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Robbins Review of Pathology - E. Klatt, V. Kumar (W B Saunders, 2000) WW PDF

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Robbins Review of Pathology - E. Klatt, V. Kumar (W B Saunders, 2000) WW PDF

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Robbins a anata aeya PATHOLOGY an <4! att VON aU USMLE-style Questions and Explained Answers Crete Rae coda ay n Tala i We, Basis of Disease, 6th Edition and Basic Pathology, 6th Edition vi Full Color Images Throughout Robbins Review of PATHOLOGY Edward C. Klatt, M.D. Professor of Pathology ‘The University of Utah Health Sciences Center Salt Lake City, Uish Vinay Kumar, M.D., F.R.C.Path. Vere A. Stembridge Chair in Pathology Department of Pathology ‘The University of Texas Southwestern Medical School Dallas, Texas W.B. SAUNDERS COMPANY ‘A Harcourt Healih Sciences Company PTiladelphis London New York St. Louis Sydney Toronto ‘< not for aale! > < He nna qponame | > < Cran ReccameronMepeHA: MOCK a QpoM. Py > ‘WB. SAUNDERS COMPANY ‘A Harcourt Heath Sciences Compeny ‘The Canis Center Independence Square West Philadelphia, Pennsyivania 19106 brary of Congress Cataloging in-Pubiction Date ‘on, Eduard. Robbins revew of punlogyEdvaraC. Kat, Viry Kumar—tst ed pom ISBN 0-7216-€280-6 | Patnlogy—Examiraions, uestens, ee. 1 Te: Review of paboogy. —U. Rebbir, Stoney L. (Staniey Leotard) I Kurar, Viegy,, WW. The ORLA 1. Patelogy. G2 4 K6Sr 00a RB110.Ks6 2000 616.07:076— < He nam mponame t > < CRAM RescamRoMMEpCHA: MOCK 8 QpoM. Py > To our students, for constant challenge and stimulation << not for salet > < He mmm nponame | > < CRAM ReaMeroMMEpCHA: NCR 2 Goo. Ey > This book is designed to provide a comprehensive review of pathology through multiple choice questions and expla- nations of the answers, The source materials are the sixth, editions of Cotran, Kumar, Collins: Robbins Pathologic Basis of Disease (PBD6) and Kumar, Cotran, Robbins: Basic Pathology (BP6). It_is intended to be a useful re- source for students at a variety of levels, including those in the allied health professions. In keeping with the style used by the USMLE, only two ‘question formats are used: single best answer and extended matching. The majority of the questions contain a clinical vignette that is followed by a series of homogenous. choices. This approach emphasizes an understanding of ‘mechanisms and manifestations of disease in a clinical con- text. Wherever possible, we have incorporated relevant lab- oratory, radiologic, and physical diagnostic findings in the questions to emphasize clinicopathologic correlations. For each question, the correct answer is provided with a brief explanation of why the correct answer is “correct” and why the other choices are “incorrect.” Each answer is referenced to Robbins Pathologic Basis of Disease and 10 Basic Pa- thology to facilitate and encourage a more complete read- ing of the topic. Pathology is a visually oriented discipline and hence we have used full color images in many of the questions. The illustrations are taken from the Robbins textbooks, so students can reinforce their study of the illus- trations in the text with questions that utilize the same images. ‘The questions are intentionally fairly difficult, with the purpose of “pushing the envelope” of student understand- ing of pathology. We hope, therefore, that this text will be useful not only prior to examinations but also during the course. We must hasten to add that no review book is @ substitute for the textbooks and other course material pro- Vided by individual instructors. The best use of this book will be after a thorough study of Robbins Pathologic Basis of Disease and/or Basic Pathology. Finally, we hope that students and instructors will find this review book to be ‘useful adjunct t0 the learning of pathology. Epwarp C. KLarr VINAY KUMAR We are very grateful to our editorial assistants, Beverly Shackelford and Carolyn Osterman, for their invaluable help in the production of the manuscript. Thanks are also due to Hazel Hacker, our Developmental Editor. and Wil- liam Schmitt, Editor-in-Chief, Medical Books, W.B. Saun- ders Company, for their support of this project. Last but not least, We are grateful to our families and colleagues for graciously accepting this additional demand on our time. EDWARD C. KLATT ‘VINAY KUMAR vil < CraN He ReccamermonMepCHA: MOCK 2 Goo. Py > PART 1 GENERAL PATHOLOGY 1. Cellular Pathology... 2. Acute and Chronic Inflammation. 3. Tissue Repair: Cellulor Growth, Fibrosis, ‘and Wound Healing........ 4 Hemognamict Disorders, Thrombosis, ANd SHOCK sess 5. Genetic Disorders, 6. Diseases of Immunity. 7. Neoplasic.. 8. Infectious Diseases .. 9. Environmental ond Nutritional Pathology....78 10. Diseases of Infancy and Childhood PART 2 DISEASES OF ORGAN SYSTEMS 11. Blood Vessels... 