Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

pathology > GI Pathology > Flashcards

GI Pathology Flashcards

1
Q

Failure of facial prominences to fuse, there are 5 facial prominences , the maxillary and medial nasal fail to fuse

A

Cleft lip and palate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Painful superficial ulceration of oral mucosa that arises with stress and resolves spontaneously it is characterised by greyish based surrounded by erythema

A

APTHOUS ULCER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Recurrent apthous ulcers, genital ulcers and uveitis (triad) which happens due to immune complex vasculitis involving small vessels

A

Behcet syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Primary infection occurs in childhood causing shallow painful red ulcers

A

herpes simplex virus 1 - oral herpes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

After primary infection with HSV1 what happens to the virus?

A

Stays dormant in the ganglia of trigeminal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What reactivates dormant HSV1?

A

Stress and sunlight cause reactivation leading to vesicles on lips (COLD SORES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Malignant neoplasm of squamous cells lining mucosa

A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the major Risk factors of squamous cell carcinoma?

A

Tobacco smoke and alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the most common location of squamous cell carcinoma?

A

Floor of the mouth is the most common location

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are leukoplakia and erythroplakia?

A

Precursor lesions of squamous cell carcinoma, they need to be biopsied to rule out the carcinoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What can be confused with leukoplakia?

A

Oral candidiasis a white patch on the mouth which can be easily scrapped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

A patch on the lateral tongue due to EBV in immuno compromised

A

Hairy leukoplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does a true leukoplakia present with

A

True leukoplakia is presented with hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Leukoplakia + blood vessels which indicate angiogenesis

A

Erythroplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Is leukoplakia or erythroplakia more likely to have dysplasia

A

Erythroplakia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Presents with bilateral inflamed parotid glands can also cause orchitis, pancreatitis and aseptic meningitis

A

Mumps
Orchitis has a risk of sterility in teens
Pancreatitis + inflamed parotid glands cause increase in serum amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

A stone obstruction in salivary glands is called

A

Sialolithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Inflammation of salivary glands due to an obstructing stone (sialolithiasis) leading to S. Aureus infection

A

Sialadenitis - usually unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q
  • Benign tumour composed of stromal and epithelial tissue which usually arises in the parotid.
  • mobile painless circumscribed mass at angle of the jaw
  • no invasion of facial nerve
  • has high risk of reoccurring due to irregular borders
A

Pleomorphic adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Most common tumour of salivary glands

A

Pleomorphic adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

When a tumour has for example - stromal (eg.cartilage) and epithelial tissue(eg glands) what is it called?

A

biphasic two types of tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

How often does pleomorphic adenoma become carcinoma and what is an indication?

A

It rarely does and damage to (facial nerve)CN VII ~palsy is the indicator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Benign cystic Timor with abundant lymphocytes with lymph node tissue and germinal centres that almost always happens in parotid glands

A

Warthin tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What the second most common salivary gland tumour that is common for smokers

A

Warthin tumour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Malignant tumour composed of MUCINOUS AND SQUAMOUS CELLS, that usually arise in parotid commonly INVOLVED FACIAL NERVE - that usually reoccurs

A

Mucoepidermoid carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q 
A congenital defect presents in new born as 4 issues 
•vomiting 
•polyhydraminous 
•abdominal distension 
•aspiration
A

Tracheoesophageal fistula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mucosa protrudes in to the lumen causing dysphasia and increased risk for oesophageal squamous cell carcinoma
•seen in Plummer Vinson syndrome with severe Fe deficiency and beefy red tongue

A

ESOPHAGEAL WEB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q
  • A false esophageal diverticulum of the mucosa and the muscular wall
  • arises above the upper esophageal sphincter at junction of esophageal and pharynx
  • presents with dysphagia and halitosis (bad breath due to food trapping and rotting)
A

Zenker diverticulum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q
  • longitudinal laceration of mucosa at gastro esophageal junction which is due to increased vomiting caused by bulimia and alcoholism
  • presents with painful hematemesis
  • risk of boerhaave syndrome (rupture of esophagus)
A

