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

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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.

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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.

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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.

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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.

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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.

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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

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 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.

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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.

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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.

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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

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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.

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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

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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.

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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.

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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".

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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

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