101 12. The Heart 10 13. Red Cells and Bleeding Disorders. 123 14. 15. 16. 7. 18. White Cells, Lymph Nodes, Spleen, and The Lung. Head and Neck The Gastrointestinal Tract ... 173 The Liver and the Biliary Tract ... The Pancreas .. The Kidney and the Lower cumey Tract . The Male Genital Tract ....... The Female Gerital Tract... The Breost .. The Endocrine System The Skin... Bones, Joints, and Soft Tissue Tumors... 274 Peripheral Nerve ond Skeletal Muscle .... The Central Nervous System. The Eye... SAM 2 pow. By > PART ] GENERAL PATHOLOGY OTCKAHMPOBAN XOTA Bbi covtt Aaa aed HAVE YOU SCANNED AT LEAST ONE BOOK ? < GaN % pemane-mounepcua! MYCAR oF pour. py > CHHAPTER Cellular Pathology PBD6 Chapter 1 - Cellular Pathology | PBD6 Chapter 2 - Cellular Pathology Il BP6 Chapter 1 - Cell Injury, Death, and Adaptation L.A 17-year-old mate infected with hepatitis A experi- fences some mild nausea for about a week and has very mild scleral icterus. Laboratory findings include elevations in the levels of the hepatic enzymes aspartate transaminase (AST) and alanine transaminase (ALT). The increase in the enzyme levels in the serum results from which of the following changes in the hepatocytes? ‘O(A) Dispersion of ribosomes ‘O(B) Autophagy by lysosomes © (C) Swelling of the mitochondria OD) Clumping of nuclear chromatin © (©) Defects in the cell membrane 2. A S4-year-old male experienced the onset of severe chest pain. An electrocardiogram demonstrated changes consistent with an acute myocardial infarction. He was given thrombolytic therapy with tissue plasminogen activa- tor (tPA). However, his serum cteatine kinase increased after this therapy. Which of the following events most likely occurred?” OLA) Reperfusion injury © @®) Cellular regeneration OC Chemical injury ‘©(D) Increased synthesis of creatine kinase © ©) Myofiber atrophy 3. A Si-yearold male has a blood pressure of 150/95 mm Hg. If this condition remains untreated for year, which of the following cellular alterations will be seen in the heart? (A) Atrophy O(B) Hyperplasia OC) Metaplasia OD) Hemosiderosis © ©) Hypertrophy 4. The aortic valve seen in the figure was discovered at the autopsy of a 72-year-old male. The heart weighed 580g, with marked left ventricular hypertrophy and. minimal coronary arterial atherosclerosis. A serum chem: istry panel revealed no abnormalities prior to. death from congestive heart failure. Which of the following pathologic processes accounts for the appearance of the valve? (A) Amyloidosis ©) Dystrophic calcification © (C) Lipofuscin deposition ‘O(D) Hemosiderosis © © Fatty change 5. A right carotid endarterectomy is performed on a 69- year-old female who had an audible broit on auscultation Of the neck. Examination of the cureited atheromatous plaque reveals a grossly yellow-tan, firm appearance. Mi- croscopically, which of the following materials can be found in abundance in the form of erystals producing long, clefilike spaces? OLA) Glycogen ‘©1B) Lipofuscin O(© Hemosiderin ©(D) Immunoglobulin © ©) Cholesterol 4m Port (GENERAL PATHOLOGY 6A 38-year-old woman experienced severe abdominal ppain with hypotension and shock that led to her death within 36 hours. From the gross appearance of the mesen- tery, seen in the figure, which of the following events has most likely occurred! ‘O(A) Hepatitis B virus infection OB) Small intestinal infarction OO Tuberculous lymphadenitis OC) Gangrenous cholecystitis © ©) Acute pancreatitis, 7. Absorption of radiant energy, such as x-rays, can result, in cell injury by causing hydrolysis of water. Which of the, following cellular enzymes protects cells from this type of injury’? OLA) Phosphotipase OG) Glutathione peroxidase OC Endonnclease O(D) Lactate dehydrogenase © © Proteases 8. In patients with emphysema due to ayantitrypsin defi- ciency, the molecular mechanism responsible for the accu- ‘mulation of -antitrypsin in hepatocytes is OLA) Excessive hepatic synthesis of a-antitrypsin ©) Retention in the endoplasmic reticulum because of poorly folded «-antitrypsin OO Decreased catabolism of c;-anttrypsin in lysosomes OC) Inability to metabolize e,-anttrypsin ‘©(E) Impaired dissociation from chaperones 9. A 63-year-old man experienced diaphoresis and sub- sternal chest pain after thrombosis of the left anterior de- scending artery. His serum creatine kinase level was ele vated. Which of the following patterns of tissue injury was ‘most likely? OC) Liquetactive necrosis O1B) Caseous necrosis OC Coagulative necrosis OD) Fat necrosis, OLE) Gangrenous necrosis, 10. After several weeks of immobilization of the leg in a plaster cast, the diameter of the calf often decreases. This < Gram H emane-nctsnepCHnY MYCAI 9 por. By > change results from which of the following alterations