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Download textbook Concise Pathology For Exam Preparation 3Rd Edition Geetika Khanna Bhattacharya ebook all chapter pdf
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Concise Pathology
For Exam Preparation
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RELX India Pvt. Ltd.
Registered Office: 818, 8th Floor, Indraprakash Building, 21, Barakhamba Road, New Delhi 110 001
Corporate Office: 14th Floor, Building No. 10B, DLF Cyber City, Phase II, Gurgaon-122 002, Haryana, India
Concise Pathology For Exam Preparation, 3rd Edition, Geetika Khanna Bhattacharya
Copyright © 2016, 2011, 2009 by RELX India Pvt. Ltd.
All rights reserved.
ISBN: 978-81-312-4421-0
eISBN: 978-81-312-4422-7
No part of this publication may be reproduced or transmitted in any form or by any means, electronic or me-
chanical, including photocopying, recording, or any information storage and retrieval system, without permis-
sion in writing from the publisher. Details on how to seek permission, further information about the Publisher’s
permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the
Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.
This book and the individual contributions contained in it are protected under copyright by the Publisher (other
than as may be noted herein).
Notice
Knowledge and best practice in this field are constantly changing. As new research and experience broaden our
understanding, changes in research methods, professional practices, or medical treatment may become necessary.
Practitioners and researchers must always rely on their own experience and knowledge in evaluating and
using any information, methods, compounds, or experiments described herein. In using such information or
methods they should be mindful of their own safety and the safety of others, including parties for whom they
have a professional responsibility.
With respect to any drug or pharmaceutical products identified, readers are advised to check the most
current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be
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to take all appropriate safety precautions.
To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors, assume any
liability for any injury and/or damage to persons or property as a matter of product liability, negligence
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Please consult full prescribing information before issuing prescription for any product mentioned in this
publication.
Typeset by GW India
Printed in India by
Dedicated to Shriya and Elaina
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Preface to the Third Edition
Evaluation, a critical and human-error prone component of the medical curriculum, contin
ues to evoke dread in students due to its sometimes “unpredictable” outcome. This book
was originally conceived for the students of Pathology, who are naturally apprehensive
about this “unpredictability”. The enthusiastic response to the previous editions, sugges-
tions received from the student community and the newer learning points now incorpo-
rated in standard textbooks, have all necessitated this Edition.
Special effort has been made to include all the latest concepts and changes in the subject
including clinical information, wherever feasible, in the chapters to accentuate the
relevance of each section to actual patient situations. The text has been presented in a
tabulated format, wherever required, to enable easy learning and recall. Definitions and
classifications have been incorporated as per World Health Organization and other stan-
dard currently accepted guidelines. Many new illustrations and flowcharts have been
added to make the book more student-friendly, particularly to the “visual learner”. Micro-
photographs and gross pictures have been introduced in all the chapters to enhance com-
prehension of the subject. At the same time, every effort has been made to restrict the
increase in page extent so that students are not overloaded with information.
In addition, complimentary access to online assessment questions and images along
with complete e-book is also provided.
The main objectives of this book remain the same:
• To allow a quick self-assessment and revision before the examination.
• To highlight the “must know” areas (the areas covered in this book are the ones that are
frequently referred to/stressed upon by examiners, and are also relevant to the student
from knowledge point of view. Proficiency in these topics will aid students’ in under-
standing their clinical subjects in the coming years).
• To enable students to learn and present their knowledge in a format that is easy to
appreciate and assess during an examination.
I am certain that this edition is more useful and convenient compared to earlier ones
and will find greater acceptability among the undergraduate pathology students.
I would be grateful for any criticism or suggestions which would make this book better
in any way. Suggestions and comments from teachers and students can be e-mailed at
gtka0612@gmail.com or indiacontact@elsevier.com.
vii
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Preface to the First Edition
As an examiner and teacher, one often encounters students who have read extensively
and have grasped the basic concepts of pathology from their textbooks, but are unable to
organize or prioritize this succinctly into the type of answers the examiners expect and
appreciate, thus, preventing them from achieving good results/scores in their assessments.
