Pathology GIT Flashcards
1
Q
Dysphagia
A
Difficulty swallowing
2
Q
Odynophagia
A
Pain on swallowing
3
Q
Heart burn
A
Burning sensation behind sternum not due to heart issue
4
Q
Main reason of acid regurgitation into mouth
A
Gastro esophageal reflux disease
5
Q
Second name of ectopic gastric mucosa
A
Inlet patch
6
Q
Where can you mostly find an ectopic gastric mucosa
A
Upper third of Esophagus
7
Q
Complications of ectopic gastric mucosa
A
Dysphagia
Esophagitis
Barrett esophagus
Adenocarcinoma (worst case)
8
Q
Which one is more common
A. Ectopic gastric mucosa
B. Ectopic pancreatic mucosa
A
A
9
Q
Pulmonary sequestration
A
Lung Parenchymal tissue in esophagus
10
Q
Atresia definition
A
Thin non canalized cord replaces a segment of the esophagus
11
Q
Is atresia compatible with life ?
A
Incompatible without repair
12
Q
Why does atresia occur mostly with fistula ?
A
Because most atresia occur near the tracheal bifurcation
13
Q
Atresia symptoms
A
Cyanosis of baby when first feeding
Chocking, coughing
Respiratory distress
Baby vomits after feeding
14
Q
Fistula definition
A
Abnormal connection between 2 organs
15
Q
Tracheoesophageal fistula symptoms
A
Aspiration
Suffocation
Pneumonia
Severe fluid and electrolytes imbalance
16
Q
Esophageal Stenosis
A
Narrowing of the lumen after fibrous thickening of the wall
17
Q
What is the cause of congenital esophageal stenosis ?
A
Due to partial apoptosis of the lumen
18
Q
How can increase peristalsis cause esophageal stenosis ?
A
Muscle hypertrophy due to high demand causing partial obstruction
19
Q
Causes of esophageal stenosis
A
Congenital Increased peristalsis causing muscle hypertrophy Inflammatory scarring ( chronic GERD) Irradiation Systemic sclerosis Caustic ingestion
20
Q
Mucosal webs
A
Semi circumferential Protusion of mucosa into lumpen ~5mm
21
Q
Mucosal webs composition
A
Fibrovascular connective tissue
22
Q
Which population is more at risk of mucosal webs
A
Women over 40 year old
23
Q
What diseases are associated with mucosal webs
A
GERD
Chronic graft versus host
Blistering skin diseases
24
Q
When can you see the
- Patterson brown Kelly syndrome
- Plummer vinson syndrome
A
Mucosal webs associated with
Cheilosis
Iron deficiency anemia
Glossitis
25
Symptoms of mucosal webs
Non progressive dysphagia ( solid food )
| Incomplete chewed food
26
Rings definition
Circumferential protusion of mucosa submucosa into the lumen and sometimes muscularis proprio hypertrophy
27
Where do you find A rings
Above gastroesophageal junction with squamous mucosa
28
Where do you find B rings
At squamocolumnar junction with gastric cardia type mucosa
29
How can you assess esophageal dysmotility
Esophageal manometry
30
Three forms of dismotility
Nutcracker esophagus
Diffuse esophageal spasm
Hypertensive lower esophageal sphincter
31
Nutcracker esophagus
High amplitude contractions with loss of coordination between inner circular and outer longitudinal
32
Diffuse esophageal spasm
Repetitive, silmutaneous contractions of distal smooth muscle
33
Diverticulae definition
Outpouch of wall due to weakness
34
Epiphrenic diverticulum
Diverticulum above lower esophageal sphincter
35
Zenker diverticulum
Impaired relaxation and spasm of cricropharyngeus muscle causing outpouch just above it
36
Complications of zenker diverticulum
Regurgitation
| Halitosis
37
Achalasia
Impaired smooth muscle relaxation increasing tone of lower esophageal sphincter preventing passage of food into stomach with possible obstruction
38
Achalasia triad
Incomplete LES relaxation
Increased LES tone
Aperistalsis of esophagus
39
Symptoms of achalasia
Progressive dysphagia ( food and liquid)
Chest pain
Regurgitation
40
Primary achalasia cause
Ganglion cell degeneration
| Vagus nerve degeneration
41
Secondary achalasia cause
Chagas’s disease with destruction of myenteric plexus
42
Achalasia like disease
```
Diabetic neuropathy
Malignancy
Amyloidosis
Sarcoidosis
Polio
```
43
Hiatal hernia
Protusion of stomach above diaphragm
44
2 forms of hiatal hernia
Axial/sliding hernia
| Non axial/paraesophageal hernia
45
Which form of hiatal hernia has higher incidence ?