in the calf muscles? OCA) Aplasia OG) Hypoplasia ‘©(©) Atrophy O() Dystrophy ‘© (E) Hyalin change 11. Which of the following cells have the highest telom- erase activity? OA) Endothelial cells, ©) Ger cells O10) Neurons OD) Neutrophils O ©) Exythrocytes 12. A 32-year-old male experiences “heartburn” with sub- sternal pain from reflux of gastric contents into the lower esophagus. After many months, the esophageal epithelium exhibits the microscopic appearance shown here. Which of the following pathologic alterations has occurred? (A) Squamous metaplasia OB) Mucosal hypertrophy OC] Colurnnar epithelial metaplasia OC) Atrophy of lamina propria OE) Goblet cell hyperplasia 13. On day 28 of the menstrual cycle in a 23-year-old female, there is menstrual bleeding that lasts for a few days, She has had these regular cycles for many years. Which of the following processes is most likely happening in the endometrium just before the onset of bleeding? OCA) Apoptosis ‘© (B) Caseous necrosis O(C) Heterophagocytosis OW) Atrophy © ©) Liquefactive necrosis 14, Many drugs that are used to treat cancer cause death of tumor cells by apoptosis. Mutational inactivation of which of the following genes can render tumor cells resist- ant to the effects of such chemotherapeutic drugs? OWA) bet2 O@) p53 O(C) NF-KB O@) PA50 O(E) Granzyme B 15. After the birth of her first child, a 19-year-old female began breast-feeding the baby. She continued breast-feed- ing for almost a year. Which of the following processes that occurred in the breast during pregnancy allowed hie to rurse the infant? O(A) Stromal hypertrophy OG) Lobular hyperplasia OC) Epithelial dyspla ©) Intracellular accumulation of fat © ©) Ductal epithelial metaplasia 16. A 22-year-old female has a congenital anemia that required multiple transfusions of red blood cells for many years. She now has no significant findings on physical examination. However, her liver function test results are abnormal. Which of the following findings would most likely appear in a liver biopsy? OLA) Steatosis in hepatocytes ©@®) Bilirubin in canaliculi OO Glycogen in hepatocytes OW) Amyloid in portal triads © ©) Hemosiderin in hepatocytes For each of the clinical histories in questions 17, 18, and 19, match the most closely associated lettered descrip” tion of a form of cellular change or injury: (A) Apoptosis (B) Atrophy (©) Caseovs necrosis (D) Coagulative necrosis (E) Dysplasia (F) Dystrophic calcification (G) Fat necrosis GH) Farry change (D Gangrenous necrosis () Hydropie change (K) Hyperplasia (L) Hypertrophy (M) Liquefactive necrosis (N) Metaplasia (©) Metastatic caeification 17. A 3-om, right middle lobe lung nodule was seen on a chest radiograph of an asymptomatic 37-year-old male. The nodule was excised with a pulmonary wedge resection by the thoracic surgeon. On sectioning by the pathologist, the nodule was sharply circumscribed and had a soft, white center. Culture of tissue from the nodule grew Mycobacte- rim tuberculosis. (— 18. A 69-year-old male has difficulty with urination. A. digital rectal examination reveals that the prostate gland is < CRAM peccameonMepeHA: MOAI 8 QpoM. Py > Chopter! CELLULAR PATHOLOGY mS palpably enlarged to about twice normal size. A transure- thral resection of the prostate is performed, and the micro- scopic appearance of the prostate “chips” obtained is that of nodules of glands with intervening stroma. ( 19. Blunt trauma to the abdomen of a 16-year-old male ‘ccurred during a vehicular accident in which be lost con- trol of the vehicle at high speed and struck a bridge abut- ‘ment. He is found to have a hemoperitoneum, and at lapa- rotomy, a small portion of the left lobe of the liver was resected because of the injury. Weeks later, the liver had regained its normal size. ( 20. Accumulation of lipofuscin granules in cells is ty cally seen in which of the following conditions? O1A) Atrophy O68) Hypertrophy OC) Hyperplasia ©(D) Metaplasia ©) Apoptosis 21. A 40-year-old male was diagnosed with an undiffer- entiated carcinoma of the lung. Despite treatment with chemotherapy, he died of widespread metastases. At au- topsy, tumor was found in many organs. Histologic exami nation revealed many foci in which individual tumor cells appeared shrunken and deeply eosinophilic. Their nuclei showed condensed aggregates of chromatin under the nu- clear membrane. ‘The process affecting these shrunken tu- ‘mor cells was triggered by the release of which of the following proteins into the cytosol? OLA) Lipotuscin (8) Cytochrome ¢ O(C) Catalase OD) Phospholipase O€) bel-2 22. Metastatic calcification is most likely to occur in which of the following conditions? ‘O(A) Tuberculosis of the lung ‘O(B) Acute hemorthagie pancreatitis ©(O) Aortic stenosis in a 70-year-old man Q(D) Vitamin D intoxication