The need for a revision or reference manual, which enables students to understand the
nuances of key principles of pathology and express them efficiently in the limited time that
is usually available to them, thus became obvious.
This book has been written with the following objectives:
• To allow a quick self-assessment and revision before the examination.
• To highlight the areas that need focus (must know areas) and are relevant to the student
from both knowledge and examination point of view. (The areas covered in this book
are the ones that are frequently referred to/stressed upon by examiners. Also, proficiency
in these topics will aid the students in understanding their clinical subjects in the com-
ing years.)
• To enable students to learn and present their knowledge in a format that is easy to ap-
preciate and assess, in the limited time available, during an examination. This book has
been primarily written for the discerning undergraduate (MBBS, BDS, and Nursing);
however, some topics are covered more extensively, and may benefit the postgraduate
as well. I welcome any criticism and suggestions that would contribute towards
enhancement of this book.
ix
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Acknowledgements
I am both delighted and humbled by the most enthusiastic reception of the first and
second editions of this book and am immensely grateful to my students for all their valu-
able insights and suggestions, which I have tried to incorporate in this edition. Their
overwhelming response keeps me going and makes the entire effort worthwhile.
I would not have been able to complete this all encompassing project without the
tremendous patience and endurance of my daughter, the valued support and guidance of
my husband, the blessings of my parents, and the constant encouragement and motivation
of my brother.
I would like to offer my sincere appreciation to my friends, particularly Dr Sonal
Sharma, who has always very generously helped me whenever required. I am also grateful
to my departmental staff for their unquestioning support and cooperation.
I am extremely thankful to my publisher, RELX India Pvt. Ltd., particularly Shabina
Nasim, Sr Manager–Education Solutions; and Goldy Bhatnagar, Sr Content Development
Specialist, for overseeing this project with great commitment and efficiency while conced-
ing to my requests for changes and amendments till the last minute. It has been an abso-
lute pleasure working with them.
Last but not the least I continue to be indebted to the authors of the various publica-
tions and reference books that I have consulted during the compilation of this book and
regret being unable to acknowledge them all, individually.
xi
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Contents
SECTION I
General Pathology 1
1 Cell Injury and Cell Death 2
2 Acute and Chronic Inflammation 31
3 Healing and Repair 53
4 Haemodynamic Disorders, Thrombosis and Shock 67
5 Diseases of Immunity 89
6 Neoplasia 123
7 Infections 150
8 Genetic and Paediatric Disorders 189
9 Environmental and Nutritional Pathology 211
SECTION II
Diseases of Organ Systems 227
10 Blood Vessels 228
11 Disorders of the Heart 254
12 Haematology 285
13 The Lung 356
14 The Oral Cavity and Gastrointestinal Tract 384
15 Diseases of the Hepatobiliary System and Pancreas 420
16 Diseases of the Kidney and Lower Urinary Tract 453
17 Male Genital Tract 489
18 Female Genital System 502
19 The Breast 522
xiii
xiv Contents
20 Endocrinology 534
21 Musculoskeletal System 569
22 The Skin 603
23 The Central Nervous System 613
Index 625
Cell in homeostasis
Cellular adaptation
FLOWCHART 1.2. Cellular adaptation.
Intracellular
accumulations
4. Cell ageing: Represents progressive accumulation over the years of sublethal injury
that manifests with either cell death or inadequate response of the cell to injury. Ageing
is influenced by genetic factors, diet and social environment as well as diseases like
atherosclerosis, diabetes and osteoarthritis.
Hyperplasia
Definition
Increase in number of cells in an organ or tissue leading to increased size/mass of the tissue
or organ. Hyperplasia takes place in cells, which are capable of synthesizing DNA. In nondivid-
ing cells, only hypertrophy occurs.
Mechanism
• Production of transcription factors that induce genes encoding growth factors, receptors
for growth factors and cell-cycle regulators.
