MCQs in Objective Pathology

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Objective Pathology

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Sumant Sharma

MDMD

Laboratory Director/ Director of Infection Control Laboratory Director/ Director of Infection Control

Prince Sultan Kidney and Heart Center Prince Sultan Kidney and Heart Center

Najran, Kingdom of Saudi Arabia Najran, Kingdom of Saudi Arabia

Yogesh Chhabra

MDMD

Director of Blood Bank and Transfusion Services Director of Blood Bank and Transfusion Services

King Khalid Hospital King Khalid Hospital

Najran, Kingdom of Saudi Arabia Najran, Kingdom of Saudi Arabia

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

New Delhi • Panama City •

New Delhi • Panama City • London • Dhaka • KathmanduLondon • Dhaka • Kathmandu

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Second

cond Edition

Edition

® ®

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Jaypee Brothers Medical Publishers (P) Ltd.

Headquarter

Jaypee Brothers Medical Publishers (P) Ltd 4838/24, Ansari Road, Daryaganj

New Delhi–110 002, India Phone: +91-11-43574357 Fax: +91-11-43574314

Email: [email protected] Overseas Offices

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Inquiries for bulk sales may be solicited at: [email protected]

This book has been published in good faith that the contents provided by the authors contained herein are original, and is intended for educational purposes only. While every effort is made to ensure accuracy of information, the publisher and the authors specifically disclaim any damage, liability, or loss incurr ed, directly or indirectly, from the use or applica-tion of any of the contents of this work. If not specifically stated, all figures and tables are courtesy of the authors.

MCQs in Objective Pathology with Explanations First Edition: 2000

Second Edition: 2012 ISBN: 978-93-5025-904-7 Printed at

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Dr Swarn Kanta Sharma

and

Dr Smita

Bade Jatan se Beeni Chadariya

Jyon ki Tyon Rakh Deeni Chadariya

After living with great care, I will give back

this life uncorrupted.

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Pathology is an oceanvast and without shores. The second edition

of this book (the first edition was entitled MCQs in Objective

Pathology authored by Dr Sumant Sharma), is an attempt to

con-dense this ocean in a drop. As Gautama Buddha described (and

later Immanuel Kant proved it to be correct) man is in the middle of

creation (Madhyam Sthith ), i.e. as far is man from the beginning of

creation, so is God from man. Man’s knowledge of Pathology also

has reached this middle point and it just makes the challenge of

knowing it all more daunting.

Buddha also described the characteristics of a good horse

(Shrestha Ashwa ). An excellent horse is one that gets up from

slumber with the sight of rider’s cane. A slightly lower standard is

given to a horse which gets up on hearing the stroke of the cane on

his friend. The worst is one that requires the stroke of the rider’s

cane to awaken.

Hurry up, flip the pages. The journey may be longer than

ex-pected. Let’s draw blood!

Sumant Sharma

Yogesh Chhabra

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Most Pathology books are written with one examination or another

in mind. The one in your hands now, is an all encompassing

work-book. You can use it to enhance your skills in the subject or use it

as a workbook to test your learning. The format of true/false is

used in many national and international licensure examinations.

Study the chapter from any comprehensive textbook and then

check your learning using this book. Give 1 mark for any correct

answer and 0 for unanswered one, Give 1 mark for any incorrect

response. In this way, a score of up to 70% should be deemed

appropriate.

For somebody, who has regular responsibilities, it is difficult to

compile such a Question Bank without the outside help from fellow

professionals. I wish to thank everyone who has been directly or

indirectly involved with the project.

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I am extremely thankful to Shri Jitendar P Vij (Chairman and

Managing Director) for his patient support to the project. I must

also mention the support given by the publishing team of M/s Jaypee

Brothers Medical Publishers, New Delhi, India, especially Ms Samina

Khan and Mr Gurnam Singh.

Lastly, I thank the past and future students of this great

sub- ject who have served as lamp-posts all throughout.

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1. Introdu ctio n to Patholog y ... 1

2. Genetic and Environ mental

Causes o f Diseases ... 37

3. Miscellaneous Topics in General Pathology ...42

4. Disord ers of Growth and Diff erentiation ... 45

5. Disord ers of Metabol ism and Homeost asis ... 48

6. Cardio vascular System ... 52

7. Blood and Bone Marro w ... 56

8. Respiratory Syst em ... 61

9. Liver, Bili ary Tract and Exocrine Pancreas ...65

10. Alimentary Tract ... 67

11. Male and Female Genital Tract and

Endocrin e Syst em ... 73

12. Breast ... 76

13. Male Genital Tract ... 78

14. Kidn ey and Urinary Tract ... 81

15. Skin, Soft Tissue and Skeletal System ...84

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Including Cell Pathology

and Immunopathology

(Including Special Diagnostic Techniques)

PRETEST

1. Which of the following are correctly matched? (R-1) A. Virchow—Invention of microscope.

B. Celsius—Work on naked eye appearance of diseased organs.

C. Pasteur—Showed the way to active immunization. D. Jenner—Laid foundation of bacteriology.

E. Mendel—Discovered principles of inheritence.

2. Which of the following are pathology subspecialities!? A. Histopathology—The diagnosis of disease by examining

altered histology of tissue sections.

B. Exfoliate cytology—Diagnosis of disease by studying body fluids secretion and excretions.

C. Toxicology—Study of defence processes in the body D. Hematology—Study of infectious processes.

E. Forensic pathology—Use of pathology for legal purposes. 3. Which of the following definitions are correct?

A. Allophenic mouse—A mouse in which two types of cells form clones of varying number in different organs.

Intr

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B. In paraffin wax technique, tissue is fixed usually in 10 percent formalin, dehydrated graded alcohols, cleared in xylol, chloroform or other solvent which is mixable with both alcohol and wax.

C. Pathogenesis—The cause of disease.

D. Etiology—The mechanism by which disease is caused E. Recombinant DNA—Artificial joining of DNA of one species (e.g. humans) to that of others (e.g. bacteria). 4. Which of the following are true about electron

micro-hyplum scopy?

A. Can differentiate between lymphoma and carcinoma as well as between adenocarcinoma and mesothelioma. B. Can be used to classify lymphomas.

C. Can employ osmium tetraoxide as a fixative as well as special stain for lipids.

D. Can differentiate between prostate cancer and gastric cancer.

E. Can locate the primary site of a squamous cell carci-noma (SCC).

5. Which of the following are true about cytology? A. FNAC preserves cellular and tissue architecture. B. Urinary cytology detects transitional cell carcinoma C. Diagnosis is not very accurate.

D. Exfoliate cytology is performed on cells aspirated by fine needle.

6. Which of the following are true?

A. A biopsy should be sent to pathology ideally fresh in saline, but is sent in 10 percent formalin 10 to 20 times the volume of specimen.

B. For immunohistochemical (IHC) analysis using immuno-flouresence of immunoperoxide method, the latter (IP) method is less advantageous.

C. A biopsy can be sent to laboratory without any infor-mation.

D. Cloning involves isolation of a particular fragments of DNA (usually a gene) and obtaining multiple copies. E. Vectors used for cloning can be plasmid vectors or

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7. Which of the following prefixes and suffixes are correctly defined? A. Hypo—deficient B. It’is—Inflammation C. Plasia—Growth abnormality D. Hetero—Dissimilar in composition E. Meta—In excess

ANSWERS

1. A. False: Inventor of microscope was Leeuwenhoek. B. True

C. False: Pasteur laid the foundation of bacteriology. D. False: Jenner showed the way to active immunization. E. True

2. A. True B. True

C. False: Toxicology is study of effect of poisons. D. False: Hematology is study of blood disorders. E. True

3. A. True: Alophenic mice are produced by implantation into a psuedopregnant female a combined embryo developed in vitro by fusing two developing eggs from two pregnant mice.

