Pathology Review-Term2

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medical school pathology lectures. Year end review of pathology. Term 2 - Haematology and gastrointestinal systems.

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Pathology Review-Term2

  1. 1. As is our Pathology, so is our Practice. -- Sir William Osler, M.D. (Father of Modern Medicine & Founding professor of John Hopkins, developed first residency program for physicians.) Pathology: The science of medicine !
  2. 2. CPC21: Week Overview 2013 Term 2 CPC 1 Title: Haematopoetic 1/2 Anaemia System: Haematopoietic system Aim: To train students in: Clinical, pathological & population studies of patients with anemia (RBC disorders) Objectives: 1. History taking & clinical examination of patients with anaemia 2. Physical examination for anaemia and related illnesses. 3. Pathophysiology of common and important rare causes of anaemia, particularly in the tropics and Indigenous populations. 4. Review of Basic sciences relating to bone marrow, red blood cell production and turnover of iron, routine blood test parameters, measurement of iron stores, and precursors important for red cell production. 5. Pathophysiology of acute anaemic processes. 6. Complications of anaemia. 7. Anaemia as a presentation for other pathologies and as an illness in itself.
  3. 3. Core Learning Issues: • Basic Science Review: – RBC life cycle, structure, functions. – Iron, B12 & Folate, Hemoglobin/bilirubin metabolism. • Major Learning: – CBC – Principles & Interpretation (reticulocytes). – Microcytic, Macrocytic & Normocytic anemia. – Overview & Classification of Anemias – Common An: IDA, MA, Hemolytic & ACD • Minor Learning: – Congenital anemia– sickle, thalassaemia, G6PD, HS. – Aplastic and hypoplastic anemia. – Disorders of excess RBC – Polycythemia. – Myelodysplastic syndromes (refractory anemia). 3
  4. 4. Haemopoiesis: Leukemia 4
  5. 5. 5
  6. 6. Blood Smear - Normal RBC crenated RBC Lymphocyte 6
  7. 7. Blood count - C.B.C / F.B.C • Haemoglobin - 15±2.5, 14 ±2.5 - gms/dl. • PCV/HCT - 0.47 ±0.07, 0.42 ±0.05 - lit/lit (%) – RBC vol – better than Hb for anemia diagnosis. • RBC count - 5.5 ±1, 4.8 ± 1 x1012/lit 33 • MCHC - Hb/PCV - 30-36 – grams/deci lit. – Hb synthesis within RBC • MCH - Hb/RBC - 29.5 ± 2.5 pg picogram (wt) 30 – Average Hb in RBC • MCV - PCV/RBC 85 ± 8 – fl femto litres (vol) 85 7
  8. 8. Reticulocyte: Immature RBC Reticular RNA - Methylene blue stain. Reticulocyte RBC (Bluish, Large (high MCV) Reticulocytes (Immature RBC)  Increased RBC production Reticulocytosis  Hemolytic anemia/bleeding 5-7 days
  9. 9. MCV Microcytic Anemia clinical Types & Diagnosis Normocytic Macrocytic Measure Ferritin Low Iron def Anemia Measure B12 + folate Normal/high Normal Anemia of chronic disease/ Congenital Hb dis. Low Megaloblastic anemia Reticulocyte count Hemolytic anemia or blood loss high low Anemia of chronic disease Renal failure Marrow failure
  10. 10. Haemopoiesis in Def. anemias Normal DNA & Hb Normal cell division Normoblasts Low DNA, Normal Hb Less Cell division Megaloblasts Normal DNA, Low Hb More cell division Micro-Normoblasts Macropoly, pancytopenia Iron Def. Anem Normal Megaloblastic 10
  11. 11. IDA – Clinical Features Angular chelitis Pale creases …Why? Bald Fissured - Glossitis 11
  12. 12. Stages of Iron Deficiency: 12
  13. 13. Hypochromic Microcytic RBC 13
  14. 14. Megaloblastic Anaemia: Marrow Hyperplasia Giant metamyelocyte - Macropolycyte Erythroblasts - Megaloblasts Megaloblastic marrow 14
  15. 15. ANEMIA OF CHRONIC DISEASE: • Defective iron transfer. • By Inflammatory mediators. •  erythropoietin production. •  Iron transfer. • IDA with normal or increased iron stores. • Does not respond to hematenic therapy. • Responds to erythropoietin or resolution of inflammation. 15