Mallory-Weiss syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q
  • Dilated submucosal vein in lower esophagus which arises secondary due to portal HTN
  • risk of rupture cuasing painless hematemisis
A

Esophageal varices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Most common cause of death from liver cirrhosis

A

Esophageal varices - the veins will rupture and the cirrhotic liver has couagulopathy so can’t close the bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Reflex of acid from stomach due to reduced tone of lower esophageal sphincter

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Risk factors of GERD

A

Alcohol, tobacco, obesity, fat rich diet, caffeine and hiatal hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How can hiatal hernia cause GERD

A

The diaphragm is important in maintaining the lower esopageal sphincter tone, so in diaphragmatic hernia the stomach can herniate in to the thorax and most common type is sliding hiatal hernia the stomac wil S herniate in to the esophagus and allowing for reflux and giving the hour glass appearance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Patient presents with heartburn (mimics cardiac chest pain) adult onset asthma and cough and damage to enamel teeth ulceration and meta plasma causing Barrett esophagus

A

GERD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Esophageal metaplasia from squamous cells to non ciliated Columnar epithelium with goblet cells

A

Butters esophagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Type is esophageal carcinoma

A

Adenocarcinoma and squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Most common esophageal carcinoma in the west occurs from metaplasia of burret esophagus occurring at the lower 1/3 of esophagus

A

Adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q
  • Malignant proliferation of squamous cells
  • most common esophageal cancer world wide and arises in the top 2/3 of the oesophagus due to irritation (eg hot tea, alcohol, tobacco, achalasia)
A

Squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

•Can’t relax lower esophageal sphincter and disordered motility leading to dysphagia and dilation due to food building up
• bird beak esophagus
•caused by ganglion cells damage of the mycenteric plexus
Cells damaged idiopathic or by chagas
•dysphagia, bad breath, LES pressure increase and increased risk of squamous cell carcinoma due to rotting food irritation of wall

A

Achalasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Lymph node cancer spread in 3 quarters of the esophagus

A

Upper 1/3 -> cervical nodes
Middle1/3-> mediastinal and tracheobronchial nodes
Lower 1/3 -> gastric and celiac nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

A congenital malformation of the abdominal wall leads to exposure of the abdominal content
“A hole in the abdominal wall”

A

Gastroschisis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

A congenital malformations - Persistent herniation of bowel in to the umbilical cord due to failure of herniated intestines to return to body cavity during development
• content are covered by peritoneum and amnion of umbilical cord

A

Omphalacele

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Congenital defects that develops after 2 weeks after birth~ it causes projectile non bilious vomiting as good can’t pass through the stenosis so it shoots back
• visible peristalsis with olive like mass in the abdomen
•hypertrophy of smooth muscle

A

Pyloric stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Acid damage to mucosa due to imbalance between acidic environment and mucosal defences

A

Acute gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Epithelial foveolar cells protect by producing - mucosa , increase HCO3- secretion and normal blood supply (absorbing acid and supply nutrients)

A

Mucosal defended

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Severe burn causing an ulcer due to hypovolemia less blood flow to the stomach and decreased nutrient supply and acid sweeping

A

Curling ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Risk factors of stomach ulcers

A 
NSAIDs 
chemotherapy 
Heave alcohol consumption 
Shock causes stress ulcers 
Severe burns (curling ulcer)
Increased intracranial pressure (Cushing ulcer)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q 
Incrwases intra cranial pressure leads to Increases vagal stimulation -> ach release which binds to parietal cells to secrete 
1) achR 
2) gastrin r
3) his r 
Leading to increased acid
A

Cushing ulcer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Acid damage to stomach results in

A

Superficial inflammation
Erosion (loss of epithelium)
Ulcer (loss of mucosal layer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Chronic inflammation of stomach mucosa