B. True

C. False: Pathogenesis is the mechanism by which disease is caused.

D. False: Etiology is the cause of disease. E. True

4. A. True

B. False: Immunohistochemistry (IHC) or gene rearrange-ment studies are required.

C. True

D. False: Immunohistochemical studies for prostate speci-fic antigen are required.

E. False

5. A. False: Cellular morphology is preserved but not the tissue architecture.

B. True

C. False: FNAC can be used to diagnose tumors in some situations and may eliminate the need for surgery.

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D. False: In exfoliate cytology cells shed or scraped from a epithelium surface are examined.

6. A. True

B. False: The immunoperoxide method provides a perma-nent slide–a major advantage over immunofluorescene. C. False: The request form should tell the site of biopsy

and patient’s age and sex besides other operative details. D. True E. True 7. A. True B. True C. True D. True

E. False: Meta denotes a change from one form to another. Excess is denoted as hyper.

CONCEPTS

Q.1. Which of the following are true about cell-cell inter-actions?

A. Occluding junctions and zona adherence are the same. B. Macula densa are also called nexus.

C. Integrins and selectins share a common role of leuko-cyte—endothelial cell interaction.

D. Cadherins prevent cancers from becoming invasive. E. Immunoglobulin superfamily molecules have a role in

recognizing and binding immunological molecules. F. Cytokines are secreted by hemopoietic cells only. G. Tyrosine kinase associated receptors cause synthesis

and secretion of various hormones.

H. G-proteins are also called guanosine nucleotide binding regulatory proteins.

Ans. A. False: Occluding junctions are called zonula occludens and adhering junctions are called zonula adherence. B. False: Macula densa is another name for desmosomes

and gap junctions are called nexus.

C. True: Besides the selectins also cause movement of leukocytes and platelets.

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mole-cules which bind adjacent cells and prevent invasion of ECM by cancer cells.

E. True: These act through other adhesion molecules and cytokines.

F. False: Cytokines can be secreted by nonhemopoietic cells too. So far about 50 cytokines have been recog-nized.

G. True: This is an example of enzyme-linked receptors which are involved in cell growth.

H. True

Q.2. Which of the following are true?

A. Cyclin E controls synthesis of mRNA and proteins required for DNA synthesis; cyclin A controls DNA repli-cation, and cyclin B controls correct daughter DNA synthesis.

B. After mitosis cyclins and cyclin dependent kinases are degraded in peroxisomes.

Ans. A. True

B. Caretaker proteins—Ubiquitins are responsible for this. Q.3. Which of the following are true?

A. Hypoxia and Ischemia result in same type of reversible injury.

B. Inability to reverse mitochondrial function after removal of causative agent and membrane damage are two defining differences between reversible and irreversible injury.

C. Intracellular accumulation of lactic acidosis is a cause of chromatin clumping.

D. Intracellular accumulation of potassium causes hydropic swelling of cell.

E. Myelin figures are found only intracellularly in reversible injury. .

Ans. A. False: Reversible injury due to ischemia blocks the nutrient supply to cells too and thus both aerobic and anaerobic respiration in the cell is compromised, resul-ting in more severe cell injury. Furthermore, highly specialized cells like myocardium, proximal tubular cells of kidney and neurons are specially dependent on aerobic respiration and are thus more severely and rapidly affected by ischemia than hypoxia alone.

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B. True C. True

D. False: Failure of energy dependent sodium potassium pump causes intracellular accumulation of Sodium. E. False: Myelin figures seen in cell injury are disintegrated

membrane blebs containing water and dissociated lipo-proteins between lamellae of membranes.They can be found both intracellularly and extracellularly.

A. Phospholipid rich amorphous densities are seen in mitochondria in irreversible cell injury.

B. Ischemia-reperfusion injury is mainly because of oxida-tive damage to cell.

C. Generation of oxygen free radicals occurs in cytoplasm. D. Superoxide oxygen is the most reactive of the oxygen

free radicals.

E. Cyanide kills by poisoning mitochondrial cytochrome oxidase.

F. Ionising radiation can injure the DNA and the cell by radiolysis of water and production of oxygen free radi-cals.

Ans. A. False: These are characteristic of reversible injury. In irreversible injury, calcium rich densities are seen. B. True

C. False: It begins within mitochondrial inner membrane. D. False: Hydroxyl radical is the most reactive.

E. True F. True

A. Cloudy swelling and hydropic swelling are the same. B. Russell’s bodies representing excessive immunoglobin

in plasma cells’ rough endoplasmic reticulum represent a form of hyalin change.

C. Hyalin degeneration occurs in rectus abdomin’s muscle in typhoid fever.

D. Mallory’s hyalin is seen in hepatocytes in cholestasis. E. Corpora amylacea represent a form of intracellular hyaline. Ans. A. False: Cloudy swelling involves excessive accumulation of sodium and water whereas in hydropic swelling mainly only water accumulates (vacuolar degeneration).

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B. True

C. True: This is called Zenker’s degeneration. D. False: It is seen in alcoholic hepatitis.

E. False: It is an example of extracellular hyaline. Q.6. Which of the following are true?

A. In hepatic Steatosis, granulomas may be found in the liver.

B. In hepatic steatosis, neutral fat accumulates both inside the hepatocytes and outside.

C. Mallory’s hyaline bodies are basically proteins. D. Albinos are more prone to skin cancers.

E. Ochronosis and alkaptonuria are synonymous.

Ans. A. True: Lipogranulomas may appear consisting of collec-tions of lymphocytes, macrophages and some multi-nucleated giant cells.

B. False: There is only intracellular accumulation. Stromal infiltration by mature adipose cells is sometimes seen in obesity; most common organs affected being the heart and pancreas.

C. True: These are intermediate filaments of cytokeratin D. True: Albinos are deficient in tyrosinase activity in skin

and have generalized hypopigmentation. This makes them more prone to develop basal cell and squamous cell cancers on excessive exposure to sun.

E. False: Ochronosis is a rare condition marked by dark pigmentation of ligaments, cartilage,fibrous tissue skin and urine. It may be caused by an inborn error of meta-bolism, alkaptonuria. This allows formation of Homo-gentisic acid, part of which is excreted in the urine and part of which is stored in tissues. But ochronosis may also be caused by chronic phenol poisoning.

Q.7. In which cases are the number of cisterns of rough endoplasmic reticulum increased and in which condi-tions are they decreased?

Ans. 1. Increased number of cisterns: In all cells with high protein production and secretion, e.g. plasma cells.

2. Decreased number of cisterns: Inactive cells with de-creased protein synthesis, e.g. in liver of undernourished patients.

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Q. 8. What is oncosis?

Ans. Irreversibly impaired metabolism (generally oxidative meta-bolism) brings about the death of cells with subsequent vacuolar swelling of cell and reactive inflammation in the absence of programmed cell death. The morphologic result is necrosis

Note _{: Cell death and necrosis are not identical. A once-living cell}

submerged and fixed in formaldehyde is chemically dead although from a structural standpoint it remains intact and “animate”.

SYNONYM OF ONCOSIS IS ACCIDENTAL

CELL DEATH

Q.1. What are oncofetal lesions of rough endoplasmic reti-culum (RER)?

