fissure
3) the internal sphincter undergo spasm due to damage
4) spasm of internal sphincter pulls apart the edges of the fissure
5) spasm decrease blood flow from posterior portion

201
Q

Anal fissure clinical presentation

A

symptoms: painful rectal bleeding (on toilet paper), pain with bowel movement, pruritus

inspection of anus: fissure in posterior midline (90% cases) or anterior midline (10% cases), chronic fissure (anal ulcer) triad of fissure + sentinel skin tags + hypertrophied papillae

DRE: sphincter spasm

202
Q

Anal fissure treatment

A

1) Conservative treatment
prevent constipation and straining: stool softener, bulking agents
symptomatic relief: Sitz bath
relaxation of internal anal sphincter to promote healing: topical calcium channel blocker, topical nitroglycerin, botox

2) Surgical treatment
lateral internal sphincterotomy to relieve sphincter spasm to increase blood flow and promote healing

fissurectomy

anal advancement flap

surgery increase risk of fecal incontinence

203
Q

Peri anal complications of Crohn’s Disease

A

~40% of patients with Crohn’s disease have peri-anal disease, which can include any of the following

anal fissure

peri-anal abscess and anal fistula

recto-vaginal fistula

anal stenosis

hemorrhoids

adenocarcinoma, which can occur in fistula tracts

peri-anal skin excoriation, skin tags

204
Q

Anal tumours anatomy

A

anal tumors classified based on anal canal vs. anal margin

anal margin = below / distal to anal verge
anal canal = above / proximal to anal verge

inner lining of anal canal is mucosa, which give rise to anal cancer (squamous cell carcinoma)

glands and ducts are found under mucosa in anal canal, which give rise to adenocarcinoma

rectum = columnar cells -> transitional zone = transitional cells -> below dentate line = squamous cells -> outside anal verge = skin cells

205
Q

Types of anal tumours

A

types of anal tumor can be differentiated based on appearance on inspection or pathology from biopsy

1) Benign tumors
inflammatory polyps
lymphoid polyps
hypertrohied anal papillae
skin tags
anal warts (condylomas)
adnexal tumor
leiomyoma
granular cell tumor
hemangioma
lipoma
Schwannomas
2) Malignant tumors
pre-cancerous lesions: anal intraepithelial neoplasia
squamous cell carcinoma
adenocarcinoma
skin: basal cell carcinoma, melanoma
GI stromal tumor
206
Q

Anal tumour by anatomical position

A

anal canal tumors: anal intraepithelial neoplasia, polyp, squamous cell carcinoma, adenocarcinoma

anal verge tumors: Bowen’s disease (squamous cell carcinoma), Paget’s disease (adenocarcinoma), squamous cell carcinoma, basal cell carcinoma, Kapok’s sarcoma, giant condyloma

207
Q

Anal cancer epidemiology

A

uncommon cancer, but incidence increasing

common in elderly (age >60)

208
Q

Anal cancer risk factors

A

HPV (type 16 and 18)

inflammatory bowel disease (Crohn’s)

sexual activity (increased sexual partners)

HIV, especially in men who have sex with men

chronic immunosuppression

smoking

family history of anal or colorectal cancer

209
Q

Anal cancer types

A

majority of anal cancer are squamous cell carcinoma

anal cancer can also be adenocarcinoma, basal cell carcinoma, lymphoma, melanoma, kaposi’s sarcoma or giant condyloma

210
Q

Anal cancer clinical presentation

A

anal cancer presents similar to hemorrhoid

rectal bleeding (bright red blood, usually on toilet paper) in 45% cases

anarectal pain or sensation of rectal mass in 30% cases

change in bowel habits: constipation, diarrhea or different caliber of stool

prolapsing sensation

lump near anus

fecal incontinence

itching or discharge from anus

constitutional symptoms: weight loss

inspection from rectal exam or scope (anoscopy, rigid sigmoidoscopy) can show a rough, bulky and friable mass (which is different from hemorrhoids that are smooth)

211
Q

Anal cancer investigations

A

Rigid sigmoidoscopy or anoscopy

Colonoscopy

CT colonography

212
Q

Anal cancer diagnosis

A

usually diagnosis based on pathology of biopsy via endoscope (anoscopy or rigid sigmoidoscopy)

213
Q

Anal cancer management

A

surgery only if stage 1 (T1N0M0)

chemotherapy with radiotherapy for almost all anal cancer (Nigro regimen)
5-FU
mitomycin or cisplatin
intermediate dose of radiotherapy

abdominal perineal resection if patient has any of the following:
recurrent disease that is resistant to chemotherapy and radiation is not recommended
persistent disease