Chapter 10 ( Gastrointestinal ) Flashcards
1
Q
Mechanism of cleft lip and palate ?
A
Due to failure of facial prominences to fuse
2
Q
Aphthous ulcer is seen as ?
A
Grayish base surrounded by erythema
3
Q
Mechanism of Behcet syndrome ?
A
Immune complex vasculitis involving small vessels
4
Q
Where does HSV remains dormant after primary infection ?
A
Ganglia of trigeminal nerve
5
Q
Causes of reactivation of HSV 1 ?
A
Stress
Sunlight
6
Q
Leukoplakia ?
A
White plaque that can’t be scrabed away
Represents : squamous cell dysplasia
7
Q
Oral candidiasis ?
A
White depositon the tongue that is easily scrapped away
Seen in immunocompromised patients
8
Q
Hairy Leukoplakia ?
A
White rough patch that arises on the lateral surface of the tongue
Seen in immunocompromised patients
Due to EBV-induced squamous cell HYPERPLASIA
NOT PREMALIGNANT !!!
9
Q
Erythroplakia ?
A
Vascularized leukoplakia
Highly suggestive of squamous cell dysplasia
10
Q
Why serum amylase is increased in mumps ?
A
Due to salivary gland or pancreatic involvement
11
Q
Organism that cause sialadenitis ?
A
Staphylococcus aureus
12
Q
Biphasic tumors composition ? Example ?
A
Stromal and epithelial tissue
Ex: Pleomorphic adenoma
13
Q
Cause of high rate of recurrence in pleomorphic adenoma ?
A
Extension of small islands of tumor through tumor capsule often leads to incomplete resection
14
Q
Warthin tumor ? Its incidence?
A
Benign cystic tumor with abundant lymphocytes and germinal centers ( lymph node-like stroma )
2nd most common tumor of the salivary gland
15
Q
Most common malignant tumor of the salivary gland ?
A
Mucoepidermoid carcinoma
16
Q
Presentation of tracheoesophageal fistula ?
A
Polyhydramnios
Vomiting , abdominal distention , aspiration
17
Q
Esophageal web mechanism ? Most common site ? Presentation ?
A
Thin protrusion of esophageal mucosa
Most often in the upper esophagus
Presents with dysphagia for poorly chewed food
18
Q
Site for zenker diverticulum ?
A
Above the upper esophageal sphincter , at the junction of the esophagus and pharynx
19
Q
Mallory-Weiss syndrome description ? Causes ? Presentation ?
A
Longitudinal laceration of the mucosa at the gastroesophageal junction
Caused by : sever vomiting due to alcoholism or bulimia
Presents with : Painful hematemesis
20
Q
Boerhaave syndrome ?
A
Rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema
21
Q
Mechanism of esophageal varices ? Presentation ?
A
Dilated submucosal veins in the lower esophagus secondary to portal hypertension
Presents with Painless hematemesis
22
Q
Distal esophageal vein drains into the portal vein via ?
A
Left gastric vein
23
Q
Most common cause of death in cirrhosis ?
A
Hematemesis due to esophageal varices
24
Q
Mechanism of Achalasia ?
A
Due to damaged ganglion cells in the myenteric plexus
Damage to the ganglion cells can be idiopathic or secondary to known insult as :
Trypanosome cruzi infection in Chagas disease
25
Site of myenteric plexus ?
Between the inner circular and outer longitudinal layers of muscularis propria
26
Presentation of GERD ?
1- heartburn
2- asthma ( adult onset ) and cough
3- damage to enamel of teeth
4- ulceration with stricture , Barrett esophagus
27
Adenocarcinoma of the esophagus incidence ? Site ?
Most common esophageal carcinoma in the west
Usually the lower one third of the esophagus
Arises from preexisting Barrett esophagus
28
Squamous cell carcinoma of the esophagus incidence ? Site ?
Most common esophageal carcinoma world wide
| In upper and middle third of the esophagus
29
Congenital malformation of the anterior abdominal wall ?
Gastroschisis
30
Time of presentation of pyloric stenosis ?
