1. Cell Injury

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Figure 1-1 Ventilation (V)-perfusion (Q) defects. A, Schematic showing normal ventilation and perfusion; B, schematic showing ventilation defect; C, schematic of perfusion defect. See text for discussion. PvCO2, partial pressure of carbon dioxide in mixed venous blood; PvO2, partial pressure of oxygen in mixed venous blood. (From Goljan EF, Sloka KI: Rapid Review Laboratory Testing in Clinical Medicine. Philadelphia, Mosby Elsevier, 2008, p 76, Fig. 3-5.) Downloaded from: StudentConsult (on 21 March 2012 08:55 PM) © 2005 Elsevier

Transcript of 1. Cell Injury

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Figure 1-1 Ventilation (V)-perfusion (Q) defects. A, Schematic showing normal ventilation and perfusion; B, schematic showing ventilation defect; C, schematic of perfusion defect. See text for discussion. PvCO2, partial pressure of carbon dioxide in mixed venous blood; PvO2, partial pressure of oxygen in mixed venous blood.

(From Goljan EF, Sloka KI: Rapid Review Laboratory Testing in Clinical Medicine. Philadelphia, Mosby Elsevier, 2008, p 76, Fig. 3-5.)

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Figure 1-2 Oxygen-binding curve (OBC). Note that at the Po2 in the tissue (ranges from 20 to 50 mm Hg) a left-shifted OBC still has an O2 saturation (Sao2) of 80% (only released 20% of its O2 to tissue), a normal-shifted OBC has an Sao2 of 50% (only released 50% of its O2 to tissue), and a right-shifted curve has an Sao2 of 20%

(released 80% of its O2 to tissue). 2,3-Bisphosphoglycerate (BPG) improves O2 delivery to tissue by stabilizing the hemoglobin (Hb) in the taut form, which decreases O2 affinity, hence facilitating the movement of O2 from Hb into tissue by diffusion.

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Figure 1-3 Oxidative phosphorylation. See text for discussion. (From Pelley J, Goljan E: Rapid Review Biochemistry, 2nd ed. St. Louis, Mosby, 2007, p 81, Fig. 5-8.)

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Figure 1-4 Watershed infarction showing a wedge-shaped hemorrhagic infarction at the junction of the anterior and middle cerebral arteries. (From Damjanov I, Linder J: Anderson's Pathology, 10th ed. St. Louis, Mosby, 1996, p 375, Fig. 17-16.)

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Figure 1-5 Hyperplasia of smooth endoplasmic reticulum (2) and damaged mitochondria (megamitochondria, 1) in alcoholic liver disease. (From MacSween R, Burt A, Portmann B, et al: Pathology of the Liver, 4th ed. London, Churchill Livingstone, 2002, p 288, Fig. 6-20.)

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Figure 1-6 Chédiak-Higashi neutrophil (arrow) and lymphocytes with giant granules. See text for discussion. (From McPherson R, Pincus M: Henry's Clinical Diagnosis and Management by Laboratory Methods, 21st ed. Philadelphia, WB Saunders, 2007, p 551, Fig. 32-7.)

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Figure 1-7 Mallory bodies. Hyaline (eosinophilic) inclusions (arrow) are present in the cytosol of hepatocytes. Many of the hepatocytes have vacuoles containing triglyceride. (From Kumar V, Fausto N, Abbas A: Robbins and Cotran's Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, p 34, Fig. 1-34A.)

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Figure 1-8 Fatty change of the liver. Vacuoles containing triglyceride are noted in most of the hepatocytes. The nucleus is displaced to the periphery. (From Kumar V, Fausto N, Abbas A: Robbins and Cotran's Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, p 36, Fig. 1-36B.)

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Figure 1-9 Radiograph showing multiple dystrophic calcifications in the pancreas in a patient with chronic pancreatitis. (From Katz D, Math K, Groskin S: Radiology Secrets. Philadelphia, Hanley & Belfus, 1998, p 155, Fig. 4.)