Ans. Deranged cisterns of RER, which occur in this form only in fetal and tumor tissue.

Types

1. Ribosome-layer complexes: These are layered aggregates of RER cisterns with interposed rows of ribosomes.

2. Annulated lamellae complexes: These are layered aggre-gates of perinuclear RER cisterns with nuclear pores. 3. Mitochondrial-lamellar-layer complexes: These are layered

aggregates of longitudinally compressed mitochondria and RER cisterns.

Q.2. What are cytoplasmic nuclei?

Ans. This is the histological correlate of onion-layered aggre-gation of smooth endoplasmic reticulum (“fingerprint dege-neration”).

Cytoplasmic nuclei are a sign of blocked enzyme syn-thesis, such as is occasionally seen in blocked or dege-nerative protein synthesis.

Q.3. Why is golgi apparatus atrophied in erythroblasts? Ans. Atrophy of golgi apparatus is the ultrastructural correlate of

disturbed protein synthesis with or without impaired post-translational protein modification. So it is typical in cells that

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lose their nuclei, e.g. erythroblasts and undifferentiated malignant tumors.

Q. 4. Give examples in which various substances accumu-late in the golgi apparatus.

Ans. Several disorders are attributed to disturbed secretion and therefore to dysfunctioning of golgi apparatus. Examples are:

1. Cholestasis: Gall drainage disorders in which gall is blocked up into cisterns of the golgi apparatus.

2. Fatty liver: Hereditary or acquired disorders of lipoprotein metabolism, lipoprotein component accumulates in cisterns of golgi of hepatocytes.

3. Achondroplasia: (Chondrodystrophica fetalis, dwarfism) Impaired proteoglycan synthesis causes proteoglycan accumulation in golgi cisterns of chondrocytes.

4. Alveolar proteinosis: Surfactant proteins accumulate in golgi cisterns of type II alveolar surface cells.

Q.5. What are oncocytes?

Ans. These are swollen cells with grainy eosinophilic cytoplasm. Pathogenesis: Mitochondrial DNA mutation disturbs ATP synthesis. This in turn causes compensatory mitochondrial proliferation. So oncocyte is a descripitive term for a cell rich in mitochondria. This is not a tumor cell. Carcinomas of salivary and thyroid glands, though, may exhibit total or partial oncocytic transformation (Oncocytic thyroid ca., Oncocytic salivary gland ca.) These tumors have mahogany brown color because of high cytochrome content.

Q.6. What are megamitochondria?

Ans. These occur in severe deficiencies (Vitamin B complex defi-ciency or alcoholism) as a result of defective mitochondrial division or fusion. They are not caused by toxic swelling. Q.7. What is “turbid swelling of parenchymal organs”? Ans. First described by R Virchow in 1852, this implies swelling

of internal organs with enlarged, doughy, turbid cut surface. Microscopically, cells are swollen with granular light cytoplasm. Ultrastructurally, swelling begins in response to the change in osmotic pressure with condensation of matrix and swelling of space between the cristae (crista type). This is followed by distribution of mitochondrial matrix and

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mito-chondrial cristae (matrix type). There is usually generalized cytoplasmic degeneration with formation of vacuoles.

Q.8. Which of the following are true about dysplasia? A. It rarely occurs in epithelial tissue.

B. It can be called atypical hyperplasia.

C. Loss of polarity in dysplasia means disorderly arrange-ment of cells from basal layer to surface layer.

D. Dysplasia always progresses to carcinoma. E. Anaplasia is a hallmark of dysplasia.

Ans. A. False: Dysplasia means disordered cellular development and often is accompanied with metaplasia and hyper-plasia. It occurs most commonly in epithelial tissue. B. True: Epithelial dysplasia is a characterized by cellular

proliferation and cytological changes.

C. False: Loss of basal polarity means nuclei lying away from basement membrane. Of course in dysplasia, dis-orderly arrangement of cells in different layers is also seen but it is not termed ‘loss of basal polarity’.

D. False: On removal of inciting stimulus which is usually chronic irritation or prolonged inflammation, changes may disappear.

E. False: Anaplasia is loss of cellular differentiation and functions is a feature of frank cancer.

SUPPLEMENTARY TOPICS—GENERAL PATHOLOGY

Q.1. Which of the following are true/false?

A. General pathology is related to basic reactions of cells and tissues to abnormal stimuli that underlie all diseases. B. Specific responses to all stimuli of specialized organs

and tissues are examined under special or systemic pathology.

C. Etiology and pathogenesis are synonymous.

D. In modern terms, intrinsic or genetic and environmental are the two groups of etiological agents of diseases. E. Understanding pathogenesis of cystic fibrosis involves

knowing the gene responsible for its causation.

F. Morphological changes in a diseased organ have nothing to do with diagnosis of etiological process.

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G. Molecular techniques like DNA microassays and immu-nological approaches for analysis diseases are no more helpful in studying diseases than traditional morpho-logical methods.

H. Rudolf Virchow has no contribution to modern pathology. I. Study of origins, molecular mechanisms and structural

changes of cell injury alone are enough to understand morphological and clinical patterns of tissue and organ injury.

Ans. A. True.

B. False: Special or systemic pathology is concerned with specific responses of specialized organs or tissues to more or less well-defined stimuli.

C. False: Etiology is the cause of a disease. Pathogenesis refers to sequences of events in the response of cells or tissues to the etiological agent. It is the mechanism of disease. So even if the genes and their mutant forms underlying a great number of diseases and the entire human gename have been mapped, functions of enco-ded proteins and how mutations induce disease are often still obscure. The latter part forms pathogenesis of a disease.

D. True: Though there are two major classes of etiological agents, concept of one cause for one disease is obso-lete. Almost all diseases known today have both genetic and environmental etiologies combined.

E. False: To know full mechanism (pathogenesis) and manifestations (Morphology) of cystic fibrosis, besides the knowledge of defective gene and gene product, the biochemical immunological and thus the morphological events leading to formation of cysts and fibrosis in lungs, pancreas and organs are required.

F. False: Molecular changes in a disease refer to structural alterations in cells or tissues that are either characteri-stic of the disease or diagnocharacteri-stic of etiologic process. Diagnostic pathology is devoted to identify nature and progression of disease by studying morphological chan-ges in tissues and chemical alterations in patients. G. False: Molecular analyses have begun to reveal genetic

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are breast cancers and tumors of lymphocytes that look morphologically identical but may have widely different courses, therapeutic responses and widely different courses, therapeutic responses and prognosis. Increasingly, such techniques extend and even supplant traditional morphological methods.

H. False: Rudolf Virchow, known as the father of modern pathology first put forth a concept in nineteenth century that virtually all forms of organ injury start with molecular or structural alterations in cells.

I. False: Different cells in tissue constantly interact with each other and an elaborate system of extracellular-matrix is necessary for integrity of organs. Cell-cell and cell-matrix interactions contribute significantly to res-ponse to injury which are as important as cell injury in defining the morphologic and clinical patterns of disease.

KEY WORDS

Etiology, pathogenesis, morphological changes, clinical significance, molecular biology, tissue, cell and organ injury, Father of modern pathology.

A. Atrophy involves decrease in number of cells of an organ. B. Adaptation, reversible injury and cell death are separate events not interlinked and can occur independently or each other.

C. Cell death can be normal.

D. Necrosis can be physiological as apoptosis can be pathological (abnormal).

E. Calcification is always pathological.

F. Cells exposed to even sublethal or chronic stimuli are always damaged.

G. Cellular aging occurs with cumulative sublethal injury with increasing life span.

Ans. A. False: Atrophy involves decrease in function and size of cells.

