GIT Disorders Flashcards
Layers of GI tract
Mucosa
Submucosa
Muscularis propria
Serosa
Topmost layer of GI tract
Mucosa
Epithelial lining of Oral cavity
Squamous epithelium
Epithelial lining of Oesophagus
Stratified squamous non keratinized epithelium
Epithelial lining of Stomach, Small intestine and Large intestine
Columnar epithelium
Epithelial lining of Anal canal
Squamous epithelium
Meissner’s plexus is located within
Submucosa
Function of Meissner’s plexus
Secretory in nature and absorptive function
Muscularis propria consists of
Inner circular and
Outer longitudinal
Aurebach’s or Myenteric plexus is located within
Muscularis propria
Aurebach’s or Myenteric plexus function
Responsible for motor activity - Peristalsis
Innermost layer of GI tract
Serosa
Serosa is absent in which part of GI tract
Oesophagus
Which layers are absent in gall bladder
Muscularis propria and
Submucosa
IBD is most commonly seen in which age group and gender
Young females
IBD happens due to
Abnormal activation of immune system against normal gut bacteria
Is IBD included in Autoimmune disorders?
NO
Which organs can be involved in IBD
GIT
Skin
Eye
Joint
Bile ducts
Clinical features of IBD due to effect on GIT
Severe abdominal colicky pain
Bloody stools
Diarrhea
Clinical features of IBD due to involvement of skin
Pyoderma gangrenosa
Effects on eye in case of IBD
Photophobia
Watery eyes
Effects on bile ducts in case of IBD
Obstructive Jaundice
Most common history in Crohn’s disesase
Smoking
In Crohn’s disesase, which part of GIT is involved
Can involve any part of GIT
Most commonly affected part of GIT in Crohn’s disesase
Ileum
Rarely affected part in Crohn’s disesase
Rectum
Superficial ulcers seen in Crohn’s disease
Aphthous ulcers
Skip lesions are seen in
Crohns disease
Irregular mucosa seen in Crohns disease can termed as
Cobblestone Mucosa
Which layers are involved in Crohn’s disease
All 4 layers are involved (Transmural inflammation)
Due to Excessive fibrosis in Crohn’s disease
Decreased size of lumen (Stricture formation)
Radiological finding due to excessive fibrosis in Crohn’s disesase
STRING SIGN
Involvement of T cells in Crohn’s disease
TH17 cell/ TH1 cell
Type of inflammation in Crohn’s disease
Granulomatous inflammation
Antibody seen in Crohn’s disease
ASCA (Anti Saccharomyces cerevisiae Antibody) +
Creeping fat is seen in which GIT disorder
Crohn’s disease
Clinical features of Crohn’s disease
Abdominal colicky pain
Bloody stools
Uveitis
Joint pain
Bile duct involvement
Skin involvement - Pyoderma gangrenosa
Complications of Crohn’s disease
Fistula formation
High risk of Kidney stones
Pathogenesis of Kidney stones in Crohn’s disease
Defective ileum - No Calcium and Bile acids absorption- Oxalate combines with Calcium and increased absorption - can lead to Kidney stones
Risk of colon cancer in Crohn’s disease
High risk
Ulcerative colitis involves which part of GI Tract
Only Large intestine or Colon
Most commonly affected part of GIT in Ulcerative colitis
Rectum
Complete inflammation of Colon is termed as
Pancolitis
Backwash ileitis is seen in which GIT disorder
Ulcerative colitis
Which layers of GIT are involved in Ulcerative colitis
Superficial layers - Mucosa and Submucosa
Chances of fistula formation in Ulcerative colitis
Low chances
Pseudopolyps can be seem in
Ulcerative colitis
Microscopic finding in Ulcerative colitis
Crypts abscess
Antibody seen in Ulcerative colitis
p-ANCA (p-Antineutrophilic Cytoplasmic antibody)
Toxic megacolon is seen in which disorder
Ulcerative colitis
Increased size of transverse colon
Bile duct involvement in Ulcerative colitis can leads to
Primary sclerosing Cholangitis
Radiological finding in Ulcerative colitis
Lead pipe appearance
T cell involved in Ulcerative colitis
TH2 cell
Type of inflammation in Ulcerative colitis
Non granulomatous inflammation
Risk of development of colon cancer in Ulcerative colitis
High risk
Mass like projections present in lumen of intestine are termed as
Intestinal polyps
Types of intestinal polyps
Non neoplastic Polyps
Neoplastic Polyps
Subtypes of Non-neoplastic Polyps
Inflammatory Polyps
Hyperplastic Polyps
Hamartomatous Polyps
Subtype of Neoplastic Polyps
Adenomatous Polyps
Which is the most dangerous subtype of Intestinal polyps
Adenomatous Polyps
Inflammatory Polyps are
Secondary to inflammation
Hyperplastic Polyps are usually present at
Rectosigmoid junction
Subtypes of Hamartomatous Polyps
Juvenile polyps
Peutz-Jegher Polyps
Juvenile polyps are usually seen in which age group
Usually seen in 1st decade of life
Mostly <5yr
Mostly affected part of GIT in Juvenile polyps
Rectum
Peutz-Jegher Polyps are usually seen in what age
Around Puberty
