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Diseases of GIT Patho-B Lab
Esophagealvarices Chronic gastritis Chronic peptic ulcer Adenocarcinoma of rectum Adenocarcinoma of Stomach Hemorrhoids Meckel’sdiverticulum Acute appendicitis TB of intestine Schistosoma Appendix Adenocarcinoma of colon
EsophagealVarices Tortuos dilated veins lying within the submucosa of the distal esophagus. Congested sub epithelial and sub mucosal venous plexus within the distal esophagus Due to diseases that impede venous blood flow from GIT to the liver via portal vein before reaching Inferior vena cava Alcoholic Liver disease – In  90% of cirrhotic patients Schistosomiasis-2nd most common cause worldwide Complication- Hemorrhage & Internal bleeding
Diagnosis Often asymptomatic utill there is a rupture Endoscopy Clinical Manifestation Increased vascular hydrostatic pressure is associated with vomiting Rupture can cause massive hematemesis Management Medical emergency Sclerotherapy Endoscopic ballontamponade Endoscopic rubber band ligation
Congested sub epithelial and sub mucosal venous plexus
Congested sub epithelial and sub mucosal venous plexus
Congested sub epithelial and sub mucosal venous plexus
Congested sub epithelial and sub mucosal venous plexus
Congested sub epithelial and sub mucosal venous plexus
Congested sub epithelial and sub mucosal venous plexus
Chronic Gastritis Defined by presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasia. Etiology:- Most common is H. Pylori infection(typically found in the antrum) Most common cause of duodenal ulcer Morphology:- Antral mucosa usually erythematous with coarse or nodular appearance. Neutophilic infiltrates within lamina propria Intraepithelianeutrophils and subepithelial plasma cells characteristic
Complication:- Peptic ulcer Disease Dysplasia and Intestinal Metaplasia Gastritis cystica Diagnosis Gastroscopy Clinical Manifestation Nausea and abdominal discomfort Management:-  H.pylori eradication if that’s the cause Primary therapy for 7 days which includes proton pump inibitor along with antibiotic(Clarithromycin, metronidazole,amoxicillin)
Atrophied Mucosa due to Chronic inflammation LPO
Atrophied Mucosa due to Chronic inflammation LPO
LPO Neutophilic infiltrates within lamina propria Intraepithelianeutrophils and subepithelial plasma cells characteristic
LPO
LPO Neutrophils
LPO
HPO Plasma cell infiltrate Gastric glands
HPO Lymphocyte & Plasma cell infiltrate
Chronic peptic Ulcer Peptic ulcers are chronic most often solitary lesions that occur in any portion of the GIT exposed to the aggressive action of acidic peptic juices. 98% of the peptic ulcers are either in the first portion of the duodenum or in the stomach(4:1 ratio) 2 conditions leading to Peptic ulcers H.pylori infection  which has a strong causal relationship with peptic ulcer development. (in person with no H.pylori infection NSAIDs are the major cause of peptic ulcers) Mucosal exposure to gastric acid and pepsin.
