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ENDOCRINE
SEVENTH EDITION
ENDOCRINE
EDITOR:
MICHAEL T. McDERMOTT, MD
Professor of Medicine and Clinical Pharmacy
University of Colorado Denver School of Medicine
Director, Endocrinology and Diabetes Practice
University of Colorado Hospital
Aurora, Colorado
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ENDOCRINE SECRETS, SEVENTH EDITION ISBN: 978-0-323-62428-2
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Henry McDermott, for making life fun.
LIST OF CONTRIBUTORS
Abdurezak A. Abdela, MBBS Tamis M. Bright, MD

Internal Medicine Associate Professor
Addis Ababa University Chief, Division of Endocrinology
Addis Ababa, Ethiopia Texas Tech University
El Paso, TX, United States
Veena R. Agrawal, MD, FRCPC
Assistant Professor Henry B. Burch, MD, FACE
Department of Internal Medicine Program Director
University of Manitoba Division of Diabetes, Endocrinology, and Metabolic
Winnipeg, MB, Canada Diseases
National Institute of Diabetes and Digestive and Kidney
Maria B. Albuja-Cruz, MD Diseases
Assistant Professor Professor of Medicine
Department of Surgery Endocrinology Division
University of Colorado Anschutz Medical Campus Uniformed Services Health Sciences University
Aurora, CO, United States Bethesda, MD, United States
Sarah L. Anderson, PharmD Anne-Marie Carreau, MD, MSc
Associate Professor Faculty of Medicine
Department of Clinical Pharmacy Université Laval
University of Colorado Skaggs School of Pharmacy and Division of Endocrinology and Nephrology
Pharmaceutical Sciences Centre de Recherche du CHU de Québec-Université
Aurora, CO, United States Laval
Clinical Pharmacy Specialist Quebec, Canada
Ambulatory Care Services
Denver Health Medical Center Ana Chindris, MD
Denver, CO, United States Endocrinology
Mayo Clinic
Harris M. Baloch, MD Jacksonville, FL, United States
Department of Endocrinology
Walter Reed National Military Medical Center Melanie Cree-Green, MD, PhD
Bethesda, MD, United States Assistant Professor
Division of Endocrinology
Linda A. Barbour, MD, MSPH Department of Pediatrics
Professor University of Colorado Anschutz Medical Campus
Medicine and Obstetrics and Gynecology Director, Multi-Disciplinary PCOS Clinic
University of Colorado School of Medicine Children’s Hospital Colorado
Aurora, CO, United States Aurora, CO, United States
Brenda K. Bell, MD Mark M. Cruz, MD
Clinical Endocrinologist Fellow
Private Practice Department of Endocrinology
Lincoln, NE, United States Walter Reed National Military Medical Center
Helen Y. Bitew, MD Bethesda, MD, United States
Assistant Professor of Medicine Shanlee M. Davis, MD, MSCS
Internal Medicine Assistant Professor
Addis Ababa University Pediatric Endocrinology
College of Health Sciences Children’s Hospital Colorado
Addis Ababa, Ethiopia University of Colorado
Mark Bridenstine, MD Aurora, CO, United States
Banner Health Clinic Stephanie Davis, MD
Loveland, CO, United States General Surgery Resident
University of Colorado Anschutz Medical Campus
Aurora, CO, United States
vi
LIST OF CONTRIBUTORS vii
Meghan Donnelly, MD Thomas Jensen, MD

Assistant Professor Assistant Professor
Obstetrics and Gynecology University of Colorado Denver
University of Colorado School of Medicine Aurora, CO, United States
Denver, CO, United States Janice M. Kerr, MD
William E. Duncan, MD, PhD, MACP Associate Professor
Professor of Medicine Endocrinology, Metabolism and Diabetes
Department of Medicine University of Colorado, Denver
Uniformed Services University Denver, CO, United States
Bethesda, MD, United States Pratima Kumar, MD, FACE
Oliver J. Fackelmayer, MD Assistant Professor, Division of Endocrinology
Surgical Resident Department of Medicine
University of Colorado Anschutz Medical Campus Dell Medical School
Department of Surgery The University of Texas at Austin
Aurora, CO, United States Austin, TX, United States
Shari C. Fox, BS, MS, MD, FACE Helen M. Lawler, MD

