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Title[Harsh Mohan] Textbook of Pathology
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LanguageEnglish
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Total Pages949
Table of Contents
                            Front Matter
	Cover
	Foreword
	Preface
Contents
Section I: General Pathology and Basic Techniques
	1. Introduction to Pathology
	2. Techniques for the Study of Pathology
	3. Cell Injury and Cellular Adaptations
	4. Immunopathology Including Amyloidosis
	5. Derangements of Homeostasis and Haemodynamics
	6. Inflammation and Healing
	7. Infectious and Parasitic Diseases
	8. Neoplasia
	9. Environmental and Nutritional Diseases
	10. Genetic and Paediatric Diseases
	11. Basic Diagnostic Cytology
Section II: Haematology and Lymphoreticular Tissues
	12. Introduction to Haematopoietic System and Disorders of Erythroid Series
	13. Disorders of Platelets, Bleeding Disorders and Basic Transfusion Medicine
	14. Disorders of Leucocytes and Lymphoreticular Tissues
Section III: Systemic Pathology
	15. The Blood Vessels and Lymphatics
	16. The Heart
	17. The Respiratory System
	18. The Eye, ENT and Neck
	19. The Oral Cavity and Salivary Glands
	20. The Gastrointestinal Tract
	21. The Liver, Biliary Tract and Exocrine Pancreas
	22. The Kidney and Lower Urinary Tract
	23. The Male Reproductive System and Prostate
	24. The Female Genital Tract
	25. The Breast
	26. The Skin
	27. The Endocrine System
	28. The Musculoskeletal System
	29. Soft Tissue Tumours
	30. The Nervous System
Appendix
Further Readings
Index
                        
Document Text Contents
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by pyogenic bacteria (e.g. staphylococci, streptococci and
pneumococci) and less frequently by fungi and parasites. The
infection may spread to the pericardium by the following
routes:
i) By direct extension from neighbouring inflammation e.g.
in empyema of the pleural cavity, lobar pneumonia, infective
endocarditis and mediastinal infections.
ii) By haematogenous spread.
iii) By lymphatic permeation.
iv) Direct implantation during cardiac surgery.

Generally, fibrinous or serofibrinous pericarditis precedes
the development of purulent pericarditis. The amount of
exudate is variable and is generally thick, creamy pus, coating
the pericardial surfaces.

Microscopically, besides the purulent exudate on the
pericardial surfaces, the serosal layers show dense
infiltration by neutrophils (Fig. 16.34). Purulent exudate
generally does not resolve completely but instead heals
by organisation resulting in adhesive or chronic
constrictive pericarditis.

4. HAEMORRHAGIC PERICARDITIS. Haemorrhagic
pericarditis is the one in which the exudate consists of
admixture of an inflammatory effusion of one of the foregoing
types alongwith blood. The causes are as under:
i) Neoplastic involvement of the pericardium
ii) Haemorrhagic diathesis with effusion
iii) Tuberculosis
iv) Severe acute infections

The outcome of haemorrhagic pericarditis is generally
similar to that of purulent pericarditis.

B. Chronic Pericarditis

Chronic pericarditis is the term used for tuberculous
pericarditis and the healed stage of one of the various forms

of acute pericarditis already described. Included under this
are: tuberculous pericarditis, chronic adhesive pericarditis,
chronic constrictive pericarditis, and the pericardial plaques.

1. TUBERCULOUS PERICARDITIS. Tuberculous peri-
carditis is the most frequent form of granulomatous
inflammation of the pericardium. The lesions may occur by
one of the following mechanisms:

i) Direct extension from an adjacent focus of tuberculosis.

ii) By lymphatic spread e.g. from tracheobronchial lymph
nodes, chronic pulmonary tuberculosis or infected pleura.

The exudate is slightly turbid, caseous or blood-stained
with sufficient fibrin. Tubercles are generally visible on the
pericardial surfaces and sometimes caseous areas are also
visible to the naked eye.

Microscopically, typical tuberculous granulomas with
caseation necrosis are seen in the pericardial wall. The
lesions generally do not resolve but heal by fibrosis and
calcification resulting in chronic constrictive pericarditis.