B. False: Adaptation, reversible injury and cell death can be considered stages of progressive impairment of cell’s normal function and structure. For instance in response

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to increased hemodynamic loads, heart muscle first becomes enlarged—an adaptation. If blood supply to myocardium is insufficient to meet with demand, muscle becomes reversibly injured and finally cell death occurs. C. True: Cell death is a normal and essential part of

em-bryogenesis, the development of organs, maintenance of homeostasis and is aim of cancer therapy.

D. False: Necrosis is a cell death that is always pathologic. Apoptosis can be pathological too when cells are damaged beyond repair and especially, if cell’s nuclear DNA is damaged.

E. False: Metabolic derangements can cause some intra-cellular accumulations of which calcium is one. However calcification also occurs normally during skeletal mine-ralization.

F. False: Damage might not occur in sublethal, chronic stimuli but cells may show subcellular alterations. G. True.

Q.3. A. Give an example of cellular adaptation involving altera-tions in protein synthesis.

B. What are the major molecular mechanisms of cellular adaptations?

C. Do estrogens have any effect on (1) DNA synthesis of uterine epithelial cells (2) Structural components of myometrial cells?

D. In hormonal hyperplasia of physiological type, some hormones may themselves act as growth factors—True or false.

E. Compensatory hyperplasia of physiological type in liver occurs only by proliferation of remaining cells—True or false.

F. Some bone marrow cells can give rise to liver cells— True or false.

Ans. A. Example 1: induction of new protein synthesis by target cells as in response of muscle cells to increased physical exercise. Example 2: Switch from one type of protein synthesis to another—Or, markedly overproducing on type of protein—cells producing various collagen types and extracellular matrix proteins in chronic inflammation and fibrosis.

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B. 1. Direct: Stimulation of cells by factors produced by res-ponding cells or other cells in environment.

2. Activation of various cell surface receptors and down-stream signalling pathways.

C. 1. Yes: Hormone induced growth of uterus involves in-crease in both number (hyperplasia)(→↑DNA synth.) and size (hypertrophy) ( ↑ Str Comp.) of smooth muscle cells and epithelial cells. Abnormal endo-metrial hyperplasia is an example of pathological hyperplasia and the consequence is mainly hyper-plasia of endometrial glands though both hypertrophy and hyperplasia of epithelial and endomyometrial cells takes place to some extent. This is a common cause of abnormal menstrual bleeding.

2. After normal menstruation, there is a rapid burst of proliferative activity that is stimulated by pituitary hormones and ovarian estrogen. It is brought to a halt by rising level of progesterone usually about 10 to 14 days before anticipated menstrual period. If by any cause the balance between estrogen and proges-terone is tripped, there is absolute or relative increase in estrogen with consequent hyperplasia of endo-metrial glands.

D. True: Hyperplasia is caused by increased local produc-tion of growth factors, increased levels of growth factor receptors on responding cells, or activation of particular intracellular signalling pathways. These changes cause production of transcription factors that turn an may cellu-lar genes including those envolving growth factors, growth factor receptors and cell cycle regulators-net result being cellular proliferation. Hormones themselves can act as growth factors and trigger source of growth factors in compensatory hyperplasia is not clear trans-cription of cellular genes.

E. False: Not only remaining cells but some new cells are also formed from stem cells. In liver, intrahepatic stem cells don not play a role in hyperplasia after hepatectomy but contribute to regeneration after some forms of liver injury like chronic hepatitis in which proliferative capacity of hepatocytes is compromised.

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F. True: Recent clinical and experimental data suggests that some bone marrow stem cells may be able to give rise to many types of differentiated, specialized cell types including hepatocytes. Then these bone marrow stem cells have a potential to repopulate damaged tissues.

Q.4. A. What is the difference between cell proliferation that occurs pathological benign hyperplasia and cancer? B. What role does tissue hyperplasia play in wound

healing?

C. Skin and mucosal tissue can be stimulated by growth factors. True or false.

Ans. A. Pathological hyperplasia (alone) regresses, if the stimu-lus for growth is taken off. Whereas growth in number of cells in cancer is because of loss of normal growth control mechanisms and goes on occurring after particular phase of initiation. Most forms of pathological hyperplasias are caused by excessive hormonal or growth factor stimulation of target organs. Benign pros-tatic hyperplasia, e.g. occurs because of stimulation by androgens.

Pathological hyperplasia however, provides a fertile soil on which cancer can arise. Thus patients of endometrial hyperplasia are more prone to endometrial cancer.

B. Hyperplasia is an important connection tissue response in wound healing in which proliferation of fibroblasts and blood vessels and in repair growth factors are res-ponsible for this hyperplasia.

C. True: Stimulation of skin epithelium can occur by growth factors in papilloma viral infections leading to skin warts. Same viruses and other viruses can also cause similar mucosal lesions.

Q.5. A. In nondividing cells like myocardial cells, both hyper-plasia and hypertrophy can occur. True or false?

B. Why is nuclear DNA content of hypertrophied cells higher than the rest of cells?

C. There’s a similarity in mechanisms of production of bul-ging muscles of men engaged in ‘pumping iron’ and cardiac hypertrophy in hypertension. True or false.

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D. When do uterus and breast physiologically grow in size? Ans. A. False: Cells capable of division can respond to stress

by both hyperplasia and hypertrophy but in nondividing cells only hypertrophy occurs. Hypertrophy refers to increase in individual cell size leading to increase in size of whole organ.

B. Because of arrest at some stage of cell cycle in these cells without undergoing metosis.

C. True: Most common stimulus for hypertrophy of muscles is increased workload. In both the examples given, the increase workload is shared by greater mass of cellular components and each muscle false is spared of excess work and so escapes injury. The enlarged muscle cell achieves a new equilibrium, permitting it to function at a higher activity level. The striated skeletal and heart muscle are able to respond to increased workload (and thus ! metabolic demands) by tremendous hypertrophy as there is no mitotic response. In chronic hemodynamic load like faulty values or HT, an imbalance occurs bet-ween demand and response of cell’s functional capacity. Greater number of myofilaments per cell permits an increase workload with a level of metabolic activity per unit volume of cell not different from that borne by normal cell. D. Uterus: During pregnancy, uterus grows massively because of hypertrophy and hyperplasia both caused by hormonal influence of estrogens on smooth muscles. Oestrogens act on hormone receptors on individual myo-metrial cells leading to hypertrophy—increase in smooth muscle protein synthesis and increase in cell size. Breast: During lactation again the stimulus is hormonal. This time it is estrogen and prolactin.

Q.6. A. Is these a conclusive and substantial evidence that dur-ing stress, hypertrophy and hyperplasia occur together? B. For a patient in cardiac failure decompensation because of previous MI, coronary and peripheral vascular athero-sclerosis is a common setting. Previous to decom-pensation, peripheral vascular atherosclerosis might have caused gene induction of which genes in heart muscle?

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C. When do the genes in heart muscle fibers switch to similar to fetal or meonatal forms from adult forms expression.

Ans. A. Hyperplasia and hypertrophy often occur together. The conclusive evidence comes from the fact that cardiac and skeletal muscles, under stress, undergo an increase in their individual fiber size as well as (a recent discovery) repopulation from some existing and precursor cells. So neither hyperplasia nor hypertrophy is ever absolute.