A

Chronic gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

types of Chronic gastritis

A

AutoImmune type and Hpylori type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q
  • T cell mediated autoimmune destruction of gastric parietal cells of the body and fundus
  • associated with antibodies against parietal cell and or internsic factor -> used for diagnosis
A

Chronic autoimmune gasteritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q 
Clinical features includ
•Atrophy of mucosa, 
•acholhydria due to decreased  in number of parietal cells with increase in gastrin level and 
•Antral G cell hyperplasia 
• megaloblastic anemia
A 
Chronic autoimmune gastritis 
#1 cause of bit B12 deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Usually in the stomach there is no inflammatory cells but in chronic gastritis there will be inducing metaplasia which causes

A

An increased risk for gastric adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

It can induce acute and chronic inflammation of the stomach and is the most common cause 90% of gastritis

A

Chronic H pylori gastritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How does H pylori work

A

H pylori ureases and proteases and it weakens mucosal defenses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Most common site of H pylori and how does it present

A

Antrum, epigastric abdminal pain with increased risk of ulceration, gastric adenocarcinoma and MALT lymphoma due to intestinal metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

H Pylori treatment and complications

A

Triple treatment = triple complications

Ulcers , malt lymphoma and adenocarcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

How does treatment of h pylori help

A

Resolves the gastritis which in turn resolves the ulcer and reverses the intestinal metaplasia

61
Q

How to test h pylori has been resolved

A

Negative urea Breath test and lack of stool antigen confirm eradication of H pylori

62
Q

Solitary mucosal ulcer involving proximal duodenum 90% or distal stomach 10%

A

Peptic ulcer disease

63
Q

What causes duodenal ulcer

A

H pylori mostly and early it’s due to ZE syndrome

64
Q

Presents with epigastirc pain improving with meals and diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner glands

A

Duodenal ulcer

65
Q

What can an ulcer of the posterior wall of the duodenum do?

A

It can cause the wall to rupture leading to bleeding from gastroduodenal artery or acute pancreatitis

66
Q

Causes of gastric ulcers

A

H pylori 70%
NSAIDS 20%
Bile reflux

67
Q

Presents with epigastric pain and worsening with meals

A

Gastric ulcers

68
Q

What’s the risk of gastric ulcer being on the lesser curvature of antrum

A

Rupture carries risk of bleeding from the left gastric artery

69
Q

Differential diagnosis for ulcers includes cancer

A

•Duodenal ulcers are almost never malignant
•gastric ulcer due to PVD, small punched out and normal surrounding tissue (benign)
Gastric ulcer due to cancer irregular, larger and piling up of mucosa

70
Q

Malignant proliferation of surface epithelial cells adenocarcinoma can be intestinal or diffuse type

A

Gastric carcinoma

71
Q

Which type of gastric carcinoma presents with
• large irregular ulcers with heaped yo margins
• most commonly involves the lesser curvature of antrum (same place as gastric ulcer)
• risk factors intestinal metaplasia due to autoimmune and H pylori chronic gastritis

A

Intestinal type

72
Q

Which type of gastric carcinoma presents with
•singer ring cells ( a cell nucleus pushed off due to mucus accumulation) that diffusely infiltrate gastric wall.
• due to the infiltration the gastric wall will undergo desmoplasia white fibrous formation (linitis pastica)
(Not associated with H pylori intestinal metaplasia or nitrosamines

A

Diffuse type

73
Q

When do gastric carcinomas present

A

Late

74
Q

What do gastric carcinomas present with

A
  • Weight, loss abdominal pain and anemia
  • Presents with acanthodians nigricans (dark skin on axilla) and lesser trelat sign (sebbrhoic keratosis over skin
  • spreads to vie how’s node
75
Q

Where does diffuse gastric carcinoma metastasis to

A

To the ovaries krukenberg tumour

76
Q

Where does intestinal gastric carcinoma metastasis to

A

Periumbilical region ( sister Mary joseph nodule)