2. CHRONIC ADHESIVE PERICARDITIS. Chronic
adhesive pericarditis is the stage of organisation and healing
by formation of fibrous adhesions in the pericardium
following preceding fibrinous, suppurative or haemorrhagic
pericarditis. The process begins by formation of granulation
tissue and neovascularisation. Subsequently, fibrous
adhesions develop between the parietal and the visceral
layers of the pericardium and obliterate the pericardial space
(Fig. 16.35,A). Sometimes, fibrous adhesions develop
between the parietal pericardium and the adjacent
mediastinum and is termed as adhesive mediastinopericarditis.
Chronic adhesive pericarditis differs from chronic
constrictive pericarditis in not embarrassing the function of
the heart. However, cardiac hypertrophy and dilatation may
occur in severe cases due to increased workload.

3. CHRONIC CONSTRICTIVE PERICARDITIS. This is
a rare condition characterised by dense fibrous or fibrocalcific
thickening of the pericardium resulting in mechanical
interference with the function of the heart and reduced
cardiac output. The condition usually results from a long-
standing preceding causes, e.g.
i) Tuberculous pericarditis
ii) Purulent pericarditis
iii) Haemopericardium
iv) Concato’s disease (polyserositis)
v) Rarely, acute non-specific and viral pericarditis.

The heart is encased in 0.5 to 1 cm thick and dense
collagenous scar which may be calcified. As a result, the heart
fails to dilate during diastole. The dense fibrocollagenous
tissue may cause narrowing of the openings of the vena
cavae, resulting in obstruction to the venous return to the
right heart and consequent right heart failure. In contrast to
chronic adhesive pericarditis, hypertrophy and dilatation do
not occur due to dense fibrous scarring. Instead, the heart
size is normal or smaller (Fig. 16.35,B).

4. PERICARDIAL PLAQUES (MILK SPOTS, SOLDIERS’
SPOTS). These are opaque, white, shining and well-
circumscribed areas of organisation with fibrosis in the

Figure 16.34 Fibrinopurulent pericarditis. The pericardium is covered
with pink serofibrinous exudates. The space between the layers of the
pericardium contains numerous inflammatory cells, chiefly PMNs.

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pericardium measuring 1 to 3 cm in diameter. They are seen
most frequently on the anterior surface of the right ventricle.
The exact cause is not known but they are generally believed
to arise from healing of preceding pericarditis. The plaque-
like lesions of pericardial thickenings are also termed milk
spots or soldiers’ spots as they were often found at autopsy in
the soldiers in World War I who carried their shoulder bags
causing pressure against the chest wall by the straps which
produced chronic irritation of the pericardium.

TUMOURS OF THE HEART

Tumours of the heart are classified into primary and
secondary, the latter being more common than the former.

PRIMARY TUMOURS

Primary tumours of the heart are quite rare, found in 0.04%
of autopsies. In decreasing order of frequency, the benign
tumours encountered in the heart are: myxoma, lipoma,
fibroelastoma, rhabdomyoma, haemangioma and lymph-
angioma. The malignant tumours are still rarer, the important
ones are: rhabdomyosarcoma, angiosarcoma and malignant
mesothelioma. Out of all these, only myxoma of the heart
requires elaboration.

MYXOMA. This is the most common primary tumour of the
heart comprising about 50% of all primary cardiac tumours.
Majority of them occur in the age range of 30 to 60 years.
Myxomas may be located in any cardiac chamber or the
valves, but 90% of them are situated in the left atrium.

Grossly, they are often single but may be multiple. They
range in size from less than 1 to 10 cm, polypoid, pedun-
culated, spherical, soft and haemorrhagic masses
resembling an organising mural thrombus. Some
investigators actually consider them to be organising
mural thrombi rather than true neoplasms.
Microscopically, the tumour shows the following features:
i) There is abundant myxoid or mucoid intercellular
stroma positive for mucin.
ii) The cellularity is sparse. The tumour cells are generally
stellate-shaped, spindled and polyhedral, scattered in the

Figure 16.35 Appearance of the heart and the pericardium in chronic
adhesive (A) and chronic constrictive pericarditis (B).

stroma. Occasional multinucleate tumour giant cells are
present.
iii) Numerous capillary-sized blood vessels are found and
the tumour cells may be aggregated around them.
iv) A few lymphocytes, plasma cells and macrophages are
seen.
v) Foci of haemorrhage and deposits of haemosiderin
granules are often present.

