GIT Disorder part 2 Flashcards
Alcohol induced esophageal disorders can be divided into
Mallory weis tear
Borhaave Syndrome
In Mallory weis tear there is
There is mucosal tear due to repeated vomiting
Sites of Mallory weis tear
90% cases - Present below gastroesophageal junction
10% cases - in lower part of Esophagus
In Borhaave Syndrome there is involvement of
Muscle layer due to repeated vomiting
Site of Borhaave Syndrome
Usually above 3-5cm from GE junction and involves posterolateral part of Esophagus
Triad seen in Borhaave Syndrome termed as
Mackler’s triad
Mackler’s triad includes
Chest pain
Repeated vomiting - Painful hematemesis(blood in vomiting)
Subcutaneous emphysema
Hamman crunch on auscultation is heard in which condition
Subcutaneous emphysema
Most common motility disorder of Esophagus
Achalasia cardia
Stimulatory neurons present in esophagus have
Acetylcholine - helps in muscle contraction
Inhibitory neurons present in esophagus have
Nitric oxide
Vasoactive intestinal peptide(VIP) - helps in muscle relaxation
In case of Achalasia cardia, there is selective loss of
Inhibitory neurons
Which part of Esophagus commonly involved in Achalasia cardia
Lower part of Esophagus - lower esophageal sphincter doesn’t works properly - incomplete relaxation of LES
Triad seen in Achalasia cardia
Increased LES tone
Aperistalsis
Incomplete LES relaxation
Primary causes of Achalasia cardia
Idiopathic
Secondary causes of Achalasia cardia
Trypanosoma cruzi (Chagas disease)
Varicella zoster
Cancer
Autoimmune disorders
Clinical features of Achalasia cardia
Dysphagia - difficulty in swallowing food
Liquids > Solid
Weight loss
Complications seen in Achalasia cardia
Regurgitation - food aspiration - can lead to lung infection - Lung abscess
High risk of development of cancer
Most common complication seen in Achalasia cardia
Lung abscess
Risk of what type of cancer in case of Achalasia cardia
Squamous cell carcinoma
Investigation of choice in Achalasia cardia
Manometry
Appearance seen in Barium swallow method in case of Achalasia cardia
“Bird-beak appearance”- Dilation of proximal part due to accumulation of food
Allgrove syndrome
Triple A disease
Achalasia
Alacrimia
ACTH resistant adrenal insufficiency
Management of Achalasia cardia
Botulinum toxin - decreases Ach activity
Surgery
Surgery performed in case of Achalasia cardia
Myotomy - Heller’s myotomy + Partial fundopligation
Epithelium present in esophagus
Stratified squamous non keratinized epithelium
Esophagus size in adult
25cm
Esophagus normal size in newborn
10cm
Serosa is not found in which part of GIT
Esophagus
How many constrictions are present in normal esophagus
4
Constrictions seen in esophagus
Upper esophageal constrictor - 6 inch- 15cm
Aortic arch - 9inch - 22.5cm
Left bronchus - 11inch - 27.5cm
Lower esophageal sphincter - 16inch - 40cm
Which constriction is narrowest
Upper esophageal constrictor - Cricopharyngeus muscle
Why there is high muscle tone in lower esophageal sphincter
To prevent backflow of stomach contents in esophagus
Esophagitis means
Inflammation of esophagal lining
Causes of esophagitis
Chemical esophagitis
Infections
Reflux esophagitis
Chemical cause of Esophagitis includes
Drugs - Bisphosphonates (Osteoporosis medicine)
Doxycycline
Infectious causes leading to esophagitis
Fungal - Candida
Virus - HSV - Punched out ulcer ,
CMV - Shallow ulcer
Biopsy taken in case of viral HSV Esophagitis
Taken from edge of ulcer
Multinucleate squamous epithelial cells
Eosinophilic Cowdry’s inclusions
Biopsy in CMV Esophagitis
Basophilic intranuclear inclusions
“Owl-eye appearance”
Commonest cause of Esophagitis
