GI Pathology Flashcards
(148 cards)
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
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
3
Q
Recurrent apthous ulcers, genital ulcers and uveitis (triad) which happens due to immune complex vasculitis involving small vessels
A
Behcet syndrome
4
Q
Primary infection occurs in childhood causing shallow painful red ulcers
A
herpes simplex virus 1 - oral herpes
5
Q
After primary infection with HSV1 what happens to the virus?
A
Stays dormant in the ganglia of trigeminal nerve
6
Q
What reactivates dormant HSV1?
A
Stress and sunlight cause reactivation leading to vesicles on lips (COLD SORES)
7
Q
Malignant neoplasm of squamous cells lining mucosa
A
Squamous cell carcinoma
8
Q
What are the major Risk factors of squamous cell carcinoma?
A
Tobacco smoke and alcohol
9
Q
What is the most common location of squamous cell carcinoma?
A
Floor of the mouth is the most common location
10
Q
What are leukoplakia and erythroplakia?
A
Precursor lesions of squamous cell carcinoma, they need to be biopsied to rule out the carcinoma.
11
Q
What can be confused with leukoplakia?
A
Oral candidiasis a white patch on the mouth which can be easily scrapped
12
Q
A patch on the lateral tongue due to EBV in immuno compromised
A
Hairy leukoplakia
13
Q
What does a true leukoplakia present with
A
True leukoplakia is presented with hyperplasia
14
Q
Leukoplakia + blood vessels which indicate angiogenesis
A
Erythroplakia
15
Q
Is leukoplakia or erythroplakia more likely to have dysplasia
A
Erythroplakia
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
17
Q
A stone obstruction in salivary glands is called
A
Sialolithiasis
18
Q
Inflammation of salivary glands due to an obstructing stone (sialolithiasis) leading to S. Aureus infection
A
Sialadenitis - usually unilateral
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
20
Q
Most common tumour of salivary glands
A
Pleomorphic adenoma
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
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
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
24
Q
What the second most common salivary gland tumour that is common for smokers
A
Warthin tumour
25
Malignant tumour composed of MUCINOUS AND SQUAMOUS CELLS, that usually arise in parotid commonly INVOLVED FACIAL NERVE - that usually reoccurs
Mucoepidermoid carcinoma
26
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A congenital defect presents in new born as 4 issues
•vomiting
•polyhydraminous
•abdominal distension
•aspiration
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Tracheoesophageal fistula
27
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
ESOPHAGEAL WEB
28
* 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)
Zenker diverticulum
29
* 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)
Mallory-Weiss syndrome
30
* Dilated submucosal vein in lower esophagus which arises secondary due to portal HTN
* risk of rupture cuasing painless hematemisis
Esophageal varices
31
Most common cause of death from liver cirrhosis
Esophageal varices - the veins will rupture and the cirrhotic liver has couagulopathy so can’t close the bleeding
32
Reflex of acid from stomach due to reduced tone of lower esophageal sphincter
GERD
33
Risk factors of GERD
Alcohol, tobacco, obesity, fat rich diet, caffeine and hiatal hernia
34
How can hiatal hernia cause GERD
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
35
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
GERD
36
Esophageal metaplasia from squamous cells to non ciliated Columnar epithelium with goblet cells
Butters esophagus
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Type is esophageal carcinoma
Adenocarcinoma and squamous cell carcinoma
38
Most common esophageal carcinoma in the west occurs from metaplasia of burret esophagus occurring at the lower 1/3 of esophagus
Adenocarcinoma
39
* 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)
Squamous cell carcinoma
40
•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
Achalasia
41
Lymph node cancer spread in 3 quarters of the esophagus
Upper 1/3 -> cervical nodes
Middle1/3-> mediastinal and tracheobronchial nodes
Lower 1/3 -> gastric and celiac nodes
42
A congenital malformation of the abdominal wall leads to exposure of the abdominal content
“A hole in the abdominal wall”
Gastroschisis
43
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
Omphalacele
44
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
Pyloric stenosis
45
Acid damage to mucosa due to imbalance between acidic environment and mucosal defences
Acute gastritis
46
Epithelial foveolar cells protect by producing - mucosa , increase HCO3- secretion and normal blood supply (absorbing acid and supply nutrients)
Mucosal defended
47
Severe burn causing an ulcer due to hypovolemia less blood flow to the stomach and decreased nutrient supply and acid sweeping
Curling ulcer
48
Risk factors of stomach ulcers
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NSAIDs
chemotherapy
Heave alcohol consumption
Shock causes stress ulcers
Severe burns (curling ulcer)
Increased intracranial pressure (Cushing ulcer)
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49
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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
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Cushing ulcer
50
Acid damage to stomach results in
Superficial inflammation
Erosion (loss of epithelium)
Ulcer (loss of mucosal layer)
51
Chronic inflammation of stomach mucosa
Chronic gastritis
52
types of Chronic gastritis
AutoImmune type and Hpylori type
53
* 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
Chronic autoimmune gasteritis
54
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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
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Chronic autoimmune gastritis
#1 cause of bit B12 deficiency
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55
Usually in the stomach there is no inflammatory cells but in chronic gastritis there will be inducing metaplasia which causes
An increased risk for gastric adenocarcinoma
56
It can induce acute and chronic inflammation of the stomach and is the most common cause 90% of gastritis
Chronic H pylori gastritis
57
How does H pylori work
