GIT Disorders Part 3 Flashcards by Richhpal Singh

Most common Malignant tumor of stomach

Gastric adenocarcinoma

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Gastric Adenocarcinoma is most prevalent in which country

Japan

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Risk factors of Gastric Adenocarcinoma

Smoked/salted foods
Low socio-economic status
Previous gastric surgery
Partial anterectomy
Pernicious anemia
Atrophic gastritis
H pylori
EBV
Tobacco use
Gastric adenomatous Polyps
Menetrier’s disease
Blood group A
Nutrient deficiencies (Zn,Mo,Se, Vit A)
Genetic factors

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Genetic risk factors of gastric Adenocarcinoma

P53 gene - Liframeni Syndrome
APC gene down regulation
Beta Catenin upregulation - increases epithelial cell proliferation
CDH1 gene - loss of E-cadherin
BRCA2 gene
HNPCC Syndrome

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Commonest site of Gastric Adenocarcinoma

Antrum (lesser curvature)

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Common site of gastric adenocarcinoma in Pernicious anemia

Fundus/Body

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Clinical features of Gastric Adenocarcinoma

Right upper quadrant discomfort
Early/recent onset dyspepsia
Post -prandial heaviness
Abdominal pain
Weight loss

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Paraneoplastic syndromes seen in Gastric Adenocarcinoma

Acanthosis nigricans - Hyperpigmentation of skin (axillary region)
Lesser Trelat sign - multiple seabouric keratosis on back and trunk
MAHA
Migratory thrombophlebitis

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Metastasis of Gastric Adenocarcinoma

Hematogenous spread - Liver, lungs, ovary
Lymphogenous spread - Lymph nodes, Ovaries

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Supraclavicular lymph node on left side is termed as

Virchow’s LN

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Axillary lymph node on left side is termed as

Irish LN

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Periumbilical skin nodules termed as

Sister Mary Joseph Nodule

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Metastasis of gastric tumor to Pouch of Douglas termed as

Blumer’s Shelf

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Investigation of choice in Gastric Adenocarcinoma

Endoscopy + Biopsy

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Gastric Adenocarcinoma can be classified on the basis of

On basis of Morphology
Depth of invasion
Lauren’s classification

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Classification of gastric Adenocarcinoma on the basis of Morphology

3 types - Exophytic growth
Flat growth
Lesion or ulcer

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Classification of gastric Adenocarcinoma on the basis of depth of invasion

Early
Late

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Which layer is involved in early gastric Adenocarcinoma

Mucosa/submucosa involvement

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Prognosis of early gastric Adenocarcinoma

Better prognosis

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Layers involved in late Gastric Adenocarcinoma

Muscle/serosa involvement

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Prognosis in late Gastric Adenocarcinoma

Bad Prognosis

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Best prognosis in which gastric Adenocarcinoma

Superficial spreading of stomach cancer

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Lauren’s classification includes

Intestinal type
Diffuse type

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In intestinal type, there is overactivity of

APC gene
Beta -Caterin

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In intestinal type, tumor cell makes

Intestinal gland like pattern

Intestinal type is seen in which age group

Elderly patients

Prognosis of intestinal type Gastric Adenocarcinoma

Better prognosis

In Diffuse type gastric Adenocarcinoma, tumor cells are

Scattered

According to Lauren's classification which type have localized tumors

Intestinal type

According to Lauren's classification,Non-localized tumor is seen in

Diffuse type

Diffuse type gastric Adenocarcinoma affects which age group

Younger patients

Mutation seen in Diffuse type gastric Adenocarcinoma

CDH1 gene mutation - loss of E cadherin

Prognosis in diffuse type gastric Adenocarcinoma

Bad prognosis

Condition seen in diffuse type gastric Adenocarcinoma due to increased connective tissue