Department of Endocrinology Assistant Professor
Colorado Permanente Medical Group Division of Endocrinology, Metabolism, and Diabetes
Denver, CO, United States University of Colorado
Michele B. Glodowski, MD
Homer J. LeMar Jr., MD
Clinical Instructor
El Paso Veterans Affairs Health Care System
New York University School of Medicine
New York, NY, United States
Vinh Q. Mai, DO, FACP, FACE
Bryan R. Haugen, MD Chief and Associate Professor
Professor of Medicine and Pathology Endocrinology, Diabetes and Metabolism
Head, Division of Endocrinology, Metabolism Walter Reed National Military Medical Center
and Diabetes Bethesda, MD, United States
Mary Rossick Kern and Jerome H. Kern Chair of
Endocrine Neoplasms Research Ayesha F. Malik, MD
University of Colorado School of Medicine Fellow
Aurora, CO, United States Endocrinology
Mayo Clinic
Matthew R. Hawkins, BSW, MMSc Jacksonville, FL, United States
Senior Instructor/Physician Assistant
Division of Endocrinology, Metabolism and Diabetes Roselyn I. Mateo, MD, MSc
University of Colorado School of Medicine Endocrinology
Aurora, CO, United States Beth Israel Deaconess Medical Center
Boston, MA, United States
James Vincent Hennessey, MD
Clinical Director Sarah E. Mayson, MD
Endocrinology Assistant Professor
Beth Israel Deaconess Medical Center Division of Endocrinology, Department of Medicine
Associate Professor University of Colorado School of Medicine
Medicine Rocky Mountain Regional Veterans Affairs Medical Center
Harvard Medical School Aurora, CO, United States
Boston, MA, United States Michael T. McDermott, MD
Professor of Medicine and Clinical Pharmacy
Thanh Duc Hoang, DO, FACP, FACE
University of Colorado School of Medicine
Director, NCC Endocrinology Fellowship Program
Director, Endocrinology and Diabetes Practice
Department of Endocrinology
Walter Reed National Military Medical Center
Associate Professor, Internal Medicine
Director, Endocrinology Division Robert C. McIntyre Jr., MD
Uniformed Services Health Sciences University Professor
Bethesda, MD, United States Department of Surgery
Sean J. Iwamoto, MD Aurora, CO, United States
Instructor of Medicine
Endocrinology, Metabolism and Diabetes Logan R. McKenna, MD
University of Colorado School of Medicine Surgical Resident
Rocky Mountain Regional VA Medical Center University of Colorado Anschutz Medical Campus
Aurora, CO, United States Aurora, CO, United States
viii LIST OF CONTRIBUTORS
Shon Meek, MD, PhD Kevin B. Rothchild, MD

Assistant Professor Assistant Professor
Endocrinology Division GI, Tumor, and Endocrine Surgery
Mayo Clinic University of Colorado Hospital
Jacksonville, FL, United States Aurora, CO, United States
Richard Millstein, DO Micol Sara Rothman, MD
University of Colorado Health Endocrinology Associate Professor of Medicine
Greeley, CO United States Endocrinology, Diabetes and Metabolism
Kerrie L. Moreau, PhD Aurora, CO, United States
Professor
Division of Geriatrics Shauna Runchey, MD, MPH
University of Colorado Anschutz Medical Campus Fellow
Aurora, CO, United States University of Colorado Anschutz Medical Campus
Research Health Scientist Denver, CO, United States
Geriatric Research Education Clinical Center (GRECC)
Mary H. Samuels, MD
Denver Veterans Administration Medical Center
Professor of Medicine
Denver, CO, United States
Program Director, Clinical and Translational Research
Wesley Nuffer, PharmD Center
Associate Professor Oregon Health & Science University
Department of Clinical Pharmacy Portland, OR, United States
University of Colorado Skaggs School of Pharmacy &
Leonard R. Sanders, MD, FACP, BC-ADM, CDE, CLS
Pharmaceutical Sciences
Director of Diabetes Care
Endocrinology
John J. Orrego, MD Montage Medical Group
Endocrinologist Monterey, CA, United States
Endocrinology and Metabolism
Virginia Sarapura, MD
Colorado Permanente Medical Group
Associate Professor
Medicine-Endocrinology
Endocrinology Department Chair
Endocrinology and Metabolism
St. Joseph Hospital