  16. 16. “The future belongs to those who believe in the beauty of their dreams.” –Eleanor Roosevelt
  17. 17. Self-pity is an opiate! --Napoleon Hill
  18. 18. Hemolytic anemia: Morphology • Abnormal shapes (here a spherocyte) • Polychromatophil (large, bluish, no central palor) • Nucleated RBC (small, pyknotic) Thalassemia 18
  19. 19. Hemolytic Anemia - Types: • Acquired/External causes: – Immune Hemolytic Anemia Commonest • Warm Antibody HA (WAHA) & Cold Ab (CAHA) • Allo immune hemolytic anemia. – Mechanical Damage • Valve, Microangiopathy (DIC), prosthesis, march – Infection induced • Clostridia, malaria, septicemia • Congenital/Internal Defects 1 • Membrane (Hereditary Spherocytosis) 2 • Enzyme defect (G6PD deficiency) 3 • Hb defects (Qual: Sickle cell dis, Quant: Thalassemias) 19
  20. 20. Autoimmune Hemolytic An: AIHA • Auto antibody binding to red cell surface antigens / Drug complex. • RBC phagocytosis in spleen or complement fixation and intravascular hemolysis. • Warm (IgG) & Cold (IgM) types. • Warm: Drugs, Ideopathic. • Cold: Infections, Lymphoma • Lab diagnosis: Coombs Test, Direct / Indirect. Warm / IgG Cold / IgM 20
  21. 21. AIHA: Lab diagnosis – Coombs test. Direct Coombs Test: (for antigen on patient RBC) Pos Neg Indirect Coombs Test: (for antibodies in the serum.) 21
  22. 22. Sickle Cell Anemia - Pathology
  23. 23. Sickle Cell Anemia • • • • • Commonest congenital hemolytic anemia. Hemoglobinopathy – β chain 6(ValGlu)  HbS Deoxigenation  cryst. Hb  rigid sickle  obstruction, hemolysis. BS - Sickle cells, anisocytosis, poikilocytosis, and target cells. Hemolytic anemia, Multiple Infarcts, autosplenectomy(adult), pigment gall stones, hemosiderosis.
  24. 24. Thalassemia: • Quantitative Hb defect. • Defective protein chain synthesis. • α, β, , , … types. • α thal  α  Hb   β (β β or β tetramers) • Decreased normal Hb. • Abnormal Hb (α/β tetramers). • Like IDA (minor) Destruction  hemolytic anemia (major) • Minor: micro hypo, target cells • Major: severe with hemolysis. Minor / Trait Major / Disease 24
  25. 25. “The only person who never makes a mistake is a person who never does anything” - Theodore Roosevelt 25
  26. 26. CPC22: Week Overview 2013 Term 2 CPC 2 Title: Haematology 2/2 System: Haematopoetic System Aim: To train students in: Clinical and pathological presentation of haematological malignancy Objectives: 1. History taking & clinical examination of patients with haematological malignancy 2. Physical examination of haematopoeitic system and related systems in malignancy. 3. Pathophysiology of haematological malignancies. 4. Review of basic sciences relating to bone marrow, red blood cell production and turnover of iron, routine blood test parameters, measurement of iron stores, and precursors important for red cell production. 5. Pathophysiology 6. Complications of haematological malignancies.
  27. 27. Normal Blood Cells: Non-Specific Immunity Eosinophil Specific Immunity Neutrophil Lymphocyte Basophil Non granular, Mononuclears Granulocytes, Polymorphs 27
  28. 28. WBC Absolute counts in disease: Penia Penia Penia Penia Neutro Philia Eosino Philia Mono cytosis Lympho cytosis
  29. 29. Granulopoiesis – Leukocytosis – Shift to left
  30. 30. Leukemia Classification • Acute Leukemias: – Acute Myeloid Leukemia - AML • AML M0, M1, M2, M3, M4, M5, M6 & M7 – Acute Lymphoid Leukemia - ALL • ALL - L1, L2 & L3 - maturity • Chronic Leukemias: – Chronic Myeloid Leukemia- CML • Eosinophilic, neutrophilic, myelomonocytic etc. – Chronic Lymphoid Leukemia - CLL • Myeloma, Hairy cell, prolymph, Sezary sy. etc.
  31. 31. ALL - AML
  32. 32. Leukemia - Clinical Features Decreased Hemopoiesis: • Anemia (low RBC) • Fever - Infections (low WBC) • Bleeding tendency (low PLT) Organ Infiltration: • Bone pain / back pain. • Lymphadenopathy. • Hepato-spleenomegaly.