Reflux esophagitis
Reflux esophagitis means
Inflammation of Esophagus due to reverse content of stomach into esophagus
Most common cause of Reverse esophagitis
Decreased tone of LES
TLESR
Full form of TLESR
Transient lower esophageal sphincter relaxation
TLESR is aggravated by which factors
Alcohol
Smoking
Fatty foods
Obesity/overeating
Pregnancy
Chocolates or coffee
Hiatal hernia
Clinical features in Esophagitis
Retrosternal chest pain - Heartburn
Sour brash
Teeth discoloration
Investigation of choice in Esophagitis
24 hour pH study
Diagnostic methods used in case of Esophagitis
Endoscopy + Biopsy
Due to Metaplasia lower end of Esophagus changes to which epithelium
Intestinal columnar epithelium
Intestinal columnar epithelium contains and secrets
Contains goblet cells - secrets acidic mucin
Goblet cells in intestinal columnar epithelium are stained by
Alcian blue
Barret’s esophagus means
Upper part - SSNK epithelium
Lower part - Intestinal columnar epithelium
In Barret’s esophagus, if changed lining less than 3cm then its termed as
Short Barret’s esophagus
In Barret’s esophagus, if changed lining is more than 3cm then its termed as
Long Barret’s esophagus
If there is metaplasia for long term them it can leads to
Mutations - increased risk of cancer - Adenocarcinoma (lower part of Esophagus)
In case of Barret’s esophagus Biopsy is usually taken from which junction
Squamocolumnar junction
Treatment of Esophagitis
Proton pump inhibitors
Prokinetic drugs
Surgical - Fundopligation
Types of esophageal tumors
Benign tumors
Malignant tumors
Bening esophageal tumor includes
Leiomyoma (M.C)
Leiomyoma
M>F
Involves 2/3rd area of lower esophagus
Asymptomatic for long time
Subtypes of Malignant esophageal tumors
Squamous cell cancer (M.c in World)
Adenocarcinoma (M.C in USA)
Squamous cell cancer usually affects which part of Esophagus
Upper 1/3rd and
Middle 1/3rd
Adenocarcinoma usually affects which part of Esophagus
Lower 1/3rd except long standing achalasia cardia
Risk factors of Squamous cell cancer
Smoking/Alcohol
Nitrosamines - Smoked food
Chronic Achalasia cardia
Hot beverages
Radiation
Tylosis et palmaris
Celiac disease
Mursik
Plummer vinson Syndrome
HPV
Triad seen in Plummer vinson Syndrome
IDA
Esophageal web
Atrophic glossitis
Risk factors of Esophageal Adenocarcinoma
Whites
Long standing GERD
Barret’s esophagus
Smoking/Alcohol
Obesity
Scleroderma
Radiation
Which bacterial infection reduces risk of esophageal Adenocarcinoma
H. Pylori - leads to gastric atrophy - acid secretion decreases - decreases risk of Barret’s esophagus
Early mutations seen in Esophageal Adenocarcinoma
P53 mutations
Late mutations seen in Esophageal Adenocarcinoma
Cyclin D1 and Cyclin E overexpression
Clinical features of Esophageal tumors
Progressive dysphagia
Weight loss
Can involve recurrent laryngeal nerve - Hoarseness
Investigation of choice in case of Esophageal tumors
Endoscopy + Biopsy
Biopsy findings in Esophageal Adenocarcinoma
Multiple glands like structures - can be diffuse or interstitial
Biopsy findings in Squamous cell carcinoma
Keratin pearls +
Barium swallow finding in case of Esophageal tumors
“Rat-Tail defects”
Most common metastasis in Esophageal tumors
Hepatic
Paraneoplastic syndrome in Esophageal tumors
Hypercalcemia
LN affected when tumors is in upper 1/3rd part of esophagus
Cervical LN
LN involved when esophageal tumor affected middle 1/3rd part of esophagus
Mediastinal LN
LN involved when Esophageal tumor present in lower 1/3rd of Esophagus
Celiac LN, Gastric LN, Cardiac LN
Treatment in case of Esophageal tumors
Esophagectomy - Partial or Total