77
Q

Gastric carcinoma usually distant metastasis to

A

Liver

78
Q

Congenital failure of small bowel to canalize and is associated with down syndrome

A

Duodenal atresia

79
Q

Congenital defect that presents with
•polyhydroamnios (can’t digest the ammniotic fluid)
•bilious vomiting (unlike pyloric stenosis with non bilious vomiting)
• distension of stomach and blind loop of duodenum (double bubble sign)

A

Duodenal atresia

80
Q

A true diverticulum (zenker is false)
•out pouching if all 3 layers of bowel wall
Arises due to failure if vitelline duct to involute
-rule of 2s->
-2% of pollution
-2inches long
- 2 feet from iliorectal junction
- seen in first 2 years of life
• present with bleeding volvulus and intussusception

A

Meckel diverticulum

81
Q

Twisting of bowel along its mesentery
• results in obstruction and disruption of blood supply (infarction)
•most common locations are sigmoid and cecum

A

Volvulus

82
Q

Telescoping of proximal segment of bowls in to the distal segment, presents with infarction and obstruction ( currant jelly stool)

A

Intussusception

83
Q

Happens due to a leading edge since it moves with the direction of peristalsis there is something it is hooking on
•in children -> most commonly cause is lymphoid hyperplasia
• in adults-> most common cause is tumour

A

Intussusception

84
Q
  • Transmural infarction occurs with embolism/ thrombosis of superior mesenteric artery or thrombosis of mesenteric vein
  • presents with abdominal pain and bloody diarrhoea and decreased bowel sounds
A

Small bowel infarction

85
Q

Happens due to not complete obstruction of the arterial supply usually due to hypotension

A

Mucosal infarction

86
Q

Immune mediated damage of small bowel villi due to gluten exposure

A

Celiac disease

87
Q

Genes associated with celiac disease

A

HLA DQ2 and HLA DQ8

88
Q

What is the most pathological component of gluten and how does it affect the bowel

A

Gliadin - it gets deamidated by tissue trans glutamase

The deamination gliadin is presented by APCs via MHC 2 -> helper T cell mediated damage

89
Q

What symptoms does celiac disease cause

A

Bloating and diarrhoea and is associated with dermatitis hepetiformis -> due to IgA deposition at top if dermal papillae resolves with gluten free diet

90
Q

Lab finding of celiac disease

A

IgA antibodies against endomysium + TG or gliadin

IgG antibodies are useful in IgA deficiency

91
Q

What is found on celiac disease biopsy

A

Flattening of villi hyperplasia of crypts and increased intraepithelial lymphocytes
Damage is mostly in duodenum less in ileum and jejunum
The symptoms resolve with gluten free diet

92
Q

What are the complications of celiac disease even with a gluten free diet

A

Small bowel carcinoma and T cell lymphoma

93
Q

Damage to small bowel villi due to unknown organism results in malabsorption
Similar to celiac disease except ->
•occurs in tropical regions
• arises after infectious diarrhoea and responds to antibiotics
• damage is mostly in jejunum (folic acid def) and ileum (vit B12 Def)

A

Tropical sprue

94
Q

•Decrease function of lactase in brush border enterocytes
•Abdominal distension
• diarrhea after milk
- continental (rare) or acquired just by aging or after a GI infection

A

Lactose intolerance

95
Q

•Systemic damage, macrophages containing tropheryma whippli
• PAS positive macrophages
• location is small vowel lamina propria
- macrophages compress lacteals
- chylimicrons cannot be transferred from enterocytes to lymphatics
- results in fat malabsorption and steatorrhea

A

Whipple disease

96
Q
  • Acute inflammation of the appendix, most common cause of acute abdomen
  • related to obstruction of the appendix by lymphoid hyperplasia (children) or fecalith(adults)
A

Acute appendicitis

97
Q

This disease is presented by peri umbilical pain, fever and nausea.
Pain localises to the RLQ the rupture results in peritonitis with guarding and rebound tenderness