OE) Amyloidosis 23. A 68-year-old female suddenly lost consciousness and, on awakening an hour later, could not speak or move her right arm and leg. Two months later, a head computed tomography (CT) scan showed a large cystic area in her left parietal lobe. Which of the following pathologic processes most likely occurred in the brain? ‘O(A) Fat necrosis, OG) Coagulative necrosis OCC) Apoptosis OD) Liquefactive necrosis O ©) Karyolysis 6 Part! GENERAL PATHOLOGY ‘Women's Hespital, Boston, 24. At autopsy, a 40-year-old male has an_ enlarged {2200 g) liver with a yellow cut surface. The microscopic appearance of this liver is shown in the figure. Before Geath, his total serum cholesterol and triglyceride levels ‘were normal, but he had a decreased serum albumin con- centration and increased prothrombin time. Which of the following activities by this man most likely led to these findings? (A) Injecting heroin ©) Playing basketball ©] Drinking beer O() Smoking OE) Ingesting aspirin Counesy of De. Scom Grater, Brigham and Women’s Hespial, Bestn, 25. The cellular change in the epidermal cell located in the midepidermis, in the figure, results from which of the following biochemical reactions? ‘< Gram Remanernciseponnt HYCAN 9 Opceer By > O(A) Activation of caspases © (B) Reduced ATP synthesis ©) Increased glycolysis ©) Activation of lipases © ) Lipid peroxidation 26. At autopsy, the heart of « 63-year-old male is only 250 g, with small right and left ventricles. The myocar dium is firm, with a dark chocolate brown color through- ‘out. The coronary arteries demonstrate very litle athero sclerosis. Which of the following substances will most likely be found in the myocardial fibers of this heart? O(A) Melanin OB) Hemosiderin OO Glycogen OD) Lipofuscin © Bilirubin 27. A pneumonectomy is performed for lung cancer diag nosed in a 69-year-old female, Examination of the hilar lymph nodes reveals a uniform dark black cut surface. ‘What is most likely to account for this appearance of these ymph nodes? (A) Smoking O(B) A bleeding disorder O© Liver failure ©) Aging OW) Metastases 28. Deposition of calcium in the renal tubular epithelium in patients with primary hyperparathyroidism is the result ‘of which of the following processes? (A) Dystrophic calcification OG) Renal tubular atrophy OW Autophagocytosis OD) Metastatic calcification © ©) Cellular aging 29. A renal biopsy is performed on a 33-year-old female ‘who has had increasing renal failure for the past week. Which of the following changes seen with electron micros- copy most likely suggests a diagnosis of acute tubular necrosis? (A) Mitochondrial swelling O(B) Plasma membrane blebs O(© Chromatin clumping O(D) Noclear fragmentation ©) Ribosomal disaggregation from endoplasmic reticu- lum 30. Reperfusion of ischemic tissues, as may occur after therapeutic use of thrombolytic agents, sometimes leads to cell death after the blood flow resumes. The biochemical basis for cell death under these circumstances. is most likely which of the following? (A) Reduction in protein synthesis ©) Increased generation of oxygen-derived free radicals ‘O(C) Increased activity of catalase O(D) Reduced oxidative phosphorylation OE) Release of calcium from endoplasmic reticulum 31. A 50-year-old male experienced several episodes of chest pain before his death. A histologic section of left ventricular myocardium taken at autopsy showed a deeply cosinophilic staining area with loss of nuclei and cross- striations in myocardial fibers. There was no hemorthage or inflammation. Which of the following conditions most likely produced these myocardial changes OA) Viral infection OG) Coronary artery thrombosis O© Blunt chest trauma OD) Antibodies directed against myocardium O() A protein-deficient diet 32, The nonpregnant uterus of a 20-year-old female measured 7 X 4 X 3 em. She became pregnant, and just before delivery of a term infant, the uterus measured 34 X 18 X 12 cm. Which of the following cellular processes was the major reason for the increase in the size of the uterus? OCA) Endometrial glandular hyperplasia ©) Myometrial fibroblast proliferation OO Endometrial stromal hypertrophy OD) Myometrial smooth muscle hypertrophy ©O(E) Vascular endothelial hyperplasia 33. A 40-year-old female with chronic congestive heart failure has a cough productive of rust-colored sputum. A sputum cytology specimen shows numerous bemosiderin- laden macrophages. Which of the following subcellular structures in macrophages is most important for the accu- mulation of this pigment? OLA) Lysosome O(B) Endoplasmic reticulum OO Ribosome OW) Golgi apparatus ©) Chromosome >———_- ANSWERS 1. (B) Ineversible cell injury is associated with loss of ‘membrane integrity. This allows intracellular enzymes to leak into the scrum. All other morphologic