Denver, CO, United States David Saxon, MD, MSc
Assistant Professor
Roger A. Piepenbrink, DO, MS, MPH, FACP, FACE
Division of Endocrinology, Metabolism, and Diabetes
Staff Physician
University of Colorado
Departments of Adult Endocrinology and Sleep Medicine
Mike O’Callaghan Federal Medical Center Aurora, CO, United States
Nellis Air Force Base Jonathan A. Schoen, MD
Las Vegas, NV, United States Associate Professor of Surgery
GI, Tumor, and Endocrine Surgery
Christopher D. Raeburn, MD
Associate Professor
Department of Surgery
University of Colorado Anschutz Medical Campus Emily B. Schroeder, MD, PhD
Aurora, CO, United States Clinician Investigator
Institute for Health Research
Aziz Ur Rehman, MD
Kaiser Permanente Colorado
Assistant Professor
Assistant Professor
Division of Endocrinology
Division of Endocrinology, Metabolism and Diabetes
Texas Tech University
El Paso, TX, United States University of Colorado School of Medicine
Richard O. Roberts III, MD, MPH
Stacey A. Seggelke, DNP, APRN, ACNS-BC, BC-ADM
Fellow Physician
Senior Instructor of Medicine
Children’s Hospital Colorado
Department of Medicine, Division of Endocrinology
Department of Pediatrics
University of Colorado Denver
Section of Endocrinology and Diabetes
LIST OF CONTRIBUTORS ix
Kenneth J. Simcic, MD† Nicole Odette Vietor, MD

Formerly Assistant Professor Department of Endocrinology, Diabetes, and Metabolism
Division of Endocrinology Walter Reed National Military Medical Center
Department of Medicine Bethesda, MD, United States
University of Texas Health Science Center at San Antonio
Robert A. Vigersky, MD
San Antonio, TX, United States
Robert H. Slover, MD Endocrinology Service
Director of Pediatrics Walter Reed National Military Medical Center
The Barbara Davis Center for Diabetes Bethesda, MD, United States
Professor of Pediatrics
Katherine N. Vu, DO
Wagner Family Chair in Childhood Diabetes
Assistant Professor
University of Colorado Denver
Endocrinology Service
Anschutz Medical Campus
Naval Medical Center San Diego
San Diego, CA, United States
Robert Smallridge, MD
Cecilia C. Low Wang, MD, FACP
Associate Professor of Medicine
Endocrinology Division
Associate Director, Fellowship/Education
Mayo Clinic
Jacksonville, FL, United States
Christine M. Swanson, MD, MCR, CCD Aurora, CO, United States
Assistant Professor
Matthew P. Wahl, MD
Assistant Professor of Medicine (Clinical)
Division of Endocrinology Metabolism, and Diabetes
University of Utah School of Medicine
Elizabeth A. Thomas, MD Salt Lake City, UT, United States
Assistant Professor
Katherine Weber, MD
Endocrinology
Kaiser Permanente
Rocky Mountain Regional Veterans Affairs Medical
Center
Aurora, CO, United States Margaret E. Wierman, MD
Carlos A. Torres, MD
William Beaumont Army Medical Center
Majlinda Xhikola, MD
Sharon H. Travers, MD
Fellow
Associate Professor
Endocrinology Division
Pediatric Endocrinology
Mayo Clinic
Jacksonville, FL, United States
Aurora, CO, United States Adnin Zaman, MD
Clinical/Research Fellow
Jennifer M. Trujillo, PharmD
Associate Professor
Clinical Pharmacy
Aurora, CO, United States Philip Zeitler, MD, PhD
Professor
Amy M. Valent, DO
Pediatrics
Assistant Professor
University of Colorado Denver Anschutz Medical Campus
Obstetrics and Gynecology
Chair
Oregon Health and Science University
Endocrinology
Portland, OR, United States
†Deceased
PREFACE
Medical and scientific investigations are progressing at an astounding pace. It is difficult for any provider, at whatever
level, to keep up with the enormous volume of primary research, case reports, review articles, and clinical practice
guidelines that are published daily in printed and online forms. The authors of the chapters in this book have carefully
reviewed and summarized each specific assigned area and have added their own opinions, based on their extensive
clinical experience, to give readers the best possible coverage of these topics in a well-organized and concise form.