  33. 33. ALL • • • • - Dense chromatin Few nucleoli Scanty cytoplasm. No cytoplasmic granules. AML • • • • Fine lacy chromatin Many nucleoli More cytoplasm Cytoplasmic granules
  34. 34. CML • • • • Middle age 40-60y Philadelphia chrom. t(9:22) Anemia, Fever & Bleeding Marked leucocytosis – >50,000 (abnormal) • Marked splenomegaly, Hepatomegaly. Clinical course  Chronic phase CLL • Elderly age • Anemia, fever & bleeding – slow over years. • Lymphocytosis & Lymphadenopathy • Marked Spleenomegaly • Common B cell (CD5 +ve) Accelerated crisis
  35. 35. Lymphoma • Definition: Neoplasms of lymphoid tissue • Etiology: Idiopathic, Genetic, Infective. • Pathogenesis: – overexpression of antiapoptotic gene – t(14-18)  bcl-2+IgM.  B Lymph. neoplasia * • Clinical: Lymphadenopathy, weight loss, Fever, Anemia. • Hodgkins lymphoma (HL) – RS cells. • Non-Hodgkins lymphoma (NHL) – no RS. – B, T & Histiocytic “B commonest”
  36. 36. Hodgkins Lymphoma: • Only Reed-Sternberg cells are malignant „B‟ cells. Others cells are reactive. • Types: • • • • Nodular sclerosis HL Lymphocyte-rich classical HL Mixed cellularity HL Lymphocyte depletion HL • More RS cells = poor prognosis. • Progresses by continuity – nearby LN first. • Staging is important for prognosis. (x NHL)
  37. 37. Hodgkins Lymphoma: • B cell lymphoma with special RS cells. • Only Reed-Sternberg cells are malignant „B‟ lymphocytes. Others cells are mixed inflammatory cells with eosinophils. • Many sub types: based on % of RS cells. • More RS cells = poor prognosis. 1. 2. 3. 4. Lymphocyte-rich classical HL Nodular sclerosis HL – commonest. Mixed cellularity HL Lymphocyte depletion HL • Spread to nearby LN not distant. • Good prognosis, cure likely* RS RS RS
  38. 38. Non-Hodgkins Lymphoma: • Large group of lymphatic malignancies. • types B, T & Histiocytic. “B common” • Clinical Features: – Fever, anemia, infections, – Lymphadenopathy. Spleen+/-. – low, intermediate & high grade. • Pathology – Lymphnode tumour – no RS cells, all one type. – Follicular / Diffuse, Small / Large / mix Cells. • Special types: – Burkitts lymphoma – lymphoblastic. – Multiple Myeloma – plasma cell.
  39. 39. NHL types- Diffuse & Nodular types
  40. 40. Lymphoma: Hodgkins Non Hodgkins Age Average age is 27.7 with two peaks, 15-24y , >55. Average age is about 67. Occurrence ~ 15% of all lymphomas ~ 85% of all lymphomas Location above the collar bone 85% Chest in 40%, more abdomen (the mediastinum), (exception lymphoblastic Extranodal in 4% lymphoma) Extranodal in ~23% & BM Affected Lymph Cells B-Lymphocytes characterized by the Reed-Sternberg Cell B, T, Histiocytes, NK Cells depending on the subtype Symptoms More likely to have systemic ("B") Symptoms Less likely to have "B“ symptoms.(27%) Progression Early diagnosis, Predictable, continuous involvement. Better prog. Late stages, less predictable more spread. Good to Worse prognosis.
  41. 41. Burkitt‟s lymphoma: B cell. • • • • • • Young children, EBV virus. Endemic in Africa High grade, fast growing, Tumour in jaw bones. Lymphoblastic lymphoma Many macrophages – “starry sky” appearance.
  42. 42. Multiple Myeloma: • Malignancy of Plasma cells (Mature B lymphocytes with Ab production) • Hyper gammaglobulinemia • Monoclonal antibody – neoplastic. • Thick viscous blood – infarctions, visual difficulties & even blindness. • Old age, males common. • Multiple, punched out Lytic bone lesions (Osteolysis) & fractures. • Immunodeficiency – infections.
  43. 43. "Creativity is inventing, experimenting, growing, taking risks, breaking rules, making mistakes, and having fun." -- Mary Lou Cook
  44. 44. MyeloProliferative Syndromes: • Neoplastic, Proliferation, Slow, chronic, & Mature cells. • JAK2 gene mutation on 9p*  Erythropoietin hypersensitivity. • Increased number (Functionally abnormal) • Extramedullary spread – Hepatosplenomegaly. • May transform to Acute Leukemia (AML). • Classification: – RBC - Polycythemia vera (PV) – WBC • Chronic Myeloid Leukemia (CML) • Chronic neutrophilic leukemia • Chronic eosinophilic leukemia/HE syndrome. – PLT - Essential Thrombocythemia (ET) – Fibroblasts - Myelofibrosis (MF)
  45. 45. ET - Blood Film & clinical. Plenty of Platelets Megakaryocyte
  46. 46. Polycythemia Rubra Vera (PV) Hypercellular Marrow, Red skin & Hepatosplenomegaly
  47. 47. MPS : MF. Hepatosplenomegaly Massive hepato-splenomegaly secondary to Extramedullary hematopoiesis due to Myelofibrosis.