Diagnosis Endoscopy Gastric ulcers may occasionalybe malignant and therefore must always be biopsied and followed up to ensure healing. Clinical manifestation  Recurrent epigastric pain- most common Occasional vomiting Anorexia Anemia in some patients with silent undetected blood loss Management Relive symptoms Induce healing Prevent recurrence H.pylori eradication
LPO Epithelial injury Morphology of PUD ** Necrotic debris ** Inflammation with     predominant neutrophils **Granulation tissue **Fibrosis
LPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
LPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
LPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
HPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
HPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
HPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
HPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
LPO Morphology of PUD ** Necrotic debris ** Inflammation with      predominant neutrophils **Granulation tissue **Fibrosis
Adenocarcinoma of Stomach Most common malignancy of stomach Classification is according to the location in stomach,gross and histologic morphology. Intestinal Adenocarcinoma- Bulky and composed of glandular structures. (slide shown in lab) Diffuse Adenocarcinoma- Infiltrative pattern composed of signet ring cells that do not form glands
Diagnosis There are no laboratory markers Upper GI Endoscopy remains the choice. Multiple biopsies from base and edge of ulcer Clinical manifestation  Early stage is asymptomatic Weight loss(most common) Epigastric pain with vomiting Virchow’s node Sister Mary Joseph sign Management Surgical resection(Partial gastrectomy common) For unrectable tumors palliative measures are taken Over all prognosis of patients with Adenocarcinoma of stomach is poor with <30% survival rate of 5 years
Bulky glandular structures Formed from previous chronic inflammation LPO
Bulky glandular structures Formed from previous chronic inflammation LPO
LPO
LPO
LPO
LPO
HPO
Hemorrhoids They arise from congestion of the internal and/or external venous plexuses around the anal canal. Also Known as Piles First Degree Piles - Bleed Second Degree Piles – Prolapse but retract spontaneously Third Degree Piles– Require manual replacement after prolapse Associated with constipation and straining Manifestation – Bright red rectal bleeding after defeacation Pain Pruritisani Mucus discharge Management –  Injection sclerotherapyor band ligation is effective in most patients Some patients require haemorrhoidectomy.
LPO
- LPO
LPO
HPO Demonstrative Congestion
HPO Demonstrative Congestion
Meckel’sDiverticulum Most common congenital anomaly of GIT Diverticulum results from the failure of the closure of the vitelline duct. Small out pouching extending from the anti mesenteric side of the bowel. Normal mucosal lining resembling small intestine
Diagnosis Scanning the abdomen by gamma counter following an IV injection of pertechnate. Clinical manifestation Bleeding results from ulceration of the ileal mucosa(Present as Recurrent Melena) Abdominal pain  Management Some are present with no complication and may be left as it is. The ones with complications like perforation require Surgery.
Ectopic Gastric mucosa
Acute Appendicitis Appendiceal inflammation is associated with obstruction in 50-80% of cases usually in the form of a fecalth and less commonly gall stone tumor or ball of worm(Oxyuriasisvermicularis) At earliest stages only scanty of neutrophilicexudate may be found throughout the mucosa,submucosa and muscularispropria.
Diagnosis Until the localization of pain occurs diagnosis is not made. CBC counts are taken if pain is manifested in RLQ, to confirm inflammation in appendix. Clinical manifestation  Epigastric pain is the initial symptom Later classically nausea,vomiting then pain becomes generalized which finally shifts to Right lower Quadrant. Management Non surgical treatment can be approached but there are chances of recurrence  and perforation. Conventional Appendectomy is performed in most cases.
LPO Tunica muscularis Wtih infiltration Of neutrophils
LPO Congestion in subserosal vessel LPO
LPO
LPO
LPO
LPO
HPO PMNs ---- Mostly Neutrophils in Tunica muscularis layer
TB of intestines Extrapulmonary TB  Upper GI involvement is rare and is usually an unexpected findings in endoscopy or laparotomy specimen Ileocecal disease accounts for approximately half of the abdominal TB cases. Commonly found in immunocompromised patients(HIV patients)
Diagnosis Diagnosis rest on obtaining histology by either colonoscopy or minilaparotomy. Cultures from obtained specimens Ultrasound/Ct may reveal thickened bowel wall,mesenteric thickening or ascites. Clinical manifestation  Exudativeascites Intestinal obstruction Fever Night sweats Anorexia  Weight loss Management Classical 4 drug therapy for TB
LPO
HPO
LPO
HPO
Schistosoma Appendix As the worm produces more eggs the lesion tends to be more extensive and widespread. Clinical feature resemble those of severe infection. Small as well as large bowel can be affected.