Overall prognosis of esophageal tumors
Bad prognosis
Parts of stomach
Cardia
Fundus - air present - On X ray gastric air bubble
Body
Antrum
Pylorus
Parietal cells of stomach secrets
Intrinsic factor - helps in Vitamin B12 absorption
HCL
Parietal cells are stimulated by
Ach
Gastrin
Histamine
Cheif cells of stomach secrets
Pepsinogen - helps in food digestion
Foveolar cells of stomach secrets
Mucus in stomach - make layer in internal lining of stomach - Protection from HCL
Endocrine or G cell in stomach secrets
Gastrin - Stimulates HCL secretion
Damagin factors in stomach
HCL
Damaging factor HCL can be aggravated by which bacteria
H. Pylori
Protective factors of Stomach
High epithelial regenerative activity - Stress, Shock
Bicarbonates - neutralizes HCL
Mucus - makes protective layer
Prostaglandins - Protective for gastric mucosa
Acute gastritis causes due to
Imbalance between damaging and protective factors
Inflitration of which cells seen in Acute gastritis
Neutrophilic infiltration
Risk factors of Acute gastritis
Alcohol intake
Stress
Drugs - NSAIDS
Anticancer drugs
Uremia
Burns
Increased intracranial tension
Ulcer seen in acute gastritis due to burns
Curling ulcer - due to burn there is dehydration - epithelial regeneration interrupted
Type of ulcer seen in acute gastritis due to increased intracranial tension
Cushing’s ulcer - Stomach only
In chronic gastritis there is infiltration of which type of cells
Lymphocytes/plasma cells inflitration
Causes of chronic gastritis
Autoimmune
H pylori
Chemical exposure
Radiation exposure/Grafts vs host disesase
Crohn’s disesase
Type of gastritis due to Autoimmune disorders
Type A gastritis
Type of gastritis due to H pylori infection
Type B gastritis
Type of gastritis due to Chemicals exposure
Type C gastritis
Most common cause of Chronic gastritis
H pylori
Type A gastritis seen in how much percent of cases
8-10%
Most common affected area in type A gastritis
Body/Fundus
Most common cause of Type A gastritis
Autoimmune disorders
CD4 T cells present in Type A gastritis can damage
Parietal cells - decreased Hcl secretion (Achlorhydria)
And due to feedback mechanism Gastrin level increases (Hypergastrinemia)
In Type A gastritis there is high risk of development of
Type 1 DM
Hashimoto disease
Pernicious anemia
Due to chronic inflammation in Type A gastritis
Can lead to intestinal metaplasia - increased risk of gastric cancer
Type B gastritis can be seen in how much percent of cases
90-92%
Bacteria responsible for Type B gastritis
H pylori
H pylori secrets
Increased Hcl secretion
Urease, Cag A, Vac-A - leads to inflammation of gastric epithelium
Most common affected area in type B gastritis
Antrum
CagA secreted from H pylori can cause
Pangastritis + Multifocal atrophy - Decreased Hcl secretion
Reactive T cells in Type B gastritis
Stimulates B cell proliferation - B cell cancer - MALTOMA
Gastropathy means
Inflammation in Gastric mucosa - Cell injury but no inflammatory cells
Menetrier’s disease usually affects which age group and gender
Middle aged males (40-60yrs)
Menetrier’s disease is example of
Hypertrophic gastropathy
In Menetrier’s disease there is increased secretion of
TGF-alpha (Transforming growth factor alpha)
TGF-alpha acts on
Epidermal growth factor receptors - increased epithelial cells - Prominent gastric rugal folds +++
“Bag of worm” appearance in seen in which gastropathy
Menetrier’s disease
Microscopic findings in gastropathy
Increased foveolar cells hyperplasia
Dilated cystic glands
Gastrin secreting tumor (GASTRINOMA) is seen in
Zollinger Ellison Syndrome
Gastrinoma can be divided into
Sporadic - Solitary in nature