• In hormonal hyperplasia, hormones themselves act as growth factors and trigger tran-
scription of genes.
• In compensatory hyperplasia, there is proliferation of remaining cells and development of
new cells from stem cells.
Types
1. Physiologic hyperplasia:
(a) Hormonal hyperplasia: Hormonal stimulation increases the functional capacity of
the tissue when needed, eg, breast and uterus in puberty, pregnancy and lactation.
(b) Compensatory hyperplasia: Increase in tissue mass after damage or partial resection,
eg, regeneration of liver after partial hepatectomy.
2. Pathologic hyperplasia: Hyperplasia due to excessive hormonal stimulation or excessive
effects of growth factors on target cells, eg, endometrial hyperplasia (occurs when bal-
ance between progesterone and oestrogen is disturbed) and benign nodular prostatic
hyperplasia or NHP (occurs due to androgen excess; Fig. 1.2).
Hypertrophy
Definition
Increase in size of the cell due to increased synthesis of structural components and not due
to cellular swelling is known as hypertrophy. Nondividing cells, eg, myocardial fibres,
undergo hypertrophy only. Dividing cells (stable cells, quiescent cells) undergo both
hyperplasia and hypertrophy.
Papillary
projection
Stroma
Proliferating
glands
FIGURE 1.2. NHP prostate showing hyperplastic glands lying back to back. The glands are lined
by two distinct layers of epithelium indicating benign nature of the lesion (H&E; 1003).
6 SECTION I General Pathology
Mechanism
Induction of genes stimulates synthesis of cellular proteins, eg, genes encoding transcrip-
tion factors, growth factors and vasoactive agents. In the heart, increased workload (me-
chanical stretch), growth factors (transforming growth factor-beta and Insulin-like growth
factor-1) and a-adrenergic hormones activate signal transduction pathways (phos-
phoinositide-3-kinase/AKT pathway and downstream signalling of G-protein coupled
receptors), which in turn activate transcription factors like GATA4 (critical transcription
factor for proper mammalian cardiac development and essential for survival of the em-
bryo), NFAT (nuclear factor of activated T cells) and MEF 2 (myocyte enhancer 2). They
work together to increase synthesis of proteins responsible for cardiac hypertrophy.
Types
1. Physiological hypertrophy: This occurs due to increased functional demand and stimula-
tion by growth factors and hormones, eg, uterine enlargement in pregnancy and breast
hypertrophy during lactation.
2. Pathological hypertrophy:
(a) Hypertrophy of cardiac muscle in systemic hypertension and aortic valve stenosis
(chronic haemodynamic overload) leading to left ventricular hypertrophy (Fig. 1.3).
(b) Compensatory hypertrophy, which occurs when an organ or tissue is called upon to
do additional work or to perform the work of destroyed tissue or of a paired organ.
Atrophy
Definition
A decrease in size of a body organ, tissue or cell along with decreased function, owing to
disease, injury or lack of use.
Mechanism
Atrophy is the result of decreased protein synthesis or increased protein degradation.
Protein degradation is mediated by
• Lysosomal acid hydrolases, which degrade endocytosed proteins (taken up from
extracellular environment, cell surface as well as some cellular components).
• Ubiquitin-proteasome pathway, which causes degradation of many cytosolic and nuclear
proteins.
Left Hypertrophy
ventricle
Right
ventricle
FIGURE 1.4. Atrophic testis showing marked loss of germ cells within the tubules, with peri-
tubular and interstitial fibrosis and proliferation of interstitial cells of Leydig (H&E; 1003).
Types
1. Physiological atrophy: Common during early development, eg, atrophy of notochord or
thyroglossal duct during fetal development and uterus after parturition.
2. Pathological atrophy:
(a) Decreased workload due to immobilization and prolonged functional inactivity
leads to disuse atrophy.
(b) In denervation atrophy, there is loss of innervation of muscle which induces its
wasting, as in polio and motor neuron disease.
(c) Atherosclerosis can cause ischaemic atrophy.