B. Blood pressure (arterial) increase is a common disease caused by atherosclerosis of peripheral and visceral vessels leading to increased risk of ischemic heart disease, if untreated for long. Hypertension causes hypertrophy (by definition only hypertrophy) of cardiac muscle fibers. During this increase in individed fiber mass of cardiac muscles, three types of genes are induced:

1. Those coding transcription factors (C-fos, C-jun) 2. These coding growths factors (TGF-b, insulin like

GF-1, IGF-1) fibrolast growth factor.

3. These coding vasoactive agents (alfa-adrenergic agonist, endothelin-1, angiotensin II)

C. During muscle hypertrophy, e.g.

1. In hypertrophied cardiac muscle fibers, b myosin chain production mostly replaces alpha-myosin heavy chain production. This leads to decreased myosin ATP-ase activity. This leads to slow utilization of ATP by myosin and then slower contraction of individual fibers. So in a given time lesser ATP’s are used and heart rate decreases (efficiency of myosin is more). 2. Re-exprasion of early developmental gives like atrial natriuretic peptide in ventrides occur. (In embryo, ANP gene is expressed in both atrium and ventricle. After birth, oly in atrium). ANP is a peptide hormone that causes increased slat and water loss by kidneys leading to decreased hemodynamic load on stressed heart.

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QUESTIONS AND ANSWERS

Q.1. Why two classes of etiology’s theory is considered obsolete?

Ans. Some single gene disorders on one hand and infections on the other gave rise two one disease—once cause concept. Two types of etiological types suggested were genetic and acquired; recent data supports role of genetic factors in acquired diseases like hypertension and DM similarly even infectious are prove to genetic susceptibility, e.g. lower repiratory tract infections in cystic fibrosis.

Q.2. Does pathogenesis involve knowing the earliest molecular event in a disease?

Ans. Yes but not only this. Pathogenesis means the full course of immmunological, biochemical and morphological processes besides the initial infectious or molecular cause. It involves the whole process from the first stimulus to ultimate manifestation of a disease. Some of the processes in many diseases like the mechanism of manifestation of alteration in genes’structure are still a subject of research.

Q.3. Why is morphological diagnosis of tumors not enough for management?

Ans. Tumor behavior also depends on its genetic profile. So studies in molecular biology of tumors which may be morphologically similar but behave differently in therapeutic response are required, e.g. slymphomas.

Q.4. What was the most pioneering concept put forth by Rudolph Virchow?

Ans. Virchow, called the father of modern pathology, put forth the cell theory. All forms of organ injury starts with molecular or structural cell injury. Though cells interact with each other and extracellular matrix ECM. ECM also maintains cells in themselves.

Q.5. What are the two types of pathogenesis identified? Ans. Casual and formal pathogenesis. Causal pathogenesis tells

why a pathogen causes a disease. This considers the environmental factors, host’s bodily disposition (suscep-tibility without regard to adaptability) and the interplay of nonspecific immune responses in producing resistance to

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some diseases. Formal pathogenesis describes the struc-tural changes observed during clinical course of a disease which culminate in the altered structural and functional state of diseased organ/body.

Q.6. Define health and disease.

Ans. WHO defines health as a condition of complete bodily, mental and social well-being. Disease is defined as a dysfunction in life-processing that alter the body or a part of body in a manner that the affected individual requires help for subjective, clinical or social reasons.

Q.7. In what way is the type of clinical course of a disease defined as regards to its development.

Ans. Peracute diseases are fulminant and usually lead to death in several days. Acute diseases are usually intense and last for a few days or weeks. Recuperation is possible. Subacute diseases are insidious in onset, clinical course lasting for weeks with doubtful recuperation. Chronic diseases are mild and progress in stages over months. Primary chronic di-seases begin without a manifest acute phase. Clinical course is episodic. Recuperation is not possible. Secondary chronic disorders occur subsequent to acute inflammation that fails to heal because of complications. Recuperation in secondary chronic diseases occurs with persisting struc-tured damage and functional deficits after the disease and subsides. The social and functional adaptability is thus res-tricted. Recurrence is resurgence of what is basically a chronic disease after a gap. Remission is temporary dis-appearance of symptoms of a disease. Death (Exitus letalis = lethal end)

Q.8. Will it be correct to say that homeostasis is a conti-nuously changing state?

Ans. Yes, but upto some extent only. The normal cell is confined to a fairly narrow range of function because of:

1. Genetic programming of metabolism, differentiation and specialization.

2. Constraints because of neighboring cells. 3. Availability of metabolic substracts.

The narrow range of functioning is the steady state or homeostasis. Within this narrow range there is

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conti-nuous change—in one of different metabolites and other substances in the cell.

Q.9. What are the triggers for muscle hypertrophy and for changes in gene expression in cardiac muscle fibers in myocardial hypertrophy?

Ans. Two groups:

1. Mechanical triggers (stretch). 2. Trophic triggers.

The trophic triggers are chiefly growth factors (IGF-α) and vasoactive amines (angiotension II, DC-adrenergic orga-nists). The latter are produced by nonmyocyte cells and myocytes themselves.

Q.10. What ultimately regulates the size of myocardial cells?

Ans. From the above discussion it is clear that environmental cues are important. Nutrients (blood supply to heart muscle) is also a limiting factor.

Q.11. Why don not heart muscles enlarge unlimitedly in response to increase burden?

Ans. There’s a limit upto which heart muscle fibers can resond to increase in their size. Any increase in burden after that leads to cardiac failure. Various factors are implicated but not confirmed. These are—limited blood supply, limited oxidative capacity adaptability of mitochondria, changes in number and type of proteins, degradation of proteins and changes in myofibril cytoskeleton. Various ultrastructural manifestations include the myocardial fibers degeneration. There may also be apoptosis or nucleosis of myocardial fibers.

Q.12. Give two examples of physiological atrophy.

Ans. Physiologic decrease in cell size that may ultimately culmi-nate in cell death can lead to decrease in entire tissue or even organ. Physiologically this is seen in (1) embryonic growth—thyroglossal of duct atrophy. (2) in uterus after parturition.

Q.13. When is atrophy accompanied by osteoporosis?

Ans. Atrophy of disuse may be accompanied by osteoporosis of disuse.

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Q.14. In which conditions is cachexia seen?

Ans. Marked muscle wasting or cachexia may be seen in protein energy malnutrition of (1) marasmus type or (2) chronic inflammatory states (because of secretion of TNF) or (3) cancer.

Q.15. What are the causes of widening of sulci and narro-wing of gyri in above 50 years persons?

Ans. Aging and compromised blood supply because of atheros-clerosis. Aging typically causes cell loss in tissues containing permanent cells: particularly in brain and heart.

Q.16. What are the other causes of atrophy?

Ans. Besides disuse, malnutrition and aging, denervation, ischemia, loss of endocrine stimulation and pressure by expanding mass can cause atrophy.

Q.17. What are the ultrastructural changes seen in atrophy? Ans. Ultrastructural changes in atrophy represent a new balance between compromised conditions and size of cell upto the limit of its viability. Atrophied muscle fibers have fewer structural and functional components like myofibrils, mito-chondria and endoplasmic reticulum.

Q.18. Can atrophy lead to cell death?

Ans. If the conditions are compromised limitlessly, cell death may result in atrophied tissue. Examples include ischemic necrosis and apoptosis in developing embryo.

Q.19. What are the mechanisms involved in atrophy?

Ans. 1. Proteolysis by lysosomal hydrolases and ubiquitin pro-teasome pathway.