A

Acute appendicitis

98
Q

What is the most common tumour of the appendix

A

Carcinoid tumour

99
Q

How does cancer of the appendix present

A

The clinical presentation of adenocarcinoma can be indistinguishable from that of acute appendicitis

100
Q

Chronic relapsing inflammation of bowel

Possibly due to an abnormal immune response to the enteric flora

A

IBD

101
Q

Clinical presentation young women teens to 30s with recurrent bouts of bloody diarrheas and abdominal pain

A

Irritable bowel disease which is of two type

Ulcerative colitis and chrohn’s disease

102
Q

IBD with wall involvement and location of
•mucosal and submucosal ulcers
• starts at rectum and can go up to cecum with continued lesions

A

Ulcerative colitis

103
Q

IBD That has the wall involvement and location
•full thickness inflammation with knife like fissures
•any where from mouth to the anus presents with skip lesions most common in terminal ileum and least common is the rectum

A

Chron’s disease

104
Q

IBD that is accociatwd with

P ANCA and primary sclerosing cholangitis

A

Ulcerative colitis

105
Q

Effect of smoking on ulcerative colitis

A

Protects against ulcerative colitis

106
Q

IBD associated with ankylosing spolynditis and sarcolitis and uveitis

A

Chrohns disease

107
Q

IBD that has a gross appearance of

  • cobblestone mucosa creeping far and strictures
  • string sign in imaging
A

Chrohns disease

108
Q

IBD with symptoms of

•RLQ. Pain (ileum) with non bloody diarrhoea

A

Chrohns disease

109
Q

IBD that has inflammation as

•lymphoid aggregates with granulomas

A

Chrohns disease

110
Q

IBD with complications of

• malabsorption, calcium oxylate stones fistulas and carcinoma

A

Chrohns disease

111
Q

Smoking and chrohns disease

A

Increases the risk of chrohns disease

112
Q

IBD with complications that include

• toxic megacolon and carcinoma

A

Ulcerative colitis

113
Q

IBD that has a gross appearance of

•pseudopolyps, loss of haustra and lead pipe on imaging

A

Ulcerative colitis

114
Q

IBD with inflammation of

•crypt abscesses with neutrophils

A

Ulcerative colitis

115
Q

IBD that has symptoms of

•left Lower quadrant pain(rectum) with bloody diarrhea

A

Ulcerative colitis

116
Q
  • Defective relaxation and peristalsis of rectum and distal sigmoid colon
  • associated with down syndrome
  • it happens due to ganglion cells fail to descend lacking both ganglion cells from myenteric and meissner plexus.
A

Hirschsprung disease

117
Q

Clinical features of this disease are fully based on obstruction
The failure to pass muconium
Massive dilation of bowel proximal to obstruction with risk of rupture

A

Hirschsprung disease

118
Q

Which type of biopsy is used for hirschsprung disease

A

Rectal suction biopsy (pulley the submucosa) it reveals the lack of ganglion cells

119
Q

What is the treatment of hirschsprung disease

A

Resection of the area lacking ganglion cells

120
Q

False diverticulum of the colon (pseudodiverticulum)

• out pouching of mucosa and submucosa through the muscularis propria

A

Colonic diverticula

121
Q

What causes colonic diverticula

A

It is related to wall stress associated with constipation, low fiber diets and commonly seen in older adults

122
Q

Where does colonic diverticula arise from

A

Arises from the vasa texts traverse muscularis propria(weak point in the colonic wall)

123
Q

What is the most common location of the colonic diverticula

A

Sigmoid is the most common location

124
Q

Complications of colonic diverticula

A
  • Rectal bleeding - it occurs right up on the wall of the vein so it won’t be hard for bleeding to occur
  • Diverticulitis - inflammation of the wall due to blocking of the diverticulum with fecal mater (left sided appendicitis)
  • Fistula due to the inflammation of the wall it can rupture and link to another tube
125
Q

Acquired malformation of mucosa and submucosal capillary beds
Usually arises in cecum and right colon due to increased wall tension