  48. 48. Myelodysplastic Syndromes: • Excess proliferation & destruction of dysplastic cells in BM  Peripheral pancytopenia. • Also known as Refractory Anemia‟s FAB classification RA : Refractory Anemia (BM Blasts <1%) RARS : RA with Ring Sideroblasts (<1%) RAEB : RA with excess blasts (<5%) RAEB in T : RAEB in transformation (5-30%) (>30% blasts in BM  Leukemia) Abnormal cells & Recurrent infections in MDS
  49. 49. Worrying is like a rocking chair, it gives you something to do, but doesn't get you anywhere. -- Anonymous. ….Instead.. join winners club….!
  50. 50. The goal of mankind is knowledge, which is is inherent in man. No knowledge comes from outside: it is all inside. What man 'learns' is really what he “discovers” by taking the cover off his own soul. Swami Vivekananda Education… from Eduse (latin) to bring out..
  51. 51. CPC23: Week Overview 2013 Term 2 CPC 3 Title: Hepatobiliary 1/2 System: Hepatobiliary System Aim: To train students in: Clinical Diagnosis & Understanding of patients with liver disease. Objectives: 1. History taking & clinical examination in patients with (breakdown of liver disease. Aim) 2. Pathophysiology of acute & chronic hepatitis. 3. Pathophysiology of cirrhosis. 4. Review of basic sciences of hepatobiliary system. 5. Professional, ethical & legal issues in alcohol & drug abuse. 6. Epidemiology of addiction, public health strategies. Note to tutors: There are two cases this week. Either case illustrates the learning issues. Please feel free to use either case (or both).
  52. 52. Liver Function Tests: Interpretation • Synthesis / Function. – Total protein & albumin low, PT?Hepatocyte Injury. – ALT, AST, LDH - high. ?? – Alk Phos – mild increase?? • Bile Duct Damage: – Alk Phos – increased ?? • Other: – GGT – alcohol use. – why? – Viral serology – Auto-Antibody panel. GGT ↑ Alcohol (centrilobular) IgG ↑ Autoimmune hepatitis IgM ↑ Primary biliary cirrhosis IgA ↑ Alcoholic cirrhosis AFP +ve Hep. Cell. Carcinoma Antimitochondrial antibody +ve Primary biliary cirrhosis Anti-smooth muscle, & ANA +ve Autoimmune hepatitis 52
  53. 53. Normal • 1.5 kg, wedge shape • 4 lobes, Right, left, (Caudate, Quadrate) • Double blood supply • Hepatic arteries • Portal – Venous blood 53
  54. 54. CPC 4.2.3 – 2013 – “yellow eyes” CASE STUDY 1 Mr. T.D. 50 year old, presents to his GP. „My stomach appears big and my wife has noticed a yellow tinge in my eyes‟. Presenting Symptoms: Abd distension, fatigue, yellow discoloration of eyes for 1 week • • • • • • • • • • Fatigue / Anorexia..? • Liver failure… Nausea, Vomiting..? • Liver failure… Haematemesis… ? • Portal Hypertension Itching..? • Obstructive jaundice. Fever..? • Hepatitis. Abdominal distension slow..? • Cirrhosis. Bleeding / Bruising..? • Vit-K deficiency. • Differential Diagnosis: hepatitis. 10 stubbies/day /more..? • Alcoholic • Hepatitis: Alcoholic/Infective/Malignant/Drug/Toxins Many Tattoos..? • Viral Hepatitis (B/C) • Acute / Chronic? Primary/Secondary? BMI – if low / High..? • Anorexia / Obesity – • “HBV / HCV, CMV, Lepto, Dengue, Melioidosis. steatosis. 54
  55. 55. Viral Hepatitis A: Serology 55
  56. 56. Viral Hepatitis B: Serology Sequence of serologic markers for hepatitis B viral hepatitis demonstrating (A) acute infection with resolution and (B) progression to chronic infection. 56
  57. 57. Pathogenesis of Hepatitis A & B: 57
  58. 58. Acute Hepatitis: • • • • Portal & Diffuse Inflammation. No clear border between inflammation & normal tissue Because of active necrosis & apoptosis at margins. Abnormal enzymes. 58
  59. 59. Liver Biopsy – Chronic Inflammation • Portal Inflammation. • No Necrosis • Liver enzymes normal 59
  60. 60. Acute viral Hepatitis: Swelling & Apoptotic cells. • Diffuse Inflammation. • Necrosis & Apoptosis. • Liver enzymes raised. 60
  61. 61. Fulminant Hepatitis: • • • • • Rapid Hepatic failure with in 2-3 weeks. Massive necrosis, shrinkage, wrinkled Only portal tracts visible Little or massive inflammation – time Complete recovery – or - cirrhosis. 61