2. Autophagy by autophagic vacuoles.

Lysosomes and proteasomes: Cytosomal hydrolases like cathepsins degrade protein molecules from the inter-cellular environment, surface of cells, environment. Ubi-quitin conjugates cytosolic and nuclear proteins and binds to large proteolytic organelles called protea-somes–leading to proteolysis. Ubiquitin proteasome pathway is involved in cancer cachexia and proteolysis by glucocorticoids and thyroxine. Insulin inhibits this. TNF also stimulates this.

Autophagy : Small membrane bound vacuoles within cell with fragments of organelles form and then fuse with

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lysosomes the latter throwing their proteolytic enzymes in the autophagic vacuoles. Some residual bodies— vascuoles with digested material may remain.

Lipofuscin or aging pigment is a form of these residual bodies causing brown coloration of organs in which it accumulates brown atrophy.

Q.20. What are the equivocal signs of death?

Ans. These are cardiac arrest, lack of pulse, cessation of breathing, areflexia and decreasing body temperature. This is referred to as clinical death.

Q.21. What are the criteria for brain death?

Ans. A patient is regarded as biologically dead where brain death has been diagnosed according to following criteria:

1. An isoelectric or flat electroencephalogram for 24 hours. 2. Two angiographic studies performed ½ an hour apart

demonstrating absent cerebral circulation.

3. Irreversible absence of spontaneous respiration. 4. Aflexia (loss of corneal and papillary reflexes). Q.22. What are the unequivocal signs of death?

Ans. Livores: After cardiac arrest, gravity causes blood in venous system to collect in lowest part of body. This produces reddish violet skin spots that can be mobilized by applying local process.

Regor mortis: Postmortem rigidity begins 3 to 6 hours after death.

Nystem’s law: Rigor mortis begins at head and spreads towards feet. Later subsides in the same manner. Occurs due to lack of ATP and subsequent coagulation of active and myosin filaments.

Antolysis or decomposition: Because of activiation of lysosomal intrinsic protease and extrinsic protease from intestinal bacteria which digest the organic components of body. Failure of tissue respiration causes lysosomal protease activation.

Q.23. The above three types of signs of death can be simu-lated in which condition?

Ans. In any condition causing reduced vital functions like barbi-turate intoxication.(apparent death).

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Q.24. Define average life expectancy, morbidity and morta-lity and lethamorta-lity.

Ans. Average life expectancy: Time period in which 50 percent of certain population group have died. The population group can be, e.g. women.

Morbidity: Number of persons per year per 100,000 popu-lation who suffer from a disease.

Mortality: Number of persons per year per 100,000 popu-lation who have died of a disease.

Lethality: Quotient obtained by dividing the number of persons who have died of a certain disease by the number of persons who have contracted that disease.

Q.25. Define epidemic autopsy, clinical autopsy and insu-rance autopsy.

Ans. Epidemic autopsy: Performed in equivocal cases involving chemical suspicious of infectious disease.

Clinical autopsy: Performed on patients who died in hospital usually a part of hospital quality assurance program. Requires consent of next of kin.

Insurance autopsy: Done when required by insurance companies when:

1. Sudden death from uncertain or unnatural causes. 2. Occupational exposure to certain pathogens.

The procedure is ordered by ensurer. This type of insurance autopsy to resolve insurance claim is almost never refused by next of kin.

Q.26. What are the two main classes of nuclei seen in cell cycle?

Ans. Interphase nucleus: Characterized by a nucleolus contai-ning RNA, loosely structured, genetically active euchroma-tin and densely structured heterochromaeuchroma-tin (genetically inactive)

Mitotic nucleus: Characterised by visible chromosomes. Q.27. What is the structure of chromosomes in metaphase?

Ans. Two strands of chromatids joined at centromere. – short arm – p (for petit)

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Q.28. What is a karyogram?

Ans. Chromosomes of a cell are shown to be arranged in a karyo-gram. This is a short formula or description of chromosomes using the following criteria:

– Total number of chromosomes. – Sex chromosome status.

– Applicable aberrations.

Q.29. Based on a computer model, which part of DNA corresponds to software and which one to hardware? Ans. The software is the program and base sequence containing

and instructions for:

1. Copying the program—DNA replication. 2. Repairing program defect—DNA repair.

3. Using subprograms to create protein (Structure and functional).

The replication process and machinery, transcription pro-cess and machinery and translation propro-cess and machinery can be compared to hardware—computer itself.

Q.30. What is a nucleosome? Ans. Nucleosome consists of:

1. A histone molecule with 2, H2A, H2B, H3 and H4 poly-peptides each.

2. One histolne H1 polypeptide 3. Limker DNA

4. DNA proper.

Diameter of a nucleosome in a solenoid model is 11 cm. A DNA double helix diameter is 2 mm.

Q.31. What are the dimensions or diameter (average) of a chromatid?

Ans. Each chromatid is a supercoil of around 700 mm diameter with each coil of single DNA strand and histone molecules (polynucleosome) being of around 30 mm diameter.

Q.32. Give an example of congenital DNA repair defect. Ans. Xeroderma pigmentosum.

It is rare. It is hereditary (because of an endonuclease defect).

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Pathogentic chain reaction: Ultraviolet radiation

↓

DNA damage in skin cells

↓

Increased DNA defects in skin cells Sequelae:

1. Skin atrophy (→Thinning of skin)→ an adaptive reaction of excessive cornification and hyperpigmentation is induced.

Mitotic dysfunction in skin cells: Skin cancers. Clinically the→following lesions are seen:

• Dry scaly skin (Xeroderma) with mottled hyper-pigmentation.

• It is a precusor of skin cancer. Later multiple skin tumors such as basal cell Ca, squamous cell Ca and malignant melanoma develop.

Q.33. What are the types of UV radiation?

Ans. Three wavelength ranges exist in UV portion of solar spectrum:

1. UVA → 280 to 400 mm

2. UVB → 280 to 320 mm→ to cause cutaneous cancers. 3. UVC → 200 to 280 mm filtered by ozone layer.

Q.34. Causation of skin cancers by UV radiation depends upon which factors?

Ans. 1. Type of UV rays.

2. Intensity of exposure.

3. Quantity of light absorbing protective mantle of melanin in skin. Fair shinned Europeans who do not tan their bodies and live near equator, e.g. Queensland Australia, have the highest incidence of cutaneous cancers. Q.35. What the subcellular level effects of UV rays?

Ans. 1. Inhibition of cell division.

2. Induction of mutations → carcinogenicity of UV rays is attributed to formation of dipyrimidine dimmers in DNA. 3. Cell death.

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Q.36. What is NER and discuss its role in UV radiation caused cutaneous tumors?

Ans. NER or nucleotide excision repair is the mechanism of repair of DNA damage such as formation of dispyrimidine dimmers by UV rays in chin cells. Steps of NER are: 1. Recognition of DNA lesion.

2. Incision of damaged portion on both sides of lesion. 3. Removal of damaged nucleotide.

4. Synthesis of normal nucleotide patch. 5. It is ligation to DNA.

In mammalian cells upto 30 or more proteins are involved. It is postulated that in excessive sunlight UV ray damage, NER is overwhelmed leading to large transcriptional errors and thus cancer.

Q.37. How does UVB radiation cause skin cancers in XP? Ans. There are basically two mechanisms:

1. Inherited inability to repair UVB damaged DNA.

XP is a heterogenous disease with at least 7 variants each caused by a defect in one of several genes involved in NER. There is extreme photosensitivity and 2000 fold increased risk of skin cancers in sun exposed skin. 2. UVB also causes mutations in oncogenes and tumor

suppressor genes.

