UHS Pathology & Microbiology 2009 Past Paper PDF

MBBS SECOND PROFESSIONAL MODEL QUESTIONS FOR ANNUAL 2009 General Pathology and Microbiology (Multiple Choice Questions) Q.1 A 22-year-old man develops marked right lower quadrant abdominal pain over the past day. On physical examination ther...

MBBS SECOND PROFESSIONAL MODEL QUESTIONS FOR ANNUAL 2009 General Pathology and Microbiology (Multiple Choice Questions) Q.1 A 22-year-old man develops marked right lower quadrant abdominal pain over the past day. On physical examination there is rebound tenderness on palpation over the right lower quadrant. Laparoscopic surgery is performed and the appendix is swollen, erythematous and partly covered by a yellowish exudate. It is removed and a microscopic section shows infiltration with numerous neutrophils. The pain experienced by this patient is predominantly the result of the formation of which of the following two chemical mediators: a) Complement C3b and IgG b) Interleukin-1 and Tumor Necrosis Factor c) Histamine and serotonin d) Prostaglandin and bradykinin e) Leukotriene and HPETE Q.2 A fifty year old woman, who is suffering from cirrhosis of the liver, presents with a distended abdomen to her physician, who taps the fluid and sends the specimen to the hospital laboratory for analysis. The fluid shows protein content and specific gravity less than 3.0 gm/dl and 1.015 respectively. The fluid is best described as: a) Exudate b) Transudate c) Effusion d) Isotonic fluid e) Serous fluid Q.3 A group of sailors was rescued from a ship that was lost for a month. They lived on fish recovered from the sea. They were all fatigued and had gums bleeding on eating anything hard. What is the most likely cause? a) Scurvy b) Vitamin K deficiency c) Ehlers-Danlos syndrome d) Osteogenesis imperfecta e) Marfan syndrome Q.4 A cholecystectomy specimen is examined fresh in the laboratory. It shows a large impacted gallstone in the neck. Fundus of the gallbladder shows engorgement of blood vessels on external surface. This is most likely due to: a) A malignant process b) Hemorrhage c) Hyperemia d) Congestion due to obstruction to outflow of blood e) Chronic inflammation Q.5 A 40 years injured male is presented in emergency with complaints of increased respiratory rate, cold extremities, rapid pulse and oliguria. On examination B.P. is 60/40mmHg, Pulse 150/min and bluish discoloration of tip of tongue and nails. Which type of shock is developed in this patient? a) Cardiogenic shock b) Neurogenic shock c) Hypovolemic shock d) Septic shock e) DIC Q.6 A 60-year old businessman lived for 40 years in Egypt. On return to Pakistan, he presents with painless gross haematuria. Cystoscopy was done by the urologist and the biopsy specimen obtained showed Transitional Cell Carcinoma. Urine examination shows pear shaped ova with large terminal spine. Which of the following is most likely responsible for this tumor: a) Schistosoma haematobium b) Schistosoma japonicum c) Schistosoma mansoni d) Wuchereria bancrofti e) Trypanosoma cruzi. Q.7 A neonate was born with signs of encephalitis, chorioretinitis, hepatosplenomegaly, fever and jaundice. The mother gave a history of fever two to three times during pregnancy. History taking revealed that she has many cats as pet. On examination of neonate intra cranial calcifications were found. IgM Ab titer was also raised. What is the most likely Microorganism responsible? a) Pneumocystis carinii b) Toxoplasma gondii c) Cytomegalovirus d) Treponema palladium e) Rubella virus Q.8 A forty year old man complains of upper abdominal pain, watery foul smelling diarrhea and flatulence for the past two weeks. He drank spring water on a camping trip near Abbotabad. Trophozoites were found on stool examination. Which is the most likely protozoan involved: a) Crytosporidium b) Giardia lamblia c) Entamoeba coli d) Trichomonas e) Acanthamoeba Q.9 A male baby is born at 39 weeks gestation with a petechial rash, low birthweight, hepatosplenomegaly and bilateral cataracts. This is thought to be due to an infection acquired while the baby was still in utero. Select the condition which is most likely to cause this clinical presentation: a) Cytomegalovirus b) Group B streptococcus c) Rubella virus d) Toxoplasma gondii e) Treponema pallidum Q.10 A forty year old woman, has blurred vision and slurred speech. She is afebrile. She is well known in her neighbourhood for her expertise in home canned vegetables and fruits. The most likely cause of her illness is? a) Clostridium perfringens toxin acting on neuromuscular junction b) Clostridium botulinum toxin acting on the neuromuscular junction c) Clostridium botulinum toxin acting on the cranial nerves d) Clostridium difficile acting on the acetylcholine receptors e) Clostridium botulinum toxin acting on the adrenergic receptors  Page 1 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) Total Marks: 45 Time Allowed: 45 Minutes Total No. of MCQs: 45 Note: THE FINAL PAPER WILL BE SIMILAR TO THE MODEL PAPER BUT WILL FOLLOW TOS EXACTLY. 1. Which of the following types of necrosis is grossly opaque and chalky white: a) Coagulation necrosis. b) Liquefaction necrosis. c) Caseous necrosis. d) Fat necrosis. e) Gangrenous necrosis. Key: d Ref: Cell Injury, Death and Adaptation. 2. Which of the following types of necrosis is most commonly associated with ischaemic injury: a) Coagulative necrosis. b) Liquifactive necrosis. c) Caseous necrosis. d) Fat necrosis. e) Gangrenous necrosis. Key: a Ref: Cell Injury, Death and Adaptation. 3. Dystrophic calcification is most closely associated with: a) Hypercalcaemia. b) Necrosis. c) Chronic irritation. d) Diminished blood flow. e) Increased work load. Key: b Ref: Cell Injury, Death and Adaptation. 4. Localized area of ischaemic necrosis is mostly associated with: a) Ascitese. b) Petechiae. c) Infarction. d) Emboli formation. e) Hematoma. Key: c Ref: Cell Injury, Death and Adaptation. 5. Metabolism is most closely associated with: a) Diminished blood supply. b) Increased work load. c) Necrosis. d) Chronic irritation. e) Hypercalcemia. Key: d Ref: Cell Injury, Death and Adaptation.  Page 2 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 6. Which of the following is a reversible change: a) Karyorrhexis. b) Pyknosis. c) Karyolysis. d) Swelling of endoplasmic reticulum. e) Gangrenous necrosis. Key: d Ref: Cell Injury, Death and Adaptation. 7. After initiation of an acute inflammatory process third in a sequence of changes in vascular flow is: a) Vasoconstriction. b) Redness. c) Leukocytic migration. d) Vasodilation. e) Slowing of the circulation. Key: d Ref: Acute and Chronic Inflammation. 8. Which of the following are thought to mediate, many of the systemic effects of inflammation are chemotactic and stimulate adhesion molecules: a) Interleukin 1 (IL-1) and tumor necrosis factor. b) C5 a and leukotriene B-4. c) C3 b. d) Leukotriene C4 , D4 and E4. e) Bradykinin. Key: a Ref: Acute and Chronic Inflammation. 9. Which of the following is the hallmark of acute inflammation: a) Neutrophils. b) Connective tissue. c) Macrophages. d) Granulation tissue. e) Granuloma formation. Key: a Ref: Acute and Chronic Inflammation. 10. Granuloma formation is most frequently associated with: a) The healing process. b) Acute inflammation. c) Wound contraction. d) Fibroblasts and neovascularization. e) A persistent irritant. Key: e Ref: Acute and Chronic Inflammation. 11. Morphologic changes seen in chronic non-specific inflammation include an increase in: a) Neutrophils, lymphocytes and liquefaction necrosis. b) Neutrophils, macrophages and fibrosis. c) Lymphocytes, plasma cells and fibrosis. d) Giant cells, macrophages and coagulative necrosis. Key: c Ref: Acute and Chronic Inflammation.  Page 3 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 12. Caseation necrosis is most characteristic of: a) Acute myocardial infarction. b) Tuberculosis. c) Acute pancreatitis. d) Cerebral infarct. e) Pulmonary pneumoconiosis. Key: b Ref: Acute and Chronic Inflammation. 13. The most characteristic feature of granulation tissue is the: a) Growth of fibroblasts and new capillaries. b) Resemblance to a granuloma. c) Character of the exudate. d) Granular scar that results. e) Presence of monocytes and fibroblasts. Key: a Ref: Healing and Repair. 