  62. 62. Clinical Spectrum of HBV inf: Acute Chronic 62
  63. 63. Cirrhosis – Portal hypertension 1. 2. 3. 4. Cirrhosis-obstruction Portal hypertension Splenomegaly transudation - Ascites 63
  64. 64. Liver Biopsy – Cirrhosis Fibrous septa Reg. nodule 64
  65. 65. Primary Biliary Cirrhosis • Autoimmune. • Females 6:1. • Pruritis, jaundice, hepatosplenomegaly (initial). • Intrahepatic Bile duct inflammation • Cholestasis (bile stained liver) 65
  66. 66. "The past, the present and the future are really one: they are today!" -Harriet Beecher Stowe The past has gone and future you cannot see. The present, when you can do something, that is the Gift (Present) with which you can make your future & past memorable. - Sai Baba
  67. 67. Chronic Alcoholism: Acetaldehyde 67
  68. 68. Alcoholic Liver Damage 68
  69. 69. Alcoholic Hepatits - Mallory's hyalin 69
  70. 70. Alcoholic Fatty Liver 70
  71. 71. Alcoholic Fatty liver: 71
  72. 72. Safe drinking… High Risk Intermediate Low Risk 72
  73. 73. Learn from the mistakes of others. You can't live long enough to make them all yourself…! 61% of 5th year students exceeded ‘sensible’ limits Drugs and alcohol were taken mainly for pleasure and were perceived as a normal part of life for many students… Capability of advising patients…? http://www.lycaeum.org/research/researchpdfs/1996_webb_1.pdf 73
  74. 74. CPC24: Week Overview 2013 Term 2 CPC 4 Title: Hepatobiliary 2/2 System: Hepatobiliary & Pancreas Aim: To train students in: Understanding of & clinical approach to diagnosis of patients with obstructive jaundice & gall bladder disease. Objectives: 1. History taking & clinical examination 2. Physical examination for liver, gall bladder, jaundice. 3. Pathophysiology of obstructive jaundice. 4. Review of Basic sciences: Bile synthesis and metabolism. 5. Professional, ethical & legal issues. 6. Epidemiology, Public Health.
  75. 75. Why! HBS: Common Clinical Presentations. 75
  76. 76. Biliary Obstructions: • Extrahepatic Obstruction: – – – – Dislodged gallstones Ca. CBD, Ca. Head of pancreas. inflammatory stricture of CBD accidental surgical ligation of CBD. • Intrahepatic Obstruction: – – – – Biliary atresia – Congenital. Primary Biliary Cirrhosis Primary Sclerosing Cholangitis. Cystic fibrosis. 95% - Cholelithiasis (+cystitis) Common Disorders: • Cholecystitis • Cholelithiasis • Choledocholithiasis. (Adeno Carcinoma)
  77. 77. Cholelithiasis: • Morphology & Types: – Mixed Chol (Ca+Bile salt)* Multiple, faceted, yellow-grey - commonest. – Rarely Pure cholesterol: Round spiky. – Bile Pigment stones (black/brown). Infection / Jaundice. % Calcium = radio opaque.
  78. 78. Complications of Cholelithiasis: • • • • • • • • • • • • • • Obstruction Sec biliary cirrhosis* Cholecystitis Cholangitis Biliary colic Jaundice Empyema Liver abscess Mucocele Pancreatitis. Peritonitis Carcinoma Fistula formation Gall stone ileus. Gallstone ileus
  79. 79. Acute Cholecystitis: • • • • • • • • • 90% Cholelithiasis. 10% non-calculous Females common. Outflow obstruction by a small gallstone. Infection – E.coli.  Empyema. Risk of perforation, peritonitis, fistula  Gall stone ileus when stone enters GIT. Serum amylase normal (high with pancreatitis). Mild jaundice in 20% - obstructive. Acute inflammation, hemorrhage, edema, neutrophils. Gangrenous cholecystitis: when obstruction is severe compromising blood supply. Green-black necrotic.
  80. 80. Chronic Cholecystitis: • • • • • Females. Recurrent / Chronic. Thick fibrotic wall. Thick bile – biliary gravel. Aschoff-Rokitansky sinuses – diverticula - Due to increased luminal pressure (obstruction) • Diffuse infiltration by chronic inflammatory cells.
  81. 81. Acute Hemorrahagic Pancreatitis - Clinical Mild Grey Turner Sign - Cullen‟s Sign Severe
  82. 82. SUMMARY: Trypsin  Kallikrein  Thrombosis - Necrosis Protease  Blood Vessel injury – Bleeding. Lipase  Fat necrosis  Inflammation.