LINITIS PLASTICA

Treatment of gastric Adenocarcinoma

Surgical Anticancer drugs

ECF Regime for gastric Adenocarcinoma

Epirubicine Cisplatin Flifluorouracil

Most common mesenchymal tumor in abdomen

Gastro-intestinal Stromal tumor (GIST)

Locations involved in GIST

Stomach > SI > LI > Esophagus

Most common site in GIST

Stomach

Rarest site in GIST

Esophagus

Cell of origin in GIST

Cell of CAJAL - Pacemaker of GI tract - controls Peristaltic activity

Mutations seen in GIST

C-Kit Mutation PDgFR-A(Platelet derived growth factor receptor alpha) mutation Succinate dehydrogenase mutation

Commonly affected age group in GIST

Elderly patients (around 60 years) , sometimes younger too

Carney Stratakis Syndrome

GIST + Paraganglioma

Mode of inheritance in Carney Stratakis Syndrome

Autosomal dominant

Mutation seen in Carney Stratakis Syndrome

SDH Mutation

Mutation in Familial GIST

NF-1 gene mutation

Carney's triad

GIST Paraganglioma Pulmonary chondroma

Due to C-Kit or PDgFR alpha mutation there is

Increased activity of different growth factors - increased Tyrosine kinase activity - cell proliferation increases - Cancer

Clinical features of GIST

Bleeding Abdominal pain Weight loss

GIST spread via

Blood vessels, No lymphatic spread

Common site of metastasis in GIST

Liver

Investigation of choice in GIST

CT Scan/PET

Findings of Biopsy in GIST

Epitheloid cells Presence of spindle cells Mixed cells

Endoscopic finding in GIST

Solitary, fleshy mass "Whorled appearance"

Immunohistochemistry markers in GIST

DOG-1(Best markers) > C-Kit(CD117) > CD34

Treatment of GIST

Surgical TKIs - Imatinib

Prognosis of GIST Depends upon

Location Mitotic index Size of tumor

Higher the mitotic index, the prognosis is

Poorer

Depending on the location GIST affecting stomach have prognosis

Good prognosis - less aggressive

If size of tumor is more than 10cm in GIST, The prognosis is

Bad

When the size of tumor is less than 5cm , then prognosis is

Good

Most common extranodal site in Non Hodgkin's Lymphoma

GIT - Stomach (MC)

Most common extranodal site in Non Hodgkin's lymphoma + HIV Patient

CNS

Preferred site of GI lymphoma in Follicular Lymphoma

Duodenum

Preferred site in Enteropathy associated T cell Lymphoma

Jejunum

In case of allogenic BM transplantation or organ Transplantation, effect of Immunosuppressive therapy

Decreased T cell activity - leads to increased B cell proliferation

Gastric Maltoma also termed as

Indolent Marginal zone Lymphoma

Role of H pylori in Gastric Maltoma

Lymphocytes proliferation in gastric mucosa

H pylori induced inflammation leads to

Formation of H pylori Specific B cells and T cells - Cytokines secretion - leads to increased BCL-10 and MALT-1 Activity

Increased BCL-10 And MALT-1 Activity stimulates

Nuclear factor kappa Beta - B cell proliferation - Leads to Low grade MALTOMA

Which mutation leads to conversion of Low grade MALTOMA to High grade MALTOMA

p16 and p53 mutations

Translocation associated Maltoma are resistant to

Antibiotics

Clinical features of Gastric Maltoma

Epigastric pain Dyspepsia

Microscopical finding from Biopsy in Gastric Maltoma

Lymphoepithilial lesion - lymphocyte infiltrates into epithelial cells - destroys glands

Immunohistochemistry markers in Gastric Maltoma

CD20 +ve CD5/CD23 -ve CD43 +ve (25%)