H pylori ureases and proteases and it weakens mucosal defenses
58
Most common site of H pylori and how does it present
Antrum, epigastric abdminal pain with increased risk of ulceration, gastric adenocarcinoma and MALT lymphoma due to intestinal metaplasia
59
H Pylori treatment and complications
Triple treatment = triple complications
| Ulcers , malt lymphoma and adenocarcinoma
60
How does treatment of h pylori help
Resolves the gastritis which in turn resolves the ulcer and reverses the intestinal metaplasia
61
How to test h pylori has been resolved
Negative urea Breath test and lack of stool antigen confirm eradication of H pylori
62
Solitary mucosal ulcer involving proximal duodenum 90% or distal stomach 10%
Peptic ulcer disease
63
What causes duodenal ulcer
H pylori mostly and early it’s due to ZE syndrome
64
Presents with epigastirc pain improving with meals and diagnostic endoscopic biopsy shows ulcer with hypertrophy of Brunner glands
Duodenal ulcer
65
What can an ulcer of the posterior wall of the duodenum do?
It can cause the wall to rupture leading to bleeding from gastroduodenal artery or acute pancreatitis
66
Causes of gastric ulcers
H pylori 70%
NSAIDS 20%
Bile reflux
67
Presents with epigastric pain and worsening with meals
Gastric ulcers
68
What’s the risk of gastric ulcer being on the lesser curvature of antrum
Rupture carries risk of bleeding from the left gastric artery
69
Differential diagnosis for ulcers includes cancer
•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
Malignant proliferation of surface epithelial cells adenocarcinoma can be intestinal or diffuse type
Gastric carcinoma
71
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
Intestinal type
72
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
Diffuse type
73
When do gastric carcinomas present
Late
74
What do gastric carcinomas present with
* 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
Where does diffuse gastric carcinoma metastasis to
To the ovaries krukenberg tumour
76
Where does intestinal gastric carcinoma metastasis to
Periumbilical region ( sister Mary joseph nodule)
77
Gastric carcinoma usually distant metastasis to
Liver
78
Congenital failure of small bowel to canalize and is associated with down syndrome
Duodenal atresia
79
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)
Duodenal atresia
80
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
Meckel diverticulum
81
Twisting of bowel along its mesentery
• results in obstruction and disruption of blood supply (infarction)
•most common locations are sigmoid and cecum
Volvulus
82
Telescoping of proximal segment of bowls in to the distal segment, presents with infarction and obstruction ( currant jelly stool)
Intussusception
83
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
Intussusception
84
* 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
Small bowel infarction
85
Happens due to not complete obstruction of the arterial supply usually due to hypotension
Mucosal infarction
86
Immune mediated damage of small bowel villi due to gluten exposure
Celiac disease
87
Genes associated with celiac disease
HLA DQ2 and HLA DQ8
88
What is the most pathological component of gluten and how does it affect the bowel
Gliadin - it gets deamidated by tissue trans glutamase
| The deamination gliadin is presented by APCs via MHC 2 -> helper T cell mediated damage
89
What symptoms does celiac disease cause
Bloating and diarrhoea and is associated with dermatitis hepetiformis -> due to IgA deposition at top if dermal papillae resolves with gluten free diet
90
Lab finding of celiac disease
IgA antibodies against endomysium + TG or gliadin
| IgG antibodies are useful in IgA deficiency
91
What is found on celiac disease biopsy
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
What are the complications of celiac disease even with a gluten free diet
Small bowel carcinoma and T cell lymphoma
93
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)
Tropical sprue
94
•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
Lactose intolerance
95
•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
Whipple disease
96
* Acute inflammation of the appendix, most common cause of acute abdomen
* related to obstruction of the appendix by lymphoid hyperplasia (children) or fecalith(adults)
Acute appendicitis
97
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
Acute appendicitis
98
What is the most common tumour of the appendix
Carcinoid tumour
99
How does cancer of the appendix present
The clinical presentation of adenocarcinoma can be indistinguishable from that of acute appendicitis
100
Chronic relapsing inflammation of bowel
| Possibly due to an abnormal immune response to the enteric flora
IBD
101
Clinical presentation young women teens to 30s with recurrent bouts of bloody diarrheas and abdominal pain
Irritable bowel disease which is of two type
| Ulcerative colitis and chrohn’s disease
102
IBD with wall involvement and location of
•mucosal and submucosal ulcers
• starts at rectum and can go up to cecum with continued lesions
Ulcerative colitis
103
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
Chron’s disease
104
IBD that is accociatwd with
| P ANCA and primary sclerosing cholangitis
Ulcerative colitis
105
Effect of smoking on ulcerative colitis
Protects against ulcerative colitis
106
IBD associated with ankylosing spolynditis and sarcolitis and uveitis
Chrohns disease
107
IBD that has a gross appearance of
* cobblestone mucosa creeping far and strictures
* string sign in imaging
Chrohns disease
108
IBD with symptoms of
•RLQ. Pain (ileum) with non bloody diarrhoea
Chrohns disease
109
IBD that has inflammation as
| •lymphoid aggregates with granulomas
Chrohns disease
110
IBD with complications of
• malabsorption, calcium oxylate stones fistulas and carcinoma
Chrohns disease
111
Smoking and chrohns disease
Increases the risk of chrohns disease
112
IBD with complications that include
• toxic megacolon and carcinoma
Ulcerative colitis
113
IBD that has a gross appearance of
| •pseudopolyps, loss of haustra and lead pipe on imaging
Ulcerative colitis
114
IBD with inflammation of
| •crypt abscesses with neutrophils
Ulcerative colitis
115
IBD that has symptoms of
| •left Lower quadrant pain(rectum) with bloody diarrhea
Ulcerative colitis
116
* 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.