Diagnosis Diagnosis depends on demonstrating eggs or serological evidence of infection. Stool examination Eosinophilia Clinical manifestation  Initially itching at the site of penetration Later 5-6 weeks Acute schistosomiasis(Katayama syndrome) may develop with allergic presentation such as urticaria,fever,Muscleaches,abdominalpain,cough,sweating. Management Objective is to kill the adult schistosome so that it stop producing eggs. (Praziquantel is the drug of choice) Surgery may be required
LPO
LPO
HPO
HPO
HPO
LPO
Adenocarcinoma of colon 98% of cancers in large intestine are adenocarcinomas. Tumors in the proximal colon tend to grow as polyp.Obstruction is uncommon When the carcinomas in distal colon are discovered the tend to be annular encircling lesions that produce so called napkin ring constrictions of the bowel and narrowing of  the lumen. Almost all cancers of colon are adenocarcinomas which range from well differentiated to Undifferentiated, frankly anaplastic masses. Many tumors produce mucin which is secreted into the gland lumina/interstitium of gut wall which facilitate the extension of this cancer and worsen the prognosis.
Diagnosis Barium enema Colonoscopy Confirmatory biopsy Digital rectal examination and fecal testing for occult blood loss Clinical manifestation  Fatigue Weakmess Weight loss Changes in bowel habits Left lower quadrant discomfort Management Chemotherapy determined on the basic of the cancer classification. Prognosis for T1 stage in 97% of patients is 5 year survival rate Palliative surgical segmental resection
LPO Invasive Adenocarcinoma of colon
LPO
LPO
Malignant glands infilrating  the surrounding tissue LPO
HPO Malignant glands infilrating  the surrounding tissue
HPO Cytologicatypia Pleomorphism
HPO Cytologicatypia Pleomorphism
HPO Cytologicatypia Pleomorphism
HPO
HPO
Rectal Adenoma(not included in practical quiz)
Thanking to the entire Universe

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Diseases of GIT

  • 1. Diseases of GIT Patho-B Lab
  • 2. Esophagealvarices Chronic gastritis Chronic peptic ulcer Adenocarcinoma of rectum Adenocarcinoma of Stomach Hemorrhoids Meckel’sdiverticulum Acute appendicitis TB of intestine Schistosoma Appendix Adenocarcinoma of colon
  • 3. EsophagealVarices Tortuos dilated veins lying within the submucosa of the distal esophagus. Congested sub epithelial and sub mucosal venous plexus within the distal esophagus Due to diseases that impede venous blood flow from GIT to the liver via portal vein before reaching Inferior vena cava Alcoholic Liver disease – In 90% of cirrhotic patients Schistosomiasis-2nd most common cause worldwide Complication- Hemorrhage & Internal bleeding
  • 4. Diagnosis Often asymptomatic utill there is a rupture Endoscopy Clinical Manifestation Increased vascular hydrostatic pressure is associated with vomiting Rupture can cause massive hematemesis Management Medical emergency Sclerotherapy Endoscopic ballontamponade Endoscopic rubber band ligation
  • 5. Congested sub epithelial and sub mucosal venous plexus
  • 6. Congested sub epithelial and sub mucosal venous plexus
  • 7. Congested sub epithelial and sub mucosal venous plexus
  • 8. Congested sub epithelial and sub mucosal venous plexus
  • 9. Congested sub epithelial and sub mucosal venous plexus
  • 10. Congested sub epithelial and sub mucosal venous plexus
  • 11. Chronic Gastritis Defined by presence of chronic inflammatory changes in the mucosa leading eventually to mucosal atrophy and epithelial metaplasia. Etiology:- Most common is H. Pylori infection(typically found in the antrum) Most common cause of duodenal ulcer Morphology:- Antral mucosa usually erythematous with coarse or nodular appearance. Neutophilic infiltrates within lamina propria Intraepithelianeutrophils and subepithelial plasma cells characteristic
  • 12. Complication:- Peptic ulcer Disease Dysplasia and Intestinal Metaplasia Gastritis cystica Diagnosis Gastroscopy Clinical Manifestation Nausea and abdominal discomfort Management:- H.pylori eradication if that’s the cause Primary therapy for 7 days which includes proton pump inibitor along with antibiotic(Clarithromycin, metronidazole,amoxicillin)
  • 13. Atrophied Mucosa due to Chronic inflammation LPO
  • 14. Atrophied Mucosa due to Chronic inflammation LPO
  • 15. LPO Neutophilic infiltrates within lamina propria Intraepithelianeutrophils and subepithelial plasma cells characteristic
  • 16. LPO
  • 18. LPO
  • 19. HPO Plasma cell infiltrate Gastric glands
  • 20. HPO Lymphocyte & Plasma cell infiltrate
  • 21. Chronic peptic Ulcer Peptic ulcers are chronic most often solitary lesions that occur in any portion of the GIT exposed to the aggressive action of acidic peptic juices. 98% of the peptic ulcers are either in the first portion of the duodenum or in the stomach(4:1 ratio) 2 conditions leading to Peptic ulcers H.pylori infection which has a strong causal relationship with peptic ulcer development. (in person with no H.pylori infection NSAIDs are the major cause of peptic ulcers) Mucosal exposure to gastric acid and pepsin.