11yrs of age
Peutz-Jegher Polyps are usually affects which part of GIT
Jejunum
Juvenile Polyposis Syndrome mode of inheritance
Autosomal dominant
Mutation seen in Juvenile Polyposis Syndrome
Gene SMAD
Risk of cancer in Juvenile Polyposis Syndrome
High
Condition with Multiple Peutz-Jegher Polyps is termed as
Peutz-Jegher Syndrome
Effect on skin in Peutz-Jegher Syndrome
Hyperpigmentation of skin
Maximum risk of cancer in which type of Polyp
Adenomatous Polyps
Which gene is defective in case of Familial adenomatous Polyposis (FAP)
APC gene
APC gene is responsible for
Decreases growth of adenomatous Polyps
If APC gene is not working properly then there is
Increased no. Of adenomatous Polyps
In case of Classical familial adenomatous Polyposis we can se
> 100 adenomatous Polyps
Turcot Syndrome
Combination of FAP and CNS Tumors
Gardener Syndrome
Combination of FAP and other type of Adenomas
In case of MUTYH-Associated Polyposis there is defect in
DNA Repair genes
Colon cancer is usually seen in which age group
Elderly patients
Colon cancer can gradually lead to which type of anemia
Gradually progressive Iron deficiency anemia - due to chronic blood loss
Colon cancer is which type of Carcinoma
Adenocarcinoma
Most common site in colon cancer
Rectum
Genetic risk factors in Colon cancer
HNPCC syndrome/LYNCH Syndrome
FAP Syndrome
Defect in HNPCC or LYNCH Syndrome
DNA repair gene defect
LYNCH SYNDROME type of inheritance
Autosomal dominant
Most common site involved in LYNCH Syndrome
Proximal colon
Subtypes of Adenomatous Polyps
Tubular
Villous
Tubulovillous
Most common subtype of adenomatous Polyps
Tubular
Maximum risk of cancer in which subtype of adenomatous Polyps
Villous - most dangerous
Non genetic risk factors of Colon cancer
Dietary lipids
Radiation exposure
Ureterosigmoidostomy
Streptococcus Bovis infection
Protective factors of Colon cancer
Dietary fibers - increases gut motility
Drugs - COX inhibitors
COX Inhibitors have protective role in cancer because
They Decreases proliferation of Adenomatous Polyps
Clinical Presentation in case of Right sided Colon cancer/Ascending colon cancer
History of LYNCH Syndrome
Ulcerative cancer - Chronic blood loss
Iron deficiency anemia
Symptoms of anemia
Clinical Presentation in case of Left sided colon cancer/Descending colon
Common site - Rectum
Rectal bleeding
Tenesmus
Spurry diarrhea
Blood in mucus
Alteration in bowel habits
Tenesmus means
Urge to defecate but can’t do so
Investigation of choice in Colon cancer
Colonoscopy + Biopsy
Detection of occult blood loss is done by which test
Guaiac test
In blood sample of Colon cancer patients, we can see increased level of
Carcinoembryonic antigen (CEA)
In Colon cancer, Radiological findings includes
Apple core appearance
NAPKIN-RING Appearance
Site of Metastasis of Colon cancer
Regional lymph nodes
Liver
Lungs
In females, when colon cancer metastasize to ovary, leading to increased size of ovary termed as
Krukenberg tumor
Tracheo-esophageal fistula means
Abnormal connection between Trachea and esophagus
In Tracheo-esophageal fistula Upper end of Esophagus have
Blind ending
In Tracheo-esophageal fistula lower end of Esophagus attached to
Trachea above bifurcation
Clinical features of Tracheo-esophageal fistula
Polyhydroamnios (too much amniotic fluid around baby during the)
Abdominal distension
High chance of development of aspirational pneumonia
In Infantile hypertrophic pyloric stenosis, we can see
Hypertrophy of muscle present in Pylorus which leads to narrowing of lumen
In case of Infantile hypertrophic pyloric stenosis, clinical Presentation is usually seen after
3-6 weeks
Infantile hypertrophic pyloric stenosis is associated with
Trisomy 18 and 21
Drugs - Erythromycin
Clinical Presentation in Infantile hypertrophic pyloric stenosis
New onset regurgitation
Vomiting after drinking milk - Non bilious vomiting
“Olive lump”
Best Diagnosis in case of Infantile hypertrophic pyloric stenosis
Ultrasonography
Treatment of Infantile hypertrophic pyloric stenosis
Pyloromyotomy - excission of excessive muscle
In Hirschsprung disease, we can see
Failure of migration of neural crest cells
Leads to constricted bowel in affected areas and dilated bowel in proximal area due to accumulation of gastric contents
Most common part of GIT affected in Hirschsprung disease/Congenital Aganglionic megacolon
Rectum
Which gene is involved in Hirschsprung disease
RET Gene
Hirschsprung disease is usually associated with
Down Syndrome
Clinical Presentation of Hirschsprung disease
Not able to pass stools because muscle not relaxing properly
Constipation
Abdominal distension
Diagnosis in case of Hirschsprung disease
Suction Biopsy - Rectum