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Pathology > Chapter 10 ( Gastrointestinal ) > Flashcards

Chapter 10 ( Gastrointestinal ) Flashcards

1
Q

Mechanism of cleft lip and palate ?

A

Due to failure of facial prominences to fuse

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2
Q

Aphthous ulcer is seen as ?

A

Grayish base surrounded by erythema

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3
Q

Mechanism of Behcet syndrome ?

A

Immune complex vasculitis involving small vessels

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4
Q

Where does HSV remains dormant after primary infection ?

A

Ganglia of trigeminal nerve

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5
Q

Causes of reactivation of HSV 1 ?

A

Stress

Sunlight

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6
Q

Leukoplakia ?

A

White plaque that can’t be scrabed away

Represents : squamous cell dysplasia

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7
Q

Oral candidiasis ?

A

White depositon the tongue that is easily scrapped away

Seen in immunocompromised patients

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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 !!!

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9
Q

Erythroplakia ?

A

Vascularized leukoplakia

Highly suggestive of squamous cell dysplasia

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10
Q

Why serum amylase is increased in mumps ?

A

Due to salivary gland or pancreatic involvement

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11
Q

Organism that cause sialadenitis ?

A

Staphylococcus aureus

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12
Q

Biphasic tumors composition ? Example ?

A

Stromal and epithelial tissue

Ex: Pleomorphic adenoma

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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

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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

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15
Q

Most common malignant tumor of the salivary gland ?

A

Mucoepidermoid carcinoma

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16
Q

Presentation of tracheoesophageal fistula ?

A

Polyhydramnios

Vomiting , abdominal distention , aspiration

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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

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18
Q

Site for zenker diverticulum ?

A

Above the upper esophageal sphincter , at the junction of the esophagus and pharynx

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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

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20
Q

Boerhaave syndrome ?

A

Rupture of esophagus leading to air in the mediastinum and subcutaneous emphysema

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21
Q

Mechanism of esophageal varices ? Presentation ?

A

Dilated submucosal veins in the lower esophagus secondary to portal hypertension
Presents with Painless hematemesis

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22
Q

Distal esophageal vein drains into the portal vein via ?

A

Left gastric vein

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23
Q

Most common cause of death in cirrhosis ?

A

Hematemesis due to esophageal varices

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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

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25
Q

Site of myenteric plexus ?

A

Between the inner circular and outer longitudinal layers of muscularis propria

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26
Q

Presentation of GERD ?

A

1- heartburn
2- asthma ( adult onset ) and cough
3- damage to enamel of teeth
4- ulceration with stricture , Barrett esophagus

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27
Q

Adenocarcinoma of the esophagus incidence ? Site ?

A

Most common esophageal carcinoma in the west
Usually the lower one third of the esophagus
Arises from preexisting Barrett esophagus

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28
Q

Squamous cell carcinoma of the esophagus incidence ? Site ?

A

Most common esophageal carcinoma world wide

In upper and middle third of the esophagus

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29
Q

Congenital malformation of the anterior abdominal wall ?

A

Gastroschisis

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30
Q

Time of presentation of pyloric stenosis ?

A

Two weeks after birth ( more commonly in males ) as :
Projectile NONBILIOUS vomiting
Visible peristalsis
Olive-like mass in the abdomen

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31
Q

Mucin layer of the stomach is produced by ?

A

Foveolar cells

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32
Q

Mechanism of Cushing ulcer ?

A

Increased intracranial pressure leads to increased stimulation of vagus nerve leads to increased acid production

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33
Q

Pathogenesis of chronic autoimmune gastritis is mediated by ?

A

T cells ( type Vl hypersensitivity reaction )

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34
Q

Clinical features of chronic autoimmune gastritis ?

A

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 )

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35
Q

How to confirm eradication of H pylori ?

A

Negative urea breath test

Lack of stool antigen

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36
Q

Mechanism of H pylori chronic gastritis ?

A

H pylori proteases and ureases along with inflammation weaken mucosal defenses
Antrum is the most common site .

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37
Q

H pylori chronic gastritis increases the risk for which cancers ?

A 
Gastric Adenocarcinoma ( intestinal type ) 
MALT lymphoma
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38
Q

Causes of duodenal ulcer ?

A

H pylori 95%

Zollinger Ellison syndrome

39
Q

Duodenal ulcer most common site ? Microscopic findings ? Presentation ?

A

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
Q

Gastric ulcer presentation ? Most common site ? Rupture result in ?

A

Epigastric pain that worsens with meals

On the lesser curvature of the antrum

Bleeding from left gastric artery

41
Q

Risk factors for gastric carcinoma intestinal type ?

A

1- Intestinal metaplasia ( due to H pylori or autoimmune )
2- Nitrosamines in smoked foods ( Japan )
3- Blood type A

42
Q

Characteristics of gastric carcinoma diffuse type ?

A

Signet ring cells that diffusely infiltrate the gastric wall
Desmoplasia results in thickening of the stomach wall ( linitis plastica )

43
Q

Presentation of Gastric carcinoma ?

A

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
Q

Sister Mary joseph nodules are seen with which type of gastric carcinoma ?

A

Intestinal type

45
Q

Krukenberg tumor is seen with which type of gastric carcinoma ?

A

Diffuse type

46
Q

Duodenal atresia is associated with ? Clinical features ?

A 
Down syndrome 
Clinically :
Polyhydramnios 
Double bubble sign 
BILIOUS vomiting
47
Q

Mechanism of Meckel diverticulum ?

A

True diverticulum

Due to failure of the vitelline duct to involute

48
Q

Most common congenital anomaly of the git ?

A

Meckel diverticulum

49
Q

Most common locations for volvulus ?