Axial hernia (95% cases)
46
Axial hernia presentation
Circumferential and bell shaped dilation
47
False diverticulum
Outpouching of mucosa and submucosa
48
True diverticulum
Outpouching of all parts of the GIT zone concerned
49
Traction diverticulum
Diverticulum near midpoint of esophagus
| Tb like Scarring due to mediastinal lymphadenitis
50
Mallory Weiss syndrome
Longitudinal tear at esophagogastric junction
51
Mallory Weiss syndrome most common in
Alcoholics because of excessive vomiting and gastric reflux
52
What would happen in case of infection in Mallory Weiss syndrome
Inflammatory ulcer
| Mediastinitis
53
Which one is most severe
Mallory Weiss syndrome
Boerrhave syndrome
Boerrhave syndrome
54
Why do you do ECG in boerrhave syndrome
Because ressembles myocardial infarction
55
Boerthave syndrome
Transmural tearing with rupture of distal oesophagus
56
Complication of boerrhave syndrome
Severe mediastinitis
57
Symptoms of boerrhave syndrome
Severe chest pain
Tachypnea
Shock
58
What are some factors that can injure oesophagus
Irritants ( alcohol, corrosive acids, hot fluids, smoking)
Chemical injury in children
Attempted suicide in adults
59
What are the desquamative diseases of esophageal injuries
chron’s disease
Bullous pemphigoid
Epiderm
60
How does stenosis manifest in adulthood
Progressive dysphagia
61
What do you see in X ray of achalasia patient
Bird beak sign
62
Most important cause of acute esophagitis
Viral and fungal infections in immunocompromised patient
63
Most common infection of esophagus
Candidiasis
64
Complication of candidiasis in esophagus
Dysphagia
65
How do you recognize candidiasis
White plaque with hemorrhagic margins
66
What are the diseases under chronic esophagitis
GERD
| Barrets esophagus
67
How is the esophagus protected from abrasion
Stratified squamous epithelium
Mucin and bicarbonate secretions
Constant LES tone
68
What is the most common cause of GERD
LES incompétence
69
Symptoms of GERD
Acid awareness
Heartburn
Odynophagia
Dysphagia
70
Morphology of GERD
```
Cell injury
Accelerated desquamation
Basal cell hyperplasia
Immature cell predominance in epithelium
Low grade inflammation
```
71
Severe GERD presentation
Ulceration
| Possible hemorrhages
72
GERD Healing process
Fibrosis
| Epithelial regeneration
73
What disease is Barrett’s disease a complication of ?
GERD
74
Barrett’s esophagus
columnar metaplasia in esophagus
75
Two criteria to diagnose Barrett’s esophagus
Endoscopy evidence of columnar epithelium ( appear as tongue of red mucosa)
Histologic evidence with biopsy to find columnar cell
Goblet cells - stain pale blue by H&E
76
What is the single most important factor to develop esophagus adenocarcinoma
Barrett’s esophagus
77
Why do you put patient with barrets esophagus disease on regular endoscopic surveillance ?
They have 100 more chances of developing cancer
78
Are benign tumors of esophagus common ?
No
79
Most common type of benign tumor of esophagus
Leiomyoma ( smooth muscle)
80
Type of benign tumors of esophagus
```
Leiomyomas ( smooth muscle)
Hemangiomas ( blood vessels)
Neurofibromas (nerves)
Lymphangiomas (lymphatic vessels)
Fibrovascular polyps/pedunculated lipomas
Squamous papillomas
Inflammatory polyps
```
81
Fibrovascular polyps morphology
Mucosal polyps with conbination of fibrous, vascular, or adipose tissue covered with normal mucosa
82
Squamous papillomas morphology
Sessile lésions with connective tissue core , and hyperplastic pappiliform squamous mucosa
83
What population most affected by malignant tumors of esophagus ?
Adult male (4x more than female)
84
Etiology of malignant esophageal tumor
Riboflavin, vit À, C, thiamine, pyridoxine deficiencies in diet
Zinc, molybdenum deficiencies
Fungal contamination
Opium usage
Thermal injury
Smoking
Alcohols
Viruses ( HPV)
Genetic alterations (p161NK4 mutation, cyclin D1, c-MYC, EGFR amplification)
85
Morphology of malignant cancer of esophagus
Pleomorphism ( disordered maturation, mitotis at surface)
86
Most common type of carcinoma in lower third of esophagus
Adenocarcinoma
87
Most common type of carcinoma in esophagus
Squamous type
88
How do squamous carcinoma start
As ulcer
89
Main presentation of esophagus carcinoma
Dysphagia
90
Main Treatment of esophagus carcinoma
Radiotherapy
| Laser therapy
91
How is long term survival of esophagus carcinoma
Poor - 5% survival in 5 years
92
Congenital anomalies of stomach
Heterotopic rest
| Pyloric stenosis
93
Pancreatic heterotopia
Pancreatic tissue in gastric submucosa , subserosal
Pancreatic tissue in intestinal submucosa, subserosal
Pancreatic tissue on pylorus with risk of obstruction
94
Which population is more affected by the congenital hypertrophic pyloric stenosis
Infants especially boys
95
What disease are associated with congenital hypertrophic pyloric stenosis
Turner syndrome, trisomy 18, esophageal atresia
96
Congenital hypertrophic pyloric stenosis clinical presentation
Regurgitation
Vomiting (persistent, projectile, non bilious)
Visible Peristalsis and mass in pyloric region or distal stomach
Edema
Inflammatory changes
97
Curative measure of Congenital hypertrophic pyloric stenosis
Surgical muscle split
98
Possible complications of peptic ulcer near pylorus
Acquired pyloric stenosis
99
Possible causes of acquired pyloric stenosis
Carcinoma, lymphomas, inflammatory fibrosis, malignant infiltration, chronic pyloric spasm
100
Two types of gastritis
Acute or chronic
101
Acute gastritis is an important cause of..
