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Pathology > GIT Disorder part 2 > Flashcards

GIT Disorder part 2 Flashcards

1
Q

Alcohol induced esophageal disorders can be divided into

A

Mallory weis tear
Borhaave Syndrome

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2
Q

In Mallory weis tear there is

A

There is mucosal tear due to repeated vomiting

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3
Q

Sites of Mallory weis tear

A

90% cases - Present below gastroesophageal junction
10% cases - in lower part of Esophagus

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4
Q

In Borhaave Syndrome there is involvement of

A

Muscle layer due to repeated vomiting

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5
Q

Site of Borhaave Syndrome

A

Usually above 3-5cm from GE junction and involves posterolateral part of Esophagus

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6
Q

Triad seen in Borhaave Syndrome termed as

A

Mackler’s triad

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7
Q

Mackler’s triad includes

A

Chest pain
Repeated vomiting - Painful hematemesis(blood in vomiting)
Subcutaneous emphysema

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8
Q

Hamman crunch on auscultation is heard in which condition

A

Subcutaneous emphysema

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9
Q

Most common motility disorder of Esophagus

A

Achalasia cardia

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10
Q

Stimulatory neurons present in esophagus have

A

Acetylcholine - helps in muscle contraction

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11
Q

Inhibitory neurons present in esophagus have

A

Nitric oxide
Vasoactive intestinal peptide(VIP) - helps in muscle relaxation

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12
Q

In case of Achalasia cardia, there is selective loss of

A

Inhibitory neurons

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13
Q

Which part of Esophagus commonly involved in Achalasia cardia

A

Lower part of Esophagus - lower esophageal sphincter doesn’t works properly - incomplete relaxation of LES

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14
Q

Triad seen in Achalasia cardia

A

Increased LES tone
Aperistalsis
Incomplete LES relaxation

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15
Q

Primary causes of Achalasia cardia

A

Idiopathic

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16
Q

Secondary causes of Achalasia cardia

A

Trypanosoma cruzi (Chagas disease)
Varicella zoster
Cancer
Autoimmune disorders

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17
Q

Clinical features of Achalasia cardia

A

Dysphagia - difficulty in swallowing food
Liquids > Solid
Weight loss

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18
Q

Complications seen in Achalasia cardia

A

Regurgitation - food aspiration - can lead to lung infection - Lung abscess
High risk of development of cancer

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19
Q

Most common complication seen in Achalasia cardia

A

Lung abscess

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20
Q

Risk of what type of cancer in case of Achalasia cardia

A

Squamous cell carcinoma

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21
Q

Investigation of choice in Achalasia cardia

A

Manometry

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22
Q

Appearance seen in Barium swallow method in case of Achalasia cardia

A

“Bird-beak appearance”- Dilation of proximal part due to accumulation of food

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23
Q

Allgrove syndrome

A

Triple A disease
Achalasia
Alacrimia
ACTH resistant adrenal insufficiency

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24
Q

Management of Achalasia cardia

A

Botulinum toxin - decreases Ach activity
Surgery

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25
Q

Surgery performed in case of Achalasia cardia

A

Myotomy - Heller’s myotomy + Partial fundopligation

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26
Q

Epithelium present in esophagus

A

Stratified squamous non keratinized epithelium

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27
Q

Esophagus size in adult

A

25cm

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28
Q

Esophagus normal size in newborn

A

10cm

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29
Q

Serosa is not found in which part of GIT

A

Esophagus

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30
Q

How many constrictions are present in normal esophagus

A

4

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31
Q

Constrictions seen in esophagus

A

Upper esophageal constrictor - 6 inch- 15cm
Aortic arch - 9inch - 22.5cm
Left bronchus - 11inch - 27.5cm
Lower esophageal sphincter - 16inch - 40cm

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32
Q

Which constriction is narrowest

A

Upper esophageal constrictor - Cricopharyngeus muscle

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33
Q

Why there is high muscle tone in lower esophageal sphincter

A

To prevent backflow of stomach contents in esophagus

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34
Q

Esophagitis means

A

Inflammation of esophagal lining

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35
Q

Causes of esophagitis

A

Chemical esophagitis
Infections
Reflux esophagitis

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36
Q

Chemical cause of Esophagitis includes

A

Drugs - Bisphosphonates (Osteoporosis medicine)
Doxycycline

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37
Q

Infectious causes leading to esophagitis

A

Fungal - Candida
Virus - HSV - Punched out ulcer ,
CMV - Shallow ulcer

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38
Q

Biopsy taken in case of viral HSV Esophagitis

A

Taken from edge of ulcer
Multinucleate squamous epithelial cells
Eosinophilic Cowdry’s inclusions

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39
Q

Biopsy in CMV Esophagitis

A

Basophilic intranuclear inclusions
“Owl-eye appearance”