Mutant forms of P53 and RAS are +. The mutations occur mainly at dipyrimidine sequences. In animal models, P53 mutations occur early than appearance of tumors.

In XP, there may also be neurological abnormalities. Q.38. What does the size of nucleus in a cell depend upon?

Ans. 1. Size of cell.

2. DNA content of nucleus. 3. Functional state of nucleus.

Q.39. In what conditions does nuclear polyploidy occur? Ans. Multiple complement chromosomes in a cells is called

polyploidy. It occurs when:

1. Proliferating cells double their DNA in synthesis phase and just before mitosis become tetraploid.

2. Where mitosis fails to occur after the synthesis phase or is followed by several additional synthesis phases.

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This occurs in some endocrine gland cells like thyroid. 3. As a morphological sign of stress induced adaptative

reactive as in.

Barbiturate above: Increased liver metabolism results in liver cells polyploidy.

Cardiac valvular defects: Mycocardium works harder and produces polyploidy.

Haploid cells are normally seen only while spermio-genesis and oospermio-genesis.

Q.40. What is nuclear aneuploidy and what is its morpholo-gical sequela?

Ans. Variation from normal euploid complement (Haploid or Diploid) of chromosomes in which individual chromosomes do not exist in their normal quantities. Morphological sequela of aneuploidy are:

1. Variability in size of nucleus (nuclear polymorphism) larger cell nucleus indicates cellular activity and smaller nucleus indicates cellular inactivity.

2. Variability in nuclear chromatin content. (Nuclear poly-chromasia).

Both polymorphism and ploychromasia are important criteria characterizing a malignant tumor.

Q.41. What are the nuclear criteria of malignancy?

Ans. 1. Nuclear polymorphism and nuclear polychromasia. 2. Proliferation measured by mitotic count in a field of

vision.

3. Dyskaryosis.

Q.42. What are the chromatin changes seen in nuclear chro-matin in different disease states?

Ans. 1. Meterochromatin condensation: Checker board type of chromatin condensation indicates arrested transcription. 2. Dyskaryosis: Irregular pattern of heterochromatin con-densation and fine aggregates gives cancer cells a salt and pepper appearance.

3. Perinuclear hyperchromatosis: Chromatin condensation along inner nuclear membrane. Early sign of cell death (apoptosis). Later it leads to total chromatin clumping or nuclear pyknosis.

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4. Karyolysis: Fading of nucleus due to chromatin dissolu-tion. Late sign of induced cell death.

5. Karyorrhexis: Nuclear burst due to chromatin fragmen-tation. Late sign of programmed cell death.

Q.43. What are the different types of nuclear inclusions seen?

Ans. 1. Cytoplasmic inclusions: Migration of portions of cyto-plasm in nucleus, associated with dysfunctional cell divi-sion in telephase causes a rounded lucency in nucleus

→_{frosted glass nucleus.}

For example papillary thyroid carcinoma.

2. Paraplasmic inclusions: Migration of portions of paraplasm in nucleus due to imagination of nuclear membrane or dysfunctional telophase.

3. Glycogen inclusions: Seen as nuclear defects after alcohol fixation—Diabetes.

4. Fatty inclusions: Following paraffin fixation, cause lipid defects in nucleus. Typical of tumors in the form of fatty tissue—Liposarcoma.

5. Immunoglobulin inclusions: PAS-positive globules (Fahey-Dutcher bodies). Malignant lymphocytic tumors like— Lympholoplasmacytic lymphoma.

6. Viral inclusion: Viral proteins arranged in paracystalline configuration.

Q.44. What is the most frequent type of metaplasia seen? Ans. Metaplasia or an adaptive response to stress in which one mature cell type (epithelial or mesenchymal) is converted to another mature cell type is most commonly of columnar to squamous epithelial type. The commonest form occurs in smokers’ respiratory columnar ciliated mucous secreting epithelium is replaced by more resistant stratified squa-mous epithelium with loss of mucous secreting function. The change may be focal or wide. Stones in excretory ducts of salivary glands, pancreas or bile ducts may also cause a change from columnar to stratified squamous epithelium. Q.45. What is the role of Vitamin A in maintaining

respiratory epithelium?

Ans. Vitamin A deficiency (retinoic acid deficiency) may cause squamous metaplasia of respiratory epithelium and excess of Vitamin A is protective against keratinization.

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Q.46. Is squamous metaplasia beneficial?

Ans. It is a double edged sword as in case of respiratory epi-thelium important function of mucous secretion is lost. Also malignant cancer can arise in metaplasmic tissue and most common cancer of respiratory epithelium is of squamous type. All this with standing, stratified squamous epithelium is more rugged and causes increased resistance to noxious stimuli.

Q.47. Can metaplasia from squamous to columnar epithe-lium occur?

Ans. Yes. Barrett’s esophagus is a condition in which lower eso-phagus after increased exposure to acid reflux from sto-mach converts from stratified squamous to glandular colum-nar type of epithelium cancer arising in this setting is most commonly adenocarcinoma.

Q.48. In connective tissue metaplasia also clearly are adap-tive response?

Ans. Connective tissue formation of the type which is not indi-genous to its site is not clearly adoptive. Example is forma-tion of bone in soft tissue in myositis ossificans in fractures. Fat and cartilage can form sometimes too.

Q.49. What is the role of stem cells in metaplasia?

Ans. Metaplasia results from reprogramming of stem cells pre-sent in the tissue or of undifferentiated mesenchymal cells in connective tissue. Precursor cells develop differently there is no change in the phenotype of differentiated, mature cells.

Q.50. What are the mechanisms involved in altered pre-cursor cells development in metaplasia?

Ans. Many tissue specific and differentiation genes are involved in coding for growth factors, cytokines and E (M compo-nents which signal for altered development of precursor cells, e.g. bone morphogenic proteins, members of TGF-B superfamily, induce chondrogenic and osteogenic ex-pression in stem cells. While suppressing differentiating into muscle or fat these growth factors act as external triggers induce specific transcription factors that lead the cascade of phenotype specific genes towards a full-developed (of different type) cell. Why the normal pathways are disrupted is not known?

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Examples:

Examples: Vitamin Vitamin AA→→ Retinoic acid regulates cell growth, Retinoic acid regulates cell growth,

differentiation and tissue pattering.

Certain cytostatic drugs:

Certain cytostatic drugs: Cause disruption of DNA methy- Cause disruption of DNA

methy-lation patterns and can transform mesenchymal cells from

lation patterns and can transform mesenchymal cells from

one cell type (fibroblast) to another (muscle, cartilage).

SUP

PL

EME

NT

AR

Y

T

OPI

CS—

CEL

L

INJURY AND INFLAMMATION

PRETEST

1.

1. Which of tWhich of the follohe following are truwing are true about cell Ie about cell Injury?njury?

A.

A. Hypothyroidism and scurvy cause delayed woundHypothyroidism and scurvy cause delayed wound

healing.

B.

B. Ultraviolet light promotes healing.Ultraviolet light promotes healing.

C.

C. Cerebral cortex and myocardium can regenerate after Cerebral cortex and myocardium can regenerate after

injury.

D.

D. Fibrinoid necrosis occurs in TB.Fibrinoid necrosis occurs in TB.

E.

E. Enzymatic lysis of adipose tissue causes fat necrosis.Enzymatic lysis of adipose tissue causes fat necrosis.

2.

2. Which Which of the of the follofollowing awing are true?re true?

A.