Acute gastrointestinal bleeding
102
Acute gastritis possible causes
```
Heavy use of NSAIDs
Alcohol
smoking
chemotherapy
ureamia
Systemic bacterial or viral infections
heavy stress ischemia
shock
suicide attempts
mechanical trauma
gastrectomy
```
103
Gastritis pathophysiology
```
Increased acid secretion
Decreased bicarbonate
Reduced blood flow
Mucus layer disruption
Epithelium damage
Acid bile regurgitation
Low PG
Lysolecithins
```
104
Acute Gastritis morphology
Moderate Edema lamina propria
Vascular congestion
Neutrophils in epithelium
Erosion ( fibrin, infiltrate)
hemorrhage (dark spots) in severe cases
105
Is acute gastritis a major cause of massive hemorrhage in alcoholics
Yes
106
Acute gastritis symptoms
```
May be asymptomatic
Nausea
pain
vomiting
hemorrhage massive
haematemesis
melaena
Fatal blood loss
```
107
Chronic gastritis presentation
Chronic mucosal inflammatory changes
Mucosal atrophy
Epithelial metaplasia
No erosion
108
Major cause of chronic gastritis
```
Chronic infection by H pylori
Autoimmunity - pernicious anemia
Toxic ( smoke and alcohol)
Post surgery
Motor and mechanical
Radiation
Granulomatous
Miscellaneous ( amyloidosis, graft versus host )w
```
109
Percentage of patients with chronic gastritis affected by h pylori
90%
110
H pylori specialized traits
Motility in viscous mucus ( flagella)
Urease which buffers acids around parasite
Adhésins ( especially in O patients)
111
What type of h pylori associated with duodenal ulcer
Cag A gene
| Vac A gene
112
2 patterns of h pylori chronic gastritis
Antral type gastritis
| Pan gastritis
113
Antral type gastritis
H pylori gastritis with high acid production and high risk of duodenal ulcer
114
Pam gastritis
Lower acid secretion , high risk of adenocarcinoma
115
Autoimmune chronic gastritis
Autoantibodies against gastric parietal cells which prevent acid production.
116
Autoimmune chronic gastritis presentation
Hypoclorrhydria
| Macrocytic anemia with vit B12 deficiency because no intrinsic factor
117
Pernicious anemia
Autoimmune gastritis + macrocytic anemia
118
Autoimmune gastritis morphology
```
Glandular atrophy
Fibrosis of lamina propria
Intestinal metaplasia with goblet cells replacing mucin cells
Absortive cells
Paneth cells
```
119
Reflux gastritis
Regurgitation of bile and alkaline duodenal juice in stomach
120
Reflux gastritis presentation
Epithelial desquamation
Compensatory Hyperplasia
Vasodilation and edema of lamina propria
121
When does reflux gastritis occur
Post operative stomach with bypass of pylorus
| Failure in pyloric competence
122
Types of chronic gastritis
Type a - immune gastritis ( less frequent) affect fundus, antibodies to parietal cells (achlorrydria and high gastrin serum)
Type b- infectious disease ( more frequent) mostly h pylori
123
Ulcers
Breach in mucosa of GIT from muscularis mucosa to submucosa or deeper
124
Most common type of ulcer
Chronic
Solitary
Présent in any part of GIT exposed to acid or peptic juices
125
Which type of peptic ulcer pénétrâtes the full thickness of muscularis propria and has base in serosal layer of organ
Chronic peptic ulcer
126
Most common location of peptic ulcer
Duodenum first part
Stomach ( antrum)
Gastro esophageal junction ( barrets esophagus)
Within margins of gastrojejunostomy
Duodenum,stomach or/and jéjunum of patient with zollinger Ellison syndrome
Within or adjacent to iléal Meckel diverticulum with ectopic gastric mucosa
127
Which type of peptic ulcer pénétrâtes muscularis mucosa but does not extend further than submucosa ?
Acute peptic ulcer
128
Main cause of acute peptic ulcer
Stress
Analgesic drugs
129
Curling ulcers
Ulcers with severe burns
130
Cushing’s ulcer
Ulcers occurring in brain damage
131
Main presentation of acute peptic ulcer
Gastric hemorrhage
132
Acute peptic ulcer heals. Scar or no ?