changes listed are associated with reversible cell injury, in which the cell ‘membrane remains intact. BP6 6-8 PBD6 7-9 2. (A) The restoration of blood flow is helpful if the existing cell damage is not great, and further damage can be prevented. However, the reperfusion of damaged cells results in generation of oxygen-derived free radicals to pro- duce a reperfusion injury. The elevation in the exeatine Kinase level is indicative of myocardial cell necrosis, not < Cran ReccamnrmonMepCHA: MOCK 8 pce. py > Chapter] CELLULAR PATHOLOGY m7 regeneration or atrophy, The tPA does not produce a chem= ical injury but induces thrombolysis to restore blood flow. BP69-10 PBD6 12-13 3. (B) The pressure load on the left ventricle results in an increase in myofilaments in the existing myofibers. ‘The result of conti ty, but the cells do not decrease in size. Metaplasia of muscle does not occur, although loss of muscle occurs with aging, with replace. ment by fibrous tissue and adipose issue. Hemosiderin ‘deposition in heart is pathologic process resulting from increased iron stores in the body. BP6 22 PBD6 33-35 4, (B) The valve is stenotic because of nodular deposits ‘of calcium. The process is “dystrophic” because calcium eposition occurs in damaged tissues. ‘The damage here results from wear and tear of aging. Amyloid deposition in the heart typically occurs within the myocardium and the vessels, The amount of lipofuscin inereases within myocar- cium with aging, With a genetic defect in iron absorption known as hereditary hemochromatosis, there is extensive myocardial iron deposition. Fatty change is uncommonly seen in myocardium, but infiltration of fat cells can occur. BP6 20 PBD6 43-44 5. (E) Cholesterol is a form of lipid commonly deposited within athcromas in arterial walls, imparting a yellow color to these plaques. Glycogen is a storage form of carbohy- rate seen mainly in liver and muscle. Lipofuscin is a brown pigment that increases with aging in cell cytoplasm, mainly in cardiac myocytes and in hepatocytes. Hemosid- cin is a storage form of iron that appears in tissues of the ‘mononuclear phagocyte system (c.g., marrow, liver. spleen) but can be widely deposited with hereditary hemochroma- tosis. Immunoglobulin occasionally may be seen as rounded globules in plasma cells (i.e., Russell bodies), BP6 18 PBD6 40 6 (E) The focal chalky-white deposits are areas of fat necrosis resulting from the release of pancreatic lipases in patients with acute pancreatitis. Viral hepatitis docs not cause necrosis in other organs, and hepatocyte necrosi from viral infections occurs mainly by means of apoptosi Intestinal infarction is a form of coagulative necrosis. Tu- berculosis produces cascous necrosis. Gangrenous necrosis is mainly coagulative necrosis but occurs over an extensive BP6 12-13 PBD6 16-17 7. (B) Intracellular mechanisms exist that deal with free radical generation, as can occur with radiant injury from irradiation. Glutathione peroxidase reduces such injury by catalyzing the breakdown of HO; Phospholipases decrease cellular phospholipids and promote cell membrane injury. Proteases can damage cell membranes and cytoskeletal pro- teins. Endonucleases damage nuclear chromatin. Lactate dehydrogenase (LDH) is present in a variety of cells, and its clevation in the serum is an indicator of cell death. BP6 9-11 PBD6 12-14 8 mM Pon! GENERAL PATHOLOGY 8. (B) Mutations in the qy-antitrypsin gene give rise to ‘,-antitrypsin molecules that cannot fold properly. The par- tially folded molecules accumulate in the endoplasmic re- ticulum (ER) and cannot be secreted. Impaired dissociation Of the cystic fibrosis transmembrane conductance regulator (CFTR) protein from chaperones is the cause of many ‘cases of cystic fibrosis. There is no abnormality in the synthesis or metabolisin of qy-antitrypsin in patients with ‘,-antitrypsin deficiency. PBD6 41 9. (C) He has an acute myocardial infarction. An ische- mic injury {© most internal organs produces a pattem of cell death called coagulative necrosis. Liquefactive necrosis ‘ceurs following ischemic injury to brain and is also the pattern seen with slbseess formation. Caseous necrosis can be seen in various forms of granulomatous inflammation, ‘ppilied by tuberculosis. Fat necrosis is usually seen in pancreas and breast tissue. Gangrenous necrosis is @ form Of coagulative necrosis that usually results from ischemia and effects limbs. BP6 12-13 PBD6 16-18 10, (©) Reduced workload causes shrinkage of cell size because of loss of cell substance, a process called atrophy. ‘Aplasia refers to lack of embryonic development; hypopla- sia is used to describe poor or subnormal development. Dystrophy of muscles refers to inherited disorders of skele- tal muscles that lead co muscle weakness and_ wasting. Hyaline