(d) Nutritional deficiency, eg, marasmus and cancer cachexia are associated with the
use of skeletal muscle as a source of energy and lead to nutritional atrophy.
(e) Loss of endocrine stimulation after menopause induces atrophy of reproductive
organs.
(f) Senile atrophy is an ageing-associated cell loss which is typically seen in tissues
containing permanent cells, eg, brain and heart or testes (Fig. 1.4).
Metaplasia
Definition
Reversible change in which there is replacement of one adult/differentiated cell type (epi-
thelial or mesenchymal) by another adult/differentiated cell type.
Mechanism
Occurs owing to altered/aberrant differentiation of stem cells due to their reprogramming.
Examples
• Columnar to squamous metaplasia in respiratory tract, in response to chronic irritation
(cigarette smoking) and vitamin-A deficiency. Stones in excretory ducts of salivary
glands, pancreas and gall bladder may also result in squamous metaplasia. Squamous
metaplasia in cervix is usually associated with chronic infection (Fig. 1.5).
• Connective tissue metaplasia (formation of cartilage, bone or adipose tissue in tissues
that normally do not contain these elements), eg, bone formation in muscle (myositis
ossificans), which occurs after bone fracture.
Note: The factors that predispose to metaplasia, if persistent, may eventually lead to induc-
tion of cancer in metaplastic epithelium, eg, metaplasia from squamous to columnar
epithelium in Barrett’s oesophagus may progress to adenocarcinoma oesophagus.
8 SECTION I General Pathology
Squamous
metaplastic
lining
Endocervical
glands
FIGURE 1.5. Section from cervix showing squamous metaplasia of the endocervical mucosa
(H&E; 1003).
Q. Define dysplasia.
Ans. Dysplasia indicates disordered cellular development characterized by
• Loss of orientation of cells with respect to one another, eg, disorderly arrangement of
the cells from basal to surface layer as in stratified squamous epithelium (architectural
disorientation).
• Lack of uniformity of individual cells (cellular pleomorphism).
• Causes of dysplasia include diverse cellular insults, including physical, chemical and
biological.
• It is typically seen in epithelial cells and may be reversible (at least in its early stage).
More severe dysplasia is known to progress to carcinoma in situ and invasive carcinoma.
• Dysplastic cells are characterized by the following cellular features:
• Accelerated cell proliferation (increased mitoses);
• Nuclear abnormalities such as hyperchromasia (increased basophilia on staining with
haematoxylin) and pleomorphism (altered nuclear size and nuclear shape; Fig. 1.6);
• Increased nuclear-cytoplasmic ratio.
Intact basement
membrane
Stroma
FIGURE 1.6. Stratified squamous epithelium showing severe dysplastic changes (diffuse
atypia and loss of maturation) (H&E; 2003).
1 Cell Injury and Cell Death 9
Ischaemia
Decreased ATP
The morphological features of necrosis vary with its type. Changes common to most
types include
1. Cytoplasmic changes
• Increased eosinophilia of the cytoplasm, which is due to
• loss of normal cytoplasmic basophilia caused by the loss of RNA and
• denaturation of cytoplasmic proteins which then bind strongly to the dye eosin:
• Glassy homogenous cytoplasm due to loss of glycogen.
• Swelling and vacuolation of the cytoplasm (occurs after enzymatic digestion has
started).
• Cellular and organelle swelling may eventually lead to discontinuities in cell and
organelle membranes and ultimately rupture.
• Formation of myelin figures (phospholipid masses derived from damaged cell
membranes).
2. Nuclear changes
The changes in nucleus appear in one of the following three patterns:
• Nuclear shrinkage and increased basophilia (pyknosis)
• Nuclear fragmentation (karyorrhexis)
• Loss or fading of basophilia due to DNase activity (karyolysis)
Morphological patterns of necrosis include
1. Coagulative necrosis
• It is the most common pattern of necrosis and is caused by ischaemic injury resulting
in hypoxic death of cells in all tissues except the brain.