No scar
133
Population more at risk of gastric ulcer
Older group , females
134
Clinical presentation of chronic peptic ulcer
Dyspepsia when chronic gastric ulcer
Odynophagia that improves when eating in duodenal
135
Classic peptic ulcer appearance
Circular or oval
Punched out
Gastri rugae converging near ulcer margin
136
Most common location of chronic gastric ulcer
Along the lesser curvature
137
Most common location of chronic duodenal ulcer
1st part of duodenum
138
Kissing ulcers
Ulcers on both posterior and anterior part of duodenum. Common in chronic peptic ulcer
139
Chronic peptic ulcer morphology
Usually solitary
Gastric ulcer can coexist with duodenal ulcer
Kissing ulcers
Circular or oval
Gastric rugae converge upon ulcer margin
Base of ulcer in gastric or duodenal mucosa
140
Microscopic feature of chronic peptic ulcer
Surface layer with neutrophils and structure less harmatoxyphilic bodies
Under : fibrinoid necrosis organized by granulation in deeper areas
Granulation tissue become fibrous scar
Small inflammation with lymphocytes eosinophils plasma
Endarteritis obliterans in arterial lesions (thrombosis and inflammation of small vessels)
141
Complication of chronic peptic ulcers
Healing and scarring ( scarring invariable can lead to pyloric stenosis which can cause gastric outlet obstruction)
Perforation when ulceration faster than repair ( gut content into peritoneal cavity)
Hemorrhage ( erosion of small blood vessels leading to iron deficiency anemia, when large blood vessels haematemesis and melaena visible)
Carcinoma ( 1% of chronic gastric ulcer)
142
Gastric outlet obstruction presentation
```
Recurrent vomiting
Dehydration
Chloride depletion
Rise in plasma bicarbonate
Hypokalemic alkalosis
```
143
Arteries involved in life threatening hemorrhage due to peptic ulcer
Left gastric artery
| Gastro duodenal artery
144
Ethipathogenesis of chronic gastric ulcer
```
Environment (h pylori)
Stress psychological
Cigarette
Anelgesic
Genetics ( especially O blood group)
Familial ( monozygotic twin)
```
145
Pathogenesis of peptic ulcer
Imbalance between mucosal defense and damaging forces (pepsin, gastric acid )
In gastric ulcer : impaired mucosal difference with in most cases h pylori present (70%)
Un duodenal ulcers : high gastric levels at night with in most cases h pylori present (90 x%)
Gastrinomas like zollinger Ellison syndrome stimulate acid secretion
146
Polyp in git
Any mass or nodule that projects above the level of the surrounding mucosa
147
2 forms of polyps
Neoplastic
Form because of excess reparative/regenerative process
148
Commonest form of polyp
Simple elongation of gastric pits separated by fibrous tissue or musky inflamed lamina propria
149
What form of polyp is unusual
True benign neoplastic epithelial polyp
150
Commonest connective tissue gastric neoplasm
Smooth muscle tumor
151
Morphology of smooth muscle tumor of stomach
Intramural tumor projecting into lumen
Sometimes presence of ulcer crater ( source of hemorrhage)
Interwoven bundles of spindle cells
Variable amount of eosinophils in cytoplasm
All of this can be seen in neural tumors too
152
Gastric strolls tumors
Unpredictable behaviors
Difficult to say if benign or malignant
(Benign would have small size, encapsulation, low mitosis, no necrosis)
153
Most common type of malignancy in stomach
Carcinoma (90-95%)
Then lymphomas (4%)
Carcinoid ( 3%)
Malignant stromal cell tumor (2%)
154
Second most common fatal malignancy in the world
Gastric cancer
155
Factors increasing gastric carcinoma
Diet ( nitrites , smoked food, salted food, pickled vegetables)
Low socioeconomic
Cigarette
```
Chronic gastritis (hypochlorridria which favors h pylori)
H pylori infection
```
Partial gastrectomy ( favors duodenal excretion reflux
Gastric adenomas ( 40% have cancer when diagnosed )
Barrett’s esophagus (gastro esophageal junction tumors )
Genetic (increased risk in group A blood , family history of gastric cancer, hereditary non polyposis colon cancer syndrome)
156
Dysplasia-carcinoma sequence in gastric cancer
Chronic gastritis to atrophy and intestinal metaplasia to pre malignant dysplasia
157
Percentage of cases where curative operation still possible
45%
158
Prognosis of gastric cancer
10-15% survival rate in 5 years
159
Basis of classification of gastric cancer
Depth of invasion
Macroscopic growth pattern
Histologic subtype
160
Depth of invasion of gastric cancer
Early or advanced based on direct spread into stomach wall
When early => mucosa of submucosa only ( 90% survival in 5 years)
When advanced => extend into or beyond main muscle coats
161
Growth pattern of gastric cancer (3 patterns)
Exophytic ( Protusion of tumor mass into lumen)
Flat or depressed (no obvious tumor mass in mucosa )
Excavated ( shallow or deep erosive crater present in wall )
162
Linitis plastica
Uncommon
Broad region of gastric wall or entire stomach infiltatred by malignancy
Rigid and thick leather bottle like stomach
163
Histological pattern of gastric cancer
Intestinal type => neoplastic intestinal glands in gastric wall
Diffuse type => gastric type mucous cell permetjfn mucosa and wall ( they are individual or in small clusters) with signet ring conformation ( peripheral nucleus)
164
First clinical presentation of gastric carcinoma
Metastasis to supraclavicular sentinel node (virchow node)
165
Location of body invaded by gastric carcinoma
Duodenum
Pancreas
retroperitoneum
166
Krukenberg tumor
Gastric carcinoma metastasis that reached one or both ovaries
167
Is gastric carcinoma insidious ?