SECONDARY TUMOURS

Metastatic tumours of the heart are more common than the
primary tumours. About 10% cases with disseminated cancer
have metastases in the heart. Most of these result from
haematogenous or lymphatic spread. In descending order
of frequency, primary sites of origin are: carcinoma of the
lung, breast, malignant lymphoma, leukaemia and malignant
melanoma. Occasionally, there may be direct extension of a
primary intrathoracic tumour such as carcinoma of the lung
into the pericardium and into the cardiac chambers.

PATHOLOGY OF CARDIOVASCULAR
INTERVENTIONS

Nowadays, with the development of surgical and non-
surgical coronary revascularisation procedures in coronary
artery disease, it has been possible to study the pathology of
native as well as grafted vessel. However, these invasive
therapeutic interventions are done in conjunction with life
style changes for modifying the risk factors. Besides, the
myocardial tissue by endomyocardial biopsy is also
accessible for histopathologic study.

ENDOMYOCARDIAL BIOPSY

Currently, it is possible to perform endomyocardial biopsy
(EMB) for making a final histopathologic diagnosis in certain
cardiac diseases. The main indications for EMB are:
myocarditis, cardiac transplant cases, restrictive heart
disease, infiltrative heart diseases such as in amyloidosis,
storage disorders etc.

EMB is done by biopsy forceps introduced via cardiac
catheter into either of the ventricles but preferably right
ventricle is biopsied for its relative ease and safety. The route
for the catheter may be through internal jugular vein or
femoral vein for accessing the right ventricle.

BALLOON ANGIOPLASTY

Balloon angioplasty or percutaneous coronary intervention
(PCI) is a non-surgical procedure that employs percutaneous
insertion and manipulation of a balloon catheter into the
occluded coronary artery. The balloon is inflated to dilate
the stenotic artery which causes endothelial damage, plaque
fracture, medial dissection and haemorrhage in the affected
arterial wall. PCI is accompanied with insertion of coronary
stents in the blocked coronaries with a success rate of
symptoms in over 95% cases. However, case selection for
PCI is important and major indications are 2 or 3 vessel block

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Tophi, 854f
TORCH complex, 190-91
Torsion testis, 706
Torticollis, 521
Toxic granules, in neutrophils, 348
Toxic shock, 109, 110-11
Toxoplasmosis, 191
TP53 gene, 213
Trace elements, 254
Tracheo-oesophageal fistula, 538
Trachoma, 508
Tram-track appearance, 671
Transaminases, 595, 898
Transcellular fluid, 93
Transcobalamin, 253, 303-04
Transcoelomic spread, 202-03, 750
Transferrin, 295
Transfusion, of blood, 339-40

complications of, 339-40
Transient ischaemic attacks (TIA), 879
Transitional cell carcinoma,

nasopharynx, 518-19
urinary bladder, 700-02

Translocations, 199, 259, 353, 355, 356f, 358
reciprocal, 259
Robertsonian, 259

Transplant rejection, 65-66
Transplantation, 65

cardiac, 460
bone marrow, 326, 365, 374

Transposition of great arteries, 425-26
Transthyretin, 83
Transudate versus exudate, 96t
Trauma to brain, 882-83
Trephine, 286-87
Treponema, 161
Trichoepithelioma, 785
Trichomoniasis, 270f
Trigone, 698
Triphenyl tetrazolium chloride (TTC), 432
Triple response, 131f
Trisomy, 258
Tropical pulmonary eosinophilia, 456, 494
Troponins, cardiac, 417, 435
Trouisier’s sign, 557
Trousseau’s syndrome, 232, 410, 503, 648
Truncus arteriosus, persistent, 425
Trypanosomiasis, 453, 538, 580
Tryptophan, 243
Tubercle, 152-53,

evolution of, 152-53, 155, 156
hard and soft, 153

Tubercle bacillus, 149
Tuberculin test, 152
Tuberculoma, brain, 877
Tuberculosis, 149-57

brain, 877
caseous necrosis in, 45, 153, 155, 156
caseous pneumonia in, 156
causative organism in, 149
cavitary, 155-56
clinical features of, 156-57
dystrophic calcification in, 52f
fibrocaseous, 155-56
hypersensitivity and immunity in, 152
incidence of, 151
intestinal, 569-71
kidney, 156, 684
liver, 162, 615-16
lymph node, 45, 154f

meninges, 876
miliary, 162
nose, 517
open, 155
oral cavity, 523
primary, 153-55
pulmonary, 154-56
secondary, 155-56
sinus tracts in, 153
spread of, 151-52
transmission of, 151