  83. 83. Chronic fibrosing Pancreatitis: Acute Hemorrhagic Acute Hemorrhagic Chronic fibrosing Carcinoma
  84. 84. Acute Hemorrhagic Pancreatitis: Acini Necrosis Fat Necrosis Normal Acini Hemorrhage
  85. 85. Pancreatic Ca with fibrosis (Chronic pancreatitis) Fibrous stroma Ca. Infiltration Malignant gl. Islet (normal) Note: dysplastic glands infiltrating into fibro (spindle cells) myxoid (pale blue) stroma.
  86. 86. Ca Pancreas Clinical Features Tumour marker: CEA & CA19–9 antigen Trousseau syndrome
  87. 87. Give someone a fish and you feed him for a day. Teach someone to fish and you feed him for a lifetime! Lao Tzu
  88. 88. CPC25: Week Overview 2013 Term 2 CPC 5 Title: GIT 1/3 System: Gastrointestinal Aim: To train students in: Understanding pathology & Clinical diagnosis of patients with upper GIT disorders. Clinical diagnosis of Acute Abdomen Objectives: 1. History taking & clinical examination of patients with upper GIT symptoms. 2. Physical examination of Abdomen. Recognition of an Acute abdomen. 3. Pathophysiology of peptic ulcer disease. 4. Pathophysiology of gastric cancer. 5. Review of Basic sciences – Anatomy & functions of upper GIT 6. Professional, Ethical & Legal issues in chronic diseases. 7. Epidemiology & Public Health issues of Helicobacter pylori. (Australian Nobel Laureate). 8. Presentation, epidemiology & Public Health issues of acute appendicitis. Risk factors and counseling.
  89. 89. Esophagus & Stomach Normal Glandular – Gastric  Normal  Squamous Oesophagus
  90. 90. Dysphagia • Dysphagia: Difficulty in swallowing. – Odynophagia: painful swallowing – inflam, ulcer, Carcinoma. • Sites: – oropharyngeal, esophageal, esophagogastric, and paraesophageal . • Symptoms: – Solids – Mechanical Obstruction – tumors/strictures. – Solids & Liquids – Motility disorders – Achalasia. – Liquids – Pharyngeal disorders. • Causes: – Local, Systemic, central. – Mechanical, neural, functional. – ulcers, tears, webs, rings, tumors, strictures, paralysis abnormal peristalsis. (stroke),
  91. 91. Esophageal Disorders: • Reflux Oesophagitis. • Barrett‟s • Stricture – Inflam. • • • • • • Mallory-Weiss. Varices Hernia Zenker diverticulum T-E Fistula. Web – IDA – P-V Sy. Herniations
  92. 92. Oesophagus motility Disorders: Achalasia Hernia-Sliding 95% Hernia-Rolling 5% Hernia: 30% incidence over 50years. (mostly asymptomatic) Achalasia: Lack of relaxation of lower sphincter.
  93. 93. Oesophagitis: • Acute: errosive, alcohol, infection. • Chronic: Acid reflux (GERD), chemical, alcohol, smoking, candida, radiation, idiopathic (eosinophilic). • Endoscopic view  Microscopy: • Acute inflammation. • Eosinophils: Few (reflux) more in Eosinophilic. Candida
  94. 94. GORD: Clinical Classification Etiology: (LES) • Alcohol, Tobacco, • Obesity, • CNS depressants, • Pregnancy, • Hiatal hernia • Delayed gastric emptying • increased gastric volume 24-hr pH Study Endoscopy Barrett‟s 1% AET +ve SI +ve Heartburn GORD Oesophagitis 24% AET -ve SI +ve AET -ve SI –ve ? MERD Non-Erosive Reflex Disease (NERD) AET: Acid Exposure Index SI: Symptom Index. MERD: minimal change.. RD (normal endoscopy) 75%
  95. 95. GERD: Pathogenesis. Normal  Hyperplasia  Dysplasia  Carcinoma Basal cell hyperplasia Inflammed Sq. Ep. Metaplastic Col. Ep. Normal Sq. Ep.
  96. 96. Squamous Carcinoma - Adenocarcinoma. Normal Normal Tumour Tumour • Less common • Upper end • Tobacco, diet, toxins. • More common • Lower end • Reflux disease (Barretts)
  97. 97. Gastritis: • Acute Gastritis: – Drugs, toxins, alcohol, Ischemia. – Infections (H.pylori transient) Normal ↑ • Chronic Gastritis: – Autoimmune: Pernicious an. (autoantibody) – Chem: NSAIDs, Bile reflux, Alcohol. – Bacterial: Helicobacter pylori. ← Acute Chronic ↓
  98. 98. H. Pylori Gastritis - Silver stain Bacteria over epithelial cells
  99. 99. Peptic Ulcer Morphology: • • • • • • Common in duodenum than stomach (4:1) > 80% single ulcer Round small, clean, punched out, <2cm*. Radiating folds. Microscopy: – – – – Superficial necrotic layer. Inflammatory cells zone. Granulation tissue zone - B Collagenous scar zone - C. Note: Radiating mucosal folds from the ulcer.. Why?