Yes
Slow growing
No symptoms at first
168
Symptoms of gastric cancer
```
Weight loss
Abdominal pain
Anorexia
Vomiting
Altered bowel habits
```
Less frequent:
Dysphagia
Anemia
Hemorrhage
169
Idiopathic inflammatory bowel disease
Chronic inflammatory conditions due to persistent action of mucosal immune system because of strong response to normal intramural flora
170
2 disorders of idiopathic inflammatory bowel disease
Crohn’s disease
Ulcerative colitis
171
Pathogenesis of inflammatory bowel disease
Failure of immune regulation
Genetic susceptibility
Environnemental triggers
172
Cronhs disease
Autoimmunity against any portion of GIT from mouth to anus
| Most often at distal small intestine and colon
173
Crohn’s disease characteristics
Sharply delimited
Transmural involvement of bowel
Non caseating granulomas
Fissuring with fistulae
174
Peak of detection of Crohn’s disease
2nd and 3rd decades
175
Clinical features of Crohn’s disease
```
Intermittent attacks with :
Mild diarrhea
Fever
Abdominal pain
Physical and emotional stress can trigger them
```
Fecal blood loss leading to anemia sometimes
In some patients => mimic acute appendicitis or acute bowel perforation with right lower quadrant pain
176
Complications of Crohn’s disease
Intestinal obstruction
177
Organs involvement stats in Crohn’s disease
Small intestine involvement in 40% cases
Small intestine and colon 30%
Colon alone 30%
178
Morphology of Crohn’s disease
Granular and dull gray serosa
Mesenteric fat around bowel surface
Thick, edematous, fibrotic Mesentery
Aphtous ulcers - small discrete shallow ulcers with hemorrhagic rims
Coarsely textured mucosa - cobblestone appearance
Longitudinal ulcers which progress into narrow deep fissures
Subsequent fibrosis leading to string sign because of narrowing ( only small amount of contrast passes through affected segment)
Fissure may cause rose thorn appearance of lumen with contrast medium
Enlarged reactive hyperplasia which contain granulomas
179
Skip lesions in Crohn’s disease
Disease separated by normal tissue
180
Earliest evidence of Crohn’s disease with naked eye
Aphtous ulcers
181
Microscopic feature of Crohn’s disease
Early => neutrophilic infiltration in epithelium which progresses to crypts
Crypt abscesses
Chronic mucosal damage with architectural distortion
Blunting of villi in small intestine
Crypts irregular and branching in colon
Mucosa metaplasia ( Paneth cell metaplasia or pyloric metaplasia in colon )
Transmural collection of lymphocytes and plasma cells
Granulomas ( non caseated ) With giant cells ( langhans type)
Réduplication,thickening and irregularity of the muscularis mucosa
Fibrosis of the submucosa muscularis propria and mucosa
Mucosal and submucosa lymphangiectasia, hypertrophy of mural nerve fibers , localized vasculitis
182
Classical Microscopic feature of Crohn’s disease
Granulomas ( only in 60% of patients tho so use summation of other histologicak findings to Diagnose patients without granulomas)
183
Complication of Crohn’s disease
Malabsorption syndrome ( due to Small intestine involvement and resection of bowel)
Fistula formation ( Between loops of bowel or enterocutaneous fistula)
Anal lesions ( 60% of patients)
Perforation , hemorrhage , toxic dilatation => rare
Malignancy over long-term
Systemic amyloidosis
184
More or less risk of malignancy in Crohn’s disease compared to ulcerative colitis
Less
185
Ulcerative colitis
Ulcero inflammatory disease which involves the mucosa the submucosal of the large intestine
186
Main location where ulcerative colitis starts
Rectum
187
Main differences between Ulcerative colitis and Crohn’s disease
Confined to the colon
| No granulomas
188
Backwash ileitis
Sometimes in ulcerative colitis involvement of the terminal ileum is seen
Maybe due to the incompetence of the ileocecal valve
189
Which disease is more common, ulcerative colitis or Crohn’s disease
Ulcerative colitis
190
What population is more at risk of ulcerative colitis
Females with an onset at 20 and 25 year old
191
Etiology of ulcerated colitis
Obscure causes so three theories ( Infection psychosomatic factors and Immunological factors)
Due to atypical immune response triggered by an infection (enteropathogenic E. coli)
192
Presentation of ulcerative colitis
Attacks of persistent bloody mucoid diarrhea which appear after long period without no symptoms