I thank each author, from mentored fellows to seasoned faculty and practitioners, for their selfless and painstaking
efforts to educate our readers with their own unique blends of knowledge, experience, and humanism.
The question-and-answer format, intended to mimic the interchanges between mentors and trainees on
rounds, has been preserved and carried on from the 1st Edition (1994) to the current 7th Edition (2019) of Endocrine
Secrets. But the original goal of 20 questions followed by short and to-the-point answers has been eclipsed by the
ever-expanding volume of research discoveries and evidence-based clinical practice guidelines for the multiple
conditions and issues in our field. As a result the chapters are necessarily longer now, with more questions and
answers than before.
I have also added numerous chapters to cover areas that were not covered in previous editions. One chapter
is devoted to case-based practical exercises in carbohydrate counting and insulin dose calculations; another tackles
the rapidly expanding field of diabetes technology; and yet another details the causes of spontaneous hypoglycemia,
including the cause and management of postbariatric surgery hypoglycemia. There are interesting new chapters on
pituitary stalk lesions, adrenal incidentalomas, and polycystic ovary syndrome. There is a specific chapter that covers
the emerging field of endocrinopathies resulting from the use of immune checkpoint inhibitors. There are now four
separate chapters on endocrine surgery. The new chapter on the care and management of transgender patients is
one of the highlights of this edition. Finally, I have included a unique and fascinating chapter detailing the state of
Endocrinology in Africa, authored by my valued colleagues from Ethiopia, Dr. Helen Y. Bitew and Dr. Abdurezak A.
Abdela.
I hope the readers of this book will find it readable, enjoyable, educational, and sufficiently comprehensive to
enable them to practice Endocrinology at the highest possible level for the benefit of all the patients who entrust their
care to them. Never stop learning. And I hope that all your patients reap the benefits of your expanding knowledge,
devotion to lifelong learning, and continuing compassion for them.
Michael McDermott, MD
Editor, Endocrine Secrets, 7th Edition
x
I
Fuel Metabolism
DIABETES MELLITUS: ETIOLOGY,
CHAPTER 1
CLASSIFICATION, AND DIAGNOSIS

Adnin Zaman and Cecilia C. Low Wang
1. What is diabetes mellitus?

Diabetes mellitus is a term that encompasses a heterogeneous group of metabolic disorders, all of which are
characterized by elevated blood glucose levels.
2. What is the origin of the term diabetes mellitus?
Although diabetes has been described in literature as ancient as the Ebers Papyrus of Egypt by Hesy-Ra (1552 bce),
the word diabetes comes from Arateus and the Greek word “diabainein” which means “siphon,” because affected
people excreted excessive amounts of urine. The term diabetes mellitus was coined by Thomas Willis of Oxford,
England, in 1675, when it was discovered that the urine of people with diabetes was sweet rather than tasteless
(insipidus).
3. What is the epidemiology of diabetes?
Approximately 1.5 million Americans are diagnosed with diabetes each year. Thirty million Americans, or nearly
9% of the population, had diabetes mellitus in 2015. Of this, 1.25 million children and adults had type 1 diabetes.
However, evidence suggests that out of the 30 million adults with diabetes, 7.2 million remain undiagnosed.
The number of individuals with prediabetes is roughly 84 million. American Indians and Alaskan Natives have
the highest rate of diabetes (15.1%), whereas non-Hispanic whites have the lowest prevalence.
4. What is the underlying pathophysiology of the two most common types of diabetes?
Type 1 diabetes results from autoimmune destruction of pancreatic beta cells causing complete or nearly com-
plete insulin deficiency. Type 2 diabetes is characterized by excessive hepatic glucose production, tissue insulin
resistance, and relative insulin deficiency, resulting in insufficient beta cell insulin production to compensate for
the increased insulin requirements. In both cases, it is ultimately the absolute or relative insulin deficiency that
results in elevated blood glucose levels.
5. Why do people get diabetes?
Type 1 diabetes occurs in people who have an inherited susceptibility (genetic—HLA related) and later a superim-
posed environmental trigger (theories have focused on food exposures, viral infections, and alterations of the
intestinal microbiome). Type 2 diabetes has an even stronger genetic influence (polygenic, but not yet well
defined) and more established environmental triggers (obesity, physical inactivity, glucocorticoid therapy).