14. The growth factor elaborated by macrophages, which recruits macrophages and fibroblasts to wound site and induces all steps in angiogenesis is: a) Vascular endothelial growth factor. b) Fibroblast growth factor. c) Epithelial growth factor. d) Platelet derived growth factor. e) Endostatin. Key: b Ref: Healing and Repair. 15. A young man of 20, got a lacerated wound on his left arm, stiched-1 week later sutures were remained-healing continued but the site became disfigured by prominent raised irregular nodular scar, in next 2 months which of the following best describes the process: a) Organization. b) Dehiscence. c) Resolution. d) Keloid formation. e) Secondary union. Key: d Ref: Healing and Repair. 16. If a rare disorder with an early onset in life is inherited in such a way that male and female offsprings are equally affected, only homozygous persons are affected, then the mode of inheritance would be: a) Autosomal dominant. b) Autosomal recessive. c) X-linked dominant. d) X-linked recessive. e) Mitochondrial inheritance. Key: b Ref: Genetic Disorders.  Page 4 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 17. A six months old baby with blue eyes, decreased pigmentation of hair and skin and a strong mousy odour is brought to you-on examination there is severe mental retardation. What will be the enzyme deficiency: a) Homogentisate oxidase. b) Phenyl Alanine oxidase. c) P-hydroxyphenyl pyruvate hyroxylase. d) Tyrosinase. e) α–glucocerebrosidase. Key: b Ref: Genetic Disorders. 18. A 39 years old male developed a testicular mass which was removed and was sent for pathological examination, along with additional studies. Which of the following is the most compelling evidence that the lesion is malignant: a) Cells of the mass infiltrate a narrow band of the tuinea albuginea. b) Two mitosis are found in every (HPF) high power field of microscope. c) Nuclei are viable in size and tend to stain. d) X-ray shows 2 round nodules in the left lung field and one in the right, were not present 2 years ago. e) The patient is found to be infertile. Key: d Ref: Neoplasia. 19. Which of the following pair does not correctly match the tumor with its causative agent: a) Anagenital carcinoma – HPV (Type 16 & 18). b) Burkitts lymphoma - EBV. c) Hepatocellular carcinoma - Hepatitis A virus. d) Carcinoma stomach - Helicobacter pylori. e) Squamous cell carcinoma skin – Ultraviolet radiation. Key: c Ref: Neoplasia. 20. Which of the following terms refer to a malignant tumor of mesenchymal origin: a) Carcinoma. b) Hepatoma. c) Hematoma. d) Sarcoma. e) Teratoma. Key: d Ref: Neoplasia. 21. Grading of cancer is based on which of the following statements: a) Size of the primary tumor. b) Spread of cancer cells to regional lymph nodes. c) Presence of blood born metastasis. d) Degree of differentiation of tumor cells, anaplasia and no. of mitosis. e) Presence of capsular invasion by tumor cells. Key: d Ref: Neoplasia.  Page 5 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 22. The chemical carcinogen, aflatoxin B-1 derived form a fungus, which contaminates grain foods most commonly induces: a) Transitional cell carcinoma of lung. b) Adenocarcinoma of rectum. c) Squamous cell carcinoma of skin. d) Hepatocellular carcinoma. e) Renal cell carcinoma. Key: d Ref: Neoplasia. 23. Which of the following is not a malignant tumor: a) Glioma. b) Lymphoma. c) Melanoma. d) Leiamyoma. e) Medulloblastoma. Key: d Ref: Neoplasia. 24. Which of the following are most frequent site of venous thrombosis? a) Veins of lower extremity. b) Pelvic veins. c) Portal vein. d) Hepatic vein. e) Pulmonary veins. Key: a Ref: Haemodynamic Disorders. 25. In a state of shock there is: a) A decreased hydrostatic pressure and increased osmotic pressure. b) Cardiovascular collapse. c) Active process leading to increased volume of blood. d) Decreased pulse rate. e) Fever. Key: b Ref: Haemodynamic Disorders. 26. The main factor responsible for world wide distribution of Entamoeba histolytica is: a) Extreme antigenic variation. b) Usual stability of its cysts in the environment. c) Wide spread distribution of mosquitoes. d) Usual motility of trophoziotes in contaminated water. e) Poor hygienic conditions of individuals. Key: b Ref: Parasitology. 27. All of the following characteristics are seen in the stool of Amoebic dysentery except one: a) RBCs in clumps. b) Charcat leyden crystals. c) Eosinophyls. d) Ghost cells. e) Macrophages. Key: d Ref: Parasitology.  Page 6 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 28. Parasite induced pernicious anaemia is caused by: a) Taenia saginata. b) Taenia solium. c) Diphyllabothrium latum. d) Echinococcus granulosus. e) Hymenolepis nana. Key: c Ref: Parasitology. 29. In malaria the form of plasmodium transmitted to man from mosquito is: a) Sporozoites. b) Gametocytes. c) Merozoites. d) Trophazoites. e) Schizonts. Key: b Ref: Parasitology. 30. The host that harbours the adult or sexually mature, parasite is called: a) Intermediate host. b) Commensal host. c) Symbiotic host. d) Reservoir host. e) Definite host. Key: e Ref: Parasitology. 31. Which of the following statements is not correct regarding Hookworm infestation: a) Hookworm infection causes anaemia. b) Man acquires infection when filariform larvae penetrate skin. c) Hookworm infection may sometimes be acquired by oral route. d) Larva passes through human lung during its life cycle. e) Hookworm infection can be diagnosed by finding trophozoites in the stool. Key: e Ref: Parasitology. 32. Which of the following bacterial substance binds to the Fc portion of immunoglobulin molecules: a) Endotoxin. b) Coagulase. c) Lipotheichoic acid. d) M. protein. e) Protein A. Key: e Ref: Virology. 33. Which of the following is associated with a deficiency of third component of complement C3: a) Pyogenic infection. b) Immune complex disease. c) Systemic lupus erythematosus. d) Glomerulonephritis. e) Xeroderma pigmentosum. Key: a Ref: Virology.  Page 7 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 34. Which of the following components enhances the binding of antigen antibody complex to macrophages: a) C1. b) C3a. c) C3b. d) C8. e) Cb6,7 complex. Key: c Ref: Virology. 35. A secretary piece is attached to IgA: a) In plasma cells. b) In epithelial cells. c) By enzyme in mucous secretion. d) By T-cells. e) By macrophages. Key: b Ref: Virology. 36. Two tests are used to detect the presence of HIV infections are: a) Agglutination and neutralization reactions. b) Compliment fixation and immunoflorescence tests. c) ELIZA and Western Blotting. d) Haemagglutination and Coamb’s Test. e) Indirect haemagglutination and Western Blotting. Key: c Ref: Virology. 37. General steps in viral multiplication cycle are: a) Adsorption, penetration, replication, maturation and release. b) Endocytosis, uncoating, replication, assembly and budding. c) Adsorption, uncoating, duplication, assembly and lysis. d) Endocytosis, penetration, replication, maturation, exocytosis. e) Adsorption, replication, uncoating and release. Key: b Ref: Virology. 38. Which of the following serum component is an indicator of post infection and subsequent immunity to hepatitis B-viral infection: a) HBS Ag. b) HBC Ag. c) HBe Ag. d) Anti HBS. e) Anti HBC. Key: d Ref: Virology. 39. Which of the following conditions is not rightly against its causative agent: a) Squamous cell carcinoma cervix = HPV (16, 18). b) Nasopharyngeal carcinoma = EBV. c) Cutaneous warte, (squamous cell papilloma) = HPV (12, 4, 7). d) Hepatocellular carcinoma = HDV. e) Gastric lymphoma = H. Pylori. Key: d Ref: Virology.  Page 8 of 8 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY MODEL PAPER (MCQs) 40. Which of the following is a RNA virus: a) Human papilloma virus. b) Human T-cell leukaemia virus. c) Hepatitis B virus. d) Epstein Barr virus. e) Cytomegalo virus. Key: b Ref: Virology. 41. The antiphagocytic property of the group A streptococcus is associated with which of the following: a) Hyaluromidase. b) Streptolysin S. c) M. protein. d) Peptidoglycan. e) C carbohydrate. Key: c Ref: Microbiology (General and Systemic). 