  100. 100. Gastric Peptic ulcer: Scar Note: Radiating mucosal folds from the ulcer.. Why?
  101. 101. Barry J Marshal, 2005 Nobel Prize….! There were a lot of people who didn't believe what we said but they couldn't keep us quiet…! A.A.Press.. 4 Oct 2005. Barry J. Marshall & J. Robin Warren was a trainee at that time…..!
  102. 102. Gastric Adeno Carcinoma: • • • • • • • Intestinal Type H.pylori Metaplasia C. gastritis / atrophy HER-2/NEU mutation Well differentiated No Signet ring cells. Gland formation. Better Prognosis • • • • • • • Diffuse Type Idiopathic/familial. No precursor lesion E-Cadherin mutations Poorly differentitated Signet ring cells No gland formation, Poor Prognosis
  103. 103. Fungating Carconoma
  104. 104. Diffuse Ca - Fibrotic Linitis Plastica / Leather bottle stomach. Endoscopy Malignant cells between fibrous stroma 
  105. 105. Gastric Carcinoma Normal Gland Malignant
  106. 106. To attain knowledge, add things every day. To attain wisdom, remove things every day. Lao Tzu
  107. 107. CPC26: Week Overview 2013 Term 2 CPC 6 Title: GIT3/3 System: GIT. Aim: To train students in: Understanding pathology & Clinical diagnosis of patients with lower GIT Conditions including Bowel Cancer & Inflammatory bowel disorders. Objectives: 1. Physical examination of abdomen. (breakdown of Aim) 2. Review of basic sciences – Lower GIT structure & function. 3. Pathology & Epidemiology of inflammatory bowel disease. 4. History taking & clinical examination of patients with Lower GIT Malignancy. 5. Genetic basis of colonic neoplasms. 6. Review of Basic sciences – Carcinogenesis, Knudson theory, hereditary syndromes of colon cancer. 7. Professional, Ethical & Legal issues in malignancies. 8. Epidemiology & Public Health issues of lower GIT malignancies (Global & Australian)
  108. 108. Etiology: Exact etiology not “Unregulated and exaggerated local immune response to Gut flora in genetically susceptible individuals” • Etiology theory: – 1. Genetic susceptibility – 2. Environmental Factor: Gut flora. – 3. Immune dysfunction/Autoimmunity. • 15% family history, 30-59% concordance in twins. • HLA: DR1B1 (UC), DR7, DQ4 (CD) - 27% • Hygiene hypothesis * NOD2 known…Caspase TNF, IL1, IL6, IL23 R
  109. 109. Whole of GIT Only Colon
  110. 110. Crohn‟s • • • • • • • • • • - vs - U. Colitis: Chronic granulomatous. Transmural – full thickness. Ulcers deep, narrow. Firm thick, narrow lumen. Fibrosis - significant. Skip Lesions & fistula Rectal bleeding 100% No significant perianal sores. Malabsorption - Fat (ileum) HLA-DR7, DQ4. IL17 - TH1 cells. • • • • • • • • • • Acute infl – edema. Superficial - mucosal inflammation. Ulcers shallow, broader. Normal/Thin wall, dilated lumen. Fibrosis - no/little. Continuous, no fistula. Rectal bleeding 75-85% perianal sores in 25-35% Malabsorption – no HLA – DRB1, - TH2 cells. NOD2* IL-23R*
  111. 111. Crohn‟s Disease: microscopy Lymphocytes Granuloma Giant cells No caseation.
  112. 112. UC - inflammation limited to mucosa, atrophy of colonic glands, normal muscle layer. Normal submucosa.
  113. 113. Diverticulosis: • Later age. (>30y) • Constipation alternating with diarrhoea. • Two types: – Acquired / False common, no muscular layer. – True rare, congenital, all layers present. E.g. Meckles.
  114. 114. Intestinal Obstructions: • Mechanical Obstruction: (commonest) – Adhesions, Hernias, Intussusception, Volvulus. • Others: – Tumors, gallstones, fecaliths, foreign bodies, Congenital stricture, atresias, Meconium in cystic fibrosis.
  115. 115. Pseudomembranous Colitis: Clostridium difficile: Controlled by normal flora. Antibiotic therapy may result in over growth of cytotoxin producing strains causing fibrinopurulent debris and mucus tightly adherent to ulcerated mucosa (pseudomembran).