Hirschsprung disease
117
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
Hirschsprung disease
118
Which type of biopsy is used for hirschsprung disease
Rectal suction biopsy (pulley the submucosa) it reveals the lack of ganglion cells
119
What is the treatment of hirschsprung disease
Resection of the area lacking ganglion cells
120
False diverticulum of the colon (pseudodiverticulum)
| • out pouching of mucosa and submucosa through the muscularis propria
Colonic diverticula
121
What causes colonic diverticula
It is related to wall stress associated with constipation, low fiber diets and commonly seen in older adults
122
Where does colonic diverticula arise from
Arises from the vasa texts traverse muscularis propria(weak point in the colonic wall)
123
What is the most common location of the colonic diverticula
Sigmoid is the most common location
124
Complications of colonic diverticula
* 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
Acquired malformation of mucosa and submucosal capillary beds
Usually arises in cecum and right colon due to increased wall tension
Angio dysplasia
126
High stress in the left colon -> diverticula
| Which lead to
Hematochezia
127
High stress on the right colon -> angio dysplasia which lead to
Hematochezia in older adults
128
* 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
Ischemic colitis
129
* Relapsing abdominal pain with bloating, flatulence and change in the bowel habits (diarrhea and constipation)
* improves with defection
* classically seen in middle aged females
IBS (IRRITABLE BOWEL SYNDROME)
130
Raised protrusion of colonic mucosa with the most common types being
•hyperplastic
•adenomatous
Colonic polyps
131
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
Hyperplastic polyp
132
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
Adenomatous polyps
133
What is the adenoma-carcinoma sequence
* 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
How to screen for polyps
Colonoscopy and testing for fecal occult blood
135
What is the goal of screening for polyps
Goal is to remove adenomatous polyps before progression to carcinoma
(In colonoscopy all polyps are removed and examined microscopically )
136
What increases the risk of a polyp to go from adenoma to carcinoma
Polio >2CM
Sessile polyp
Villous histology
137
* Autosomal dominant disorder charchtarized by 100s to 1000s of adenomatous colonic polyps
* Due to inherited APC mutation
* the colon and rectum are removed prophylactically
Familial adenomatous polyposis
138
A syndrome which consists of Familial adenomatous polyposis and osteomas with fibromatosis
Gardner syndrome
139
A syndrome of which a person has Familial adenomatous polyposis and with CNS tumours
Turcot syndrome
140
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Sporadic hamartoma (benign) polyp arising in children <5years
Usually solitary rectal polyp-> prolapses and bleeds
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Juvenile polyp
141
* Multiple juvenile polyps in stomach
| * only with a large number of juvenile polyps is there an increased risk progression to carcinoma
Juvenile polyposis
142
* Hamartomatous polyps throughout the GI tract
* Mucocutaneous hyperpigmentation on lips, oral mucosa and genital skin
* increased risk of colorectal cancer breast and GYN cancer
Peutz-jeghers syndrome
143
Carcinoma arising from colonic or rectal mucosa (peak incidence is 60-70 years)
Colorectal carcinoma
144
Most common pathway for colorectal carcinoma (80%)
Adenoma carcinoma sequence
145
2nd most common pathway for colorectal carcinoma
MSI micro satellite instability
146
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
HNPCC hereditary non polyposis colorectal carcinoma
147
Serum tumour marker for colorectal carcinoma
CEA - not useful for screening but usful to asses treatment and detecting reoccurrence
148
Screening for colorectal carcinoma
Begins at the age of 50
| Colonoscopy and fecal occult blood