Two weeks after birth ( more commonly in males ) as :
Projectile NONBILIOUS vomiting
Visible peristalsis
Olive-like mass in the abdomen
31
Mucin layer of the stomach is produced by ?
Foveolar cells
32
Mechanism of Cushing ulcer ?
Increased intracranial pressure leads to increased stimulation of vagus nerve leads to increased acid production
33
Pathogenesis of chronic autoimmune gastritis is mediated by ?
T cells ( type Vl hypersensitivity reaction )
34
Clinical features of chronic autoimmune gastritis ?
1- Atrophy of mucosa with intestinal metaplasia
2- Achlorhydria with increased gastrin levels and ANTRAL G CELL HYPERPLASIA
3- Megaloblastic anemia due to lack of intrinsic factor
4- increased risk for Gastric Adenocarcinoma ( intestinal type )
35
How to confirm eradication of H pylori ?
Negative urea breath test
| Lack of stool antigen
36
Mechanism of H pylori chronic gastritis ?
H pylori proteases and ureases along with inflammation weaken mucosal defenses
Antrum is the most common site .
37
H pylori chronic gastritis increases the risk for which cancers ?
```
Gastric Adenocarcinoma ( intestinal type )
MALT lymphoma
```
38
Causes of duodenal ulcer ?
H pylori 95%
| Zollinger Ellison syndrome
39
Duodenal ulcer most common site ? Microscopic findings ? Presentation ?
Anterior duodenum , when present in posterior duodenum , rupture may lead to bleeding from gastroduodenal artery or acute pancreatitis
Microscopically : hypertrophy of Brunner glands
Presents with epigastric pain that improves with meals
40
Gastric ulcer presentation ? Most common site ? Rupture result in ?
Epigastric pain that worsens with meals
On the lesser curvature of the antrum
Bleeding from left gastric artery
41
Risk factors for gastric carcinoma intestinal type ?
1- Intestinal metaplasia ( due to H pylori or autoimmune )
2- Nitrosamines in smoked foods ( Japan )
3- Blood type A
42
Characteristics of gastric carcinoma diffuse type ?
Signet ring cells that diffusely infiltrate the gastric wall
Desmoplasia results in thickening of the stomach wall ( linitis plastica )
43
Presentation of Gastric carcinoma ?
1- Acanthosis negricans ( dark thickening of axillary skin )
2- Leser Trelat sign ( acute seborrheic keratosis all over the skin )
3- Early satiety
4- weight loss , abdominal pain , anemia
44
Sister Mary joseph nodules are seen with which type of gastric carcinoma ?
Intestinal type
45
Krukenberg tumor is seen with which type of gastric carcinoma ?
Diffuse type
46
Duodenal atresia is associated with ? Clinical features ?
```
Down syndrome
Clinically :
Polyhydramnios
Double bubble sign
BILIOUS vomiting
```
47
Mechanism of Meckel diverticulum ?
True diverticulum
| Due to failure of the vitelline duct to involute
48
Most common congenital anomaly of the git ?
Meckel diverticulum
49
Most common locations for volvulus ?
In elderly : Sigmoid colon
| In young adults : Cecum
50
Most common cause of intussusception in children and adults ?
1- in children : Lymphoid hyperplasia ( ex : due to rotavirus ) usuallu arises in the terminal ileum leading to intussusception into the cecum
2- in adults : Tumor
51
Cause of transmural infarction of the small bowel ?
Thrombosis or Embolism of the superior mesenteric artery
| Thrombosis of the mesenteric vein
52
Cause of mucosal infarction of the small bowel ?
Marked hypotension
53
Cause of temporary deficiency of Lactase enzyme ?
After small bowel infection ( as Lactase is highly susceptible to injury )
54
Mechanism of Celiac disease ?
Immune-mediated damage of small bowel villi due to gluten exposure , associated with HLA-DQ2 and DQ8
Gliadin is deaminated by tissue transglutaminase (tTG) —> deaminated gliadin is presented by APCs via MHC class ll —> Helper T cells mediate tissue damage
55
Mechanism of Dermatitis Herpetiformis in Celiac disease ?