  • 22. Diagnosis Endoscopy Gastric ulcers may occasionalybe malignant and therefore must always be biopsied and followed up to ensure healing. Clinical manifestation Recurrent epigastric pain- most common Occasional vomiting Anorexia Anemia in some patients with silent undetected blood loss Management Relive symptoms Induce healing Prevent recurrence H.pylori eradication
  • 23. LPO Epithelial injury Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 24. LPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 25. LPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 26. LPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 27. HPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 28. HPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 29. HPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 30. HPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 31. LPO Morphology of PUD ** Necrotic debris ** Inflammation with predominant neutrophils **Granulation tissue **Fibrosis
  • 32. Adenocarcinoma of Stomach Most common malignancy of stomach Classification is according to the location in stomach,gross and histologic morphology. Intestinal Adenocarcinoma- Bulky and composed of glandular structures. (slide shown in lab) Diffuse Adenocarcinoma- Infiltrative pattern composed of signet ring cells that do not form glands
  • 33. Diagnosis There are no laboratory markers Upper GI Endoscopy remains the choice. Multiple biopsies from base and edge of ulcer Clinical manifestation Early stage is asymptomatic Weight loss(most common) Epigastric pain with vomiting Virchow’s node Sister Mary Joseph sign Management Surgical resection(Partial gastrectomy common) For unrectable tumors palliative measures are taken Over all prognosis of patients with Adenocarcinoma of stomach is poor with <30% survival rate of 5 years
  • 34. Bulky glandular structures Formed from previous chronic inflammation LPO
  • 35. Bulky glandular structures Formed from previous chronic inflammation LPO
  • 36. LPO
  • 37. LPO
  • 38. LPO
  • 39. LPO
  • 40. HPO
  • 41. Hemorrhoids They arise from congestion of the internal and/or external venous plexuses around the anal canal. Also Known as Piles First Degree Piles - Bleed Second Degree Piles – Prolapse but retract spontaneously Third Degree Piles– Require manual replacement after prolapse Associated with constipation and straining Manifestation – Bright red rectal bleeding after defeacation Pain Pruritisani Mucus discharge Management – Injection sclerotherapyor band ligation is effective in most patients Some patients require haemorrhoidectomy.
  • 42. LPO
  • 43. - LPO
  • 44. LPO
  • 47. Meckel’sDiverticulum Most common congenital anomaly of GIT Diverticulum results from the failure of the closure of the vitelline duct. Small out pouching extending from the anti mesenteric side of the bowel. Normal mucosal lining resembling small intestine
  • 48. Diagnosis Scanning the abdomen by gamma counter following an IV injection of pertechnate. Clinical manifestation Bleeding results from ulceration of the ileal mucosa(Present as Recurrent Melena) Abdominal pain Management Some are present with no complication and may be left as it is. The ones with complications like perforation require Surgery.
  • 50.
  • 51.
  • 52.
  • 53.
  • 54. Acute Appendicitis Appendiceal inflammation is associated with obstruction in 50-80% of cases usually in the form of a fecalth and less commonly gall stone tumor or ball of worm(Oxyuriasisvermicularis) At earliest stages only scanty of neutrophilicexudate may be found throughout the mucosa,submucosa and muscularispropria.