A. The myofibroblastic differentiation of fibroblast causesThe myofibroblastic differentiation of fibroblast causes

contraction of granulation tissue.

B.

B. Endarteritis obliterans and leukemia can be caused byEndarteritis obliterans and leukemia can be caused by

radiation exposure for a long time.

C.

C. Apoptosis Apoptosis is is pathological pathological event.event.

D.

D. Apoptosis Apoptosis is is an an energy energy dependent dependent pigmentation pigmentation of of DNADNA

by non-lysosomal endonucleases.

3.

A.

A. Endothelial cells and plasma cells are capable of Endothelial cells and plasma cells are capable of

phagocytosis of particulate matter in acute inflammation.

B.

B. Lymphocytes and plasma cells contribute in chromicLymphocytes and plasma cells contribute in chromic

inflammation.

C.

C. In vascular phase of inflammatory response, neutrophilsIn vascular phase of inflammatory response, neutrophils

and monocytes move towards periphery of

microcircula-tory vessels a process called pavementing.

tory vessels a process called pavementing.

D.

D. TT-lymphocytes produce antib-lymphocytes produce antibodies.odies.

E.

E. Transudate is noninflammatory fluid with few cellular Transudate is noninflammatory fluid with few cellular

elements.

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4.

A.

A. Unidirectional movement of Unidirectional movement of leukocytes towards leukocytes towards a a stimu-

stimu-lus is called diapedesis.

lus is called diapedesis.

B.

B. Macrophages are found in glomeruli.Macrophages are found in glomeruli.

C.

C. Hepatocytes have greater regenerative capacity thanHepatocytes have greater regenerative capacity than

myocardial cells.

D.

D. Mast cells have metachromatic granules.Mast cells have metachromatic granules.

5.

A.

A. Features of acute inflammation are in following chro-Features of acute inflammation are in following

chro-nological order:

nological order:

a

a CoContntraractction ion of of ararteteririololeses

b.

b. ArtArterieriolar olar diladilatattationion

c.

c. AcActitive hve hypypererememiaia

d. Inflammatory exudates

e. Swelling and pain

f. Slowing of blood flow.

B.

B. Cytoplasmic micropinocytotic vesicles are increased for Cytoplasmic micropinocytotic vesicles are increased for

increasing membrane permeability in acute

inflamma-tion.

tion.

C.

C. C3a, C5a, 5-HTC3a, C5a, 5-HT, Kallikrein, Kallikrein, PGE2 are involved in incr, PGE2 are involved in increa-

ea-sed vascular

sed vascular permeabilitypermeability..

D.

D. In a granuloma, there is polymorphonuclear leuko-In a granuloma, there is polymorphonuclear

leuko-cytosis, cell debris and fibrin.

cytosis, cell debris and fibrin.

E.

E. Collagen type found in dermis, tendon, bone, cornea,Collagen type found in dermis, tendon, bone, cornea,

and dentin is type IV.

6.

A.

A. Fab fragment consists of light chain and part of heavyFab fragment consists of light chain and part of heavy

chain.

B.

B. Papain digestion of monomeric immunoglobulin resultsPapain digestion of monomeric immunoglobulin results

in production of an antibody binding fragment.

C.

C. Fc, Fragment consists of C-terminal ends of heavyFc, Fragment consists of C-terminal ends of heavy

chains.

7.

A.

A. IgM class specific antibody production is a primaryIgM class specific antibody production is a primary

antibody response.

B.

B. IgA class antibody has 4 J-chains.IgA class antibody has 4 J-chains.

C.

C. Mast cells degranulation is a property of IgE.Mast cells degranulation is a property of IgE.

D.

D. Lymphocyte surface antigen receptor is a property of Lymphocyte surface antigen receptor is a property of

IgD. The deep (or

IgD. The deep (or para) cortex is the T-lymphocyte zonepara) cortex is the T-lymphocyte zone

of lymph node and enlarges during antigenic stimulation.

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E.

E. The deep (or para) cortex is the T-lymphocyte zone of The deep (or para) cortex is the T-lymphocyte zone of

lymph node and enlarges during antigenic stimulation.

8.

8. Which of the folloWhich of the following are true about Twing are true about T-lymp-lymphocythocytes?es?

A.

A. Helper T-lymphocytes and T4 positive cells.Helper T-lymphocytes and T4 positive cells.

B.

B. Cells bearing both T4 and T9 are common thymocytes.Cells bearing both T4 and T9 are common thymocytes.

C.

C. Prothymocytes are T10 positive cells.Prothymocytes are T10 positive cells.

D.

D. Suppressor T-lymphocytes are T9 positive cells.Suppressor T-lymphocytes are T9 positive cells.

E.

E. In the unstimulated lymph node, there are localizedIn the unstimulated lymph node, there are localized

aggregates of lymphocytes in superficial cortex.

9.

A.

A. Following antigenic stimulation, para cortex enlargesFollowing antigenic stimulation, para cortex enlarges

resulting in B-lymphocyte proliferation.

B.

B. Macrophages have a surface receptor for C3b.Macrophages have a surface receptor for C3b.

C.

C. C5a promotes emigration and accumulation of C5a promotes emigration and accumulation of neutrophilneutrophil

polymorphs and macrophages.

D.

D. Extrinsic allergic alveolitis is an immune complex,Extrinsic allergic alveolitis is an immune complex,

Arthus (type

Arthus (type 3) reaction 3) reaction to bacterial to bacterial spores on spores on mouldymouldy

hay.

E.

E. Rheumatoid arthritis is an organ specific autoimmuneRheumatoid arthritis is an organ specific autoimmune

disease.

10

10.. Which of thWhich of the followie following are true about aung are true about autoimmutoimmunene

disease?

A.

A. In Di-George syndrome, there is defective B-cell functionIn Di-George syndrome, there is defective B-cell function..

B.

B. In infantile sex-linked agammaglobulinemia there isIn infantile sex-linked agammaglobulinemia there is

selective B-cell defect (Bruton type).

C.

C. In severe combined immunIn severe combined immuno deficiency, o deficiency, there is defectivethere is defective

B-cell and T-cell function.

D.

D. Wiskott-Aldrich syndrome is characterized by abnormalWiskott-Aldrich syndrome is characterized by abnormal

platelets and defective T-cell function alone.

ANSWERS

1 1.. AA.. TrueTrue B. B. FalseFalse C. C. FalseFalse D. D. FalseFalse E. E. TrueTrue 2 2.. AA.. TrueTrue B. B. FalseFalse

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C. False D. False

3. A. False: Neutrophils, macrophages and eosinophil are the main phagocytes in acute inflammation.

B. True

C. Flase: The process described is called margination. Pavementing is adhering of inflammatory cells to vascular endothelium.

D. False: B-lymphocytes produce immunoglobulins. E. True

4. A. False: The described process is chemotaxis. Diapedesis is movement of white cells out of the vessel through gaps in endothelial cells. B. True C. True D. True 5. A. True B. True C. True

D. False: This description is that of an abscess. Granuloma is characterized by chronic inflammation.

E. False: Type neollagen is seen in basement membranes. Type I is seen in the said places.

6. A. True

B. False: There are two antibody binding fragments. C. True

7. A. True: IgM appears in a small quantity within 7 days of exposure to antigen.

B. False: IgA is selected by plasma cells as a dimmer, i.e. two molecules, linked together by one polypeptide-J chain. C. True D. True E. True 8. A. True B. True C. True

D. False: These are T8 positive cells. E. True