Due to IgA deposition at the tips of dermal papillae , resolves with gluten free diet
56
Laboratory findings of Celiac disease ?
1- IgA antibodies against : endomysium , tTG , gliadin
IgG antibodies are also present and useful in diagnosis of individuals with IgA deficiency ( increased risk for IgA deficiency in Celiac disease )
2- duodenal biopsy reveals :
flattening of villi
Hyperplasia of crypts
Increased intraepithelial lymphocytes
57
Damage distribution to different sites of the bowel in Celiac disease ?
Most prominent in Duodenum
| Jejunum and ileum are less involved
58
Late complications of celiac disease ?
Small bowel carcinoma
| T cell lymphoma ( EATL )
59
Mechanism of Tropical Sprue ?
Damage to small bowel villi due to unknown organism resulting in malabsorption
Arises after infectious diarrhea and responds to Antibiotics
60
Damage distribution to the bowel in Tropical Sprue ?
Most prominent in Jejunum and Ileum
| Less common in Duodenum
61
Mechanism of Whipple disease ?
Systemic tissue damage charcterized by macrophages loaded with Tropheryma Whippelii organisms , partially destroyed organisms are present in macrophages lysosomes ( positive for PAS )
Classic site of involvement is small bowel lamina propria where :
Macrophages compress lacteals
Chylomicrons can’t be transferred from enterocytes to lymphatics resulting in fat malabsorption and steatorrhea
62
Sites of involvements in Whipple disease ?
```
Small bowel lamina propria
Synovium of joints ( arthritis )
Cardiac valves
LN
CNS
```
63
Mechanism of carcinoid syndrome and carcinoid heart disease ?
Carcinoid tumor often secrets Serotonin which is released into portal circulation and metabolized by Liver by Monoamine Oxidase into 5-HIAA
Metastasis of carcinoid tumor into liver allows serotonin to bypass liver metabolism
Serotonin is released into hepatic vein and leaks into systemic circulation via hepatosytemic shunts resulting in carcinoid tumor and carcinoid heart disease
64
Carcinoid syndrome presentation ? Triggered by ?
Bronchospasm
Diarrhea
Flushing of skins
Triggered by : alcohol or emotional stress which stimulate serotonin release from the tumor
65
Carcinoid heart disease is characterized by ?
Right sided valve fibrosis ( increased collagen ) leading to TR and PS
66
Why left sided valvular lesions aren’t seen in cardiac carcinoid disease ?
Due to presence of Monoamine Oxidase in the Lung which metabolized serotonin into 5-HIAA
67
Mechanism of carcinoid tumor ? Its site ? Its appearance ?
Malignant proliferation of neuroendocrine cells , low grade malignancy
Tumor cells contains neurosecretory granules that are positive for Chromogranin
Grows as submucosal polyp like nodule anywhere in the gut specially the small bowel
68
Ulcerative colitis wall involvement ? Location ? Presentation ?
Mucosal and submucosal ulcers
Begins in the rectum and can extend proximally to the cecum ( involvement is continuous ) other parts of the git is unaffected
Left lower quadrant pain with bloody diarrhea
69
Ulcerative colitis microscopic and gross findings ? Complications ? Associations ?
Micro : Crypt abscesses with neutrophils
Gross : pseudopolyps , loss of haustra ( lead pipe on imaging )
Complications : Toxic megacolon and carcinoma
Associations :
Primary sclerosing cholangitis
p-ANCA positive
Joints problems : ankylosing spondylitis , sacroilitis , migratory polyarthritis
70
Crohn disease wall involvement ? Location ? Symptoms ?
Full thickness inflammation with knife like fissures
Anywhere from mouth to anus with skip lesions
The most common site : terminal ileum
The least common site : rectum
Right lower quadrant pain with non bloody diarrhea
71
Crohn disease microscopic and gross findings ? Complications ? Associations ?
Micro : Lymphoid aggregates and Granulomas(40% of cases )
Gross : Cobble stone mucosa , Creeping fat , strictures ( string sign on imaging )
```
Complications :
Malabsorption with nutritional deficiency
Ca oxalate nephrolithiasis
Fistula formation
Carcinoma ( in colon is involved )
```
Associations : Erythema nodosum and Uveitis
72
Smoking effect on inflammatory bowel diseases risk ?