42. Which of the following is correct sequence of steps in performing Gm. Stain: a) Safranin stain, crystal violet stain, iodine solution. b) Crystal violet stain, decolorization, safranin stain, iodine solution. c) Safranin stain, iodine solution, decolorization, crystal violet stain. d) Crystal violet stain, iodine solution, decolorization, safranin stain. e) Iodine solution, crystal violet, decolorization, safranin. Key: d Ref: Microbiology (General and Systemic). 43. The most reliable method for diagnosis of primary syphilis is the: a) VDRL Test. b) FTA-ABS. c) Microhemagglutinine. d) Dark field examination of chancre material. e) Treponema pallidum immobilization test. Key: c Ref: Microbiology (General and Systemic). 44. The pathogenisis of which of the following organisms is most likely to involve invasion of the intestinal mucosa: a) Vibrio chalerae. b) Enteroloxigenic E. coli. c) Shigella somei. d) Clostridium botulinum. e) Pseudomonas aerogenosa. Key: c Ref: Microbiology (General and Systemic). 45. Which of the following tests does not correspond with the respective disease: a) Casoni’s Test for Hydatid disease. b) Frei’s Test in Infectious mononuclease. c) Schick’s Test for Diphtheria. d) Wasserman’s Test for syphilis. e) Widal Test for typhoid. Key: b Ref: Microbiology (General and Systemic).  MBBS SECOND PROFESSIONAL MODEL PAPER FOR ANNUAL 2009 General Pathology and Microbiology (Short Essay Questions) Max. Marks 70 Time Allowed 2 hours 1. a) Define chronic inflammation. Give TWO characteristics of chronic inflammation. 1,1 b) Enumerate THREE causes of chronic inflammation. 3 2. The causes of cell injury range from the gross physical trauma of a motor vehicle accident to the single gene defect that results in a defective enzyme underlying a specific metabolic disease: a) Mention six major categories in which they can be grouped. 3 b) List four potentially toxic agents encountered daily in our polluted environment. 2 3. An American PREDATOR fired two HELL FIRE missiles on a remote house in North Waziristan. Many family members died, but a few survived despite lack of medical or surgical treatment. There was excessive loss of cells and tissues and large defects were created on the body surfaces with extensive loss of normal architecture: a) What will be this type of healing known as? 1 b) How does it differ from primary healing? 4 4. A 35-year old female patient of type II diabetes mellitus cut her hand with a knife in the kitchen; the wound failed to heal even after two weeks: a) What cause/causes of delayed healing you would suspect in this patient? 1 b) List four other local/systemic factors that influence wound healing. 4 5. A child brought to a pediatrician was found to be mentally retarded, had flat facies with epicanthal fold, Siamese crease, abundant neck skin, umbilical hernia and hypotonia with increased gap between first and second toe: a) What is this child suffering from? 1 b) What is the chromosomal abnormality and what is its cause? 1 c) In addition to phenotypic abnormality and mental retardation, name three other clinical features worthy of note? 3 6. Name five CHEMICAL CARCINOGENS which can affect LUNG, SKIN, PROSTATE, STOMACH and the HEMOPOITIC SYSTEM of the body. (One Each) 5 7. Tuberculosis is an important public health problem in Pakistan and WHO has declared it a global emergency: a) What is the basis of tuberculin test? 1 b) Give four other examples of T Cell-Mediated type IV hypersensitivity? 4 8. Now Sexually transmitted diseases (STD's) are amongst the commonest infectious diseases worldwide. More than 20 STD's have been identified. The incidence of STD's is rising, in the last few decades. a) Name SIX diseases or infections included in the list of STD’s by the WHO. 3 b) Mention FOUR reasons attributed to this increase. 2 9. Women of child bearing age are far more prone to UTI's then men because of the shortened urethra: a) Enlist two bacteria in order of frequency which can cause UTI in women of child bearing age. 1 b) Give four risk factors, which predispose to UTI. 4 10. Mycobacterium tuberculosis has a complex cell wall which confers many properties to the organism: a) Why is heating required in the staining process in the Zeihl Neelson method? 1 b) Name four complex lipids and the properties they confer to the Mycobacterium. 4 11. The above mentioned newspaper reported the following news item. SMUG AS A BUG: “He was so sure he was right and conventional medical wisdom wrong about the cause of stomach ulcers that he swallowed bacteria to prove his point. Now once-skeptical peers are talking about a possible Nobel prize. MELISSA SWEET reports.” Saturday, August 2, 1997 Finally Barry Marshall and Robin Warren, got half the Nobe l prize each, in 2005, by proving that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before: a) Which bacteria was one of them talking about? 1 b) How were Koch’s postulates fulfilled to prove, whether an organism was pathogenic in the disease it caused in this case. Narrate in less than seventy words? 4 12. a) Name the protozoan which affects the maximum women in the world. 1 b) Give its route of infection. 2 c) Mention two symptoms produced by this protozoan. 2 13. a) What is the name given to the study of the most common infectious 1 agents? b) Give three properties of the infectious agent which makes them differ from bacteria. 3 c) Name an infectious particle smaller than this particle. 1 14. Nearly 300 of the 100,000 to 200,000 species (depending on how they are classified) are thought to cause disease. a) What is the study of these organisms known as? 1 b) Classify mycosis in FOUR groups. 4  Page 1 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Total No. of SEQs: 15 Total Marks: 45 Time 2 hours 15 min. Note: 3 Marks for each question. Note: THE FINAL PAPER WILL BE SIMILAR TO THE MODEL PAPER BUT WILL FOLLOW “TOS” EXACTLY. Q.1 Write down various steps of healing in a clean uninfected surgically incised wound with reference to changes at different time periods. (3) Topic Specification: Healing and Repair. Key of Q.1: Such a process of healing is also called as Healing by Primary Intention-The incision causes death of a limited number of epithelial and connective tissue cells as well as disruption of epithelial basement membrane continuity-The narrow Incisional space immediately gets filled with clotted blood cells. Dehydration of surface clot forms the well known scab that covers the wound. -Changes within 24 hours: Neutrophils start moving towards fibrin clot. -Changes within 24-48 hours: Spurs of epithelial cells move form wound margin. -Changes by day 3: Neutrophils replaced by macrophages and granulation tissue starts developing. -Changes by day 5: Granulation tissue fills the incised gap, neovascularisation is maximum, collagen is abundant, epidermis recovers its normal thickness. -Changes by 2nd week: Continued collagen accumulation, prolif of fibroblasts-leucocyte infilt, oedema and increased vascularity disappears. -Changes by end of 1st month: Scar made up of cellular infiltrate, CT devoid of inflam. Infiltrate and is covered by intact epidermis. Dermal appendages of the area-permanently last. Reference: Robbins Pathology, 7th Edition, Healing and Repair, Pages 112-113  Page 2 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.2 A. What are nuclear changes seen in a necrotic cell. (1) B. Define steatasis, give morphologic appearance of liver in this condition. (2) Topic Specification: Cell Injury, Death and Cellular Adaptation. Key of Q.2: Key A: (1) Nuclear changes seen in a necrotic cell are all due to non-specific breakdown of DNA and they are: Karyolysis: Basophilia of chromatin fades away presumably due to DNA-ase activity. Pyknasis: Nuclear shrinkage and increased basophilia DNA condenses into solid shrinken basophilic mass. Karryorrhexis: Pyknatic or partially pyknatic nucleus unfergoes fragmentation and disappears in a day or two. Key B: (2) Steatasis or falty change is abnormal accumulation of triglycerides within parenchymal cells. Liver: Gross-There may be no change in mild/ early cases. But with progressive accumulation liver enlarges and becomes increasingly yellow soft and greasy with stretched capsule and starts weighing 3-6 Kg. Microscopically: falty changes begins as small vacuoles in the cytoplasm with central nucleus but in progressive accumulation the vacuoles coalesee, became larger and push the nucleus to one side-occasionally rupture of these lipocytes may form lipocysts. Reference: Robbins Pathology, 7th Edition, Cell Injury, Death and Cellular Adaptation, Part A Pages 21/ Part B Pages 35, 36.  