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40
Q

Commonest cause of Esophagitis

A

Reflux esophagitis

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41
Q

Reflux esophagitis means

A

Inflammation of Esophagus due to reverse content of stomach into esophagus

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42
Q

Most common cause of Reverse esophagitis

A

Decreased tone of LES
TLESR

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43
Q

Full form of TLESR

A

Transient lower esophageal sphincter relaxation

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44
Q

TLESR is aggravated by which factors

A

Alcohol
Smoking
Fatty foods
Obesity/overeating
Pregnancy
Chocolates or coffee
Hiatal hernia

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45
Q

Clinical features in Esophagitis

A

Retrosternal chest pain - Heartburn
Sour brash
Teeth discoloration

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46
Q

Investigation of choice in Esophagitis

A

24 hour pH study

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47
Q

Diagnostic methods used in case of Esophagitis

A

Endoscopy + Biopsy

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48
Q

Due to Metaplasia lower end of Esophagus changes to which epithelium

A

Intestinal columnar epithelium

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49
Q

Intestinal columnar epithelium contains and secrets

A

Contains goblet cells - secrets acidic mucin

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50
Q

Goblet cells in intestinal columnar epithelium are stained by

A

Alcian blue

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51
Q

Barret’s esophagus means

A

Upper part - SSNK epithelium
Lower part - Intestinal columnar epithelium

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52
Q

In Barret’s esophagus, if changed lining less than 3cm then its termed as

A

Short Barret’s esophagus

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53
Q

In Barret’s esophagus, if changed lining is more than 3cm then its termed as

A

Long Barret’s esophagus

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54
Q

If there is metaplasia for long term them it can leads to

A

Mutations - increased risk of cancer - Adenocarcinoma (lower part of Esophagus)

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55
Q

In case of Barret’s esophagus Biopsy is usually taken from which junction

A

Squamocolumnar junction

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56
Q

Treatment of Esophagitis

A

Proton pump inhibitors
Prokinetic drugs
Surgical - Fundopligation

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57
Q

Types of esophageal tumors

A

Benign tumors
Malignant tumors

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58
Q

Bening esophageal tumor includes

A

Leiomyoma (M.C)

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59
Q

Leiomyoma

A

M>F
Involves 2/3rd area of lower esophagus
Asymptomatic for long time

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60
Q

Subtypes of Malignant esophageal tumors

A

Squamous cell cancer (M.c in World)
Adenocarcinoma (M.C in USA)

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61
Q

Squamous cell cancer usually affects which part of Esophagus

A

Upper 1/3rd and
Middle 1/3rd

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62
Q

Adenocarcinoma usually affects which part of Esophagus

A

Lower 1/3rd except long standing achalasia cardia

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63
Q

Risk factors of Squamous cell cancer

A

Smoking/Alcohol
Nitrosamines - Smoked food
Chronic Achalasia cardia
Hot beverages
Radiation
Tylosis et palmaris
Celiac disease
Mursik
Plummer vinson Syndrome
HPV

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64
Q

Triad seen in Plummer vinson Syndrome

A

IDA
Esophageal web
Atrophic glossitis

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65
Q

Risk factors of Esophageal Adenocarcinoma

A

Whites
Long standing GERD
Barret’s esophagus
Smoking/Alcohol
Obesity
Scleroderma
Radiation

66
Q

Which bacterial infection reduces risk of esophageal Adenocarcinoma

A

H. Pylori - leads to gastric atrophy - acid secretion decreases - decreases risk of Barret’s esophagus

67
Q

Early mutations seen in Esophageal Adenocarcinoma

A

P53 mutations

68
Q

Late mutations seen in Esophageal Adenocarcinoma

A

Cyclin D1 and Cyclin E overexpression

69
Q

Clinical features of Esophageal tumors

A

Progressive dysphagia
Weight loss
Can involve recurrent laryngeal nerve - Hoarseness

70
Q

Investigation of choice in case of Esophageal tumors

A

Endoscopy + Biopsy

71
Q

Biopsy findings in Esophageal Adenocarcinoma

A

Multiple glands like structures - can be diffuse or interstitial

72
Q

Biopsy findings in Squamous cell carcinoma

A

Keratin pearls +

73
Q

Barium swallow finding in case of Esophageal tumors

A

“Rat-Tail defects”