change is the name given to a nonspecific, pink, sassy eosinophilic appearance of cells. BP6 21-22 PBD6 35-36 11. (B) Germ cells have the highest telomerase activity, and the telomere length therefore can be stabilized in these cells. This allows germ cells to retain the ability to divide. Normal somatic cells have no telomerase activity, and telo- meres. progressively shorten with each cell division until growth arrest occurs. PED6 47 12. (©) Inflammation has resulted in replacement of nor rmal squamous epithelium by intestinal-type columnar epi- thelium with goblet cells. Such conversion of one adult cell type to another type is called metaplasia. The thickness of the mucosa is normal. The lamina propria has some inflam ‘matory cells but is not atrophic. BP6 22-23 PBD6 36-37 13, (A) This is an example of orderly, programmed cell death (apoptosis) through hormonal stimuli. ‘The endomie- trium breaks down, sloughs off. and then regenerates. Ca- scous necrosis is Iypical of granulomatous inflammation, resulting most commonly from mycobacterial. infection Heterophagocytosis is typified by the clearing of an area of necrosis through macrophage ingestion of the necrotic cells, With cellar atrophy, there is often no visible necro- sis. but the tissues shrink in size. something that would happen to the endometrium after menopause. Liquefactive necrosis ean occur in any tissue after acute bacterial infec- tion or in the brain after ischemia, BP6 13-14 PBD6 18-19 ‘< GRAN m gemane-mompepcnat MYCARL 97 QpoNZ. py > 14, (B) On DNA damage induced by chemotherapeutic drugs (or other agents), normal p53 genes tigger the cells to undergo apoptosis. When p33 is inactivated, this path- way of cell death can be blocked. rendering the chemother- apy less effective. bel-2 and NF-KB favor cell survival Cytochrome P450 does not affect apoptosis. Granzyme B is found in cytotoxic cells and not tumor cells. It triggers ptosis BP6 155-156 PBD6 25 15. (B) Lobules increase under hormonal influence t0 provide for lactation. The breast stroma plays no role in lactation and may increase in pathologic processes. Epithe- lial dysplasia denotes disordered growth and maturation of epithelial cells that may progress to cancer. Accumulation Of fat within the cells is 2 common manifestation of suble- thal cell injury ot, uncommonly, hecause of inborn errors in fat metabolism. Epithelial metaplasia in the breast is a pathologic process. BP6 22 PBD6 32-33 16. (B) Fach unit of blood contains 250 mg of iron. ‘The body has no mechanism for getting rid of excess iron. A. small amount of iron is lost with normal desquamation of epithelia, and menstruating women lose a bit more. The excess iron becomes storage iron, or hemosiderin. Over time, hemosiderosis involves more and more tissues of the body, particularly the liver. Initially, the hemosiderin de- posits are found in Kupffer cells in the liver and other mononuclear phagocytes in the bone marrow, spleen, and lymph nodes. With great excess of iron, liver cells also accumulate iron. Steatosis usually occurs with ingestion of hhepatotoxins such as alcohol. Bilirubin, a breakdown prod- ‘uct of blood, can be passed out in the bile so that a person does not become jaundiced. Amyloid is an abnormal pro- tein derived from a variety of precursors such as immuno ‘globulin light chains BP6 19 PBD6 42-43 17, (©) The cheeselike appearance gives this form of ne- crosis its name —caseous necrosis. In the lung, tuberculosis and fungal infections are most likely to produce this pat- tern of tissue injury. BP6 13. PBD6 17 18, (K) Nodular prostatic hyperplasia (also-known as be- nign prostatic hyperplasia, ot BPH) is a common condition in older males that results from proliferation of both pros- tatic glands and stroma. The prostate becomes more sensi- tive to androgenic stimulation with age. This is an example of pathologie hyperplasia, BP6 22 PBDG 32-33, 19. (K) The liver is one of the few organs that can at least partially regenerate itself in the human body. This is @ form of compensatory hyperplasia. The stimuli to hepato. cyte mitotic activity cease when the liver has attained its normal si BP6 22 PBD6 32-33 20. (A) Atrophy is often associated with increased de- struction of subcellular components by autophagy. The cel- lular components (¢.g., mitochondria, endoplasmic reticu- um) are digested by the lysosomal enzymes. Some of the cell debris resist digestion and persist as insoluble material in the lysosomes. Lipofuscin granules represent undigested ‘material that results from lipid peroxidation, BP6 19 PBD6 26, 36 21, (B) This histologic picture is typical of apoptosis pro- @uced by chemotherapeutic agents. ‘The release of cyto- chrome from the mitochondria is @ key step in many forms ‘of apoptosis, and it leads to the activation of