Page 3 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.3 Define Acute inflammation and write down its: A: three major components. (1) B: write down process of increased vascular permeability in response to acute inflammation. (2) Topic Specification: Acute and Chronic Inflammation. Key of Q.3: Key A: (1) Acute inflammation is rapid or immediate response of body to injurious agent, that serve to deliver mediators of host defence, leucocytes and plasma proteins. Its three major components are: a. Alteration in vascular caliber leading to in increase in blood flow. b. Structural changes in the microvasculature that permit plasma proteins and leucocytes to leave the circulation. c. Emigration of leucocytes from micro circulation their accumulation in the focus of injury and their activation to eliminated offending agent. Key B: (2) Increased vascular permeability- a hall mark feature of acute inflammation- leading to escape of protein rich fluid (exudates) in extra vascular tissue. -Loss of proteins from plasma → ↓ intravascular osmotic pressure and ↑ in osmotic pressure → in extra vascular interstitial fluid. - ↑ Hydrostatic pressure due to increased blood flow in dilated blood vessels → leads to a marked outflow of fluid and its accumulation in interstitium → with net ↑ in extra vascular fluid → oedema. - Endothelium becomes leaky because of: Formation of gaps in venular endothelium. Direct endothelial injury → endothelial cell necrosis and detachment. Delayed prolonged leakage. Leucocyte mediated entothelial injury. ↑ Transcytosis Leakage from new blood vessels. Reference: Robbins Pathology, 7th Edition, Acute and Chronic Inflammation Pages Part A 49, Part B 50, 51.  Page 4 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.4 What is a macrophage? Write down its role in chronic inflammation. (1+2=3) Topic Specification: Acute and Chronic Inflammation. Key of Q.4: (1) Macrophage is a dominant cell of chronic inflammation and is one of the components of mononuclear phagocyte system. This system is consists of closely related cells of bone marrow origin blood monocytes and tissue macrophages, diffusely scattered in different organs. Mononuclear phagocytes arise from a common precursor in the bone marrow which gives rose to blood monocytes-from the blood monocytes migrate into various tissues and differentiate into macrophages. (2) In chronic inflammation macrophage accumulation persists and is mediated by different mechanisms. a. Recruitment of monocytes from the circulation. b. Local proliferation of macrophages. c. Immobilization of macrophages at the site of inflammation. Reference: Robbins Pathology 7th Edition, Acute and Chronic Inflammation Pages 79, 80, 81.  Page 5 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.5 Explain Virchow’s Triad in thrombosis. (3) Topic Specification: Haemodynamic Disorders (Thrombo-Embolic Diseases and Shock). Key of Q.5: Vrichow’s Triad reflects three primary influences in thrombus formation which are: 1. Endothelial Injury: A dominant influence and can by itself lead to thrombosis, particularly in heart and arterial circulation where normally high flow states might otherwise hamper clotting by preventing platelet adhesion or dilating coagulation factors. Physical loss of endothelial extracellular matrix (ECM) → platelet adhesion and release of tissue factors and local depletion of PGI2 and Pas-however it is important that endothelium need not be descended or physically disrupted to contribute to development of thrombosis, any perturbation in dynamic balance of the pro and anti thrombotic SH effects of endothelium can influence local clotting SH events. 2. Turbulence of Blood Flow or Stasis: This factor contributes to arterial and cardiac thrombosis by causing endothelial injury / dysfunction as well as by forming counter currents and local packets of stasis. Stasis is a major factor in the development of venous thrombi.-stasis or turbulence therefore: a. Disrupt laminar flow of blood. b. Prevent dilution of activated clotting factors by fresh flowing blood. c. Retard inflow of clotting factors inhibitors and permit thrombi formation. d. Premate endothelial cell activation. 3. Hypercoagulability: Contributes less frequently to thrombotic states, but is an important component in the equation-any alteration in the coagulation pathway predisposes to coagulation. Reference: Robbins Pathology, 7th Edition, Haemodynamic Disorders (Thrombo-Embolic Diseases and Shock).  Page 6 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.6 A. Define how autosomal dominant disorders are manifested? (1) B. Tabulate the system and the disorder caused by autosomal dominant disorders. (2) Topic Specification: Genetic Disorders. Key of Q.6: Key A: (1) Autosomal dominant disorders are manifested in the heterozygous state, so at least one parent of an index case is usually affected. If both male and female are affected and both can transmit the condition- if an affected person marries an unaffected one, every child has one in two of having the disease. Key B: (2) Autosomal Dominant Disorders Sr.# System Disorders 1. Nervous Huntington Disease, Neurofibromatosis, Myotonic Dystrophy, Tuberous Scterosis. 2. Urinary Polycystic Kidney Disease. 3. Gastrointestinal Familial Polyposis Coli. 4. Hematopoietic Hereditary Sphesacytosis, Van-Wille-Brand Disease. 5. Skeletal Marfan Syndrome, Ehlers-Danlos Syndrome, Osteogenisis Imperfecta, Achandroplasia. 6. Metabolic Familial Hypercholesterolemia, Acute Intermittent Porphyria. Reference: Robbins Pathology, 7th Edition, Genetic Disorders, Part A Page 150, Part B Page 151.  Page 7 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.7 A. Make a flow chart showing general scheme ofevents in chemical carcinogenesis. (2) B: Enumerate any three of DNA oncogenic viruses with reference to malignancies they can cause. (1) Topic Specification: Neoplasias. Key of Q.7: Key A: (2)  Page 8 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Key B: (1) 1. Human Papilloma Virus: (Type 16,18 and less commonly 31, 33, 35, 51). 2. Epstein Barr Virus (EBV): Burkitt’s Lymphoma, Nasopharyngeal Carcinoma. 3. Hepatitis B Virus (HBV): Hepatocellular Carcinoma. Reference: Robbins Pathology, 7th Edition, Neoplasias, Part A Page 321, Part B Pages 324, 325, 326, 327.  Page 9 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.8 Name any six tumor markers, also mentioning the tumors they are used for. (3) Topic Specification: Neoplasias. Key of Q.8: (0.5 each) 1. Human Chorionic Gonadotrophin-HCG = Trophoblastic Tumours, Non Seminomatous Testicular Tumours. 2. α–Fetoprotein = Hepatocellular Carcinoma, Non Seminomatous Testicular Tumours. 3. Carcino-Embryonic Antigen-CEA = Carcinoma of Colon, Pancreas, Stomach etc. 4. Prostatic Specific Antigen-PSA = Carcinoma Prostate. 5. CA-125 = Ovarian Cancer. 6. Calcitonin = Medullary Carcinoma Thyroid. (or any other) Reference: Robbins Pathology, 7th Edition, Neoplasias, Page 339.  Page 10 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.9 Compare Th1 and Th2 lymphocytes in terms of the following: A. the cytokines they produce. (1+1) B. whether they promote cell mediated immunity or antibody production. (1) Topic Specification: Immunology. Key of Q.9: Key A: Th1 Lymphocytes Produce Cytokines: (1) 1. Interleukin-2 (IL-2). 2. Interferon-gamma (IFN-gamma). 3. Lymphotoxin. 4. Tumor Necrosis Factor-beta (TNF-beta) Th2 Lymphocytes Produce Cytokines: (1) 1. Interleukins-2. 2. Interleukis-4. 3. Interleukins-5. 4. Interleukins-10 & 13. Key B: (1) Th1-lymphocytes recognize antigens presented by macrophages and function primarily to activate and heighten cell mediated immunity. Th2- lymphocytes recognize antigens presented by B-lymphocytes. They produce cytokines that primate antibody production. Reference: Microbiology and Immunology by Ernest Jawetz, 9th Edition Chapter 58-Page 404-05.  