Initial attack can be explosive with serious bleeding and fluids and electrolytes imbalance
Can have sudden cessation of bowel function and toxic megacolon
Cramps relieved by defecation
Constipation in small number of patients
Stress can cause an attack
193
First manifestation of ulcerative colitis
Bloody diarrhea with mucus
| lower abdominal pain and cramps relieved by defecation
194
Morphology of ulcerative colitis
Continues in distribution
Disease maximal In the rectum
Severe active inflammation
Extensive broad-based ulceration of mucosa in distal colon or throughout its length
Ulcers with irregular outline and orientation
Pseudopolyps ( Protusion of regenerating mucosa )
No mural thickening
Normal serosal surface
195
Proctitis
Ulcerative colitis confined to the rectum
196
Distal colitis
Ulcerative colitis confined to the rectosigmoid
197
Pancolitis
Ulcerative colitis extending to the cecum
198
Presentation of ulcerative colitis in severe cases
```
Muscularis propria damage
Neural plexus damage
progressive dilatation
swelling
gangrene of the colon
mixed acute and chronic inflammatory cell infiltration in mucosa
Crypts abscesses
Goblet cell depletion
```
199
Rectal biopsy in long-standing ulcerative colitis
Crypt atrophy
shortfall and distortion
metaplastic (paneth cells)
Dysplasia and progression to Franck carcinoma on epithelium
200
Ulcerative colitis complications
Locally :
Malignancy (2% but 10% if disease for more than 25years)
Hemorrhage (generally chronic blood loss with iron deficiency anemia)
electrolyte disturbances due to severe diarrhea toxic dilatation ( leading to perforation and fecal peritonitis)
Systemic :
Skin lesions with pigmentation erythema nodosum and pyoderma gamgrenosum
Liver with fatty change
Chronic Pericholangitis ( Can lead to sclerosing cholangitis and biliary obstruction and cirrhosis)
Eyes complications with iritis, uveitis, episcleritis
Joints complications (Arthritis , spinal disease, ankylosing spondylitis)
201
Higher risk of cancer in ulcerative colitis associated with
Onset of disease in childhood severe first attack
pancolitis
continuous symptoms rather than intermittent
202
Population more at risk of appendicitis
Adolescents and young adults
203
Sequence of events in appendicitis
Pain from Periumbilical region to the right lower quadrant
Nausea / vomiting
Abdominal tenderness
Mild fever
High WBC
Right flank or pelvic pain in retoceacal appendix
Left upper quadrant pain in mal rotated colon
204
Predisposing factors to appendicitis
Faecoliths/faecalith - hard pellets of feces due to dehydration and compaction
Food residue
Enterobius worm
Lymphoid hyperplasia
appendix diverticulum
Tumor
Sometime no evident obstruction
Specific inflammation ( yersinia pseudotunerculosis, typhoid, actinomycoses)
UC and CDs
205
Appendicitis morphology
Bridge in epithelium and acute inflammation of mucosa
Neutrophilic exudate in mucosa ( can spread)
Congestion of subserosal vessels
Dull granular red membrane serosal of appendix (early stage)
Fibrino purulent exudate over serosa ( later stage )
Infection by bowel flora so mucosal ulcers with exudate and fibrin into lumen
Abscess formation in wall ( suppurative necrosi in mucosa) can cause peritonitis if affect all layers
Superimposed ischaemia (caused by build up of fluid exudate + blood vessel damage + thrombosis)
Distal part of appendix can become gangrenous and perforate
206
Histology of appendicitis
Neutrophilic infiltration of muscularis propria
207
Complications of acute appendicitis
```
Perforation leading to peritonitis
Abscess and fistula
Bacteremia
Inflammation thrombosis septicemia
Portal vein and liver abscess
Fibrosis and obstruction of neck of appendix forming mucocele which can rupture => Mucus can get into the peritoneal cavity
```
208
Appendicitis like diseases
```
Mesenteric lymphadenitis (virus etiology )
Acute salpingites
Ectopic pregnancy
Mittelschmerz
CF
Meckels diverticulitis
```
209
Colonic diverticulosis
Outpouching of the mucosa and submucosa due to weakness in muscularis propria
210
Meckel diverticulum
Congenital diverticulae of all three layers of the bowel wall due to failure of involution of the vitelline duct
50% cases with heterotopic rest of gastric mucosa or pancreatic tissue
211
Diverticula of jéjunum and ileum, rare or common ?