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Figure 1-10 A, Atrophy of the brain. Note the narrow gyri and widened sulci. The meninges have been stripped from the right half of the brain. B, Pancreas in a patient with cystic fibrosis showing dilated ducts filled with thickened eosinophilic material. The ducts are surrounded with fibrous tissue. C, Left ventricular hypertrophy, showing the thickened free left ventricular wall (right side) and the thickened interventricular septum. The right ventricle wall (left side) is of normal thickness. D, Benign prostatic hyperplasia. The prostatic glands show infolding into the glandular spaces. E, Barrett's esophagus showing an extensive area of glandular metaplasia with numerous goblet cells. A small section of squamous epithelium remains on the right. F, Section of bronchus from a smoker showing focal squamous metaplasia (long arrow).

Normal ciliated, pseudostratified columnar epithelium is present on the right (short arrow). G, Squamous dysplasia of the cervix, a precursor of squamous cell carcinoma. There is a lack of orientation of the squamous cells throughout the upper two thirds of the epithelium. Many of the nuclei are enlarged (arrows), are hyperchromatic, and

have irregular nuclear margins. (A from Kumar V, Abbas A, Fausto N, Mitchell, R: Robbins Basic Pathology, 8th ed. Philadelphia, WB Saunders, 2007, p 5, Fig. 1-4; B, D, and E from Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, pp 169, 249, 111, Figs. 9-6, 12-32, 6-26, respectively; C and G from Kumar V, Fausto N, Abbas A: Robbins and Cotran's Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, pp 561, 1075, Figs. 12-3A; 22-19C, respectively; F from Corrin

B: Pathology of the Lungs. London, Churchill Livingstone, 2000, p 460, Fig. 13.1.1.)Downloaded from: StudentConsult (on 21 March 2012 08:55 PM)

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Figure 1-11 A, Acute myocardial infarction (MI) showing coagulation necrosis. This section of myocardial tissue is from a 3-day-old acute MI. The outlines of the myocardial fibers are intact; however, they lack nuclei and cross-striations. A neutrophilic infiltrate is present between some of the dead fibers. B, Acute MI showing a

pale infarction of the posterior wall of the left ventricle (bottom left). C, Hemorrhagic infarction of lung. There is a roughly wedge-shaped area of hemorrhage extending to the pleural surface. The arrow shows an embolus in one of the pulmonary artery tributaries. D, Dry gangrene involves the first four toes. The dark black areas of

gangrene are bordered by light-colored, parchment-like skin. E, Cerebral infarction showing liquefactive necrosis of the cerebral cortex leaving a large cystic cavity. F, Wet gangrene of the leg. Note the pus at the closing edges of the below-the-knee amputation site. G, Caseous granuloma showing a central area of acellular, necrotic

material (asterisk) surrounded by activated macrophages (epithelioid cells), lymphocytes, and multiple multinucleated Langhans-type giant cells. H, Enzymatic fat necrosis in acute pancreatitis. Dark areas of hemorrhage are present in the head of the pancreas (left side), and focal areas of pale fat necrosis (arrow) are present in the peripancreatic fat. (A from Damjanov I, Linder J: Pathology: A Color Atlas. St. Louis, Mosby, 2000, 375, Fig. 17-15; B from Damjanov I, Linder J: Anderson's Pathology,

10th ed. St. Louis, Mosby, 1996, p 374, Fig. 17-13; C, E, G, and H from Kumar V, Fausto N, Abbas A: Robbins and Cotran's Pathologic Basis of Disease, 7th ed. Philadelphia, WB Saunders, 2004, pp 138, 1365, 83, 943, Figs. 4-19A, 28-16, 2-33, 19-5, respectively; D from Damjanov I: Pathology for the Health-Related Professions,

2nd ed. Philadelphia, WB Saunders, 2000, p 18, Fig. 1-24; F from Grieg JD: Color Atlas of Surgical Diagnosis. London, Mosby-Wolfe, 1996, p 6, Fig. 2-2.)Downloaded from: StudentConsult (on 21 March 2012 08:55 PM)

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Figure 1-12 Apoptosis in viral hepatitis. The arrow shows a shrunken eosinophilic staining cell with pyknotic nucleus within a clear space. (From Damjanov I: Pathophysiology. Philadelphia, Saunders Elsevier, 2009, p 301, Fig. 8.22.)

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