Tuberculous meningitis, 876
Tubular necrosis, acute (ATN), 679-80
Tubules,

diseases of, 678-80
structure of, 651-52

Tubulointerstitial disease, 680-85
Tumoral calcinosis, 779
Tumour host interrelationship, 228-32
Tumour markers, 233-34, 709, 720
Tumour necrosis factor (TNF), 25-26, 109,

138-39, 146, 230, 381
Tumours (also see under Neoplasia), 192-235

anaplasia in, 197
angiogenesis in, 199, 215
benign versus malignant, 194
characteristics of, 194-204
classification of, 193t
cytomorphology of, 197-99
diagnosis of, 232-35
differentiation in, 197
epidemiology of, 205-07
etiology and pathogenesis of, 208-28
functional changes in, 198
genetic abnormalities in, 199
grading of, 204
gross features of, 196
growth rate of, 194-96
inflammatory reaction in, 199-200
invasion of, 200-04
metastasis in, 200-04
microscopic features of, 196-200
phenotype of, 196
spread of, 200-04
staging of, 205
stem cells in, 196
stroma of, 199
vascular invasion of, 201-02

Tunicae, arteries, 390
Turban tumour, 786
Turbulence, 116, 133
Turcot’s syndrome, 586
Turk cell, 349
Turner’s syndrome, 258
Typhoid fever, 571-72
Typhoid ulcers, 572f
Tyrosinase, 40

U

Ubiquitin, 26
UICC staging, 205
Ulcer,

amoebic, 187-88
aphthous, 522-23
Curling’s, 113, 550
Cushing’s, 550
peptic, 549-54
rodent, 784-85

stress, 550
Ulcerative colitis, versus Crohn’s disease, 566t
Ultimate carcinogens, 218
Ultraviolet light, 34, 221
Unicameral, bone cyst, 839-40
Union, wounds, 168-69

primary, 168
secondary, 168-69

Urachal abnormalities, 698
Urachal cyst, 698
Uraemia, 655-56
Uraemic manifestations, 655-56
Urate nephrolithiasis, 692
Ureter, normal structure of, 698
Ureterocele, 698
Urethra, normal structure of, 698
Urethral carcinoma, 702
Urethral caruncle, 702
Urethritis, 699-700
Uric acid stones, 692
Urinary bladder, 698-700

normal structure of, 698
tumours of, 700-702

Urinary calculi, 690-92
Urinary cytology, 273, 276
Urinary tract infection (UTI), 681, 682, 698
Urinary tract, lower, 698-702
Urine analysis, 652
Urobilinogen, 593
Urolithiasis, 690-92
Uropathy, obstructive, 690-93
Urothelial tumours, 700-02
Urticaria, 97, 770
Urticaria pigmentosa, 770
Uveal melanoma, 512
Uveitis, 508

V

Vaccines, hepatitis, 614
Vaccinia, 186, 773
Vagina, 723-24

normal structure of, 723
tumours of, 723-24

Vaginal smear, 268-72, 275
Vaginitis, 723

monilial, 270, 723
Valvular deformities, 426, 449-51
Valvulitis, rheumatic, 440-41
van den Bergh diazo reaction, 593
Vanillyl mandellic acid (VMA), 800
Varicella-zoster infection, 186, 773
Varices, 539-40, 631-32
Varicocele, 706
Varicosities, 409
Variola, 186, 773
Vasa recta, 650
Vasa vasora, 390
Vascular purpuras, 331
Vascular permeability, 130-33

alterations of, 131
mechanisms of, 131-33

Vascular tumours, 411-16
Vasculitis, 400-05

allergic, 402-03
hypersensitvity, 402-03, 404
leucocytoclastic, 403f
lymphocytic, 403