74
Q

Most common metastasis in Esophageal tumors

A

Hepatic

75
Q

Paraneoplastic syndrome in Esophageal tumors

A

Hypercalcemia

76
Q

LN affected when tumors is in upper 1/3rd part of esophagus

A

Cervical LN

77
Q

LN involved when esophageal tumor affected middle 1/3rd part of esophagus

A

Mediastinal LN

78
Q

LN involved when Esophageal tumor present in lower 1/3rd of Esophagus

A

Celiac LN, Gastric LN, Cardiac LN

79
Q

Treatment in case of Esophageal tumors

A

Esophagectomy - Partial or Total

80
Q

Overall prognosis of esophageal tumors

A

Bad prognosis

81
Q

Parts of stomach

A

Cardia
Fundus - air present - On X ray gastric air bubble
Body
Antrum
Pylorus

82
Q

Parietal cells of stomach secrets

A

Intrinsic factor - helps in Vitamin B12 absorption
HCL

83
Q

Parietal cells are stimulated by

A

Ach
Gastrin
Histamine

84
Q

Cheif cells of stomach secrets

A

Pepsinogen - helps in food digestion

85
Q

Foveolar cells of stomach secrets

A

Mucus in stomach - make layer in internal lining of stomach - Protection from HCL

86
Q

Endocrine or G cell in stomach secrets

A

Gastrin - Stimulates HCL secretion

87
Q

Damagin factors in stomach

A

HCL

88
Q

Damaging factor HCL can be aggravated by which bacteria

A

H. Pylori

89
Q

Protective factors of Stomach

A

High epithelial regenerative activity - Stress, Shock
Bicarbonates - neutralizes HCL
Mucus - makes protective layer
Prostaglandins - Protective for gastric mucosa

90
Q

Acute gastritis causes due to

A

Imbalance between damaging and protective factors

91
Q

Inflitration of which cells seen in Acute gastritis

A

Neutrophilic infiltration

92
Q

Risk factors of Acute gastritis

A

Alcohol intake
Stress
Drugs - NSAIDS
Anticancer drugs
Uremia
Burns
Increased intracranial tension

93
Q

Ulcer seen in acute gastritis due to burns

A

Curling ulcer - due to burn there is dehydration - epithelial regeneration interrupted

94
Q

Type of ulcer seen in acute gastritis due to increased intracranial tension

A

Cushing’s ulcer - Stomach only

95
Q

In chronic gastritis there is infiltration of which type of cells

A

Lymphocytes/plasma cells inflitration

96
Q

Causes of chronic gastritis

A

Autoimmune
H pylori
Chemical exposure
Radiation exposure/Grafts vs host disesase
Crohn’s disesase

97
Q

Type of gastritis due to Autoimmune disorders

A

Type A gastritis

98
Q

Type of gastritis due to H pylori infection

A

Type B gastritis

99
Q

Type of gastritis due to Chemicals exposure

A

Type C gastritis

100
Q

Most common cause of Chronic gastritis

A

H pylori

101
Q

Type A gastritis seen in how much percent of cases

A

8-10%

102
Q

Most common affected area in type A gastritis

A

Body/Fundus

103
Q

Most common cause of Type A gastritis

A

Autoimmune disorders

104
Q

CD4 T cells present in Type A gastritis can damage

A

Parietal cells - decreased Hcl secretion (Achlorhydria)
And due to feedback mechanism Gastrin level increases (Hypergastrinemia)

105
Q

In Type A gastritis there is high risk of development of

A

Type 1 DM
Hashimoto disease
Pernicious anemia

106
Q

Due to chronic inflammation in Type A gastritis

A

Can lead to intestinal metaplasia - increased risk of gastric cancer

107
Q

Type B gastritis can be seen in how much percent of cases

A

90-92%

108
Q

Bacteria responsible for Type B gastritis

A

H pylori

109
Q

H pylori secrets

A

Increased Hcl secretion
Urease, Cag A, Vac-A - leads to inflammation of gastric epithelium

110
Q

Most common affected area in type B gastritis

A

Antrum

111
Q

CagA secreted from H pylori can cause

A

Pangastritis + Multifocal atrophy - Decreased Hcl secretion

112
Q

Reactive T cells in Type B gastritis

A

Stimulates B cell proliferation - B cell cancer - MALTOMA

113
Q

Gastropathy means

A

Inflammation in Gastric mucosa - Cell injury but no inflammatory cells

114
Q

Menetrier’s disease usually affects which age group and gender

A

Middle aged males (40-60yrs)

115
Q

Menetrier’s disease is example of

A

Hypertrophic gastropathy

116
Q

In Menetrier’s disease there is increased secretion of

A

TGF-alpha (Transforming growth factor alpha)

117
Q

TGF-alpha acts on

A

Epidermal growth factor receptors - increased epithelial cells - Prominent gastric rugal folds +++

118
Q

“Bag of worm” appearance in seen in which gastropathy

A

Menetrier’s disease

119
Q

Microscopic findings in gastropathy

A

Increased foveolar cells hyperplasia
Dilated cystic glands

120
Q

Gastrin secreting tumor (GASTRINOMA) is seen in

A

Zollinger Ellison Syndrome

121
Q

Gastrinoma can be divided into

A

Sporadic - Solitary in nature
Familial(25%) - Multiple endocrine neoplasia -1 (MEN-1)