Rare
212
Population at risk of colonic diverticulae
Above 60 years old , 50% prevalence
Rate under 30
213
Morphology of colonic diverticulum
Flask like or spherical outpouching
Majority in sigmoid colon
Appear alongside teniae coli
Elastic
Compressible
Easily emptied of fecal contents
214
Histology of colonic diverticulum
Thin wall
Flat or atrophied mucosa
Attenuated or absent musucularis propria
Inflammation due to obstruction and or perforation
Fibrotic thickening ( can ressemble colonic cancer)
215
Complication of colonic diverticulum
Pericolic abscess
Sinus tracts
Pelvic peritonitis
Generalized peritonitis
216
Cholera pathogen involved
Comma shaped gram negative vibrio cholera
217
Number of great long lasting cholera epidemics
7
218
Which aero type of cholera associated with severe diarrhea
01 serotype
219
Pathogenesis of cholera disease
Invade lumen and secrete enterotoxin ( cholera toxin)
cAMP increases in cell which promote chloride and bicarbonate secretion with sodium and water secretion
Water secreted with small mucus ( 14L/day) leading to severe dehydration and electrolyte imbalance
220
Histology of cholera
Congestion of mucosal lamina propria
Moninuclear inflammatory cells infiltration
Hyperplasia of peyers patches
221
Thyphoid fever pathogen involved
Salmonellae typhi
222
Epidemiology of thyphoid fever
Underdeveloped countries
| Sanitary conditions insufficient
223
Presentation of thyphoid fever
```
Bacteremia
Fever
Chills
Reticuloendothelial involvement
Rash
Abdominal pain
Prostration
Intestinal bleeding
Shock
```
224
Typhoid fever pathogenesis
Salmonella invade epithelial cells and tissue macrophages
Proteins for adhesions and recruitment of host cytoskeletal proteins
225
Morphology of typhoid fever
Phagocytes proliferation
Reticuloendothelial and lymphoid tissue enlargement
Payers patches in terminal ileum
Oval ulcers with long axis in direction of bowel flow to
Enlarged, soft, bulging spleen ( pale red pulp)
Liver with parenchymal necrosis with phagocytiez mononuclear cell replacing hepatocytes forming typhoid module
Hall bladder colonized
226
Microscopy of typhoid fever
Macrophages withbbacteria and erythrocytes and nuclear debris
Lymphocytes and plasma cells with paucity of neutrophils
227
Ameobiasis pathogen
Entamoeba hystolitica
228
Presentation of amoeobiasis
Dysentery
Liver abscess
Intestinal pain
Fever
229
Ameobiasis payhogenesis
Cyst form release trophozoites
Attach colonic epithelium (lectin, channel forming protein, cysteine proteinases)
lyse colonic epithelial cells
230
Morphology of amoebiasis
Involves mostly caecum and ascending colon
Invade crypts
Flask shaped ulcers at muscularis mucosa
231
Microscopy of amoebiasis
Neutrophilic infiltrâtes in mucosa
Ulcers with few inflammatory hosts
Areas of liquefactive necrosis
Ameboema - napkin like constrictive lesion, profuse granulation
Parasite can embolies to the liver and produce liver absces
232
Bacterial enterocolitis
Various entities causing diarrheal illnesses
233
Pathogens involved in diarrhea caused by ingestion of preformed toxin
Staph aureus
Vibrios
Clostridium perfringens
234
Pathogens involved in diarrhea caused by toxigenic organism
E. coli
Shigella
They release enterotoxins
235
Pathogens involved in diarrhea caused by entrain as I’ve organism that destroy mucosal epithelial cells
Yersinia enterocolitica
236
Presentation of ingestion of preformed bacterial toxins
Symptoms in matter of hours
Explosive diarrhea
Acute abdominal distress
237
Presentation of infection with enteric pathogens
Incubation from hours to days
Diarrhea
Dehydration
Disentery
238
Presentation of insidious infections
Can present as subacute disease resembling CD
239
Bacterial enterocolitis complications
Dehydration
Sepsis
Perforation
Death
240
Necrotizing enterocolitis
Acute necrotizing inflammation of small and large intestine
241
What is most common acquired GIT energy of neonates
Necrotizing enterocolitis
242
Peak incidence of necrotizing enterocolitis
When infants start on oral food
243
Etiology of necrotizing enterocolitis
```
Combination of :
Ischemic injury
Pathogenic colonization
Excess proteins in lumen
Immaturity of neonate gut
```
244
Is necrotizing enterocolitis most prevalent in formula fed infants ?
Yes
245
Primary location affected by necrotizing enterocolitis
Terminal ileum
| Ascending colon
246
Necrotizing enterocolitis presentation
Early => bowel mucosa with edema, hemorrhage, necrosis
After
Full thickness is hemorrhagic, inflamed, grangenous
Bacterial overgrowth
Mural gas formation
Features of repairs ( epithelial regeneration, granulation, fibrosis)
Can have sepsis , perforation and shock
Distended tender abdomen
Ileus
Diarrhea with frank blood
247
Long term complications of necrotizing enterocolitis
Short bowel syndrome
| Malabsorption
248
Main origin of tumors in small and large intestine
Epithelial
249
Most common host of primary neoplasm in body
Colon
250
70% of all malignancies in GIT are
Adenocarcinoma
251
Main classification of intestinal tumors
Non neoplastic polyps
Neoplastic epithelial lesion
Neoplastic mesenchymal lesions
Other
252
Types of non neoplastic polyps
Hyperplastic polyps
Harmatomatous polyps
Inflammatory polyps
Lymphoid polyps
253
Type of neoplastic epithelial lesions
Benign ( tubular adeno ma, tubulovillous adenoma, villous)
Malignant ( adenocarcinoma, carcinoid tumors, anal zone carcinoma)
254
Type of neoplastic mesenchymal lesions
Benign ( leiomyoma, lipoma, neuroma, angioma)
Malignant ( leiomyosarcoma, liposarcoma, malignant spindle cel tumor, kaposis sarcoma)
Lymphoma
255
Hyperplastic polyps
Epithelial polyps
Seems mostly in 6th and 7th decade
Nipple like , hemispheric, moist protrusions of mucosa
Common in recto segmoid colon
Formed Glands and crypts with non neoplastic epithelial cells
256
Harmatomous polyps
Juvenile polyps ( sporadic or due to rare autosomal dominant juvenile polyposis syndrome)
80% in rectum
Large, round , smooth, slightly lobulated, stalked
Bulk of polyp with lamina propria enclosing abundant cystically dilated glands
Congested or ulcerated surface
Peutz jeghers polyps
Rare autosomal dominant syndrome
Multiple harmatomatous polyps in entire GIT
Melanotic mucosa
Cutaneous pigmentation around lips , oral mucosa, face, genitalia , palms
Large , pedunculated, firm lobulated contour
Connective tissue and well formed smooth muscle into polyp
257
Inflammatory polyps
Inflamed regenerating and reparative mucosa after ulceration
Granulation tissue
Seen in long CD and UD
258
Lymphoid polyps
Mucosal bumps with intra mucosal lymphoid tissue
259
Neoplastic epithelial lesions incidence
20-30% before 40 yo
40-50% after 60
260
most common type of neoplastic epithelial lesions
Tubular
261
Interdépendant features of malignancy risk of adenomatous polyp
Polyp size
Histologic architecture
Severity of epithelial dysplasia
262
In what type of neoplastic epithelial lesions is cancer more common
40% - sessile villous adenoma bigger than 4 cm
263
Colorectal tubular/tubulovillous adenoma mostly asymptomatic. So how is discovered
During anemia or occult bleeding evaluations
264
Why are villous adenoma more frequently symptomatic?