A

In elderly : Sigmoid colon

In young adults : Cecum

50
Q

Most common cause of intussusception in children and adults ?

A

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
Q

Cause of transmural infarction of the small bowel ?

A

Thrombosis or Embolism of the superior mesenteric artery

Thrombosis of the mesenteric vein

52
Q

Cause of mucosal infarction of the small bowel ?

A

Marked hypotension

53
Q

Cause of temporary deficiency of Lactase enzyme ?

A

After small bowel infection ( as Lactase is highly susceptible to injury )

54
Q

Mechanism of Celiac disease ?

A

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
Q

Mechanism of Dermatitis Herpetiformis in Celiac disease ?

A

Due to IgA deposition at the tips of dermal papillae , resolves with gluten free diet

56
Q

Laboratory findings of Celiac disease ?

A

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
Q

Damage distribution to different sites of the bowel in Celiac disease ?

A

Most prominent in Duodenum

Jejunum and ileum are less involved

58
Q

Late complications of celiac disease ?

A

Small bowel carcinoma

T cell lymphoma ( EATL )

59
Q

Mechanism of Tropical Sprue ?

A

Damage to small bowel villi due to unknown organism resulting in malabsorption
Arises after infectious diarrhea and responds to Antibiotics

60
Q

Damage distribution to the bowel in Tropical Sprue ?

A

Most prominent in Jejunum and Ileum

Less common in Duodenum

61
Q

Mechanism of Whipple disease ?

A

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
Q

Sites of involvements in Whipple disease ?

A 
Small bowel lamina propria 
Synovium of joints ( arthritis ) 
Cardiac valves 
LN
CNS
63
Q

Mechanism of carcinoid syndrome and carcinoid heart disease ?

A

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
Q

Carcinoid syndrome presentation ? Triggered by ?

A

Bronchospasm
Diarrhea
Flushing of skins
Triggered by : alcohol or emotional stress which stimulate serotonin release from the tumor

65
Q

Carcinoid heart disease is characterized by ?

A

Right sided valve fibrosis ( increased collagen ) leading to TR and PS

66
Q

Why left sided valvular lesions aren’t seen in cardiac carcinoid disease ?

A

Due to presence of Monoamine Oxidase in the Lung which metabolized serotonin into 5-HIAA

67
Q

Mechanism of carcinoid tumor ? Its site ? Its appearance ?

A

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
Q

Ulcerative colitis wall involvement ? Location ? Presentation ?

A

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
Q

Ulcerative colitis microscopic and gross findings ? Complications ? Associations ?

A

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
Q

Crohn disease wall involvement ? Location ? Symptoms ?

A

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
Q

Crohn disease microscopic and gross findings ? Complications ? Associations ?

A

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
Q

Smoking effect on inflammatory bowel diseases risk ?

A

Protect against Ulcerative colitis

Increases risk for Crohn disease

73
Q

Mechanism of Hirschsprung disease ?

A

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
Q

Hirschsprung disease is associated with ?

A

Down syndrome

75
Q

Clinical features of Hirschsprung disease ? Diagnosis ? Ttt ?

A

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
Q

Colonic diverticula mechanism ? Associated with ? Site ? Complications ?

A

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
Q

Angiodysplasia of the colon mechanism ? Site ? Presentation ?

A

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
Q

Hereditary hemorrhagic telangiectasia mode of inheritance ? Site ? Presentation ?

A

Autosomal dominant resulting in thin walled blood vessels

Especially in mouth and GIT

Presents by bleeding due to rupture

79
Q

Ischemic colitis most common site ? Most common cause ? Presentation ?

A

At the splenic flexure ( watershed area of SMA

Atherosclerosis of SMA

Presentation : postprandial pain , weight loss , infarction results in pain and bloody diarrhea

80
Q

Hyperplastic polyps mechanism ? Site ? Microscopical appearance ?

A

Due to hyperplasia of the glands ( benign with no malignant potential )

Site : usually in the left colon ( rectosigmoid )

Micro : Serrated appearance

81
Q

Adenomatous polyp mechanism ?

A

Due to neoplastic proliferation of the glands ( benign but premalignant , can progress to adenocarcinoma by adenoma-carcinoma sequence )

82
Q

Most common types of colonic polyps ?

A

1st : Hyperplastic polyps

2nd : Adenomatous polyps

83
Q

Adenoma-carcinoma sequence ?

A

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
Q

Role of Aspirin in Colonic polyps ttt ?

A

Impedes progression from adenoma to carcinoma

85
Q

Screening for polyps is done by ?

A

Colonoscopy

Testing for fecal occult blood

86
Q

Greatest risk for progression from adenoma to carcinoma in colonic polyps ?

A

1- Size > 2 cm
2- Sessile growth
3-Villous histology

87
Q

On colonoscopy , which type of colonic polyps is removed ?

A

All polyps are removed and examined microscopically ( because on colonoscopy hyperplastic and adenomatous polyps looks identical )

88
Q

Mechanism of Familia adenomatous polyps ?

A

Autosomal dominant

Inherited APC mutation on chromosome 5

89
Q

Gardner syndrome ?

A

FAP
Fibromatosis
Osteomas

90
Q

Turcot syndrome ?

A 
FAP
CNS tumors ( medulloblastoma and glial tumors )
91
Q

Fibromatosis ?

A

Non neoplastic proliferation of fibroblasts , arises in retroperitoneum ( desmoid ) and locally destroys tissue

92
Q

Peutz Jeghers syndrome mode of inheritance ? Presentation ? Increase risk for ?

A 
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
Q

Tumor marker of colorectal carcinoma ? Its usage ?

A

CEA

Assessing ttt response
Detecting recurrence

Pathology (18 decks)

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