  116. 116. Polyps of Colon: Hyperplastic Polyp Villous Tubular Adenoma Adenoma AdenoCarcinoma
  117. 117. Polyps of Colon: Hyperplastic - 90% - no/low malignant potential Villous Adenoma 1% high malignant potential Tubular Adenoma 9% - malignant potential Tubulovillous Adenoma - mixed
  118. 118. Hereditary Colon Cancer Sy. *Rare • HNPCC (Lynch Syndrome) (10%). – AD, Mutation in DNA mismatch repair genes MMR – increased risk of GI and non-GI cancers – Few adenomatous polyps. • Familial Adenomatous Polyposis (1%). – AD, mutation in APC gene on 5q21 – >100 - 2500 polyps throughout GIT duodenum* – virtually 100% risk of carcinoma by 50years.
  119. 119. Pathogenesis 1. – Adenoma Ca Path More common – 70%
  120. 120. Pathogenesis 2. – Mismatch pathway (also in sporadic Right type). Less common – 10-15%
  121. 121. Left sided Ca Colon – Constricting – Napkin ring (Gross) Apple core (Xray)
  122. 122. Adeno Carcinoma / Normal
  123. 123. Ca Colon – Dukes Staging - Prognosis.
  124. 124. “When we accept without questioning, we forfeit the power to control our own lives" Bryce Courtenay knowledge is power and ignorance is enslavement. To question is the key to learning…!
  125. 125. CPC27: Week Overview 2013 Term 2 CPC 7 Title: Head and Neck 1/1 System: Respiratory Tract Aim: To train students in clinical approach & diagnosis of patients with symptoms of Upper Respiratory Tract Infection (URTI). Objectives: 1. History taking & clinical examination in Patients with URTI. 2. Physical examination of head & neck. 3. Pathophysiology and Microbiology of URT & URTIs 4. Review of Basic sciences – Anatomy of Head & Neck. 5. Professional, Ethical & Legal issues. 6. Epidemiology, Public Health.
  126. 126. Leukoplakia - Erythroplakia Leukoplakia Erythroplakia Leuko+Erythroplakia
  127. 127. Progression of oral neoplasia Cigarette, Alcohol & Tobacco. C
  128. 128. Dental Pathology: • Caries: – Tooth decay, Mineral dissolution acid, carbs, bacteria. – Role of fluoride and oral hygiene • Gingivitis: – Junctional mucosa, hygiene. Plaque/calculus. – Inflammation of soft tissue around the teeth • Periodontitis: – Inflam. of supp. structures. – Important in IE, pulmonary and brain abscess
  129. 129. Oral Pathology: • Irritation Fibroma: – Fibrous scar, Rx excision – Along bite line or a gingivo-dental margin • Pyogenic granuloma: – Chronic ginvitis. Children, pregnancy. • Aphthous ulcers: – Common, painful, shallow ulcers, cause obscure. • Glossitis: – Trauma, dentures, – Infections – herpes, candida, syphilis – Anemia – IDA, Meg.
  130. 130. Nasal Polyp (inflammatory): • • • • Chronic/recurrent URTI Allergy, hypersensitivity Mucosal inflam. Polyp Eosinophils.
  131. 131. Laryngeal Neoplasms: • Vocal cord nodules: singers/smokers nodules. Irritation, Fibrous, may bleed, no malignancy. • Recurrent (Juvenile) Papillomatosis: children, multiple HPV (6,11). • Single papillomas in adults. • Laryngeal Carcinoma: Persistent hoarseness of voice. Smokers (less with alcohol, radiation). Vocal cords, SCC usu. (95%)
  132. 132. Nasopharyngeal Carcinoma • Africa (children) & China (adults)...! • EBV, Diet, likely environment important. • Undifferentiated carcinoma with plenty of reactive lymphocytes. • Can be keratinising SCC, non keratinising SCC and undiff Ca • Locally invasive, spread. • 50% 3y survival.
  133. 133. Sialadenitis: • • • • Acute / chronic, Traumatic, viral, bacterial, autoimmune, xerostomia  infections. Parotid most common. Complications – calculus (sialolithiasis) or fibrosis  duct obstruction  Recurrent sialadenitis. • Mumps, Sjogren‟s (autoimmune), S aureus, S viridans.
  134. 134. Pleomorphic Adenoma • Mixed tumor, Most common (60%) • Adults, Slow growing, Asymptomatic. • Single, Irregular, nodular, Well defined borders, less mobile. • Mature Epithelial & connective tissue. • Recurrence common. Other tumours: • Warthin‟s tumour (lymphoepithelioma) • Mucoepidermoid Ca. • Adenoid cystic carcinoma • Adeno / Squamous Cell Ca.
  135. 135. Education must award character & self-confidence, the courage to depend on one’s own strength. - Sai Baba

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