Page 11 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.10 State a disease caused by each of the following protozoans and indicate have they are transmitted to humans: (3) a. Entamoeba histolytica. b. Giardia lamblia. c. Trichomonas vaginalis. d. Toxoplasma gondii. e. Cryptosporidium. f. Plasmodium species. Topic Specification: Virology. Key of Q.10: a. Entamoeba Histolytica, causes amoebic dysentery and extra intestinal amaebiasis (liver abscess). The organism produces protective cysts which pass out of the intestines of infected host and are ingested by the next host (faeco-oral soute). (0.5) b. Giardia Lamblia, can cause a gastro-intestinal infection-“giardiasis” – cysts pass out of the intestines of the infected host (fecal-oral route). (0.5) c. Trichomonas vaginalis- infects vagina and male urinary tract- does not produce a cyst and is transmitted sexually. (0.5) d. Toxoplasma Gandii-causes toxoplasmosis, contracted by inhaling or ingesting cysts from the feces of infected domestic cats or by ingesting raw meat of infected animal. Infects brain, heart or lungs of people of immunosuppressed, but is wild in those who have normal immune system-can also be transmitted congenitally and infect the nervous system of infected child. (0.5) e. Cryptosporidium causes diarrhea and is transmitted by fecal oral route. (0.5) f. Plasmodium Species- a haemoparasite and causes malaria of different kinds with different species and transmitted parantarilly by bite of Anopheles Mosquito. (0.5) Reference: Text Book of Medical Parasitology CKJ Pamikar, Chapter 5 Page 61-81.  Page 12 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.11 Describe how certain viruses may contribute to the development of tumours. (3) Topic Specification: Parasitology. Key of Q.11: Virus Plays a Role in Cancer Development Both Directly and Indirectly. Directly: (1.5) 1. By integrating into the host cell’s chromosomes. Some viruses may alter the normal function of the proto-oncogenes and tumour suppressor genes, as is seen the HPV and HBV. 2. In case of cervical cancer, carcinogenic strains of HPV, produces and oncoprotein called E6. two variants of tumor suppressor gene known as P-53 produces a suppressor protein, that is much more susceptible to degradation by E6. Indirectly: (1.5) 1. The viruses may induce immunosuppression so that cancer cells are removed by immune responses as in the case of HIV/AIDS. 2. They may cause long term damage to tissues resulting I na large scale cell regeneration which increase the chances of natural mutation in proto-oncogenes and tumor suppressor genes, as in the case of HBV and HCV. Reference: Microbiology and Immunology, Ernest Jawetz, 9th Edition, Chapter 43, Page 306.  Page 13 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.12 A. Define the following: 1. Pathogenicity. (1) 2. Virulence. (1) B. Name four things an organism must be able to do, to cause an infectious disease. (1) Topic Specification: Microbiology General. Key of Q.12: Key A: Pathogenicity and virulence are terms that refer to an organism’s ability to cause disease. Pathogenicity is used with respect to differences between microbial species. (1) Virulence denotes differences between strains of the same species- in practice they are often used interchangeably. (1) Key B: (1) To cause disease an organisms must: 1. Maintain a reservoir before and after infection (humans, animals, environment etc.). 2. Leave the reservoir and gain access to the new host. 3. Colonize the body, and 4. Harm the body. Reference: Microbiology and Immunology, Ernst Jawetz, 9th Edition Chapter 07.  Page 14 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.13 A female infant was delivered by a midwife at home, within one day of birth she develops meningitis and dies next day. a. Name 2 most common organisms which are most likely to cause this disease. (1) b. Name 3 risk factors which increase the chances of a new born acquiring this infection. (1) c. Name 3 laboratory tests which can be helpful in identifying the causative agent. (1) Topic Specification: Microbiology General. Key of Q.13:- a: (1) 1. Group B-beta hemolytic streptococci. 2. E. coli. b: (1) 1. Prematurity. 2. Prolonged rupture of membranes. 3. Group B-streptococcal carriage in birth canal. c: (1) 1. Gm. stain of CSF. 2. Culture of CSF. 3. Blood culture. Reference: Microbiology and Immunology Ernst Jawetz, 9th Edition, Chapter 15.  Page 15 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.14 A. Describe 2 characteristics which make mycobacteria leprae different from other mycobacteria. (1) B. Differentiate between tuberculoid and lepramatous leprosy. (1) C. Name 2 causes of responsible for disfigurement in leprosy. (1) Topic Specification: Microbiology Systemic (Special) Key of Q.14: Key A: (1) It is a strict parasite that has not been grown in artificial media or tissue culture. It is slowest growing of all the species. Key B: (1) Sr.# Features Tuberculoid Leprosy (TL) Lepramatous Leprosy (LL) 1. Type of One or few macular Many erythromatous and lesion depigmented lesions eith granulomatous skin lesions little tissue damage with masked tissue damage 2. Number of Few Many acid fast bacilli 3. Likelihood of Low High transmitting leprosy 4. Cell Present Reduced or absent mediated response to M. leprae 5. Lepramin Positive Negative Test Key C: (1) 1. Loss of sensations results in burns and trauma. 2. Resorption bones results in loss of nose and finger tips. 3. Infiltration of skin and nerves results in thickening and folding. Reference: Microbiology and Immunology, Ernst Jawetz, 9th Edition, Chapter 21, Pages 167-168.  Page 16 of 16 BDS SECOND PROFESSIONAL EXAMINATION 2007 GENERAL PATHOLOGY AND MICROBIOLOGY Model Paper (SEQs) Q.15 Write briefly the mechanism of sterilization by: A. Autoclaving. (1.5) B. Pasteurization. (1.5) Topic Specification: Microbiology Systemic (Special). Key of Q.15: Key A: Autoclaving: (1.5) Most frequently used method of sterilization by moist heat because bacterial spores are resistant to boiling (100°C at sea level) they must be exposed to a higher temperature, which can only be achieved under increased pressure – for this purpose an autoclave chamber is used in which steam at a pressure of 15 lb/in2 reaches a temperature of 121°C and is held for 15-20 min. this Clostridium botulinum. Sterilization by dry heat on the other hand requires temperature in the range of 180°C for 2 hours. Key B: Pasteurization: (1.5) Used primarily for milk, consists of heating the milk to 62°C for 30 min. followed by rapid cooling (Flash Pasteurization at 72°C for 15 seconds is often used). This is sufficient to kill the vegetative cells of the milk born pathogen i.e Mycobacterium Bovis, Salmonella, Streptococcus Listeria and Brucella, but not sterilize milk. Reference: Medical Microbiology and Immunology, 7th Edition by Ernst Jawetz, Page 86. 1. Hyperplasia is an increase in the number of cells in an organ or tissue, usually resulting in increased volume of the organ or tissue. 2. Hypertrophy refers to an increase in the size of cells, resulting in an increase in the size of the organ. 3. Atrophy is the shrinkage in the size of the cell by loss of cell substance. 4. Metaplasia is defined as a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type. 5. Cell swelling is the earliest sign of a reversible cell injury. 6. Free radical is a chemical species that have a single unpaired electron in an outer orbit. 7. Necrosis is a spectrum of morphological changes that follow cell death in a living tissue largely resulting from the progressive degradative action of enzymes on the lethally injured cell. 8. Necrosis has six major type; coagulative, Caseous, Liquefactive, fibrinoid,gangrenous and Fat. 9. Apoptosis (Greek falling off) is defined as a pathway of programmed cell death that is aimed at a highly regulated intracellular programme in which cells destined to death by activated enzyme that degrade the cell’s DNA and nuclear and cytoplasmic proteins. 10. Morphologically an apoptotic cell shows: a) cell shrinkage, b) chromatin condensation c) formation of cytoplasmic blebs and apoptotic bodies, d) phagocytosis by macrophages. 11. Apoptosis has two phases a) Initiation phase extrinsic and intrinsic pathways b)Execution phase c)phagocytosis of dead cell. 12. Genes promoting apoptosis are: bax,bak,bim www.mbbsstudystuff.wordpress.com 1 13. Genes inhibiting apoptosis are bcl 2 family. 