Familial(25%) - Multiple endocrine neoplasia -1 (MEN-1)
In Zollinger Ellison Syndrome there is increased secretion of
Increased Gastrin secretion
Increased Hcl secretion
Clinical features of Zollinger Ellison Syndrome
Abdominal pain - duodenal ulcers
Diarrhea
Diagnosis in Zollinger Ellison Syndrome
Serum gastrin levels high - >1000pg/ml
Basal acid output increases
Treatment of Zollinger Ellison Syndrome
PPIs
Surgical
In Peptic Ulcer disease there is damage to
Epithelial lining - Erosions
In Peptic Ulcer disease there is involvement of which layer of GIT
Mucosa - ulcer
Causes of Peptic Ulcer disease
H pylori
NSAIDs
Smoking
Uremia
Stress
Most common cause of Peptic ulcer disease
H pylori infection
Locations of Petic ulcer disease
1st part of duodenum (Anterior wall)
Stomach - Antrum (lesser curvature)
Gastroesophageal junction
Meckel’s diverticulum
Meckel’s diverticulum means
Presence of ectopic gastric mucosa
High risk of Peptic ulcer disease in which blood group
O
High risk of development of gastric cancer in which blood group
A
Most common site of Duodenal ulcers
1st part of duodenum - anterior wall
Duodenal ulcers have strong association with
H pylori
Clinical features of Duodenal ulcers
Epigastric pain
Pain decreases after eating food - Weight gain
Brunner glands hypertrophy is seen in
Duodenal ulcers
Duodenal ulcers are benign or malignant
Purely benign
High chances of melena(bloody stools) in which ulcers
Duodenal ulcers
Common location of gastric ulcers
Antrum - Lesser curvature (Incisura angularis)
Clinical features of Gastric ulcers
Epigastric pain
Pain increases after taking food
Weight loss
Gastric ulcers are benign or malignant
Pre malignant condition
High chances of hematemesis in which ulcers
Gastric ulcers
Most common complication of Peptic ulcer disease
Bleeding
Complications of Peptic ulcer disease
Bleeding
Perforation
Gastric outlet obstruction
Malignancies
Source of bleeding in Gastric ulcer
Left gastric artery
Source of bleeding in Duodenal ulcers
Gastro-duodenal artery
Due to perforation, acid can reach to
Pancreatic glands - can cause Pancreatitis
Peritoneal folds - Peritonitis
Prognosis in case of perforation in Peptic ulcer disease
Poor prognosis
Site of gastric outlet obstruction
At first part of duodenum
Most common cause of gastric carcinoma
Gastric outlet obstruction
In gastric outlet obstruction there is
Fibrous tissue deposition - narrows lumen - stomach contents can’t move forward - accumulation of gastric contents
Due to repeated episodes of vomiting in gastric outlet obstruction
Loss of HCL - Metabolic alkalosis, Hypochloremia
Loss of fluid - RAAS activation - increased Aldosterone secretion - Hypokalemia and aciduria
Risk of malignancy in which type of ulcers
Gastric ulcers
Diagnostic methods used in Peptic ulcer disease
Urea breathe test
Endoscopy + Biopsy
CLO Test (Campellobacter like organisms)
Urea breath test method
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
Investigation of choice in Peptic ulcer disease
Endoscopy + Biopsy
Finding of Benign ulcers in endoscopy
Small in size/ Solitary
Regular folds
Clean base
Usually at lesser curvature
Findings of Malignant ulcer in Endoscopy
Large size
Multiple ulcers
Non clean base - Necrotic material
Heaping of margins
Irregular rugal folds
Usually at greater curvature
Zones seen microscopically in Peptic ulcer disease
Necrosis
Infiltration
Granulation tissue
Zone of fiborsis
In CLO test
Urea is mixed with Phenol red - Urease convert’s Urea to ammonia - Color changes to RED
Management of Peptic ulcer disease
Proton pump inhibitors - 1
Antibiotics - 2 TRIPLE DRUG THERAPY for 2 weeks