caspases. bel- 2 is an antiapoptotic protein that prevents cytochrome c release and prevents caspase activation, Lipofuscin is a pigmented residue representing undigested cellular organ- celles in autophagic vacuoles. Catalase is a scavenger of H,O;. Phospholipases are activated during necrosis and ‘cause cell membrane damage, BP6 13-15 PBD6 22-24 22, (D) Metastatic calcification of tissues occurs when there is marked hypercalcemia, and calcium is precipitated within interstitial tissues, particularly the lung, kidney, and stomach. Hypercalcemia can have a variety of causes, in- cluding hyperparathyroidism, bone destruction due to me- tastases, paraneoplastic syndromes, and, less commonly, vi- tamin D intoxication or sarcoidosis. Tuberculosis of ‘the lung results in eascous necrosis and dystrophic calcification in the damaged tissues. Pancreatitis may be the result of hypercalcemia, but the pancreas demonstrates fat necrosis that_ may develop dystrophic calcification. So-called senile calcific aortic stenosis is a form of dystrophic calcification in a person whose serum calcium level is normal. With ‘amyloidosis, there is deposition of the emyloid protein in a variety of tissues, but calcification does. not occur, and hypercalcemia is: not a complication, BP6 20. PBDE 45 23. (D) The high lipid coment of central nervous system (CNS) tissues results in liquefactive necrosis as a conse- quence of ischemic injury, as in this ease of a “stroke.” Fat necrosis is seen in breast and pancreas tissues. Coagulative necrosis is the typical result of ischemia in most solid organs. Apoptosis affects single cells and typically is not grossly. visible. Karyolysis refers to fading away of cell nuclei in dead cells. BP6 12-13 PBD6 16-17 24. (©) This is fatty change (steatosis) of the liver, with id vacuoles seen in many of the hepatocytes. Abnormali- in lipoprotein metabolism can lead to steatosis. Alcohol is a hepatotoxin that produces hepatic steatosis. Decreased serum albumin levels and inereased prothrombin time sug- gest alcohol-induced liver damage. Drug abuse with heroin has surprisingly few organ-specific pathologic findings. Ex- cercise has little direct effect on hepatic function. Smoking directly damages lung tissue but has no direct effect on the liver. Aspirin has a significant effect on platelet function, not on hepatocytes. BP 17-18 PBDS 39-40 < Cra ReccaMM-roMMepCHA: MOCK = pce. PY > Chapter} CEWULAR PATHOLOGY m9 25, (A) This cell is shrunken and converted into a dense coxinophilic mass. The surrounding cells are normal, and there is no inflammatory reaction. This pattern is typical of apoptosis. Caspase activation is a universal feature of apop- tosis, regardless of the initiating cause. Reduced ATP syn- thesis and increased glycolysis occur when a cell is sub- jected to anoxia, These changes are reversible. Lipases are ‘activated in enzymatic fat necrosis. Lipid peroxidation oc- ‘curs when the cell is injured by free radicals BP6 13-14 PBD6 18-20 26. (D) Lipofuscin is 2 “wear and tear” pigment that in- creases with aging, particularly in liver and in myocardium. ‘The pigment has minimal effect on cellular function in ‘most cases. Rarely, there is marked lipofuscin deposition in a small heart, so-called brown atrophy. Melanin pigment is responsible for skin tone: the more melanin, the darker the skin, Hemosiderin és the breakdown product of hemo- globin that contains the iron, Hearts with excessive iron Geposition tend to be large. Glycogen is increased with some inherited enzyme disorders and, when the heart is involved, increases heart size. Bilirubin, another breakdown product of hemoglobin, imparts a yellow appearance (ic- terus) to tissues. BP6 19 PBD6 42 21. (A) Anthracotic pigmentation is common in lung and hilar lymph nodes. ‘This is carbon pigment inhaled from polluted air. The tar in cigarette smoke is a good source of such carbonaceous pigment. Hemorthage can resolve, with formation of hemosiderin. pigmentation that impacts a brown color to tissues. Hepatic failure may result in jaun- dice, with a yellow color. Older persons. generally have more anthracotic pigment, but this is not inevitable with aging — persons living in rural areas will have less. Metas- tases impart a tan to white appearance to tissues. BP6 19° PBDS 42 28. (D) Deposition of calcium in normal healthy tissues from prolonged hypercalcemia is called metastatic calcifica tion. This may occur in hyperparathyroidism. Dystrophic calcification refers to calcium deposition in injured tissues, with normal serum calcium levels. BP6 20 PBD6 45 29, (D) The loss of the nucleus results in cell death. All ther cellular morphologic changes represent reversible cel- lular injury. The plasma membrane and intracellular organ- elles remain functional unless severe damage