• There is preservation of the basic architectural outlines and type of tissue can be
recognized but cellular details are lost.
1 Cell Injury and Cell Death 13
Viable cardiac
myocytes
Infarcted
myocardium
FIGURE 1.7. Infarcted myocardium surrounded by viable cardiac myocytes (H&E; 1003).
• Cell injury leads to increasing intracellular acidosis, which denatures not only struc-
tural proteins but also enzymatic proteins, and so blocks the proteolysis of the cell,
thereby preventing loss of architecture of the tissue.
• On gross examination, the affected tissue is pale in colour and firm in texture.
• Microscopically, increased eosinophilia of the cytoplasm and decreased basophilia of
the nucleus are observed. Myocardial infarction is an excellent example in which
acidophilic, coagulated anucleate cells are seen (Fig. 1.7).
Mechanism of evolution of coagulative necrosis is shown in Flowchart 1.7.
Decreased pH
Full thickness
liquefactive
necrosis of the
bowel
Disintegrating
neutrophils/debris
3. Gangrenous necrosis
This is a clinical term, not a specific pattern of necrosis. It is usually used in context
of the lower limbs, which have lost their blood supply and have undergone necrosis,
initially coagulative (dry gangrene), and later liquefactive due to secondary bacterial
infection and immigrating leukocytes (wet gangrene) (Table 1.6).
Mechanism of evolution of gangrenous necrosis is shown in Flowchart 1.9.
4. Caseous necrosis
• This type of necrosis is typically associated with tuberculous infection.
• On gross examination, the necrotic areas appear cheesy white (caseous). Micro-
scopically, the debris appears amorphous, eosinophilic and granular (Fig. 1.9), and
is surrounded by a distinct inflammatory reaction called granulomatous reaction.
• Tissue architecture is completely obliterated unlike coagulative necrosis (Table 1.5).
Dystrophic calcification may be seen.
5. Enzymatic fat necrosis
• It refers to a focal area of fat destruction that converts adipocytes to necrotic cells
with shadowy outlines and basophilic calcium deposits, surrounded by an inflam-
matory reaction (Fig. 1.10).
• It is typically seen in acute pancreatitis and traumatic fat necrosis of breast.
Mechanism of evolution of enzymatic fat necrosis in acute pancreatitis is shown in Flowchart 1.10.
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carelessly discovered a resemblance between the said starved poet and your
humble servant, the consequence of which was that your humble servant
bought up, at no inconsiderable expense, all the copies of the said print, and
committed them to the flames. And now, if I were to see my own features
prefixed to my own writings; if I were to imagine to myself your curiosity,
my public, criticizing expression of countenance as well as expression of
thought, and lines of face as well as lines of metre, I could not endure it—I
should faint! Yes, I should positively faint.
I have another reason; another very momentous one. I once heard a lady
criticizing the “Lines to——.” How beautiful were the criticisms; and how
beautiful was the critic! I would have given the riches of Mexico for such a
review, and such a reviewer. But to proceed with my story—thus were the
remarks wound up:—“Now do, Mr. Courtenay, tell me who is the author?
What an interesting looking man he must be!”
From that moment I have been enwrapt in most delightful day-dreams. I
have constantly said to myself, “Peregrine, perhaps at this moment bright
eyes are looking on your effusion; and sweet voices are saying, ‘What a
pretty young man Mr. Courtenay must be!’” And shall I publish my picture,
and give them the lie? Oh, no! I will preserve to them the charity of their
conjectures, and to myself the comfort of their opinion.
And now what rests for me but to express my gratitude to all who have
assisted me by their advice or their support, and to beg, that if, in
discharging my part to the best of my abilities, it has been my misfortune to
give offence to any one of them, he will believe that I sinned not
intentionally, and forgive me as well as he can.
I have also to return thanks to many gentlemen who have honoured me
by marks of individual kindness. It would be painful for me to leave this
spot without assuring them, that in all places, and under all circumstances, I
shall have a lively recollection of the attention they have shown me, and the
interest they have expressed in my success.
But most of all, I have to speak my feelings to him who, at my earnest
solicitations, undertook to bear an equal portion of my fatigues and my
responsibility—to him who has performed so diligently the labours which
he entered upon so reluctantly—to him who has been the constant
companion of my hopes and fears, my good and ill fortune—to him who, by
the assiduity of his own attention, and the genius of the contributors whose
good offices he secured, has ensured the success of the Etonian.
I began this letter in a light and jesting vein, but I find that I cannot keep
it up. My departure from Eton and the Etonian is really too serious a
business for a jest or a gibe. I have felt my spirits sinking by little and little,
until I have become downright melancholy. I shall make haste, therefore, to
come to a conclusion. I have done, and I subscribe myself (for the last
time),
My dear Public,
Your obliged and devoted servant,
Peregrine Courtenay.
ABDICATION OF THE KING OF CLUBS.
We, Peregrine, by Our own choice, and the public favour, King of Clubs,
and editor of the Etonian, in the ninth month of Our reign, being this day in
possession of Our full and unimpaired faculties both of mind and body, do,
by these presents, address Ourselves to all Our loving subjects, whether
holding place and profit under Us, or not.
Inasmuch as We are sensible that We must shortly be removed from this
state of trial, and translated to another life, leaving behind Us all the
trappings of royalty, all the duties of government, all the concerns of this
condition of being, it does seem good to Us, before We are withdrawn from
the eyes of Our dearly beloved friends and subjects, to abdicate and divest
Ourselves of all the ensigns of power and authority which We have hitherto
borne; and We do hereby willingly abdicate and divest Ourselves of the
same.
And be it, by all whom it may concern, remembered, that the cares and
labours of Peregrine, sometime King of Clubs, are henceforth directed to
another world; and that if any one shall assume the sceptre and the style of
Peregrine, the first King of Clubs, such person is a liar and usurper.
Howbeit, If it shall please Our trusty subjects and counsellors to set upon
Our Throne a rightful and legitimate successor, We will that the allegiance
of Our people be transferred to him; and that he be accounted supreme over
serious and comic, verse and prose; and that the treasury of Our Kingdom,
with all that it shall at such time contain, song, and sonnet, and epigram,
and epic, and descriptions, and nondescripts, shall be made over forthwith
to his charge and keeping.
And for all acts, and writings, made and done during the period of Our
reign, to wit, from the twentieth day of October, anno Domini eighteen
hundred and twenty, to the twenty-eighth day of July, eighteen hundred and
twenty-one, inclusive, we commit them to the memory of men, for the
entertainment of our friends and the instruction of posterity.
Further, If any one shall take upon himself the office of commenting
upon any of the deeds and transactions which have taken place under Our
administration, whether such comment shall go forth in plain drab or in
gaudier saffron and blue, We recommend to such person charity and
forbearance, and in their spirit let him say forth his say.
And be it hereby known, that for all that has been said or done against
Us, during the above-mentioned period, whether by open hostility or secret
dislike, We do this day publish a general and hearty Amnesty: And We will
that all such offences be from henceforth committed to oblivion, and that no
person shall presume to recall to Our recollection such sins and treasons.
And We also entreat that if, in the course of a long and arduous
administration, it has been Our lot to inflict wounds in self-defence, or to
wound, unknowingly, those who were unconnected with Us, the forgiveness
which We extend to others will be extended by others to Us.
And We do, from this day, release from all bond, duty, and obligation
those who have assisted Us by their counsel and support; leaving it to all
such persons to transfer their services to any other master, as seemeth to
them best.
We decree that Our punchbowl be henceforth consecrated to Our lonely
hours and our pleasant recollections; that no one do henceforth apply his
lips to its margin; and that all future potentates in this state of Eton do
submit to assemble their privy council around a coffee-pot or an urn.
And We most earnestly recommend to those dear friends, whom We
must perforce leave behind Us, that in all places and conditions they
continue to perform their duties in a worshipful manner, always
endeavouring to be a credit to the Prince whom they have so long honoured
by their service.
And now, as Our predecessor, Charles of Germany, in the meridian of his
glory, laid down the reins of empire, exchanging the court for the cloister,
and the crown for the cowl—even so do We, Peregrine of Clubs, lay down
the pen and the paper, exchanging celebrity for obscurity, punch for algebra,
the printing-office for Trinity College. And We entreat all those who have
Our welfare at heart to remember Us sometimes in their orisons. And so We
depart.
Peregrine.
Given in our Club-room, this twenty-eighth
day of July, A.D. 1821.
THE UNION CLUB.
A.D. 1823.
Public debts,
Epithets,
Foul and filthy, good and great,
Glorious wars,
British tars,
Beat and bruise
Parlez-vous,
Frenzy, frown,
Commons, Crown,
Ass and pannier,
Rule Britannia!—
How I love a loud debate!”
Then the Church shakes her rattle, and sends forth to battle
The terror of Papist and sinner,
Who loves to be seen as the modern Mæcenas,
And asks all the poets to dinner.
Indian Stories,
Damn the Tories,
None but he can rule the State,
Wise magicians,
Politicians,
Foreign lands,
Kings and wands,
Fiends and fairies,
Dromedaries,
Laugh at Boodle’s,
Cock-a-doodles—
How I love a loud debate!”
Then up gets a youth with a visage of truth,
An omen of good to our islands,
Who promises health and abundance of wealth
To our Oatlands, and Wheatlands, and Ryelands.
And the honourable gentleman, after making the grand tour in a hand
canter, touching cursorily upon Rome, Constantinople, Amsterdam,
Philadelphia, and the Red Sea; with two quotations, two or three hundred
similes, and two or three hundred thousand metaphors, proceeds to the tune
of
[14]“We, Mr. President, have indeed awful examples to direct us or deter.
Have we not seen the arms of the mighty overpowered, and the counsels of
the wise confounded? Have not the swords of licentious conquest, and the
fasces of perverted law, covered Europe with blood, and tears, and
mourning? Have not priests and princes and nobles been driven in beggary
and exile to implore the protection of rival thrones and hostile altars?
Where is the sacred magnificence of Rome? Where the wealth and
independence of Holland? Where the proud titles of the German Cæsars?
Where the mighty dynasty of Bourbon? But is there yet one nation which
has retained unimpaired its moral and political strength? One nation, whose
shores have ever been accessible to a suppliant, and never to an enemy?
One nation which, while the banners of her foes have been carried in
triumph to half the capitals of the world, has seen them only suspended over
her shrines as trophies? One nation, which, while so many cities have been
a prey to hostile fires, has never seen her streets lighted up but with the
blaze of victorious illumination? History and posterity will reply, ‘That
country was England.’ Let them not talk to us of their philosophy and their
philanthropy, their reason and their rights! We know too well the oratory of
their Smithfield meetings, and the orgies of their midnight clubs! We have
seen the weapons which arm, and the spirit which nerves them. We have
heard the hyæna howl, till the raving which excited dismay provokes
nothing but disgust. Amid the railings of disappointed ambition, and the
curses of factious hate; amid the machinations of the foully wicked, and the
sophistries of the would-be wise, we will cling to our fathers’ banner—we
will rally round our native rock. Mr. President, that banner is the Charta of
our rights—that Rock is the British Constitution!”
“Bravo!” “Can’t say I quite caught the line of argument.” “Argument!
Fiddlestick! Quite gone out except for opponencies; and then for the
language, and the feeling, and the style, and all that sort of thing—oh!
nobody can deny that it was all
Oratoric,
Metaphoric,
Similes of wondrous length;
Illustration,
Conflagration,
Ancient Romans,
House of Commons,
Clever Uriel
And Ithuriel,
Good old king,
Everything!—
How I love a loud debate!”
With his sayings and saws, his hems and his haws,
Another comes up to the scratch;
While Deacon and Law unite in a yaw! [Yawning.
And the President looks at his watch.
Admirable,
Bang the table,
‘Sir, although its getting late,’
Opposition,
Repetition,
Endless speeches,
Leather breeches,
Taxes, hops,
Turnip-tops,
Leather ’em, lather ’em,
Omnium-gatherum—
How I love a loud debate!”
Quite divine
Peregrine,
Never shall we see his mate;
Fun and flams,
Epigrams,
Leering, lying,
Versifying,
Nodding, noting,
Quibbling, quoting,
‘Thief!’ and ‘Bore!’
‘Lie!’ no more—
How I love a loud debate!”
Then up gets the glory of us and our story,
Who does all by logic and rule,
Who can tell the true diff’rence ’twixt twopence and threepence,
And prove Adam Smith quite a fool.
“Do you take trifle?” said Lady Olivia to my poor friend Halloran.
“No, Ma’am, I am reading philosophy,” said Halloran; waking from a fit
of abstraction, with about as much consciousness and perception as exists in
a petrified oyster, or an alderman dying of a surfeit. Halloran is a fool.
A trifle is the one good thing, the sole and surpassing enjoyment. He
only is happy who can fix his thoughts, and his hopes, and his feelings, and
his affections, upon those fickle and fading pleasures, which are tenderly
cherished and easily forgotten, alike acute in their excitement and brief in
their regret. Trifles constitute my summum bonum. Sages may crush them
with the heavy train of argument and syllogism; schoolboys may assail
them with the light artillery of essay and of theme; Members of Parliament
may loathe, doctors of divinity may contemn—bag wigs and big wigs, blue
devils and blue stockings, sophistry and sermons, reasonings and wrinkles,
Solon, Thales, Newton’s “Principia,” Mr. Walker’s “Eidouranion,” the
King’s Bench, the bench of Bishops—all these are serious antagonists; very
serious! But I care not; I defy them; I dote upon trifles; my name is Vyvyan
Joyeuse, and my motto is “Vive la Bagatelle!”
There are many persons who, while they have a tolerable taste for the
frivolous, yet profess remorse and penitence for their indulgence of it; and
continually court and embrace new day-dreams, while they shrink from the
retrospect of those which have already faded. Peace be to their everlasting
laments and their ever-broken resolutions! Your true trifler, meaning your
humble servant, is a being of a very different order. The luxury which I
renew in the recollection of the past is equal to that which I feel in the
enjoyment of the present, or create in the anticipation of the future. I love to
count and recount every treasure I have flung away, every bubble I have
broken; I love to dream again the dreams of my boyhood, and to see the
visions of departed pleasures flitting, like Ossian’s ghosts, around me, “with
stars dim twinkling through their forms.” I look back with delight to a youth
which has been idled away, to tastes which have been perverted, to talents
which have been misemployed; and while in imagination I wander back
through the haunts of my old idlesse, for all the learning of a Greek
professor, for all the morality of Sir John Sewell, I would not lose one
single point of that which has been ridiculous and grotesque, nor one single
tint of that which has been beautiful and beloved.
Moralists and misanthropists, maidens with starched morals and matrons
with starched frills, ancient adorers of Bohea and scandal, venerable
votaries of whispering and of whist, learned professors of the
compassionate sneer and the innocent innuendo, eternal pillars of gravity
and good order, of stupidity and decorum—come not near me with your
spare and spectacled features, your candid and considerate criticism. In you
I have no hope, in me you have no interest. I am to speak of stories you will
not believe, of beings you cannot love; of foibles for which you have no
compassion, of feelings in which you have no share.
Fortunate and unfortunate couples, belles in silks and beaux in
sentimentals, ye who have wept and sighed, ye who have been wept for and
sighed for, victims of vapours and coiners of vows, makers and marrers of
intrigue, readers and writers of songs—come to me with your attention and
your salts, your sympathy and your cambric; your griefs, your raptures,
your anxieties, all have been mine; I know your blushing and your paleness,
your self-deceiving and your self-tormenting.