14. Initiator caspase are 8 & 9, while executioner caspases are mainly 3 & 6. 15. Dystrophic calcification is always seen in damaged tissues while metastatic calcification may occur in normal tissues whenever there is hyperplasia. 16. Inflammation is a complex reaction to injurious agents such as microbes and damaged, usually necrotic cells that consists of vascular responses, migration and activation of leukocytes, and systemic reactions. 17. Inflammatory response consist of TWO main components: vascular & cellular, and divided into TWO main patterns: Acute and Chronic. 18. Vasodilatation is one of the earliest manifestation of acute inflammation, if follows a transient vasoconstriction of arterioles lasting few seconds. 19. Increased vascular permeability leading to the escape of a protein-rich fluid (exudate) into the extravascular tissue in the HALL MARK of acute inflammation. 20. Formation of endothelial gaps in venules is the most common cause of vascular leakage. 21. Leukocytes Adhesion molecular families have a major classes: a) Selectins (E,L & P types), b) Integrins, c) Immunoglobulin family of adhesion molecules and d) Mucin like glycoproteins. 22. Selectins mainly involved in rolling of leukocytes, PECAM in transmigration and immunoglobulin family in adhesions. 23. Chemotaxis is defined as uni directional migration of leukocytes towards the site of injury under chemical gradient action. 24. Most important chemotactic agents are C5a,LTB4 and bacterial products. www.mbbsstudystuff.wordpress.com 2 25. Major opsonins are: C3b & Fc fragment of IgG proteins. 26. H202-MPO-Halide systein is the most efficient bactericidal system in neutrophils. 27. Chediak-Higashi Syndrome is an autosomal recessive condition characterized by failure of fusion of phagosome with lysosome. 28. Chronic granulomatous disease of childhood results from inherited defects in the components of NAPDH oxidase which generates superoxide, leading to body infections. 29. Vasoactive amines are histamine and serotonin which are the main players of early inflammation. 30. Plasma Proteins are: Complement system proteins, clotting system and fibrinolytic system. 31. Prostaglandins are vasodilators. 32. MAC (C5B6789) is the membrane attack complex, which finally kills the bacteria. 33. Activated Hageman factor initiates FOUR systems involved in inflammatory responses Kinin, Clotting, fibrinolytic and complement system 34. SRS-A (slow releasing substance of anaphylaxis) constitutes LTC4, LTD4 & LTE4 promote vasoconstriction, bronchospasm & increased vascular permeability. 35. Lipoxins are bioactive products generated from transcellular biosynthetic mechanisms involving neutrophils and platelets. 36. IL-1 & TNF are two of the MAJOR cytokines that mediate inflammation. 37. Major chemokines include: IL-8, MCP-1, eotaxin, MIP-1, Lymphotactin and RANTES. 38. Nitric oxide plays major role in production of vasodilation by relaxing vascular smooth muscle in ischemic conditions. www.mbbsstudystuff.wordpress.com 3 39. The major mediators of pain are Bradykinin & Prostaglandins 40. Potent vasodilators are : Vasoactive Amines, Prostaglandins & NO. 41. Acute inflammation is defined as a rapid response to an injurious agent that serves to deliver mediators of host defense – leukocytes and plasma proteins to the site of injury. 42. Chronic inflammation is defined as an inflammation of prolonged duration, in which active inflammation, tissue destruction and attempts at repair are proceeding simultaneously. 43. Neutrophils are the main cells of acute inflammation (exudates) while Mononuclear cells (with one nucleus are the main cells of chronic inflammation.Mononuclear cells include Lymphocytes, Monocytes, Macrophages and Plasma cells. 44. Macrophages are the prima donna (main working cell) of chronic inflammation, while lymphocytes are present in increased number. 45. Granuloma is a focus of chronic inflammation, consisting of microscopic aggregation of macrophages that are transformed into epithelium like cells surrounded by a collar of mononuclear leukocytes. Don’t confuse it with Granulation tissue which has capillaries, fibroblasts, and a variable amount of inflammatory cells. 46. Classical tuberculous granulomas is composed of epithelioid cells, Langhan’s multinucleated giant cells, caseation necrosis and collar of lymphocytes. There are two types of Granulomas: Immune & foreign body. 47. There are 3 types of cells in the body: Continously dividing labile cells, Quiscent or stable cells and Permanent Non- dividing cells. 48. Stem cells are cells characterized by their prolonged self renewal capacity and by the asymmetric replication. They are of two types: embryonic & adult stem cells. www.mbbsstudystuff.wordpress.com 4 49. VEGF & fibroblast Growth factor are mainly involved in angiogenesis. 50. TGF-B is a growth inhibitor for most epithelial cells and leukocytes, potent fibrogenic agent and a strong anti- inflammatory effect. 51. Extracellualr matrix is formed of these groups of molecules : a) fibronectin b) adhesive glycoproteins and c) proteoglycans & hyaluronic acid. 52. Collagens is the most common protein in the animal world, with 27 types discovered so far. Types I, II, III, V & X) are fibrillar and most common while type IV is non fibrillar. 53. Healing by 2nd intention differs from 1st intention in three ways; a) inflammatory reaction is more intense, b) Much more granulation tissue forms and c) wound contraction phenomenon. 54. Accumulation of excessive amounts of collagen may give rise to a hypertrophic scar while if scar tissue grows beyond the boundaries of the original wound and does not regress, it is called keloid. 55. Edema is defined as accumulation of fluid in the interstitial tissue spaces and body cavities. 56. Local increased volume of blood in a particular tissue leads to Hyperemia and congestion. Hyperemia is an active process, resulting from augmented tissue inflow because of arteriolar dilation while Congestion is a passive process resulting from impaired outflow from tissue. 57. Heart failure cells are hemosiderin laden macrophages seen in chronic pulmonary congestion. 58. Petechiae are minute 1 to 2 mm hemorrhages into skin, mucous membranes or serosa surfaces, while >3 mm hemorrhages are called Purpura and more larger > 1 to 2 cm subcutaneous hematomas are called Ecchymoses. www.mbbsstudystuff.wordpress.com 5 59. Virchow’s triad include: a) Endothelial injury b) Stasis or turbulent blood flow & c) blood hypercoagulability. 60. Of the inherited causes of hypercoagulability, mutation in the factor V gene and prothrombin gene are the most common. 61. Lines of Zahn are laminated lines produced by alternating pale layers of platelets admixed with some fibrin and darker layers containing more red cells. 62. Fate of thrombus include: propagation embolization, dissolution, organization and recanalization. 63. Embolus is a detached intravascular solid, liquid or gaseous mass that is carried by the blood to a site distant from its point of origin. The phenomenon is called embolism. 64. Infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage in a particular tissue. 65. The most dominant histologic characteristic of infarction is ischemic coagulative necrosis. 66. Shock is the systemic hypoperfusion caused by reduction either in cardiac output or in the effective circulating blood volume, and resulting in hypotension followed by impaired tissue perfusion and cellular hypoxia. 67. Major types of shock include: cardiogenic, hypovolemic, septic, neurogenic and anaphylactic. 68. Mutation is defined as a permanent change in the DNA. 69. Marfan’s syndrome is a disorder of the connective tissue of the body, characterized by changes in the skeleton, eyes and cvs. Mainly cause by defects in an extracellular glycoprotein Firbillin-1. 70. Ehlers-Danlos Syndrome comprise a clinically and genetically heterogenous groups of disorders that result from some defect in the syntesis or structure of fibrillar collagen. www.mbbsstudystuff.wordpress.com 6 71. Amyloid is a pathologic proteinaceous substance deposited between cells in various tissues and organs of the body in a wide variety of clinical settings. 