Associated with overt rectal bleeding
265
Majority of tubular adenoma located in
Colon (90%)
| Rectosigmoid (1/2)
266
Tubular adenoma microscopy
Stalk - fibromuscular tissue , prominent blood vessels, non neoplastic mucosa cover
Raspberry like head- neoplastic epithelium, all degree of dysplasia,
267
Villous adenoma major location
Rectum
| Rectosigmoid
268
Villous adenoma morphology
Sessile
Cauliflower like masses
Finger like Projection in surrounding normal mucosa with dysplatic columnar epithelium
269
Tubulovillous adenoma
Intermediate adenoma between tubular and villous lesions
270
Familial adenomatous polyposis
Lot of adenomatous polyps
| Mostly always progress to colon adenocarcinoma
271
Number of polyps required for FAP diagnosis
At least 100 polyps
272
Gardners syndrome
```
Variant of FAP with same polyps but with on top :
Multiple osteomas
Epidermal cysts
Fibromatosis
Dental abnormalities
Duodenal and thyroid cancer
```
273
Turcot syndrome
Multiple adenomatous polyps + CNS tumor
274
Major type of cancer in large intestine
Adenocarcinoma(95%)
275
Adenocarcinoma of large intestine characteristics
Arise in polyps
| Symptoms early when still curable by resection
276
Adenocarcinoma of large intestine incidence
60-70 yo
UC or one polyposis syndrome preexisting in young people
Affect men and women the same
277
Make:ratio in rectal cancer
2:1
278
Rectal adenocarcinoma etiology
Dietary ( low insoluble vegetables fiber , high CHO, high fat, low protective micronutrient
279
Cæcal and right colonic cancers clinical characteristics
```
Fatigue
Weakness
Iron deficiency anemia
Bulky and bleeding
Discovered at early stage
```
280
Left sided colonic cancers characteristics
Occult bleeding
Changes in bowel habit
Cramps lower quadrant discomfort
281
Why do cancer of rectum and sigmoid have poorer prognosis
More infiltrative at time of diagnosis
282
What does iron deficiency anemia in an old man means
Git cancer until proven otherwise
283
Sites of metastasis spread of colorectal tumors
Regional lymph nodes
Liver
Lungs
Bones
284
colorectal carcinoma classification
By stages
A- mucosa limited
B1- stops at muscularis propria (nodes neg)
B2- penetrates muscularis propria
C1- stops at muscularis propria (nodes pos)
C2- penetrates muscularis propria
D- distant metastatic spread
285
Proximal colon Colorectal carcinoma morphology
Polypoid
| Fungating masses
286
Distal colon Colorectal carcinoma morphology
Annular
Encircling lesions that produce constrictions
Napkin rings - mid region ulcerated , beaded, firm, heaped
287
Carcinoid tumors
Tumors of neuroendocrine cells
| Slow growing mostly arising from gut
288
Most common site of gut carcinoid
Appendix
289
Appendix carcinoid tumor morphology
Bulbous swelling of tip which can obliterate lumen
290
carcinoid tumor morphology
Appendix -> Bulbous swelling of tip which can obliterate lumen
in other part of the gut -> Intramural or submucosa masses / Small polypoid or plateau like elevations
Overlying intact or ulcerated mucosa
Solid yellow tan appearance or transection
291
Histology of carcinoid tumor morphology
Cells from discrete islands , trabeculae, glands, or undifferentiated sheets
Monotonous similar cells
Scant pink granular cytoplasm
Round to oval stipples nucleus
292
What type of tumors can produce gastrinoma, somatostatinoma, vipoma, insulinoma?
Carcinoïd tumors
293
Cause of carcinoid syndrome
Excess serotonin production
294
Clinical features of carcinoid syndrome
```
Vasomotor disturbances (cutaneous flushes)
Intestinal hypermotility
Asmathic broncho constrictive attack
Hepatomegaly
Systemic fibrosis
```