Protect against Ulcerative colitis
| Increases risk for Crohn disease
73
Mechanism of Hirschsprung disease ?
Defective relaxation and peristalsis of rectum and distal sigmoid colon
Due to failure of ganglion cells ( neural crest derived ) to descend into myenteric and submucosal plexus
74
Hirschsprung disease is associated with ?
Down syndrome
75
Clinical features of Hirschsprung disease ? Diagnosis ? Ttt ?
1- Failure to pass meconium
2- empty rectal vault on DRE
3- megacolon with risk of rupture
Diagnosis by Rectal SUCTION biopsy which reveals lack of ganglion cells
Ttt by resection of involved segment
76
Colonic diverticula mechanism ? Associated with ? Site ? Complications ?
False diverticulum
Associated with : constipation , straining , low fiber diet
Site : where the vasa recta traverse the muscularis propria ( weak point in colonic wall )
The most common location : Sigmoid colon
Complications : hematochezia , diverticulitis , fistula
77
Angiodysplasia of the colon mechanism ? Site ? Presentation ?
ACQUIRED malformation of mucosal and submucosal capillary bed
In the cecum and right colon ( due to high wall tension )
Presents as hematochezia due to rupture
78
Hereditary hemorrhagic telangiectasia mode of inheritance ? Site ? Presentation ?
Autosomal dominant resulting in thin walled blood vessels
Especially in mouth and GIT
Presents by bleeding due to rupture
79
Ischemic colitis most common site ? Most common cause ? Presentation ?
At the splenic flexure ( watershed area of SMA
Atherosclerosis of SMA
Presentation : postprandial pain , weight loss , infarction results in pain and bloody diarrhea
80
Hyperplastic polyps mechanism ? Site ? Microscopical appearance ?
Due to hyperplasia of the glands ( benign with no malignant potential )
Site : usually in the left colon ( rectosigmoid )
Micro : Serrated appearance
81
Adenomatous polyp mechanism ?
Due to neoplastic proliferation of the glands ( benign but premalignant , can progress to adenocarcinoma by adenoma-carcinoma sequence )
82
Most common types of colonic polyps ?
1st : Hyperplastic polyps
| 2nd : Adenomatous polyps
83
Adenoma-carcinoma sequence ?
Describes the molecular progression from normal colonic mucosa to adenomatous polyps to carcinoma :
1- APC gene mutations ( sporadic or germline ) : increase risk fro formation of polyps
2- K-ras mutation leads to formation of polyps
3- p53 mutation and increased expression of COX : allow for progression to carcinoma
84
Role of Aspirin in Colonic polyps ttt ?
Impedes progression from adenoma to carcinoma
85
Screening for polyps is done by ?
Colonoscopy
| Testing for fecal occult blood
86
Greatest risk for progression from adenoma to carcinoma in colonic polyps ?
1- Size > 2 cm
2- Sessile growth
3-Villous histology
87
On colonoscopy , which type of colonic polyps is removed ?
All polyps are removed and examined microscopically ( because on colonoscopy hyperplastic and adenomatous polyps looks identical )
88
Mechanism of Familia adenomatous polyps ?
Autosomal dominant
| Inherited APC mutation on chromosome 5
89
Gardner syndrome ?
FAP
Fibromatosis
Osteomas
90
Turcot syndrome ?
```
FAP
CNS tumors ( medulloblastoma and glial tumors )
```
91
Fibromatosis ?
Non neoplastic proliferation of fibroblasts , arises in retroperitoneum ( desmoid ) and locally destroys tissue
92
Peutz Jeghers syndrome mode of inheritance ? Presentation ? Increase risk for ?
```
Autosomal dominant disorder
Hamartomatous polyps throughout the git
Mucocutaneous hyperpigmentation ( freckle like spots ) on lips , oral mucosa , genital skin
```
Increase risk for colorectal , breast , gynecologic cancers
93
Tumor marker of colorectal carcinoma ? Its usage ?
CEA
Assessing ttt response
Detecting recurrence