72. Neoplasm is an abnormal mass, the growth of which exceeds and in uncoordinated with that of the normal tissue and persists in the same excessive manner after cessation of the stimuli which evoked the change. 73. Tumor has two basic components: Parenchyma & stroma, while tumors are of two types: Benign and Malignant. 74. Benign tumors are well differentiated, grow slowly and don’t show invasion and metastases, while Malignant tumors range from well to undifferentiated, grow fast and show invasion and metastasis. 75. Single most important feature to differentiate benign from malignant tumor is METASTASIS. 76. Carcinomas mostly use lymphatic routes and sarcomas mostly use hematogenous routes of spread. 77. Four types of genes are normally working in human body: a) proto-oncogens b) antioncogenes, c) apoptotic genes and d)DNA repair genes 78. Proto-oncogenes are changed to oncogenes by three processes: mutation, translocation and amplification. 79. Major oncogenes are; RAS, ERB-B1, RET, KIT, ABL, C-MYC & N- MYC. 80. Major antioncogenes are: RB, TP53, W.-1, NF-1, BRCA-1, APC. 81. Oncogenic viruses include; Human Papilloma virus, Hepatitis B virus, Epstein Barr virus ,Kaposi Sarcoma Herpes viruses & Human T-Cell leukemia virus (The only oncogenic RNA virus). 82. Chemical carcinogenesis is a multistep process, divided into initiation and promotion phases. 83. Major chemical carcinogens associated as include: Asbestos with Mesothelioma, Aniline dyes with TCC, Nitrates-Gastric www.mbbsstudystuff.wordpress.com 7  carcinoma, Aflatoxin with HCC, Vinyl chloride with Angiosarcoma Liver. 84. Radiation induced malignancies include leukemias and papillary carcinoma thyroid. 85. Major paraneoplastic synbdromes include, Cushing syndrome, ADH secretion by small cell carcinoma lung, Hypercalcemia by Squamous cell carcinoma lung, hypoglycemia by Fibrosarcoma and HCC, Polycythemia by RCC and hypertrophia osteoarthropathy by CA lung. 86. Major tumor markers included : HCG for Choriocarcinoma, calcitonin for medullary carcinoma thyroid, alpha fetoprotein- HCC and Non-seminomatous germ cell tumor testis, CEA-CA colon, PAP For CA prostate, CA-125 for Ovarian CA , Ca 19-9 for CA Colon and pancreas ,CA 15-3 for CA breast. 87. Major immunomarkers for epithelial tumors are cytokeratin, for mesenchymal tumor – vimentin, for leukocyte origin tumor – leukocyte common antigen, S100 for neural origin tumors and for skeletal muscle tumors – desmin. 88. Type I hypersensitivity (“anaphylactic”) or “immediate hypersensitivity”) is the result of antigen binding to IgE on the surface of mast cells and basophils. These instantly degranulate and release active substances into the surrounding tissue. 89. Type II cytotoxic hypersensitivity, antibodies attach to antigens on the surfaces of a cell and then something injures or destroys the cell. 90. In type III immune-complex hypersensitivity reaction, “Soluble antigens” precipitate with antibodies, usually this happens 2-4 hours after exposure. This sort of tissue injury is mediated by antigen-antibody complexes (“immune complexes”). 91. Type IV Hypersensitivity reaction is called “delayed hypersensitivity”. It is mediated by sensitized CD4+T lymphocytes which process antigens in association with class II HLA molecules and release lymphokines. www.mbbsstudystuff.wordpress.com 8 92. Immune reactions are divided into two broad categories: A) Humoral immunity-B-cell lymphocyte mediated via production of antibody and Often develops as a response to soluble antigens, and B) Cellular immunity-T-Cell lymphocyte mediated. CD4+helper lymphocytes: help B cells make antibody and also help to generate cytotoxic T cells. 93. Major histocompatibility complex is present on all nucleated cells. 94. The HLA system is a key factor in most Transplant rejection reactions. Reactions are mediated by either T lymphocytes or by antibody. 95. Toll like receptors are membrane proteins that recognize a variety of microbe derived molecules and stimulate innate immune responses against the microbes. 96. CD4 molecule is a high affinity receptor for HIV 97. Major autoimmune disease include Hashimoto’s thyroiditis, Rheumatoid Arthritis, Sjogren’s syndrome, ankylosing spondylitis. 98. Gamma interferon is one of the cytokine to activate macrophages and also play major Role in Granuloma formation. 99. Cytokines are mediators released from one cell and modulate the actions of another cell. 100. Squamous cell carcinoma is characterized by sheets, groups and clusters of pleomorphic malignant epithelial cells with high N/C ratio,hyperchromatic nuclei and pale cytoplasm.Keratin epithelial pearls,intercellular bridges and individual cell keratinization are seen. 101. Adenocarcinoma is characterized by back to back closely packed glands lined by pleomorphic malignant epithelial cells with high N/C ratio,hyperchromatic nuclei and eosinophilic cytoplasm.Wall sharing is often noted. www.mbbsstudystuff.wordpress.com 9 102. Two types of vaccines include: Live vaccines; Measles, Mumps, Rubella, Varicella, Polio etc and Killed vaccines: Rabies, Polio, Hepatitis A. 103. Protooncogenes are converted into oncogenes. 104. p53 works by DNA repair and promoting apoptosis. 105. RB gene activates and Works in hypophosphorylated form. 106. RAS gene protooncogene protein is GTP bound and Works with GAP in cooridination with GTPase. 107. Gliomas and BCC are highly malignant but dont usually metastasize. 108. AFB is acid fase bacillus ( Mycobacterium tuberculosis ) and called so because it resists decolourization by Concentrated Acids. 109. Tigered lipid effect is seen in Herat. 110. Major complement proteins include : Opsonization by C3b Chemotaxis by C5a Anaphylatoxin C3a, C4a, C5a Membrane breakdown and killing C5b,6,7,8,9 MAC complex Enhancement of antibody production C3b 111. FNAC and biopsy are key investigations to early diagnose a tumor. 112. Active Immunity is the resistance induced after contact with foreign antigens eg microorganisms, immunization with live or killed infectious agents, exposure to microbial products (toxins, toxoids) Passive immunity is resistance based on antibodies preformed in another host eg administration of antibody against tetanus, botulism, diphtheria, rabies etc. 113. Sudden death is majorly linked with embolism. www.mbbsstudystuff.wordpress.com 10 114. 24 to 48 hours post acute inflammation ,monocytes start accumulating. 115. ubiquitin proteosome pathway & autophagic vacuoles are mainly involved in atrophy. 116. Reserve stem cells are main players in metaplasia. 117. Mechanical and trophic factors are involved in hypertophy. 118. Eosinophils are players in allergic infections. 119. Sequence of events in acute inflammation is : Transient asoconstriction,vasodilation stasis, margination, rolling, adhesion, diapedesis, chemotaxis and phagocytosis. 120. Macrophages seen as a part of reticuloendothelial system include: Osteoclasts – bone,microglia – brain,kupffer cells – liver,alveolar macrophages – lung.Sinus histiocytes – lymph nodes. 120. Tuberculosis is the leading cause of granuloma in Pakistan. 121. Major granulomatous causes include: sarcoidosis, leprosy, cat scratch disease, fungal infections. 122. Grading of a tumor is based on differentiation,atypia and mitoses. 123. Staging of a tumor is based on TNM – tumor,nodes,metastasis. 124. Major autosomal dominant disorders include: Skeletal – Marfan; syndrome Nervous – Huntington disease,neurofibromatosis Gastrointestinal – familial polyposis coli Urinary – polycystic kidney disease Haematopoietic – hereditary spherocytosis 125. Major intracellular accumulations are : Melanin – melanoma,bile – cholestasis,carbon – anthracosis,copper – Wilson disease lipofuscin – aging www.mbbsstudystuff.wordpress.com 11 126. Fatty change is also known as steatosis. 127. Point mutations are often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another e.g RAS. 128. Giant cells are cells containing more than one nucleus. 129. Major giant cells are : Langhan giant cells – Tuberculosis, Tuton giant cells – xanthoma Warthin finkeldey giant cells – measles, Reed Sternberg cells – Hodgkin Lymphoma Foreign body giant cells – foreign body 130. IgG fixes complement and crosses placenta. 131. IgM is the most heavy antibody. 132. IgE is the allergic reaction player antibody. 133. Ig A is found in secretions. 