  • 55. Diagnosis Until the localization of pain occurs diagnosis is not made. CBC counts are taken if pain is manifested in RLQ, to confirm inflammation in appendix. Clinical manifestation Epigastric pain is the initial symptom Later classically nausea,vomiting then pain becomes generalized which finally shifts to Right lower Quadrant. Management Non surgical treatment can be approached but there are chances of recurrence and perforation. Conventional Appendectomy is performed in most cases.
  • 56. LPO Tunica muscularis Wtih infiltration Of neutrophils
  • 57. LPO Congestion in subserosal vessel LPO
  • 58. LPO
  • 59. LPO
  • 60. LPO
  • 61. LPO
  • 62. HPO PMNs ---- Mostly Neutrophils in Tunica muscularis layer
  • 63. TB of intestines Extrapulmonary TB Upper GI involvement is rare and is usually an unexpected findings in endoscopy or laparotomy specimen Ileocecal disease accounts for approximately half of the abdominal TB cases. Commonly found in immunocompromised patients(HIV patients)
  • 64. Diagnosis Diagnosis rest on obtaining histology by either colonoscopy or minilaparotomy. Cultures from obtained specimens Ultrasound/Ct may reveal thickened bowel wall,mesenteric thickening or ascites. Clinical manifestation Exudativeascites Intestinal obstruction Fever Night sweats Anorexia Weight loss Management Classical 4 drug therapy for TB
  • 65. LPO
  • 66. HPO
  • 67. LPO
  • 68. HPO
  • 69. Schistosoma Appendix As the worm produces more eggs the lesion tends to be more extensive and widespread. Clinical feature resemble those of severe infection. Small as well as large bowel can be affected.
  • 70. Diagnosis Diagnosis depends on demonstrating eggs or serological evidence of infection. Stool examination Eosinophilia Clinical manifestation Initially itching at the site of penetration Later 5-6 weeks Acute schistosomiasis(Katayama syndrome) may develop with allergic presentation such as urticaria,fever,Muscleaches,abdominalpain,cough,sweating. Management Objective is to kill the adult schistosome so that it stop producing eggs. (Praziquantel is the drug of choice) Surgery may be required
  • 71. LPO
  • 72. LPO
  • 73. HPO
  • 74. HPO
  • 75. HPO
  • 76. LPO
  • 77. Adenocarcinoma of colon 98% of cancers in large intestine are adenocarcinomas. Tumors in the proximal colon tend to grow as polyp.Obstruction is uncommon When the carcinomas in distal colon are discovered the tend to be annular encircling lesions that produce so called napkin ring constrictions of the bowel and narrowing of the lumen. Almost all cancers of colon are adenocarcinomas which range from well differentiated to Undifferentiated, frankly anaplastic masses. Many tumors produce mucin which is secreted into the gland lumina/interstitium of gut wall which facilitate the extension of this cancer and worsen the prognosis.
  • 78. Diagnosis Barium enema Colonoscopy Confirmatory biopsy Digital rectal examination and fecal testing for occult blood loss Clinical manifestation Fatigue Weakmess Weight loss Changes in bowel habits Left lower quadrant discomfort Management Chemotherapy determined on the basic of the cancer classification. Prognosis for T1 stage in 97% of patients is 5 year survival rate Palliative surgical segmental resection
  • 80. LPO
  • 81. LPO
  • 82. Malignant glands infilrating the surrounding tissue LPO
  • 83. HPO Malignant glands infilrating the surrounding tissue
  • 87. HPO
  • 88. HPO
  • 89. Rectal Adenoma(not included in practical quiz)
  • 90.
  • 91.
  • 92.
  • 93.
  • 94.
  • 95.
  • 96.
  • 97.
  • 98.
  • 99.
  • 100.
  • 101.
  • 102.
  • 103.
  • 104.
  • 105. Thanking to the entire Universe