causes loss of ‘membrane integrity. BP6 11-12 PBD6 8-10 30. (B) Reperfusion injury is clinically important in myo- cardial infarction and stroke. Paradoxically, the oxygen that flows in with blood can be converted to free radicals by parenchymal and endothelial cells and infiltrating leuko- cytes. Catalase is a scavenger of free radicals. All other changes listed occur in sublethal cell injury. BP6 11 PBD6 14-15 31. (B) The deep eosinophilic staining, loss of nuclei, and the loss of cell structure suggest an early ischemic 10m Pont GENERAL PATHOLOGY injury, resulting in coagulative necrosis. This is typically caused by loss of blood flow. Viral infection could cause necrosis of the myocardium, but this is usually accompa nied by an inflammatory infiltrate consisting of lympho cytes and macrophages. Blunt trauma produces hemor- thage. An immunologic injury may produce focal cell injury but not widespread ischemic injury. Lack of protein leads to a catabolic state with gradual decrease in cell size but it does not cause ischemic changes. BP6 6-7 PBD6 7 32, (D) The increase in uterine size is primarily the result Of an increase in myometrial smooth muscle cell size. ‘The endometrium also increases in size, but it remains just a ing «© the muscular wall and does not contribute as ‘< GRAN m Zemane-mompepcnms MYCARA oF QpomE. py > much to the size change. There is litle stroma in myome- trium and a greater proportion in endometrium, but this contributes @ smaller percentage to the size gain than docs muscle. The vessels are a minor but essential component t0 this process. BP6 22 PBDS 33-35 33. (A) Heterophagocytosis by macrophages requires that endocytosed vacuoles fuse with lysosomes to degrade the ‘engulfed material. With congestive failure, extravasation of red blood cells (RBCs) into alveoli occurs, and pulmonary macrophages must phagocytose the RBCs, breaking down the hemoglobin and recycling the iron by hemosiderin for- BP6 15-16 PBD6 25-26 PBD6 Chapter 3 - Acute and Chronic Inflammation 'BP6 Chapter 2 - Acute and Chronic Inflammation 1. The products of the complement system are involved in all of the following steps or phases of the inflammatory response except OLA) Chemotaxis, OB) Increased vascular permeability © (C) Nevtrophil activation OW) Phagocytosis ‘© ©) Killing of bacteria in the phagocytic vacuole 2. After the leukocytes leave the vasculature, their migra- tion in tissues to the site of infection or injury is mediated. by which of the following substances acting as a chemntac- tic Factor? (A) Bradykinin O(B) Chemokines O(©) Histamine O() Prostaglandins © ©) Complement C3a 3. A 53-year-old female has had a high fever with cough productive of yellowish sputum for the past 2 days. Aus- caultation of the chest reveals a few crackles in both lung bases. A chest radiograph reveals bilateral patchy pulmo- nary infiltrates. Which of the following inflammatory cell types will be seen in greatly increased numbers in a spu- tum specimen? OCA) Macrophages OG) Neutrophils OC] Mast cetls OC) Small lymphocytes © €) Langhans giant cells 4, Two weeks after an acute myocardial infarction, the necrotic myocardium has largely been replaced by capil- laries, fibroblasts, and collagen. A variety of inflammatory cells are present.’ Which of the following inflammatory cell types in such a lesion plays an important part in the heal- ing. process? (A) Macrophages ©(B) Plasina cells OO Neutrophils ©) Eosinophils ©) Epithelioid cells 5. Aspirin is often used for its anti-inflammatory effects. Which of the following features of the inflammatory r- sponse is affected by aspirin? OA) Vasodilation OB) Chemotaxis OO Phagocytosis ©(D) Emigration of leukocytes © (E) Release of leukocytes fom the bone marrow 6 A G-ycarold male child presents with a history of recurrent infections with pyogenic bacteria (¢.g.. Staphylo- coccus aureus, Streptococcus penumoniae). After infec- tions, there is an expected increase in the total white blood cell (WBC) count and neutrophilic leukocytosis. However, histologic examination of tissues reveals very few neutro” phils. An analysis of patient's neutrophil function in spe- cially constructed tubes lined with human endothelium shows a defect in rolling. A defect or deficiency affecting Which of the following molecules is likely to be responsi- ble for the increased susceptibility to infection in this pa- tient? OLA) Sclectins QB) Integrins ‘O(C) Leukotriene B, OD) C3b © (E) NADPH oxidase 7. A 32-year-old female has had a chronic cough with fever for the past month. A chest radiograph shows many sinall, ill-defined nodular opacities in all lung fields. A transbronchial biopsy reveals interstitial infiltrates. with lymphocytes, plasma cells, and epithelioid macrophages.

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