A

Angio dysplasia

126
Q

High stress in the left colon -> diverticula

Which lead to

A

Hematochezia

127
Q

High stress on the right colon -> angio dysplasia which lead to

A

Hematochezia in older adults

128
Q
  • Ischemic damage to the colon usually to the splenic flexure
  • Atherosclerosis to the superior mesenteric artery is the most common cause
  • Presents as postprandial pain and weight loss
  • infarctionresults in pain and bloody diarrhoea
A

Ischemic colitis

129
Q
  • Relapsing abdominal pain with bloating, flatulence and change in the bowel habits (diarrhea and constipation)
  • improves with defection
  • classically seen in middle aged females
A

IBS (IRRITABLE BOWEL SYNDROME)

130
Q

Raised protrusion of colonic mucosa with the most common types being
•hyperplastic
•adenomatous

A

Colonic polyps

131
Q

It is the most comon type of colonic polyps happens due to hyperplasia of glands has serrated appearance (saw tooth) on microscopy
•usually arises in the left colon (rectosigmoid)
• benign no malignant potential

A

Hyperplastic polyp

132
Q

2nd most common type of colonic polyps it is a neoplasticism proliferation of glands
•benign but pre malignant as it may progress to adenocarcinoma via the adeno carnioma sequence

A

Adenomatous polyps

133
Q

What is the adenoma-carcinoma sequence

A
  • APC mutation causes risk of polyp (both copies need to be knocked out)
  • KRAS mutation allows for polyp formation
  • P53 induces malignancy (increased cox so aspirin protects)
134
Q

How to screen for polyps

A

Colonoscopy and testing for fecal occult blood

135
Q

What is the goal of screening for polyps

A

Goal is to remove adenomatous polyps before progression to carcinoma
(In colonoscopy all polyps are removed and examined microscopically )

136
Q

What increases the risk of a polyp to go from adenoma to carcinoma

A

Polio >2CM
Sessile polyp
Villous histology

137
Q
  • Autosomal dominant disorder charchtarized by 100s to 1000s of adenomatous colonic polyps
  • Due to inherited APC mutation
  • the colon and rectum are removed prophylactically
A

Familial adenomatous polyposis

138
Q

A syndrome which consists of Familial adenomatous polyposis and osteomas with fibromatosis

A

Gardner syndrome

139
Q

A syndrome of which a person has Familial adenomatous polyposis and with CNS tumours

A

Turcot syndrome

140
Q 
Sporadic hamartoma (benign) polyp arising in children <5years 
Usually solitary rectal polyp-> prolapses and bleeds
A

Juvenile polyp

141
Q
  • Multiple juvenile polyps in stomach

* only with a large number of juvenile polyps is there an increased risk progression to carcinoma

A

Juvenile polyposis

142
Q
  • Hamartomatous polyps throughout the GI tract
  • Mucocutaneous hyperpigmentation on lips, oral mucosa and genital skin
  • increased risk of colorectal cancer breast and GYN cancer
A

Peutz-jeghers syndrome

143
Q

Carcinoma arising from colonic or rectal mucosa (peak incidence is 60-70 years)

A

Colorectal carcinoma

144
Q

Most common pathway for colorectal carcinoma (80%)

A

Adenoma carcinoma sequence

145
Q

2nd most common pathway for colorectal carcinoma

A

MSI micro satellite instability

146
Q

Inherited mutation in DNA mismatch repair enzymes
•increased risk for colorectal, ovarian and endometrial carcinoma
•colorectal carcinoma that arises de novo(no history of polyps) at early age

A

HNPCC hereditary non polyposis colorectal carcinoma

147
Q

Serum tumour marker for colorectal carcinoma

A

CEA - not useful for screening but usful to asses treatment and detecting reoccurrence

148
Q

Screening for colorectal carcinoma

A

Begins at the age of 50

Colonoscopy and fecal occult blood

pathology (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions