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GLOSSARY
A2 aortic second sound EBV Epstein-Barr virus
ABGs arterial blood gases ECG electrocardiogram
ACE angiotensin converting EEG electroencephalogram
enzyme ELISA
enzyme-linked
AF atrial fibrillation immunosorbent assay
AIDS
acquired immunodeficiency EMG electromyogram
syndrome ENT ear, nose, and throat
ALS amyotrophic lateral EOM extraocular movement
sclerosis ESR erythrocyte sedimentation
ANA antinuclear antibody rate
ARDS
acute respiratory distress FDA US Food and Drug
syndrome Administration
bid two times daily FEV1 forced expiratory volume

biw twice a week in first second
bp blood pressure GFR glomerular filtration rate
BUN blood urea nitrogen GI gastrointestinal
CAPD
continuous ambulatory G6PD glucose-6-phosphate
peritoneal dialysis dehydrogenase
CBC complete blood count Hb hemoglobin
CF complement fixation Hct hematocrit
CHF congestive heart failure HDL high-density lipoprotein
CLL chronic lymphocytic HIV human immunodeficiency
leukemia virus
CML chronic myeloid leukemia hs at bedtime
CMV cytomegalovirus HSV herpes simplex virus
CNS central nervous system ICU intensive care unit
CPK creatine phosphokinase IFN interferon
CSF cerebrospinal fluid Ig immunoglobulin
CT computed tomography IL interleukin
CVP central venous pressure IM intramuscular
CXR chest x-ray IP intraperitoneal
DIC disseminated intravascular IV intravenous
coagulation IVC inferior vena cava
DVT deep venous thrombosis IVP intravenous pyelogram
Kasper_HMOM19-IFC.indd 1 4/4/16 1:51 PM

Kasper_HMOM19-FM.indd 1 4/6/16 9:26 AM
EDITORS
Dennis L. Kasper, MD, MA(HON)
William Ellery Channing Professor of Medicine,
Professor of Microbiology and Immunobiology,
Department of Microbiology and Immunobiology,
Harvard Medical School; Division of Infectious Diseases,
Brigham and Women’s Hospital,
Boston, Massachusetts
Anthony S. Fauci, MD, ScD(HON)

Chief, Laboratory of Immunoregulation;
Director, National Institute of Allergy and Infectious Diseases,
National Institutes of Health, Bethesda, Maryland
Stephen L. Hauser, MD
Robert A. Fishman Distinguished Professor and Chairman,
Department of Neurology,
University of California, San Francisco,
San Francisco, California
Dan L. Longo, MD
Professor of Medicine, Harvard Medical School;
Senior Physician, Brigham and Women’s Hospital;
Deputy Editor, New England Journal of Medicine,
J. Larry Jameson, MD, PhD

Robert G. Dunlop Professor of Medicine;
Dean, Perelman School of Medicine at the University of Pennsylvania;
Executive Vice President, University of Pennsylvania for the Health
System, Philadelphia, Pennsylvania
Joseph Loscalzo, MD, PhD

Hersey Professor of the Theory and Practice of Medicine,
Harvard Medical School; Chairman, Department of Medicine, and
Physician-in-Chief, Brigham and Women’s Hospital,

EDITORS
Dennis L. Kasper, MD
Anthony S. Fauci, MD
Stephen L. Hauser, MD
Dan L. Longo, MD
J. Larry Jameson, MD, PhD
Joseph Loscalzo, MD, PhD
New York Chicago San Francisco Athens London Madrid

Mexico City Milan New Delhi Singapore Sydney Toronto

Copyright © 2016 by McGraw-Hill Education. Previous editions copyright © 2013, 2009, 2005,
2002, 1998, 1995, 1991, 1988 by The McGraw-Hill Companies, Inc. All rights reserved. Except
as permitted under the United States Copyright Act of 1976, no part of this publication may be
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without the prior written permission of the publisher.
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CONTENTS
Contributors. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xv
Preface. . ... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xvii
Acknowledgments.. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xix
SECTION 1 CARE OF THE HOSPITALIZED PATIENT
1 Electrolytes/Acid-Base Balance....................................................1
2 Diagnostic Imaging in Internal Medicine..................................23
3 Procedures Commonly Performed by Internists......................26
4 Principles of Critical Care Medicine...........................................31
5 Pain and Its Management...........................................................35
6 Assessment of Nutritional Status...............................................40
7 Enteral and Parenteral Nutrition...............................................43
8 Transfusion and Pheresis Therapy.............................................46
9 Palliative and End-of-Life Care...................................................48
SECTION 2 MEDICAL EMERGENCIES
10 Cardiovascular Collapse and Sudden Death.............................57

11 Shock............................................................................................61
12 Sepsis and Septic Shock..............................................................65
13 Acute Pulmonary Edema............................................................69
14 Acute Respiratory Distress Syndrome.......................................71
15 Respiratory Failure......................................................................73
16 Confusion, Stupor, and Coma....................................................76
17 Stroke...........................................................................................82
18 Subarachnoid Hemorrhage........................................................91
19 Increased Intracranial Pressure and Head Trauma..................93
20 Spinal Cord Compression...........................................................98
21 Hypoxic-Ischemic Encephalopathy..........................................100
22 Status Epilepticus......................................................................101
23 Diabetic Ketoacidosis and Hyperosmolar Coma....................104
24 Hypoglycemia............................................................................107
25 Oncologic Emergencies.............................................................109
26 Anaphylaxis...............................................................................114
27 Bites, Venoms, Stings, and Marine Poisonings.......................115

vi CONTENTS
SECTION 3 COMMON PATIENT PRESENTATIONS
28 Fever, Hyperthermia, and Rash................................................127

29 Generalized Fatigue..................................................................131
30 Weight Loss................................................................................135
31 Chest Pain..................................................................................137
32 Palpitations................................................................................141
33 Dyspnea......................................................................................142
34 Cyanosis.....................................................................................145
35 Cough and Hemoptysis.............................................................146
36 Edema.........................................................................................150
37 Abdominal Pain.........................................................................154
38 Nausea, Vomiting, and Indigestion.........................................158
39 Dysphagia..................................................................................162
40 Diarrhea, Malabsorption, and Constipation...........................167
41 Gastrointestinal Bleeding.........................................................174
42 Jaundice and Evaluation of Liver Function.............................178
43 Ascites........................................................................................187
44 Lymphadenopathy and Splenomegaly...................................189
45 Anemia and Polycythemia........................................................194
46 Azotemia and Urinary Abnormalities......................................197
47 Pain and Swelling of Joints.......................................................203
48 Back and Neck Pain...................................................................207
49 Headache...................................................................................215
50 Syncope......................................................................................222
51 Dizziness and Vertigo...............................................................226
52 Acute Visual Loss and Double Vision......................................229
53 Weakness and Paralysis............................................................233
54 Tremor and Movement Disorders............................................236
55 Aphasia.......................................................................................239
56 Sleep Disorders..........................................................................241
57 Dysuria and Bladder Pain.........................................................245
SECTION 4 OTOLARYNGOLOGY
58 Sore Throat, Earache, and Upper

Respiratory Symptoms.............................................................247

CONTENTS vii
SECTION 5 DERMATOLOGY
59 General Examination of the Skin.............................................255

60 Common Skin Conditions.........................................................258
SECTION 6 HEMATOLOGY AND ONCOLOGY
61 Examination of Blood Smears and Bone Marrow...................265

62 Red Blood Cell Disorders..........................................................267
63 Leukocytosis and Leukopenia..................................................274
64 Bleeding and Thrombotic Disorders.......................................277
65 Myeloid Leukemias, Myelodysplasia, and
Myeloproliferative Syndromes................................................283
66 Lymphoid Malignancies............................................................293
67 Skin Cancer................................................................................305
68 Head and Neck Cancer..............................................................308
69 Lung Cancer...............................................................................310
70 Breast Cancer.............................................................................316
71 Tumors of the Gastrointestinal Tract......................................321
72 Genitourinary Tract Cancer......................................................333
73 Gynecologic Cancer...................................................................338
74 Prostate Hyperplasia and Carcinoma......................................342
75 Cancer of Unknown Primary Site.............................................345
76 Paraneoplastic Endocrine Syndromes.....................................348
77 Neurologic Paraneoplastic Syndromes...................................352
SECTION 7 INFECTIOUS DISEASES
78 Infections Acquired in Health Care Facilities..........................357

79 Infections in the Immunocompromised Host.........................362
80 Infective Endocarditis...............................................................372
81 Intraabdominal Infections........................................................382
82 Infectious Diarrheas..................................................................386
83 Sexually Transmitted and Reproductive Tract Infections.....399
84 Infections of the Skin, Soft Tissues, Joints, and Bones..........415
85 Pneumococcal Infections..........................................................422
86 Staphylococcal Infections.........................................................425

viii CONTENTS
87 Streptococcal/Enterococcal Infections, Diphtheria,

and Infections Caused by Other Corynebacteria
and Related Species..................................................................434
88 Meningococcal and Listerial Infections...................................443
89 Infections Caused by Haemophilus, Bordetella,
Moraxella, and HACEK Group Organisms...............................448
90 Diseases Caused by Gram-Negative Enteric
Bacteria and Pseudomonas.......................................................453
91 Infections Caused by Miscellaneous
Gram-Negative Bacilli...............................................................462
92 Anaerobic Infections.................................................................469
93 Nocardiosis, Actinomycosis, and Whipple’s Disease.............477
94 Tuberculosis and Other Mycobacterial Infections.................482
95 Lyme Disease and Other Nonsyphilitic
Spirochetal Infections...............................................................494
96 Rickettsial Diseases...................................................................500
97 Mycoplasma pneumoniae, Legionella Species, and
Chlamydia pneumoniae.............................................................510
98 Chlamydia trachomatis and C. psittaci.....................................514
99 Herpesvirus Infections..............................................................516
100 Cytomegalovirus and Epstein-Barr Virus Infections..............525
101 Influenza and Other Viral Respiratory Diseases.....................530
102 Rubeola, Rubella, Mumps, and Parvovirus Infections...........538
103 Enteroviral Infections................................................................543
104 Insect- and Animal-Borne Viral Infections..............................546
105 HIV Infection and AIDS.............................................................554
106 Fungal Infections.......................................................................568
107 Pneumocystis Infections............................................................583
108 Protozoal Infections..................................................................586
109 Helminthic Infections and Ectoparasite
Infestations................................................................................599
SECTION 8 CARDIOLOGY
110 Physical Examination of the Heart...........................................613

111 Electrocardiography.................................................................618
112 Noninvasive Examination of the Heart...................................622
113 Congenital Heart Disease in the Adult....................................627

CONTENTS ix
114 Valvular Heart Disease..............................................................632

115 Cardiomyopathies and Myocarditis........................................639
116 Pericardial Disease....................................................................644
117 Hypertension.............................................................................649
118 Metabolic Syndrome.................................................................656
119 ST-Segment Elevation Myocardial
Infarction....................................................................................658
120 Unstable Angina and Non-ST-Elevation
Myocardial Infarction................................................................668
121 Chronic Stable Angina..............................................................672
122 Bradyarrhythmias.....................................................................677
123 Tachyarrhythmias.....................................................................679
124 Heart Failure and Cor Pulmonale.............................................687
125 Diseases of the Aorta................................................................693
126 Peripheral Vascular Disease.....................................................696
127 Pulmonary Hypertension..........................................................699
SECTION 9 PULMONOLOGY
128 Respiratory Function and Pulmonary

Diagnostic Procedures..............................................................705
129 Asthma.......................................................................................711
130 Environmental Lung Diseases..................................................715
131 Chronic Obstructive Pulmonary Disease.................................718
132 Pneumonia, Bronchiectasis, and Lung Abscess......................722
133 Pulmonary Thromboembolism and Deep-Vein
Thrombosis................................................................................730
134 Interstitial Lung Disease...........................................................734
135 Diseases of the Pleura and Mediastinum................................740
136 Disorders of Ventilation............................................................744
137 Sleep Apnea...............................................................................745
SECTION 10 NEPHROLOGY
138 Acute Renal Failure...................................................................747

139 Chronic Kidney Disease and Uremia........................................752
140 Dialysis.......................................................................................754
141 Renal Transplantation..............................................................756

x CONTENTS
142 Glomerular Diseases.................................................................759

143 Renal Tubular Disease...............................................................769
144 Urinary Tract Infections and Interstitial Cystitis....................775
145 Nephrolithiasis..........................................................................779
146 Urinary Tract Obstruction.........................................................782
SECTION 11 GASTROENTEROLOGY
147 Peptic Ulcer and Related Disorders.........................................785

148 Inflammatory Bowel Diseases..................................................790
149 Colonic and Anorectal Diseases...............................................794
150 Cholelithiasis, Cholecystitis, and Cholangitis.........................799
151 Pancreatitis................................................................................804
152 Acute Hepatitis..........................................................................809
153 Chronic Hepatitis.......................................................................816
154 Cirrhosis and Alcoholic Liver Disease......................................826
155 Portal Hypertension..................................................................831
SECTION 12 ALLERGY, CLINICAL IMMUNOLOGY, AND RHEUMATOLOGY
156 Diseases of Immediate-Type Hypersensitivity.......................835

157 Primary Immune Deficiency Diseases.....................................840
158 Systemic Lupus Erythematosus, Rheumatoid Arthritis,
and Other Connective Tissue Diseases....................................843
159 Vasculitis....................................................................................850
160 Ankylosing Spondylitis.............................................................854
161 Psoriatic Arthritis.......................................................................857
162 Reactive Arthritis.......................................................................859
163 Osteoarthritis.............................................................................861
164 Gout, Pseudogout, and Related Diseases...............................863
165 Other Musculoskeletal Disorders.............................................867
166 Sarcoidosis.................................................................................870
167 Amyloidosis...............................................................................873
SECTION 13 ENDOCRINOLOGY AND METABOLISM
168 Disorders of the Anterior Pituitary and Hypothalamus.........877

169 Diabetes Insipidus and Syndrome of Inappropriate
Antidiuretic Hormone...............................................................883

CONTENTS xi
170 Thyroid Gland Disorders...........................................................886

171 Adrenal Gland Disorders..........................................................895
172 Obesity.......................................................................................901
173 Diabetes Mellitus.......................................................................904
174 Disorders of the Male Reproductive System...........................912
175 Disorders of the Female Reproductive System......................917
176 Hypercalcemia and Hypocalcemia...........................................924
177 Osteoporosis and Osteomalacia..............................................931
178 Hypercholesterolemia and Hypertriglyceridemia..................936
179 Hemochromatosis, Porphyrias, and Wilson’s Disease...........942
SECTION 14 NEUROLOGY
180 The Neurologic Examination....................................................947

181 Seizures and Epilepsy...............................................................956
182 Dementia....................................................................................968
183 Parkinson’s Disease...................................................................976
184 Ataxic Disorders........................................................................981
185 ALS and Other Motor Neuron Diseases...................................984
186 Autonomic Nervous System Disorders....................................988
187 Trigeminal Neuralgia, Bell’s Palsy, and
Other Cranial Nerve Disorders.................................................995
188 Spinal Cord Diseases.............................................................. 1002
189 Tumors of the Nervous System............................................. 1008
190 Multiple Sclerosis................................................................... 1012
191 Acute Meningitis and Encephalitis....................................... 1020
192 Chronic and Recurrent Meningitis........................................ 1031
193 Peripheral Neuropathies, Including
Guillain-Barré Syndrome....................................................... 1040
194 Myasthenia Gravis.................................................................. 1050
195 Muscle Diseases...................................................................... 1053
SECTION 15 PSYCHIATRY AND SUBSTANCE ABUSE
196 Psychiatric Disorders............................................................. 1063

197 Psychiatric Medications......................................................... 1071
198 Eating Disorders..................................................................... 1079

xii CONTENTS
199 Alcohol Use Disorder.............................................................. 1080

200 Narcotic Abuse........................................................................ 1084
SECTION 16 DISEASE PREVENTION AND HEALTH MAINTENANCE
201 Routine Disease Screening.................................................... 1087

202 Cardiovascular Disease Prevention...................................... 1092
203 Prevention and Early Detection of Cancer........................... 1094
204 Smoking Cessation................................................................. 1102
205 Women’s Health..................................................................... 1104
SECTION 17 ADVERSE DRUG REACTIONS
206 Adverse Drug Reactions........................................................ 1107
Index................................................................................................. 1109

NOTICE
Medicine is an ever-changing science. As new research and clinical experience
broaden our knowledge, changes in treatment and drug therapy are required.
The authors and the publisher of this work have checked with sources believed
to be reliable in their efforts to provide information that is complete and gener-
ally in accord with the standards accepted at the time of publication. However,
in view of the possibility of human error or changes in medical sciences, nei-
ther the authors nor the publisher nor any other party who has been involved
in the preparation or publication of this work warrants that the information
contained herein is in every respect accurate or complete, and they disclaim all
responsibility for any errors or omissions or for the results obtained from use
of the information contained in this work. Readers are encouraged to confirm
the information contained herein with other sources. For example and in par-
ticular, readers are advised to check the product information sheet included
in the package of each drug they plan to administer to be certain that the
information contained in this work is accurate and that changes have not been
made in the recommended dose or in the contraindications for administration.
This recommendation is of particular importance in connection with new or
infrequently used drugs.

CONTRIBUTORS
ASSOCIATE EDITORS
S. ANDREW JOSEPHSON, MD
Professor; Senior Executive Vice Chairman, Department of Neurology, University
of California, San Francisco, San Francisco, California
CAROL A. LANGFORD, MD, MHS
Harold C. Schott Endowed Chair; Director, Center for Vasculitis Care and
Research, Department of Rheumatic and Immunologic Diseases, Cleveland Clinic,
Cleveland, Ohio
LEONARD S. LILLY, MD
Professor of Medicine, Harvard Medical School; Chief, Brigham and Women’s/
Faulkner Cardiology, Brigham and Women’s Hospital, Boston, Massachusetts
DAVID B. MOUNT, MD
Associate Physician, Brigham and Women’s Hospital; Assistant Professor of
Medicine, Harvard Medical School; Renal Division, Brigham and Women’s
Hospital, Boston, Massachusetts
EDWIN K. SILVERMAN, MD, PhD
Professor of Medicine; Chief, Channing Division of Network Medicine, Harvard
Medical School, Boston, Massachusetts
NEERAJ K. SURANA, MD, PhD
Instructor in Pediatrics, Harvard Medical School; Assistant in Medicine, Boston
Children’s Hospital, Boston, Massachusetts
Numbers indicate the chapters written or co-written by the contributor.

ANTHONY S. FAUCI, MD
26, 42, 43, 47, 59, 60, 105, 150-167
GREGORY K. FOLKERS, MPH
105, 153, 159
STEPHEN L. HAUSER, MD
3, 5, 16-22, 48-56, 77, 180-200, 204
J. LARRY JAMESON, MD, PhD
2, 6, 7, 23, 24, 29, 30, 118, 168-179, 198, 201, 205
S. ANDREW JOSEPHSON, MD
5, 16-22, 48-56, 77, 180-197, 199, 200, 204
DENNIS L. KASPER, MD
12, 27, 28, 57, 58, 78-104, 106-109, 132, 144
SHYAMASUNDARAN KOTTILIL, MD
153
CAROL A. LANGFORD, MD
26, 42, 43, 47, 59, 60, 105, 150-167
LEONARD S. LILLY, MD
10, 11, 13, 31, 32, 34, 110-117, 119-127
DAN L. LONGO, MD
8, 9, 25, 37-41, 44, 45, 61-76, 147-149, 203
xv

xvi CONTRIBUTORS
JOSEPH LOSCALZO, MD, PhD

4, 10, 11, 13-15, 31-36, 46, 110-117, 119-143, 145, 146, 202
DAVID B. MOUNT, MD
36, 46, 138-143, 145, 146
EDWIN K. SILVERMAN, MD, PhD
4, 14, 15, 33, 35, 128-137
NEERAJ K. SURANA, MD, PhD
12, 27, 28, 57, 58, 78-104, 106-109, 132, 144

PREFACE
Harrison’s Principles of Internal Medicine (HPIM), the premier medical textbook
for students and clinicians, provides a detailed body of information important to an
understanding of the biological and clinical aspects of quality patient care. Harrison’s
Manual of Medicine aims to fulfill a different need: As a concise, fact-rich resource for
bedside care, the Manual presents clinical information drawn from the 19th edition
of HPIM, covering the key features of the diagnosis, clinical manifestations, and
treatment of the major diseases that are likely to be encountered on a medical service.
First published in 1988, the Manual has become ever more useful with the rapid
expansion of medical knowledge and the increasing time constraints associated with
heavy patient-care responsibilities in modern health care settings. The Manual’s
popularity and value reflect its abbreviated format, which has proven extremely
useful for initial diagnosis and management in time-restricted clinical settings. In
particular, the book’s full-color format allows readers to locate and use information
quickly. In addition, numerous tables and graphics facilitate decisions at the point
of care.
The Manual has been written for easy and seamless reference to the full text of
the 19th edition of HPIM, and the Editors recommend that the full textbook be
consulted as soon as time allows. Although not a substitute for in-depth analysis of
clinical problems, the Manual serves as a ready source of informative summaries that
will be useful “on the spot” and that will prepare the reader for more in-depth analy-
sis through more extensive reading at a later time. Like previous editions, this latest
edition of the Manual is intended to keep up with the continual evolution of internal
medicine practices. To this end, every chapter from the prior edition has been closely
reviewed and updated, with substantial revisions and new chapters provided where
appropriate. The 19th edition of the Manual is available in print and in portable
format for the smartphone and tablet.
xvii

ACKNOWLEDGMENTS
The Editors and McGraw-Hill wish to thank their editorial staff, whose assistance
and patience made this edition come out in a timely manner:
From the Editors’ offices: Patricia Duffey; Gregory K. Folkers; Andrew Josephson,
MD; H. Clifford Lane, MD; Carol A. Langford, MD; Julie B. McCoy; Anita Ortiz;
Elizabeth Robbins, MD; Marie E. Scurti; and Stephanie Tribuna.
From McGraw-Hill: James F. Shanahan, Kim J. Davis, and Catherine H. Saggese.
The Editors also wish to acknowledge contributors to past editions of this Manual,
whose work formed the basis for many of the chapters herein: Tamar F. Barlam, MD;
Gerhard P. Baumann, MD; Eugene Braunwald, MD; Punit Chadha, MD; Joseph B.
Martin, MD, PhD; Michael Sneller, MD; Kenneth Tyler, MD; Sophia Vinogradov,
MD; and Jean Wilson, MD.
xix

SECTION 1 CARE OF THE HOSPITALIZED PATIENT
1 Electrolytes/Acid-Base Balance
SODIUM
Disturbances of sodium concentration [Na+] result in most cases from abnormali-
ties of H2O homeostasis, which change the relative ratio of Na+ to H2O. Disorders
of Na+ balance per se are, in contrast, associated with changes in extracellular fluid
volume, either hypo- or hypervolemia. Maintenance of “arterial circulatory integrity”
is achieved in large part by changes in urinary sodium excretion and vascular tone,
whereas H2O balance is achieved by changes in both H2O intake and urinary H2O
excretion (Table 1-1). Confusion can result from the coexistence of defects in both
H2O and Na+ balance. For example, a hypovolemic pt may have an appropriately low
urinary Na+ due to increased renal tubular reabsorption of filtered NaCl; a concomi-
tant increase in circulating arginine vasopressin (AVP)—part of the defense of effec-
tive circulating volume (Table 1-1)—will cause the renal retention of ingested H2O
and the development of hyponatremia.
HYPONATREMIA
This is defined as a serum [Na+] <135 mmol/L and is among the most common
electrolyte abnormalities encountered in hospitalized pts. Symptoms include nausea,
vomiting, confusion, lethargy, and disorientation; if severe (<120 mmol/L) and/or
abrupt, seizures, central herniation, coma, or death may result (see Acute Symptom-
atic Hyponatremia, below). Hyponatremia is almost always the result of an increase
TABLE 1-1 OSMOREGULATION VERSUS VOLUME REGULATION

Osmoregulation Volume Regulation
What is sensed Plasma osmolality Arterial filling
Sensors Hypothalamic Carotid sinus
osmoreceptors
Afferent arteriole
Atria
Effectors AVP Sympathetic nervous system
Thirst Renin-angiotensin-aldosterone
system
ANP/BNP
AVP
What is affected Urine osmolality Urinary sodium excretion
H2O intake Vascular tone
Note: See text for details.
Abbreviations: ANP, atrial natriuretic peptide; AVP, arginine vasopressin; BNP,
brain natriuretic peptide.
Source: Adapted from Rose BD, Black RM (eds): Manual of Clinical Problems in
Nephrology. Boston, Little Brown, 1988; with permission.
Kasper_HMOM19-Sec01_p001-p056.indd 1 4/5/16 2:16 PM

2 SECTION 1 Care of the Hospitalized Patient
in circulating AVP and/or increased renal sensitivity to AVP; a notable exception is

in the setting of low solute intake (“beer potomania”), wherein a markedly reduced
urinary solute excretion is inadequate to support the excretion of sufficient free H2O.
The serum [Na+] by itself does not yield diagnostic information regarding total-body
Na+ content; hyponatremia is primarily a disorder of H2O homeostasis. Pts with
hyponatremia are thus categorized diagnostically into three groups, depending on
their clinical volume status: hypovolemic, euvolemic, and hypervolemic hyponatre-
mia (Fig. 1-1). All three forms of hyponatremia share an exaggerated, “nonosmotic”
increase in circulating AVP, in the setting of reduced serum osmolality. Notably,
hyponatremia is often multifactorial; clinically important nonosmotic stimuli that
can cause a release of AVP and increase the risk of hyponatremia include drugs, pain,
nausea, and strenuous exercise.
Laboratory investigation of a pt with hyponatremia should include a measure-
ment of serum osmolality to exclude “pseudohyponatremia” due to hyperlipidemia
or hyperproteinemia. Serum glucose also should be measured; serum Na+ falls by
1.4 mM for every 100-mg/dL increase in glucose, due to glucose-induced H2O efflux
from cells. Hyperkalemia may suggest adrenal insufficiency or hypoaldosteronism;
increased blood urea nitrogen (BUN) and creatinine may suggest a renal cause.
Urine electrolytes and osmolality are also critical tests in the initial evaluation of
hyponatremia. In particular, a urine Na+ <20 meq/L is consistent with hypovolemic
hyponatremia in the clinical absence of a “hypervolemic,” Na+-avid syndrome such
as congestive heart failure (CHF) (Fig. 1-1). Urine osmolality <100 mosmol/kg is
suggestive of polydipsia or, in rare cases, of decreased solute intake; urine osmolal-
ity >400 mosmol/kg suggests that AVP excess is playing a more dominant role,
whereas intermediate values are more consistent with multifactorial pathophysiology
(e.g., AVP excess with a component of polydipsia). Finally, in the right clinical set-
ting, thyroid, adrenal, and pituitary function should also be tested.
Hypovolemic Hyponatremia
Hypovolemia from both renal and extrarenal causes is associated with hypona-
tremia. Renal causes of hypovolemia include primary adrenal insufficiency and
hypoaldosteronism, salt-losing nephropathies (e.g., reflux nephropathy, nono-
liguric acute tubular necrosis), diuretics, and osmotic diuresis. Random “spot”
urine Na+ is typically >20 meq/L in these cases but may be <20 meq/L in diuretic-
associated hyponatremia if tested long after administration of the drug. Nonrenal
causes of hypovolemic hyponatremia include GI loss (e.g., vomiting, diarrhea,
tube drainage) and integumentary loss (sweating, burns); urine Na+ is typically
<20 meq/L in these cases.
Hypovolemia causes profound neurohumoral activation, inducing systems that
preserve arterial circulatory integrity, such as the renin-angiotensin-aldosterone
(RAA) axis, the sympathetic nervous system, and AVP (Table 1-1). The increase
in circulating AVP serves to increase the retention of ingested free H2O, leading
to hyponatremia. The optimal treatment of hypovolemic hyponatremia is volume
administration, generally as isotonic crystalloid, i.e., 0.9% NaCl (“normal saline”).
If the history suggests that hyponatremia has been “chronic,” i.e., present for 48 h,
care should be taken to avoid overcorrection (see below), which can easily occur as
AVP levels plummet in response to volume-resuscitation; if necessary, the adminis-
tration of desmopressin (DDAVP) and free water can reinduce or arrest the correc-
tion of hyponatremia (see below).
Hypervolemic Hyponatremia
The edematous disorders (CHF, hepatic cirrhosis, and nephrotic syndrome) are often
associated with mild to moderate degrees of hyponatremia ([Na+] = 125–135 mmol/L);
occasionally, pts with severe CHF or cirrhosis may present with serum [Na+]
<120 mmol/L. The pathophysiology is similar to that in hypovolemic hyponatremia,
except that arterial filling and circulatory integrity are decreased due to the specific

Kasper_HMOM19-Sec01_p001-p056.indd 3
Assessment of volume status
Hypovolemia Euvolemia (no edema) Hypervolemia

• Total body water ↓ • Total body water ↑ • Total body water ↑↑
• Total body sodium ↓↓ • Total body sodium ←→ • Total body sodium ↑
UNa >20 UNa <20 UNa >20 UNa >20 UNa <20
Renal losses Extrarenal losses Glucocorticoid deficiency Acute or chronic Nephrotic syndrome
Diuretic excess Vomiting Hypothyroidism renal failure Cirrhosis
Mineral corticoid deficiency Diarrhea Stress Cardiac failure
Salt-losing deficiency Third spacing of fluids Drugs
Bicarbonaturia with Burns Syndrome of inappropriate
renal tubal acidosis and Pancreatitis antidiuretic hormone
metabolic alkalosis Trauma secretion
Ketonuria
Osmotic diuresis
Cerebral salt wasting
syndrome
4/5/16 2:16 PM
FIGURE 1-1 The diagnostic approach to hyponatremia. See text for details. (From S Kumar, T Berl: Diseases of water metabolism, in Atlas of Diseases of the Kidney,
RW Schrier [ed]. Philadelphia, Current Medicine, Inc, 1999; with permission.)
3
etiologic factors, i.e., cardiac dysfunction, peripheral vasodilation in cirrhosis, and

hypoalbuminemia in nephrotic syndrome. The degree of hyponatremia is an indi-
rect index of the associated neurohumoral activation (Table 1-1) and an important
prognostic indicator in hypervolemic hyponatremia.
Management consists of treatment of the underlying disorder (e.g., afterload
reduction in heart failure, large-volume paracentesis in cirrhosis, immunomodu-
latory therapy in some forms of nephrotic syndrome), Na+ restriction, diuretic
therapy, and, in some pts, H2O restriction. Vasopressin antagonists (e.g., tolvaptan
and conivaptan) are also effective in normalizing hyponatremia associated with both
cirrhosis and CHF.
Euvolemic Hyponatremia
The syndrome of inappropriate ADH secretion (SIADH) characterizes most cases
of euvolemic hyponatremia. Other causes of euvolemic hyponatremia include hypo-
thyroidism and secondary adrenal insufficiency due to pituitary disease; notably,
repletion of glucocorticoid levels in the latter may cause a rapid drop in circulating
AVP levels and overcorrection of serum [Na+] (see below).
Common causes of SIADH include pulmonary disease (e.g., pneumonia, tuberculosis,
pleural effusion) and central nervous system (CNS) diseases (e.g., tumor, subarachnoid
hemorrhage, meningitis); SIADH also occurs with malignancies (e.g., small cell carci-
noma of the lung) and drugs (e.g., selective serotonin reuptake inhibitors, tricyclic anti-
depressants, nicotine, vincristine, chlorpropamide, carbamazepine, narcotic analgesics,
antipsychotic drugs, cyclophosphamide, ifosfamide). Optimal treatment of euvolemic
hyponatremia includes treatment of the underlying disorder. H2O restriction to <1 L/d
is a cornerstone of therapy, but may be ineffective or poorly tolerated. However, vaso-
pressin antagonists are predictably effective in normalizing serum [Na+] in SIADH.
Alternatives include the administration of loop diuretics to inhibit the countercurrent
mechanism and reduce urinary concentration, combined with oral salt tablets to abro-
gate diuretic-induced salt loss and attendant hypovolemia.
Acute Symptomatic Hyponatremia

Acute symptomatic hyponatremia is a medical emergency; a sudden drop in serum
[Na+] can overwhelm the capacity of the brain to regulate cell volume, leading to
cerebral edema, seizures, and death. Women, particularly premenopausal women,
are particularly prone to such sequelae; neurologic consequences are comparatively
rare in male pts. Many of these pts develop hyponatremia from iatrogenic causes,
including hypotonic fluids in the postoperative period, prescription of a thiazide
diuretic, colonoscopy preparation, or intraoperative use of glycine irrigants. Polydip-
sia with an associated cause of increased AVP may also cause acute hyponatremia,
as can increased H2O intake in the setting of strenuous exercise, e.g., a marathon.
The recreational drug Ecstasy (methylenedioxymethamphetamine [MDMA]) can
cause acute hyponatremia, rapidly inducing both AVP release and increased thirst.
Severe symptoms may occur at relatively modest levels of serum [Na+], e.g., in the
mid-120s. Nausea and vomiting are common premonitory symptoms of more severe
sequelae. An important concomitant is respiratory failure, which may be hyper-
capnic due to CNS depression or normocapnic due to neurogenic, noncardiogenic
pulmonary edema; the attendant hypoxemia amplifies the impact of hyponatremic
encephalopathy.
TREATMENT HYPONATREMIA
Three considerations are critical in the therapy of hyponatremia. First, the pres-
ence, absence, and/or severity of symptoms determine the urgency of therapy
(see above for acute symptomatic hyponatremia). Second, pts with hyponatremia
that has been present for >48 h (“chronic hyponatremia”) are at risk for osmotic
demyelination syndrome, typically central pontine myelinolysis, if serum Na+ is

Electrolytes/Acid-Base Balance CHAPTER 1 5
corrected by >10–12 mM within the first 24 h and/or by >18 mM within the first
48 h. Third, the response to interventions, such as hypertonic saline or vasopressin
antagonists, can be highly unpredictable, such that frequent monitoring of serum
Na+ (initially every 2–4 h) is imperative.
Treatment of acute symptomatic hyponatremia should include hypertonic
saline to acutely increase serum Na+ by 1–2 mM/h to a total increase of 4–6 mM;
this increase is typically sufficient to alleviate acute symptoms, after which correc-
tive guidelines for “chronic” hyponatremia are appropriate (see below). A number
of equations and algorithms have been developed to estimate the required rate
of hypertonic solution; one popular approach is to calculate a “Na+ deficit,” where
the Na+ deficit = 0.6 × body weight × (target [Na+] – starting [Na+]). Regardless of
the method used to determine the rate of administered hypertonic saline, the
increase in serum [Na+] can be highly unpredictable, due to rapid changes in
the underlying physiology; serum [Na+] should be monitored every 2–4 h during
and after treatment with hypertonic saline. The administration of supplemental
O2 and ventilatory support can also be critical in acute hyponatremia, if pts
develop acute pulmonary edema or hypercapnic respiratory failure. IV loop
diuretics will help treat associated acute pulmonary edema and will also increase
free H2O excretion by interfering with the renal countercurrent multiplier system.
It is noteworthy that vasopressin antagonists do not have a role in the manage-
ment of acute hyponatremia.
The rate of correction should be comparatively slow in chronic hyponatremia
(<10–12 mM in the first 24 h and <18 mM in the first 48 h), so as to avoid osmotic
demyelination syndrome. Vasopressin antagonists are highly effective in SIADH and
in hypervolemic hyponatremia due to heart failure or cirrhosis. Abnormalities in
liver function tests have been reported during the use of tolvaptan; hence, therapy
with this agent should be restricted to 1–2 months with close monitoring of liver
function. Should pts overcorrect serum [Na+] in response to vasopressin antago-
nists, hypertonic saline, or isotonic saline (in chronic hypovolemic hyponatremia),
hyponatremia can be safely reinduced or stabilized by the administration of the
vasopressin agonist DDAVP and the administration of free H2O, typically IV D5W;
again, close monitoring of the response of serum [Na+] is essential to adjust therapy.
Alternatively, the treatment of pts with marked hyponatremia can be initiated with
the twice-daily administration of DDAVP to maintain constant AVP bioactivity,
combined with the administration of hypertonic saline to slowly correct the serum
[Na+] in a more controlled fashion, thus reducing upfront the risk of overcorrection.
HYPERNATREMIA
This is rarely associated with hypervolemia, where the association is typically iat-
rogenic, e.g., administration of hypertonic sodium bicarbonate. More commonly,
hypernatremia is the result of a combined H2O and volume deficit, with losses of
H2O in excess of Na+. Elderly individuals with reduced thirst and/or diminished
access to fluids are at the highest risk of hypernatremia due to decreased free H2O
intake. Common causes of renal H2O loss are osmotic diuresis secondary to hyper-
glycemia, postobstructive diuresis, or drugs (radiocontrast, mannitol, etc.); H2O
diuresis occurs in central or nephrogenic diabetes insipidus (DI) (Chap. 168). In pts
with hypernatremia due to renal loss of H2O, it is critical to quantify ongoing daily
losses in addition to calculation of the baseline H2O deficit (Table 1-2).
TREATMENT HYPERNATREMIA
The approach to correction of hypernatremia is outlined in Table 1-2. As with
hyponatremia, it is advisable to correct the H2O deficit slowly to avoid neuro-
logic compromise, decreasing the serum [Na+] over 48–72 h. Depending on the
blood pressure or clinical volume status, it may be appropriate to initially treat

TABLE 1-2 CORRECTION OF HYPERNATREMIA

H2O Deficit
1. Estimate TBW: 50–60% body weight (kg) depending on body composition
2. Calculate free-water deficit: [(Na+ – 140)/140] × TBW
3. Administer deficit over 48–72 h
Ongoing H2O Losses
4. Calculate free-water clearance, CeH2O:
 U + UK 
CeH2 O = V  1 − Na
 SNa 
where V is urinary volume, UNa is urinary [Na+], UK is urinary [K+], and SNa is
serum [Na+].
Insensible Losses
5. ~10 mL/kg per day: less if ventilated, more if febrile
Total
6. Add components to determine H2O deficit and ongoing H2O loss; correct
the H2O deficit over 48–72 h and replace daily H2O loss.
Abbreviation: TBW, total-body water.
with hypotonic saline solutions (1/4 or 1/2 normal saline); blood glucose should
be monitored in pts treated with large volumes of D5W, should hyperglycemia
ensue. Calculation of urinary electrolyte-free H2O clearance is helpful to estimate
daily, ongoing loss of free H2O in pts with nephrogenic or central DI (Table 1-2).
Other forms of therapy may be helpful in selected cases of hypernatremia. Pts
with central DI may respond to the administration of intranasal DDAVP. Stable
pts with nephrogenic DI may reduce their polyuria with hydrochlorothiazide
(12.5–50 mg/d). This diuretic is thought to increase proximal H2O reabsorption
and decrease distal solute delivery, thus reducing polyuria. Pts with lithium-
associated nephrogenic DI may respond to amiloride (2.5–10 mg/d), which
decreases the entry of lithium into principal cells in the distal nephron by inhibit-
ing the amiloride-sensitive epithelial sodium channel (ENaC). Notably, however,
most pts with lithium-induced nephrogenic DI can adequately accommodate by
increasing their H2O intake. Occasionally, nonsteroidal anti-inflammatory drugs
(NSAIDs) or COX-2 inhibitors have also been used to treat polyuria associated with
nephrogenic DI, reducing the negative effect of local prostaglandins on urinary
concentration; however, the nephrotoxic potential of NSAIDs typically makes
them a less attractive therapeutic option.
POTASSIUM
Because potassium (K+) is the major intracellular cation, discussion of disorders
of K+ balance must take into consideration changes in the exchange of intra- and
extracellular K+ stores. (Extracellular K+ constitutes <2% of total-body K+ content.)
Insulin, β2-adrenergic agonists, and alkalosis tend to promote K+ uptake by cells;
acidosis, insulinopenia, or acute hyperosmolality (e.g., after treatment with mannitol
or D50W) promotes the efflux or reduced uptake of K+. A corollary is that tissue
necrosis and the attendant release of K+ can cause severe hyperkalemia, particularly
in the setting of acute kidney injury. Hyperkalemia due to rhabdomyolysis is thus
particularly common, due to the enormous store of K+ in muscle; hyperkalemia may
also be prominent in tumor lysis syndrome.

The kidney plays a dominant role in K+ excretion. Although K+ is transported

along the entire nephron, it is the principal cells of the connecting segment and cor-
tical collecting duct that play a dominant role in K+ excretion. Apical Na+ entry into
principal cells via the amiloride-sensitive epithelial Na+ channel (ENaC) generates a
lumen-negative potential difference, which drives passive K+ exit through apical K+
channels. This relationship is key to the bedside understanding of potassium disorders.
For example, decreased distal delivery of Na+ tends to blunt the ability to excrete K+,
leading to hyperkalemia. Abnormalities in the renin-angiotensin-aldosterone system
(RAAS) can cause both hypo- and hyperkalemia; aldosterone has a major influence
on potassium excretion, increasing the activity of ENaC channels and the basolateral
Na+/K+-ATPase, thus amplifying the driving force for K+ secretion across the lumi-
nal membrane of principal cells.
HYPOKALEMIA
Major causes of hypokalemia are outlined in Table 1-3. Atrial and ventricular
arrhythmias are the most serious health consequences of hypokalemia. Pts with
concurrent Mg deficit and/or digoxin therapy are at a particularly increased risk of
arrhythmias. Hypokalemia can directly prolong the QT interval and is a significant
cofactor in arrhythmias due to other causes of a prolonged QT interval. Other clini-
cal manifestations include muscle weakness, which may be profound at serum [K+]
TABLE 1-3 CAUSES OF HYPOKALEMIA

I. Decreased intake
A. Starvation
B. Clay ingestion
II. Redistribution into cells
A. Acid-base
1. Metabolic alkalosis
B. Hormonal
1. Insulin
2. Increased β2-adrenergic sympathetic activity: post–myocardial
infarction, head injury, theophylline
3. β2-Adrenergic agonists: bronchodilators, tocolytics
4. α-Adrenergic antagonists
5. Thyrotoxic periodic paralysis
6. Downstream stimulation of Na+/K+-ATPase: theophylline, caffeine
C. Anabolic state
1. Vitamin B12 or folic acid administration (red blood cell production)
2. Granulocyte-macrophage colony-stimulating factor (white blood cell
production)
3. Total parenteral nutrition
D. Other
1. Pseudohypokalemia
2. Hypothermia
3. Familial hypokalemic periodic paralysis
4. Barium toxicity: systemic inhibition of “leak” K+ channels
(Continued)

TABLE 1-3 CAUSES OF HYPOKALEMIA (CONTINUED)

III. Increased loss
A. Nonrenal
1. Gastrointestinal loss (diarrhea)
2. Integumentary loss (sweat)
B. Renal
1. Increased distal flow and distal Na+ delivery: diuretics, osmotic
diuresis, salt-wasting nephropathies
2. Increased secretion of potassium
a. Mineralocorticoid excess: primary hyperaldosteronism (APAs),
PAH or UAH, IHA due to bilateral adrenal hyperplasia and adrenal
carcinoma, familial hyperaldosteronism (FH-I, FH-II, congenital
adrenal hyperplasias), secondary hyperaldosteronism (malignant
hypertension, renin-secreting tumors, renal artery stenosis, hypo-
volemia), Cushing’s syndrome, Bartter’s syndrome, Gitelman’s
syndrome
b. Apparent mineralocorticoid excess: genetic deficiency of
11β-dehydrogenase-2 (syndrome of apparent mineralocorticoid
excess), inhibition of 11β-dehydrogenase-2 (glycyrrhetinic/
glycyrrhizinic acid and/or carbenoxolone; licorice, food products,
drugs), Liddle’s syndrome (genetic activation of ENaC)
c. Distal delivery of nonreabsorbed anions: vomiting, nasogastric
suction, proximal renal tubular acidosis, diabetic ketoacidosis,
glue sniffing (toluene abuse), penicillin derivatives (penicillin,
nafcillin, dicloxacillin, ticarcillin, oxacillin, and carbenicillin)
3. Magnesium deficiency, amphotericin B, Liddle’s syndrome
Abbreviations: APA, aldosterone-producing adenoma; ENaC, epithelial Na+
channels; IHA, idiopathic hyperaldosteronism; PAH, primary adrenal hyperplasia;
UAH, unilateral adrenal hyperplasia.
<2.5 mmol/L, and, if hypokalemia is sustained, hypertension, ileus, polyuria, renal

cysts, and even renal failure.
The cause of hypokalemia is usually obvious from history, physical examination,
and/or basic laboratory tests. However, persistent hypokalemia may require a more
thorough, systematic evaluation (Fig. 1-2). Initial laboratory evaluation should
include electrolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete
blood count, and urinary pH, osmolality, creatinine, and electrolytes. Serum and
urine osmolality are required for calculation of the transtubular K+ gradient (TTKG),
which should be <3 in the presence of hypokalemia (see also Hyperkalemia). Alter-
natively, a urinary K+-to-creatinine ratio of >13-mmol/g creatinine (>1.5-mmol/
mmol creatinine) is compatible with excessive K+ excretion. Further tests such as
urinary Mg2+ and Ca2+ and/or plasma renin and aldosterone levels may be necessary
in specific cases.
TREATMENT HYPOKALEMIA
The goals of therapy in hypokalemia are to prevent life-threatening and/or seri-
ous chronic consequences, to replace the associated K+ deficit, and to correct the
underlying cause and/or mitigate future hypokalemia. The urgency of therapy
depends on the severity of hypokalemia, associated clinical factors (cardiac
disease, digoxin therapy, etc.), and the rate of decline in serum K+. Pts with a

prolonged QT interval and/or other risk factors for arrhythmia should be moni-
tored by continuous cardiac telemetry during repletion. Urgent but cautious K+
replacement should be considered in pts with severe redistributive hypokalemia
(plasma K+ concentration <2.5 mM) and/or when serious complications ensue;
however, this approach has a risk of rebound hyperkalemia following acute
resolution of the underlying cause. When excessive activity of the sympathetic
nervous system is thought to play a dominant role in redistributive hypokale-
mia, as in thyrotoxic periodic paralysis, theophylline overdose, and acute head
injury, high-dose propranolol (3 mg/kg) should be considered; this nonspecific
β-adrenergic blocker will correct hypokalemia without the risk of rebound hyper-
kalemia. It should be noted that hypokalemia is refractory to correction in the
presence of Mg++ deficiency, which also should be corrected when present; renal
wasting of both cations may be particularly prominent after renal tubular injury,
e.g., from cisplatin nephrotoxicity.
Oral replacement with K+-Cl- is the mainstay of therapy in hypokalemia. Potas-
sium phosphate, oral or IV, may be appropriate in pts with combined hypokalemia
and hypophosphatemia. Potassium bicarbonate or potassium citrate should be
considered in pts with concomitant metabolic acidosis. The deficit of K+ and the
rate of correction should be estimated as accurately as possible; renal function,
medications, and comorbid conditions such as diabetes should also be consid-
ered so as to gauge the risk of overcorrection. In the absence of abnormal K+
redistribution, the total deficit correlates with serum K+ such that serum K+ drops
by approximately 0.27 mM for every 100-mmol reduction in total-body stores.
Notably, given the delay in redistributing potassium into intracellular compart-
ments, this deficit must be replaced gradually over 24–48 h, with frequent moni-
toring of plasma K+ concentration to avoid transient over-repletion and transient
hyperkalemia if otherwise appropriate. If hypokalemia is severe (<2.5 mmol/L)
and/or if oral supplementation is not feasible or tolerated, IV KCl can be adminis-
tered through a central vein with cardiac monitoring in an intensive care setting,
at rates that should not exceed 20 mmol/h. KCl should always be administered in
saline solutions, rather than dextrose; the dextrose-induced increase in insulin can
acutely exacerbate hypokalemia.
Strategies to minimize K+ losses should also be considered. These measures
may include minimizing the dose of non-K+-sparing diuretics, restricting Na+
intake, and using clinically appropriate combinations of non-K+-sparing and
K+-sparing medications (e.g., loop diuretics with angiotensin-converting enzyme
inhibitors).
HYPERKALEMIA
Causes are outlined in Table 1-4; in most cases, hyperkalemia is due to decreased
renal K+ excretion. However, increases in dietary K+ intake can have a major effect in
susceptible pts, e.g., diabetics with hyporeninemic hypoaldosteronism and chronic
kidney disease (CKD). Drugs that impact on the RAA axis are also a major cause of
hyperkalemia.
The first priority in the management of hyperkalemia is to assess the need for
emergency treatment (ECG changes and/or K+ ≥6.0 mM). This should be fol-
lowed by a comprehensive workup to determine the cause (Fig. 1-3). History
and physical examination should focus on medications (e.g., ACE inhibitors,
NSAIDs, trimethoprim/sulfamethoxazole), diet and dietary supplements (e.g.,
salt substitute), risk factors for acute kidney failure, reduction in urine output,
blood pressure, and volume status. Initial laboratory tests should include elec-
trolytes, BUN, creatinine, serum osmolality, Mg2+, and Ca2+, a complete blood
count, and urinary pH, osmolality, creatinine, and electrolytes. A urine [Na+]
<20 meq/L suggests that distal Na+ delivery is a limiting factor in K+ excretion;

Kasper_HMOM19-Sec01_p001-p056.indd 10
10
Yes Yes No further

Move to therapy Emergency? Hypokalemia (Serum K+<3.5 mmol/l) Pseudohypokalemia?
workup
No No
Treat accordingly Yes Clear evidence History, physical examination Clear evidence of Yes Treat
and re-evaluate of low intake & basic laboratory tests transcellular shift accordingly
No No
-Insulin excess
-β2-adrenergic agonists
Urine K+ -FHPP
-Hyperthyroidism
-Barium intoxication
-Theophylline
<15 mmol/day OR <15 mmol/g Cr >15 mmol/g Cr OR >15 mmol/day -Chloroquine
Extrarenal loss/remote renal loss Renal loss
Acid-base status TTKG
>4 <2
Metabolic acidosis Normal Metabolic alkalosis ↑ Distal K+ secretion ↑ Tubular flow

-GI K+ loss -Profuse -Remote diuretic use -Osmotic diuresis
sweating -Remote vomiting or
bp and/or Volume
stomach drainage
-Profuse sweating
4/5/16 2:16 PM
Another random document with
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Fig. 25. Charcoal sketch of native spearing kangaroo, Pigeon Hole, Victoria River
(× 2/5). Tracing.
Another method is to apply the paint in the form of a water mixture,

similar to that described when discussing the ochre drawings. For
this purpose, especially when an important event is pending, a
number of men are chosen to attend to the “make up” of the
performers. The assistants kneel beside those who are to act, and
apply the paste with their fingers. The most delicate parts to handle
are the eyelids. The actor is required to close his eyes whilst the
artist carefully applies the paste to the lids; but it occasionally
happens that some of the material slips on to the eyeball and is
rubbed against it before the sufferer can give the alarm. Vide Plate
XLV, 2.
We have already referred to the coloured down decorations which
are attached with human blood to the bodies of the performers taking
part in sacred and other ceremonies, and we have also mentioned a
ground drawing known as “Etominja” (Plate XXXVII), which is
constructed in a similar way. Some of the latter (e.g. the “walk-about”
of the “Tjilba Purra Altjerra Knaninja”) are very large; others, as for
instance that connected with the “Erriakutta” or yelka ceremony, are
constructed over the entire surface of mounds which cover many
square feet of ground.
Having briefly reviewed the different methods of art production in
vogue in Australia, we shall proceed to consider a number of the
designs in greater detail, deduce their origin, trace their evolution,
and, where possible, give their interpretation. It will be realized at the
outset that some of the designs are crude in the extreme, whilst
others are undeniably shapely and quite up to the standard of an
average European’s artistic proficiency. The latter remarks apply
best to actual representations of natural forms. It must be
remembered that the artistic reproductions an aboriginal makes are
invariably from memory; the primitive artist never draws with a model
in front of him. If we were to ask a number of Europeans to draw, say
a horse from memory, there is no doubt we should receive a great
variety of results in response to our request. So, among the
aboriginal artists, there is a great diversity of talent which is more
individual than tribal.
If, for instance, we study the different attempts at representing the
form of one of the most familiar subjects we could ask an aboriginal
to experiment upon—the ubiquitous kangaroo —we should find by
comparison of the productions placed before us, a very marked
difference in quality. Compare, for instance, the two pictures of
kangaroo on Plate XLVII. They are the works of men of the same
tribe, are all similarly drawn, and come from the same locality. Yet, in
the upper picture, the outline and proportions of the two animals are
so incorrect that it is very doubtful whether many people not
acquainted with the locality would guess what animal the pictures
are intended to represent. In the lower picture, however, anybody
acquainted with the shape of a kangaroo would have no hesitation in
pronouncing his diagnosis. The characteristic attitude, the large tail,
the disproportion between the front and hind limbs, and the shape of
the head are quite true enough to nature to permit of correct
identification.
Fig. 26. Carving depicting a quarrel between a man and his gin. Arunndta tribe (×
1/2). Tracing.
The three designs are all drawn in charcoal, the figures in the first
two cases being outlined with a white pipe-clay line, and in the
second case with one of yellow ochre. If we wish to go one better
still, we need only study the pipe-clay drawing on bark by a native of
the Katherine River district shown on Plate XLIX, 1—a very
creditable picture of a dead kangaroo.
Some of the designs one meets with are so accurately drawn that
a scientific determination of the species becomes possible. Look for
a moment at the fish, portrayed in pipe-clay, shown in Plate XLVIII.
The piscine nature of the form, here depicted on rocks, is not only
apparent, but it is possible to say with some certainty that the two
shown swimming belong to the Toxotes, which are commonly called
Archer Fish. The form shown in Plate XLIX, 4, is unquestionably
meant to be one of the Therapon species. Both kinds of fish are
known to be living in the Katherine River, not far from the site at
which these pictures were drawn.
But if, on the other hand, some of the designs are so poor as to be
barely recognizable or even quite unrecognizable by us, how does
the aboriginal manage? When the artist is present, he can explain.
But he is not always available!
If, by way of illustration, we were asked to say definitely what the
meaning of the central figure on Plate L, 1, was we should in all
probability want to know more about it before committing ourselves.
But an aboriginal can give us a correct reply immediately. The
locality at which the photograph was obtained is north of the
Musgrave Ranges in central Australia. But that does not give us any
clue. After studying the picture more closely, we might be able to
distinguish the outline of a quadruped, the four legs being shown,
one behind the other, in a row, and a big head on the right-hand side,
in a position suggesting that the animal is feeding. But these are
characteristics common to many animals!
So far, therefore, we have seen nothing to suggest the class of
animal we are dealing with. When we look again, we might note that
there is a crude image of a human being shown on the back of the
animal; and behind this is a structure which might stand for a saddle.
We guess the answer and claim that the group is a very poor
drawing of a man on horseback.
But there are other animals a man could ride! And when we look
again, we observe that the second leg of the animal, counting from
the right, has a peculiar enlargement attached to its lower end. That
structure is the key to the riddle; it represents the track of the animal!
Those familiar with the great beast of burden, now used extensively
in central Australia, will recognize the two-toed spoor of a camel.
This method of pictorial elucidation is by no means exceptional.
We have already noticed something similar in the ancient carvings at
Port Hedland, where the human foot-print is added to disperse any
doubt which may be entertained in so far as the correct interpretation
of the figure is concerned. A similar device is well exemplified in the
accompanying sketch of an ochre drawing of a human form from the
Glenelg River district in the northern Kimberleys of Western Australia
(Fig. 15). In the carving of an emu from the King Sound district,
which is reproduced in Plate XLII, 2, we noticed the same sort of
thing.
Fig. 27. Ochre-drawing of spear-boomerang duel, Arunndta tribe (× 1/2). Tracing.
The cases before us are not accidental, but we have acquainted

ourselves with the recognized determinative system of Australian
pictographs which is quite analogous to that known to have been
practised by the ancient Egyptians. Consider, for instance, the
character signifying “to love”—a human figure in profile with one
hand lifted to the level of the mouth. The same figure, with a few
parallel wavy lines, signifying water, drawn against it, means no
longer “to love,” but “to drink.” The wavy lines in this instance are the
determinative. In the Australian illustrations given above, we have
selected samples which are easily followed, but there are many
cases where the reading would be quite impossible if it were not for
the presence of the little, subsidiary, determinative sketch.
In his endeavour to make the meaning of some of his designs
clear, a native often embodies as many features as possible, quite
regardless as to whether in reality they would all be visible in the one
plane he is drawing. In the picture of a crocodile appearing on a
boabab-nut from the Derby district in Western Australia, shown in
Fig. 16, it will be observed that the reptile, in spite of having its dorsal
surface represented, has its vent indicated. The long, slender muzzle
of this figure, by the way, makes it clear that the smaller species of
the two northern Australian crocodiles (C. Johnstoni) is intended.
The human figure, too, very often appears half in full and half in
profile.
The aboriginal is a keen observer, and takes careful note of many
things besides a kangaroo, a snake track, or other similar natural
objects which may lead him to his daily bread. When travelling in the
Buccaneer Archipelago in the far north-west I remember one of the
natives drawing my attention to a peculiar formation in the clouds,
and saying, in the Sunday Island dialect: “Arrar ninmiddi,” which
means, literally: “Cloud knee.” My instructor proceeded to draw the
extraordinary shape he could see with his finger upon the hatchway
of the pearling lugger we were sailing in, after which he completed
the figure of a man. I was struck with this man’s faculty of
observation, because the cloud effect he referred to was rather out
of the common and projected from a cirro-cumulus like the bent limb
of a swastica.
It is in this way that many inspirations come to the cave artist.
Repeatedly one has occasion to notice how a pre-existing feature or
defect in the rock face—a crevice, a floor, a concretion—becomes
the centre piece of a design drawn to suit it. The feature one finds
most commonly embodied in a cave drawing is a small hole. This
often figures in the place of an animal’s eye, or a hole into which a
snake is disappearing. A local bulge in the rock may also be taken in
as part of a design and represent portion of a head or body.
Not only does the artist embody suitable natural features in his
designs, but, conversely, he also applies his knowledge of form to
explain already existing phenomena in the world about him. The
embodiment of his artistic ideas in his poetical explanations of
Nature’s wonders plays, as might be expected, an important role in
his mythology. These remarks apply especially to any striking
characteristics in the sky. When among the tribes of the Musgrave
Ranges, I ascertained that the black-looking gap in the Milky Way,
close to the Southern Cross, which is commonly known as the Coal
Sack, was referred to as “Kaleya Pubanye,” that is, the “Resting
Emu.”
Fig. 28. Charcoal sketch of ceremonial dance, Pigeon Hole, Victoria River (× 1/6).
Tracing.
In the north of Australia, the Larrekiya, Wogait, and other tribes

have adopted a similar designation for a series of dark spaces along
the Milky Way. But they have extended the idea considerably in that
the Coal Sack represents only the head of a gigantic emu, the beak
of which is pointed towards the Musca constellation (i.e. towards the
south). A small star of the Southern Cross group very appropriately
stands for the eye of the bird; the nebulous effect usually
surrounding this star gives it an extra life-like appearance. The neck
is but faintly discernible near the head, but becomes clearly visible in
the neighbourhood of the nearer Pointer; it passes between the two
Pointers and curves slightly towards the constellation of Lupus.
Within the constellation of Norma, the dark space widens
considerably and represents the body of the emu. The blunt tail turns
sharply towards, and into, the constellation of Scorpio. A nebulous
patch lying practically on the point of junction between the imaginary
areas of Ara, Scorpio, and Norma affords a good division between
the legs of the bird, whilst another lying between μ and ζ of the
Scorpion group separates the tail. The lower portions of the legs are
not very clear, but some of the more imaginative natives maintain
that they can distinguish three toes on each extremity. There is no
doubt the primitive eye has herein discovered a striking similarity
between an optical phenomenon in the southern sky and a living
creature, which is of great importance in the hunting field, and at the
same time plays a prominent role in tribal folk-lore. They refer to this
emu by the name of “Dangorra.” Vide Fig. 17.
PLATE XLII
1. Rock carvings, Flinders Ranges.
2. Emu design carved into the butt of a boabab tree, King Sound.
Fig. 29. Remarkable cave drawing, Glenelg River, N.W. Australia
As affording a means of comparison, a hunting scene is

reproduced carved upon the surface of a club by aborigines of
Victoria. The little group is composed of an aboriginal hunter who in
one hand is poising a spear and in the other is carrying a
boomerang; behind him are two emus standing in much the same
position as that assumed to be the case in the heavenly image just
described.
The Minning at Eucla recognize only the long neck of the emu in
the sky, and refer to it as “Yirrerri”; on the Nullarbor Plains the same
portion is looked upon as the heavenly tjuringa of the emu.
Fig. 30. Pictograph of lizard, natural and conventional form.
Speaking generally, there is perhaps no other creature living which

figures so frequently in aboriginal art, both on the cave wall and in
the dance, as the great struthious bird of Australia. This is no doubt
due in the first place to the admirable way in which it lends itself for
the purposes mentioned; its antics in the field suggest many tricks
for mimicry at a corrobboree, and its distinctive form supplies the
artist with a model which never fails to attract the attention of the
artistically inclined among his people. In Plate XLIX, 2, we have a
pipeclay drawing of an emu from the Katherine River which is rather
exceptional in that it shows the bird more en face than is usual; the
proportions are, on the whole, good, except that the head is screwed
upwards in a rather strange way. On a boomerang from Broome
(Fig. 18), we have a series of engraved emu pictures, all in profile,
and in different attitudes.
On the whole, an aboriginal’s pictures are flat and without
perspective. He takes the inspiration direct from nature and
reproduces the subject singly, and as a separate entity; a number of
such designs are drawn side by side with or without pictographic
sequence. But there are countless occasions upon which artists,
especially the more gifted, prefer to draw a real scene from life,
combining subject with action. Environment or surroundings rarely, if
ever, receive attention.
Take as a very simple illustration the lizard shown in the pipeclay
rock drawing from the Katherine River (Plate XLIX, 3). The general
shape of the body, together with the large and well-differentiated
head, strongly suggests a species of the large monitor which is
common throughout the district. The interesting feature about the
picture is, however, the life which is indicated by the fact that the
reptile is drawn in the act of shooting out a long, split tongue.
Fig. 31. Normal, conventional, and emblematic representations of turtle.

Fig. 32. Normal, conventional, and emblematic representations of frog.
Again, in the charcoal sketch of two crows from the Pigeon Hole
district (Fig. 19), one bird is represented in an attentive attitude, as
though on the point of flying away, while the other is very
characteristically shown in the act of cawing.
One could produce an almost endless variety of decorated figures,
representing men and women performing at ceremonial dances and
corrobborees to illustrate the life and action which is embodied in
aboriginal art. In Fig. 20 a selected number of pipe-clay drawings
from the Humbert River, Northern Territory, have been grouped
together to serve this purpose.
Fig. 33. Normal, conventional, and emblematic representations of echidna.
The most interesting effects, however, are those brought about by

a combination of two or more figures. How different, for instance, the
two kangaroo shown together in Fig. 21 seem to those previously
discussed (Plate XLVII). These are charcoal drawings from Pigeon
Hole on the Victoria River, and in them the hopping movement of the
animals is indicated very clearly. The animal in the rear is in full
flight, as the erect position of the tail and the general holding of the
body betray; but the one in the lead is on the point of drawing up and
is turning its head back towards its mate.
How realistic, too, the little bark drawing is from east of Port
Darwin (Fig. 22), in which a bird of prey is shown mounted upon a
wallaby or kangaroo, with its claws and beak embedded in the flesh
of its victim.
PLATE XLIII
1. Carved boabab nut, King Sound.
2. “Wanningi” from north-western Australia.
3. Slate scrapers used by the extinct Adelaide tribe for trimming skins.
A neat pipe-clay drawing from the remote Humbert River district is
presented in Fig. 23. The group, which is three feet in length, is
composed of a central figure of a man who is holding one arm on
each side towards a dog, as if offering them something to eat or for
the purpose of patting them. The dogs seem to be giving their
attention to the man.
Fig. 34. Conventionalized “Ladjia” or yam Tjuringa pattern.
Two more charcoal drawings from Pigeon Hole, though roughly

sketched by the artist, depict very graphically scenes from the hunt.
In one (Fig. 24), the hunter is in the act of stalking a buffalo or
bullock with his spear held in readiness to throw, while in the other
the attitude of the hunter indicates that the spear has just been
thrown and is entering the body of the prey, a kangaroo (Fig. 25).
The carving of an Arunndta man, reproduced in Fig. 26, is most
effective. An angry husband has been caught by the artist in the act
of punishing his wife with a waddy. The placement of the legs of the
two persons indicates stability on the part of the man engaged in the
flagellation, and a swinging movement on the part of the woman who
is being held back by her hand.
Fig. 35. A dog-track.
We have already seen the carved representations of two stages in

a stone-knife duel by an Arunndta tribesman (Fig. 4), and here, in
Fig. 27, an ochre drawing is reproduced which is, if anything, more
animated than any previously discussed. A spear-boomerang duel is
being fought, during which each of the combatants is protecting
himself with a shield. The artist has evinced considerable talent in
portraying the men just at the moment when both are bounding
through the air towards each other, the one on the left parrying his
opponent’s spear, while the other, on the right, is preparing to
receive the blow from the boomerang.
Fig. 36. A kangaroo-track.
One might now go a step further in analyzing aboriginal art. The

productions we have studied so far embody the ideas of form, life,
and action; and, it might be added, occasionally one finds a very fair
sense of composition as well. Such, indeed, might already be said to
be true of several of the pictures discussed above, but a finer
specimen lies before us in the charcoal drawing from Pigeon Hole
(Fig. 28). This faithfully portrays a scene from a gala ceremony, in
which the body of performers, fully “dressed” for the occasion, are
acting before the leader, who, in his turn, is being supported by two
others in the foreground. It must be admitted that the composition of
this group of figures is remarkably good, and, what is quite
exceptional, a very successful attempt has been made at
perspective. All figures are shown in different attitudes of dancing.
The impression this charcoal drawing gives one, at first glance, is
that of a rough sketch in crayon resembling the outline a European
artist might make on his canvas prior to starting upon the actual
painting.
Fig. 37. A rabbit track.
Leaving that section of aboriginal art which deals essentially with

designs copied directly from Nature in a sense more or less purely
artistic and æsthetic, we shall turn our attention to a few types which
are more specialized.
Fig. 38. Emu tracks.
From a study of his religious ideas, we have learned that the

aboriginal identifies himself with some mystic, natural creature or
object, which he adopts as his “totem.” It would only be reasonable
to expect, therefore, that some of the drawings represent these
objects; and that they are recognized by the natives as having
particular personal or family significance. Looked at from a modern
standpoint, these designs are really the equivalent of a family crest,
and are claimed only by those rightfully entitled to them. This
explanation must be given for many of the naturalistic designs
appearing on rocks, trees, grave posts, and personal belongings.
These “totemic” crests or symbols being hereditary, we have before
us a primitive form of heraldry, a conception we have already learned
to be covered by the word “Kobong,” originally introduced by Sir
George Grey from the north-west of Australia.
Fig. 39. Pictographic
representation of nesting emu.
Fig. 40. A lizard track.
We have also ascertained that some of the central as well as

north-western tribes of Australia believe that the earliest tribal
ancestors originally were more animal than human in appearance,
and adopted the shape of a man only at a later period; that they can,
however, return to the animal form whenever they desire; and that
others remain semi-human. It is not surprising, therefore, to find
amongst their drawings and carvings representations which are
partly human and partly animal in outline; these are honest attempts
at perpetuating the traditional appearance of the ancestral beings of
the tribe. In the photograph attached hereto (Plate LI, 1), taken at
Forrest River, two pictures of such creatures are to be found which
are drawn in ochre. There were many others, from three to five feet
in length, reptilian in shape, some with human hands and feet, others
with hair shown upon the head, and in most of them the sex unduly
prominent. These remarkable designs are, therefore, not naturalistic,
but have been evolved on purely fictional or mythological lines,
based upon the tradition of the tribe and upon the imagination of the
artist.
Fig. 41. A snake or snake-track.

From the consideration of these artistic effigies of their Demigods,
it is not a big step forwards which brings us face to face with the
sacred tribal drawings. During initiation ceremonies, especially of the
now practically extinct south-eastern tribes of Australia, gigantic
figures resembling a human being were moulded into the surface of
the ground and subsequently tinted with ochre, which were
supposed to conceal the Great Spirit or Deity, which, like the “Altjerra
Knaninja” of central Australia, watched over the proceedings as the
young men passed from a condition of adolescence to that of
permanent manhood; numerous carvings and ochre drawings were
also made upon the trunks of any trees nearby.
Not only during the initiation ceremonies are these practices
resorted to, but when a sacred observance is contemplated,
especially those having to do with the “totem,” elaborate designs are
painted in ochre upon the surrounding surfaces of rocks and trees
which depict an act connected with the traditional origin of the sacred
object.
A classical illustration is to be found in the MacDonnell Ranges, at
Emily Gap. According to Arunndta belief, it was at this spot that the
early semi-human ancestors of the witchedy grub or “Utnguringita”
alighted from Altjerringa. They brought with them large numbers of
the grub, which they cooked and ate. The territory dominated by
these ancient beings extended from Heavitree Gap to Emily Gap,
and across to Jessie Gap. On the western wall of the first-named
gap, known by the natives as “Ndariba,” an inclined slab of rock, not
high above the level of the sandy bed of the Todd River, contains a
series of peculiar concentric iron stains which are regarded as the
impressions of the stern of an Utnguringita Altjerra who sat there,
and, as he collected grubs, moved forwards. The Utnguringita came
into frequent conflict with the Dingo or “Knullia” people whose
country lay immediately west of Heavitree Gap, but, nevertheless,
they blessed the land with many eggs, which developed into larvæ
and supplied the tribe with food.
Fig. 42. Human foot-prints and trail.
Eventually the Utnguringita ancestors returned to Altjerringa, but

they left a number of stone tjuringas in Emily Gap, which are
supposed to be occupied by the spirits whenever a sacred ceremony
is performed on the spot. On the eastern stony wall of this gap some
rather imposing designs are to be seen, which originally must have
occupied most of the area available. The drawings are very old; their
origin dating back long before the recollections of the present
generation. It is wonderful how well the work has withstood the
denuding action of the weather for so long. The natives tell you that
the old Altjerringa men applied the pigment to the rock and that they
mixed it with the “knudda” (fat) of the grubs. It is more likely that the
ochres were mixed with emu fat; in places the pigment seems as
though it were chemically combined with the rock, and it could only
be removed by chipping the surface. The designs in their present
condition (Plate LI, 2) consist of a series of parallel, vertical lines,
alternately coloured red and white, and capped by horizontal bands
of the same colours, the white of which containing three or four red
dots. What the original designs may have been like, it is now difficult
to say, but the natives maintain that they included the images of
some women they call “Aluggurra,” who were waiting at the foot of
the cliff while the men were concealing their tjuringas in the rocks
and nooks above. To the present day, the old men of the local
Arunndta group store their ceremonial objects in the same sanctuary,
thinking that the sacred figures on the wall will protect them from the
hands of inquisitive intruders.
There remains yet another class of ochre drawing which deserves
mention. I allude to the famous discovery of Sir George Grey in
1837. There is perhaps no other Australian drawing, old or modern,
which has been so freely discussed and criticized. During an
expedition in the northern Kimberleys of Western Australia, it was my
good fortune to re-discover several drawings of this type in
practically the same locality as that recorded by Sir George Grey,
near the Glenelg River. One figure was perfect, others were partly
obliterated or incomplete. The best design was in a cave near the
top of a prominent bluff the local Worora people call Berrial; it was
drawn in ochre upon a steep face of rock immediately under an
overhanging ledge of quartzite. The figure was unquestionably that
of a human being, although it measured fully nine feet in length. It lay
fully extended, upon its left side, with its arms placed straight against
its sides. It reminded one forcibly of a Buddha in a Ceylonese
temple. What made the figure seem un-Australian was that it was
clothed in a long, striped garment, resembling a priestly gown, from
which only the head, hands, and feet were excluded. A loosely-fitting
belt is also shown. As seems common to all these drawings, the
facial features are only indicated by the eyes and nose, the mouth
being omitted. Another characteristic, which is shared by all other
drawings, is that the head is surrounded by a number of peculiar,
concentric bands, through which, and from which, many lines
radiate, giving the structure the effect of a halo surrounding the head
of a saint. The picture bore an unmistakable likeness to the type
illustrated by Sir George Grey, and was drawn in red, brown, black,
and white. Vide Fig. 29 and Plate L, 2.
Fig. 43. “A man is tracking a rabbit.” Simple example of pictography.
There is no doubt about these curious drawings, now more or less

adopted by the local tribe, having originated under some exotic
influence. It is historically known that for centuries past excursions
have been made to the north of Australia by Macassans and other
eastern people, who may have been responsible for the first drawing
of a figure of so sacerdotal an appearance, which the aborigines
have since learned to copy so perfectly. It has also been speculated
that shipwrecked sailors might be responsible for the representation

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SECTION 1 CARE OF THE HOSPITALIZED PATIENT

SECTION 2 MEDICAL EMERGENCIES

10 Cardiovascular Collapse and Sudden Death.............................57

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SECTION 3 COMMON PATIENT PRESENTATIONS

28 Fever, Hyperthermia, and Rash................................................127

58 Sore Throat, Earache, and Upper

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59 General Examination of the Skin.............................................255

SECTION 6 HEMATOLOGY AND ONCOLOGY

61 Examination of Blood Smears and Bone Marrow...................265

SECTION 7 INFECTIOUS DISEASES

78 Infections Acquired in Health Care Facilities..........................357

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87 Streptococcal/Enterococcal Infections, Diphtheria,

110 Physical Examination of the Heart...........................................613

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114 Valvular Heart Disease..............................................................632

128 Respiratory Function and Pulmonary

138 Acute Renal Failure...................................................................747

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142 Glomerular Diseases.................................................................759

147 Peptic Ulcer and Related Disorders.........................................785

SECTION 12 ALLERGY, CLINICAL IMMUNOLOGY, AND RHEUMATOLOGY

156 Diseases of Immediate-Type Hypersensitivity.......................835

SECTION 13 ENDOCRINOLOGY AND METABOLISM

168 Disorders of the Anterior Pituitary and Hypothalamus.........877

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170 Thyroid Gland Disorders...........................................................886

180 The Neurologic Examination....................................................947

SECTION 15 PSYCHIATRY AND SUBSTANCE ABUSE

196 Psychiatric Disorders............................................................. 1063

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199 Alcohol Use Disorder.............................................................. 1080

SECTION 16 DISEASE PREVENTION AND HEALTH MAINTENANCE

201 Routine Disease Screening.................................................... 1087

SECTION 17 ADVERSE DRUG REACTIONS

206 Adverse Drug Reactions........................................................ 1107

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JOSEPH LOSCALZO, MD, PhD

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