134. ABL gene is seen translocated in CML. 135. Lines of Zahn confirms a thrombus.They are alternate layers of platelets with fibrin and RBCs’ 136. Psamomma bodies are lamellated bodies of dystrophic calcification seen in meningioma,papillary carcinoma thyroid and serous ovarian malignant tumors. 137. Nuclear changes in a necrotic cell include: pyknosis, karyolysis, karryorrhexis and loss of nucleus. 138. Macrophages get accumulated in chronic inflammation by continuous recruitment,proliferation and immobilization. 139. Ischemic injury leads to coagulative necrosis. www.mbbsstudystuff.wordpress.com 12 140. Major sensitive cell components: maintenance of integrity of cell membrane, aerobic respiration, protein synthesis, genetic integrity 141. Liquefactive necrosis: Usually caused by focal bacterial infections, because they can attract polymorphonuclear leukocytes. 142. Coagulative necrosis is characterised by the preservation of cellular and tissue architecture 143. Fat Necrosis: A term for necrosis in fat, caused either by release of pancreatic enzymes from pancreas or gut (enzymic fat necrosis) or by trauma to fat, either by a physical blow or by surgery (traumatic fat necrosis). 144. Caseous necrosis – cheese like : A distinct form of coagulative necrosis seen in mycobacterial infections (e.g., tuberculosis), or in tumor necrosis, in which the coagulated tissue no longer resembles the cells, but is in chunks of unrecognizable debris 145. Gangrene ("gangrenous necrosis") is not a separate kind of necrosis at all, but a term for necrosis that is advanced and visible grossly with super added putrefaction. 146. Fibrinoid necrosis occurs in the wall of blood vessels when endothelium and smooth muscle cells are injured and dying. 147. Unlike necrosis, where the cell dies by swelling and bursting its content in the area, which causes an inflammatory response, apoptosis is a very clean and controlled process where the content of the cell is kept strictly within the cell membrane as it is degraded. 148. The extrinsic pathway of apoptosis is initiated through the stimulation of the transmembrane death receptors, such as the Fas receptors, located on the cell membrane. 149. In contrast, the intrinsic pathway of apoptosis is initiated through the release of signal factors by mitochondria within the cell www.mbbsstudystuff.wordpress.com 13 150. In males bronchogenic carcinoma and in females breast carcinoma are at the top. 151. Preneoplastic conditions include: Cirrhosis of liver, Atypical hyperplasia of endometrium, Leukoplakia, Inflammatory bowel disease, Adenomatous colonic polyps 152. Initiator chemicals - Cause irreversible damage to DNA, but at maximum they can cause severe dysplasia. 153. Promoter chemicals itself cannot induce cancer,they propagate or enhance the effects of initiators 154. Known chemical carcinogens include :A- Asbestos - Lung, mesothelioma. GI tract (esophagus, stomach, large intestine) b- Arsenic - Lung, skin, hemangiosarcoma c- Beryllium - Lung d- Cadmium - prostate e. Benzene - Leukemia 155. Ionizing radiation leads to dysjunction  random fusion  mutation. 156. Exposure long term of radiations lead to leukemia and thyroid cancers. 157. Initiation, Latent stage, Promotion and Malignant transformation are recognizable stages in carcinogenesis. 158. Mast cells are the main source of histamine and platelets the main source of serotonin. 159. Thromboxane A2 (TXA2), from platelets, aggregates platelets, constricts blood vessels. Great for hemostasis. 160. Prostacyclin (PGI2), from the vessel wall, prevents platelet aggregation, dilates vessels. Great for whenever hemostasis is unnecessary. 161. Suppurative or purulent inflammation is characterized by the production of large amounts of pus or purulent exudate consisting of neutrophils, necrotic cells, and edema fluid. www.mbbsstudystuff.wordpress.com 14 162. An ulcer is a local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing (shedding) of inflammatory necrotic tissue. 163. Teratoma is a tumor derived from more than one germ cell layer. 164. Seminomas,Melanomas,Hepatomas are malignant tumors. 165. Extent to which the tumor cell resemble its parent cell is differentiation. 166. Ranges of differentiation include: well, moderately, poorly, undifferentiated (anaplasia). 167. A malignant cells shows: high N/C ratio,hyperchromatic nuclei, prominent nucleoli, scanty cytoplasm and pleomorphism. 168. Carcinoma in situ is : Full-thickness dysplasia extending from the basement membrane to the surface of the epithelium. 169. Dysplasia :Atypical proliferation of cells characterized by nuclear enlargement and failure of differentiation which falls short of malignancy 170. The change that occurs in the stroma as tumor invades is called desmoplasia 171. Benign tumors never locally invade and Malignant tumors always invade the surrounding tissues. 172. Carcinoma of the ovary spreads through seeding of body cavities. 173. Commonest places for mets deposits are liver and lungs. 174. Perineural spread is seen by carcinoma of prostate and pancreas (2 P’s ). 175. Nuclear damage is the hall mark of irreversible cell injury. www.mbbsstudystuff.wordpress.com 15 176. Scientific study of structural changes and functional consequences of injurious stimuli on cells, tissues and organs is Pathology. 177. Metaplasia is a two edges sword because it can lead to dysplasia and the original function of cells is lost. 178. Metaplasia can lead to dysplasia. 179. ALTHOUGH ATROPHIC CELLS MAY HAVE DIMINISHED FUNCTION,THEY R NOT DEAD. 180. Pathologic hyperplasia constitutes a fertile soil in which cancerous proliferation may eventually arise like bph and endometrial hyperplasia. 181. Dysplasia can regress and does not always lead to cancer. 182. Transudates are fluid accumulations that are essentially salt- water, accumulated because of pressure problems. Exudates are protein-rich fluid accumulations, due to leaky vessels. 183. In disseminated intravascular coagulation, the clotting cascades are activated throughout the body. This is bad, since it tends to shut down organs due to microthrombi, and also causes bleeding due to consumption of clotting factors and activation of plasmin. 184. Some people reserve the word "thrombus" for the ante- mortem kind, and call post-mortem thrombi "clots". 185. Arterial thrombi usually occur over ruptured atherosclerotic plaques, less often at sites of other vascular disease or old surgery. 186. Vegetations are thrombi that occur on cardiac valves. They may be loaded with bacteria ("bacterial endocarditis"), or sterile ("marantic", "verrucous", "bland"; also the thrombi of acute rheumatic fever). 187. Embolus" comes from the Greek for "bottle stopper". www.mbbsstudystuff.wordpress.com 16 188. Pulmonary embolization is one of the great killers of hospitalized patients, and that ante-mortem diagnosis is notoriously unsatisfactory even today. 189. A paradoxical embolus (* crossed embolus) is one from the systemic veins that passes through a right-to-left intracardiac shunt (i.e., a birth defect), to occlude a systemic artery. 190. Long bone fractures are the main cause of fat embolism. 191. Tumor emboli are bits of cancer that invaded a vein and then broke off. Renal cell carcinoma is famous for this. 192. White infarcts ("anemic infarcts", from "an-", not, and "-eme", blood) are usual when arteries are occluded in solid organs 193. Red infarcts ("hemorrhagic infarcts", sounds like an oxymoron but isn't) result when veins are occluded, or when arteries are occluded in loose tissues (bowel) or with a dual blood supply, or when the organ was already very congested. 194. Monocytes are the largest cells in blood stream. 195. Histiocytes are mature tissue macrophages. 196. Cell membrane damage is the first sign of irreversible cell injury. 197. Lysosomal leakage confirms irreversible cell injury. 198. Choristomas and hemartomas are not neoplasms. 199. FGF,TGF,VEGF,EGF are main growth factors. 200. Endothelium gets leaky in acute inflammation due to: 1) formation of endothelial gaps in venules 2) cytoskeletal reorganization 3) increased transcytosis 4) direct endothelial injury 5) leukocyte dependent injury 6) delayed prolonged leakage 7) leakage from new blood vessels www.mbbsstudystuff.wordpress.com 17