Treatment of H pylori associated Gastric Maltoma

Antibiotics

Treatment of High grade MALTOMA

Anticancer drugs

Malabsorption means

Not proper digestion of nutrients and minerals from intestine

Classical symptoms of Malabsorption disorders

Chronic diarrhea - Steatorrhea Abdominal pain Feeling of heaviness Weight loss

Celiac sprue is also known as

Gluten sensitive Enteropathy

Celiac sprue is genetically associated with

HLA DQ2, HLA DQ8 +ve

Celiac sprue is associated with which Autoimmune disorders

Type 1 DM Sjogren Syndrome Thyroiditis IgA Nephropathy

Celiac sprue associated with which Syndromes

Down Syndrome Turner Syndrome Ataxia Autism Depression/Epilepsy

Commonly affected part of GIT in Celiac sprue

Small intestine Duodenum > Jejunum

Gluten is found naturally in which products

Wheat Barley Rye Oat

Gluten is converted to

Gliadin

Formation of Gliadin from Gluten can leads to activation of

CD8 and CD4 T cell

Activation of CD4 and CD8 cells due to gliadin leads to

Auto- antibody formation Cytokines secretion Epithelial cell damage

Autoantibodies formed in Celiac sprue

Anti-transglutminase antibody Anti-Endomysial antibody Anti-gliadin antibody

IgA antibodies in Celiac sprue leads to involvement of which organ

Skin - dermatitis herpetiformis

Clinical features of Celiac sprue

Diarrhea Abdominal pain Stunted growth Flatulence Nutrient deficiencies (Iron/Folic acid) - Anemia

Diagnosis of Celiac sprue is done through

Clinical history Intestinal biopsy Serology

Site of intestinal biopsy in Celiac sprue

Duodenum

Findings of Duodenal biopsy in case of Celiac sprue

Villous atrophy Crypts hyperplasia Lymphocytic infiltration

In Celiac sprue, there is increased risk of which cancers

Enteropathy associated T cell Lymphoma Small intestine Adenocarcinoma Esophageal cancer ( Squamous cell)

Serological findings in Celiac sprue

Anti transglutaminase antibody - most sensitive Ab Anti Endomysial antibody - overall best Ab

Treatment of Celiac sprue

Stop gluten containing diet Nutritional supplementation In case of Dermatitis herpetiformis - DAPSONE

Stages of Celiac sprue

Latent disease Silent disease Clinic disease

Findings in Latent disease

Serology +ve

Findings in silent disease

Serology +ve, Villous atrophy Asymptomatic

Findings in clinical disease

Serology +ve, Villous atrophy Symptomatic

Environmental enteropathy also termed as

Tropical sprue

Most common cause of Environmental enteropathy

E coli

Which parts of GIT involved in Environmental enteropathy

Total involvement of Small intestine - decreases iron/folic acid/B12

Treatment of Environmental enteropathy

Antibiotics

Risk of cancer in environmental enteropathy

No risk

Causative agent of Whipple's disease

Tropheryma whipplei

Pathogenesis of Whipple's disease

Phagocytosis of Tropheryma whipplei by Macrophages - leads to involvement of lamina propria - Fat malabsorption

Organs affected in Whipple's disease

Intestine Joints LN Cardiovascular system CNS

Triad seen in Whipple's disease

Diarrhea Weight loss Arthralgia

Diagnostic method used in Whipple's disease

Intestinal biopsy

Finding of intestinal biopsy on routine staining in Whipple's disease

Macrophages infiltration in lamina propria (Foamy macrophages)

Finding of intestinal biopsy on Electromicroscopy in Whipple's disease

Bacteria - Rod shaped bacilli present inside Macrophages

Finding of intestinal biopsy on PAS stain in Whipple's disease

Diastase resistance granules

Treatment of Whipple's disease

Antibiotics - Cotrimoxazole

Anal cancer is type of which carcinoma

Squamous cell carcinoma

Main cause of anal cancer

Human Papilloma virus - HPV 16,18

Why surgery is not preferred in case of Anal cancer

Risk of damage to anal sphincter - can lead to fecal incontinence

Chemoradiation Regime used in anal cancer is termed as

Nigro's regime