Vasoactive amines, 136-37

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Vasopressin, 98, 794
VDRL, 162
Vegetations, distinguishing features of, 447t
Veins, 409-11

normal structure of, 409
varicose, 409

Vena caval syndrome, 410
Venous congestion, 105-06
Ventricular hypertrophy, 55, 421-22
Ventricular septal defect (VSD), 423
Verocay bodies, 893
Verrucae, 224, 440, 771-72
Verrucous carcinoma, 527, 542, 784
Vesalius, 3
Vesico-ureteric reflux, 682
Vessels, 390-416

tumour and tumour-like lesions of, 411-16
Villonodular tenosynovitis, 855
Villous atrophy, 575
Vimentin, 16, 23-24, 861
Vincent’s angina, 517
Viral diseases, 183t
Viral hepatitis, (also see under Hepatitis, viral),

605-14
Viral oncogenesis, 222-28

DNA, 222, 224-26, 224t
RNA, 223-24, 227-28, 227t

Virchow cells, 160
Virchow’s node, 200
Virchow’s sign, 557
Virchow-Robin space, 872
Virchow, Rudolf, 5
Virilism, adrenal, 798
Virtual microscopy, 19
Viruses and human cancer, 228
Viruses, diseases caused by, 183t
Vital reaction, 44
Vital staining, 288
Vitalism, theory of, 3
Vitamins, disorders of, 246-55

A, 247-48
B1, 252-53
B2, 253
B3, 253
B6, 253
B12,
B-complex, 252
B12 metabolism, 303-04
biotin, 253-54
C, 251-52
choline, 254
D, 248-50
E, 250
fat-soluble, 247-51

flavonoids, 254
folate, 253
folate metabolism, 304-05
K, 250-51
niacin, 253
water-soluble, 251-54

Vitellointestinal duct, 561-62
Vitiligo, 40
Vocal nodules, 519-20
Volkman’s ischaemic

contracture, 172
Volvulus, 563
von Gierke’s disease, 261-62
von Hippel-Lindau syndrome, 694, 829
von Kossa stain, 13t, 51
von Recklinghausen’s disease, 206, 893
von Willebrand’s disease, 336
Vulva, 721-24

normal structure of, 721
tumours of, 722-24

W

Waldenstrom’s
macroglobulinaemia, 384

Wallerian degeneration, 172, 892
Walthard cell rests, 738
Warthin’s tumour, 535
Warts, 224, 771-72
Wassermann reaction, 162
Water-soluble vitamins, 251-54
Water, total body, 93

deficiency of (dehydration), 102
excess of (overhydration), 102

Watershed (border zone) infarcts, brain, 880
Watson, Crick, 6
Wax-D, 152
Wear and tear pigment, 43
Webs, oesophageal, 539
Wegener’s granulomatosis, 403, 495, 517

limited form, 402
Weights and measurements,

normal organs, 896-97
Wermer’s syndrome, 829
Wernicke’s encephalopathy, 252
Wet-fixed versus air-dried smear, 280t
Wheal, 131
Whipple’s disease, 576
White blood cells, diseases of, 342-86
White lesions, 525-26, 714, 721-22
Whooping cough, 178
Wilms’ tumour, 696-98
Wilson’s disease, 628

Wilmut, Ian, 7
Wintrobe, MM, 6
Wolffian cyst, 723
Working formulation for clinical usage, 366
Wound,

complications of, 169-70
contraction of, 167
healing of, 167-73
strength, 170

Woven bone callus, 830
Wry neck, 521
Wuchereria bancrofti, 97, 190

X

X-chromosome, 23, 257
X-linked disorders, 260t
X-ray crystallography, 82
Xanthelasma, 39
Xanthine stones, 692
Xanthofibroma, 855
Xanthogranuloma, 864
Xanthogranulomatous pyelonephritis, 683
Xanthomas, 39, 626
Xenograft, 65
Xeroderma pigmentosum, 215, 770, 783
Xerophthalmia, 247
Xerostomia, 81, 533

Y

Y-chromatin, 257, 275
Yellow atrophy, acute, 613
Yellow fever, 183-84
Yolk sac tumour,

ovary, 748
testis, 711

Z

Zahn, infarct of, 129
lines of, 117

Zarda, 237
Zeiss glands, 508
Zenker’s degeneration, 35
Zenker’s fluid, 371
Ziehl-Neelsen staining, 149, 157
Zollinger-Ellison syndrome, 545, 829
Zonal necrosis, liver, 604-05
Zones, hepatic lobules, 592f
Zonula adherens, 25
Zonula occludens, 24-25
Zoster virus infection, 186, 773

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