122
Q

In Zollinger Ellison Syndrome there is increased secretion of

A

Increased Gastrin secretion
Increased Hcl secretion

123
Q

Clinical features of Zollinger Ellison Syndrome

A

Abdominal pain - duodenal ulcers
Diarrhea

124
Q

Diagnosis in Zollinger Ellison Syndrome

A

Serum gastrin levels high - >1000pg/ml
Basal acid output increases

125
Q

Treatment of Zollinger Ellison Syndrome

A

PPIs
Surgical

126
Q

In Peptic Ulcer disease there is damage to

A

Epithelial lining - Erosions

127
Q

In Peptic Ulcer disease there is involvement of which layer of GIT

A

Mucosa - ulcer

128
Q

Causes of Peptic Ulcer disease

A

H pylori
NSAIDs
Smoking
Uremia
Stress

129
Q

Most common cause of Peptic ulcer disease

A

H pylori infection

130
Q

Locations of Petic ulcer disease

A

1st part of duodenum (Anterior wall)
Stomach - Antrum (lesser curvature)
Gastroesophageal junction
Meckel’s diverticulum

131
Q

Meckel’s diverticulum means

A

Presence of ectopic gastric mucosa

132
Q

High risk of Peptic ulcer disease in which blood group

A

O

133
Q

High risk of development of gastric cancer in which blood group

A

A

134
Q

Most common site of Duodenal ulcers

A

1st part of duodenum - anterior wall

135
Q

Duodenal ulcers have strong association with

A

H pylori

136
Q

Clinical features of Duodenal ulcers

A

Epigastric pain
Pain decreases after eating food - Weight gain

137
Q

Brunner glands hypertrophy is seen in

A

Duodenal ulcers

138
Q

Duodenal ulcers are benign or malignant

A

Purely benign

139
Q

High chances of melena(bloody stools) in which ulcers

A

Duodenal ulcers

140
Q

Common location of gastric ulcers

A

Antrum - Lesser curvature (Incisura angularis)

141
Q

Clinical features of Gastric ulcers

A

Epigastric pain
Pain increases after taking food
Weight loss

142
Q

Gastric ulcers are benign or malignant

A

Pre malignant condition

143
Q

High chances of hematemesis in which ulcers

A

Gastric ulcers

144
Q

Most common complication of Peptic ulcer disease

A

Bleeding

145
Q

Complications of Peptic ulcer disease

A

Bleeding
Perforation
Gastric outlet obstruction
Malignancies

146
Q

Source of bleeding in Gastric ulcer

A

Left gastric artery

147
Q

Source of bleeding in Duodenal ulcers

A

Gastro-duodenal artery

148
Q

Due to perforation, acid can reach to

A

Pancreatic glands - can cause Pancreatitis
Peritoneal folds - Peritonitis

149
Q

Prognosis in case of perforation in Peptic ulcer disease

A

Poor prognosis

150
Q

Site of gastric outlet obstruction

A

At first part of duodenum

151
Q

Most common cause of gastric carcinoma

A

Gastric outlet obstruction

152
Q

In gastric outlet obstruction there is

A

Fibrous tissue deposition - narrows lumen - stomach contents can’t move forward - accumulation of gastric contents

153
Q

Due to repeated episodes of vomiting in gastric outlet obstruction

A

Loss of HCL - Metabolic alkalosis, Hypochloremia
Loss of fluid - RAAS activation - increased Aldosterone secretion - Hypokalemia and aciduria

154
Q

Risk of malignancy in which type of ulcers

A

Gastric ulcers

155
Q

Diagnostic methods used in Peptic ulcer disease

A

Urea breathe test
Endoscopy + Biopsy
CLO Test (Campellobacter like organisms)

156
Q

Urea breath test method

A

Mix radioactive labeled urea 14 with water - Put breath analyser on mouth - If H pylori urease convert’s Urea14 into 14CO2 - release detected by breath analyser

157
Q

Investigation of choice in Peptic ulcer disease

A

Endoscopy + Biopsy

158
Q

Finding of Benign ulcers in endoscopy

A

Small in size/ Solitary
Regular folds
Clean base
Usually at lesser curvature

159
Q

Findings of Malignant ulcer in Endoscopy

A

Large size
Multiple ulcers
Non clean base - Necrotic material
Heaping of margins
Irregular rugal folds
Usually at greater curvature

160
Q

Zones seen microscopically in Peptic ulcer disease

A

Necrosis
Infiltration
Granulation tissue
Zone of fiborsis

161
Q

In CLO test

A

Urea is mixed with Phenol red - Urease convert’s Urea to ammonia - Color changes to RED

162
Q

Management of Peptic ulcer disease

A

Proton pump inhibitors - 1
Antibiotics - 2 TRIPLE DRUG THERAPY for 2 weeks

Pathology (14 decks)

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