6. How is diabetes diagnosed?
Diabetes is diagnosed through laboratory testing; there are several criteria for the diagnosis of diabetes. Ideally,
two tests on different occasions are needed to confirm the diagnosis:
a. Hemoglobin A1c (HbA1c)  6.5% (HbA1c of 5.7%–6.4% establishes a diagnosis of prediabetes
b. Fasting plasma glucose  126 mg/dL. Fasting is defined as no caloric intake for at least 8 hours
c. Random plasma glucose  200 mg/dL in a patient with classic symptoms of hyperglycemia
d. Oral glucose tolerance test with a 2-hour plasma glucose  200 mg/dL after a 75-g load of anhydrous
glucose dissolved in water
7. What is the current classification for different types of diabetes?
Previously, diabetes was classified as type 1, type 2, gestational, or “secondary” diabetes. The most current classifi-
cation of diabetes includes type 1, type 2, type 3c (pancreatogenous), gestational (type 4), latent autoimmune
diabetes of adulthood (LADA), and maturity-onset diabetes of the young (MODY), among many others.
European investigators have recently proposed that types of diabetes be divided into five relatively distinct
groups, which may offer greater predictability for diabetes-related outcomes:
Cluster 1 (severe autoimmune diabetes)—early-onset disease, low body mass index (BMI), poor metabolic control,
insulin deficiency, glutamic acid decarboxylase antibody (GAD Ab) positive
Cluster 2 (severe insulin-deficient diabetes)—similar to cluster 1, but GAD Ab negative
Cluster 3 (severe insulin-resistant diabetes)—high BMI and insulin resistance
Cluster 4 (mild obesity-related diabetes)—high BMI, but no insulin resistance
Cluster 5 (mild age-related diabetes)—similar to cluster 4, but higher age at diagnosis, and with modest metabolic
derangements
8
DIABETES MELLITUS: ETIOLOGY, CLASSIFICATION, AND DIAGNOSIS 9
Table 1.1. Classification of Diabetes Based in Antibody Status and Beta Cell Function.
A1 A2
b1 A1/b1 A2/b1
Presence of autoantibodies but preserved b-cell Absence of autoantibodies and preserved b-cell
function (ex. LADA) function (ex. type 2 DM)
b2 A1/b2 A2/b2
Presence of autoantibodies and absent b-cell Absence of autoantibodies with absent
function (ex. type 1 DM) b-cell function (ex. type 3c DM)
DM, Diabetes mellitus; LADA, latent autoimmune diabetes of adulthood.
Another way to classify diabetes is to consider antibody status and beta cell function (Ab6), which places all
forms of diabetes along a spectrum. In this system, for example, type 1 diabetes would be reclassified as autoim-
mune positive and beta cell negative (A1/b2) to indicate that it is a disease of hyperglycemia in the presence of
autoimmunity with no beta cell production of insulin. Similarly, one might think of LADA as A1/b1 (autoimmune
disorder of pancreas but with continued beta cell function) and type 2 diabetes as A2/b1 and postpancreatectomy
diabetes as A2/b2 (Table 1.1).
8. What is the natural history of type 1 diabetes?
The natural history of type 1 diabetes involves lifelong requirement for insulin therapy. Soon after the diagnosis of
type 1 diabetes is made, there is often a “honeymoon phase,” during which beta cells are still able to produce
small amounts of insulin. Patients usually still require insulin during this time but at generally smaller doses than
later in the course of their diabetes. Without insulin therapy, patients develop a life-threatening condition known
as diabetic ketoacidosis (DKA; see Chapter 2). If hyperglycemia is not adequately controlled, patients may
suffer from chronic complications of diabetes, such as retinopathy, diabetic kidney disease, and neuropathy.
9. What is the natural history of type 2 diabetes?
In individuals with type 2 diabetes, generally there is some degree of insulin resistance in the initial stages, but
eventually, insulin deficiency develops and worsens over time. Diabetes (with hyperglycemia) does not develop
until pancreatic beta cells become incapable of producing enough insulin to compensate for the individual’s
insulin resistance. Noninsulin medications are often effective in restoring euglycemia initially, but multiple agents
are often needed over time to maintain glycemic control. If patients are on several noninsulin agents but have not
achieved their goal HbA1c, insulin can be added to the regimen. Some patients with type 2 diabetes may ultimately
require basal-bolus insulin therapy (as with type 1 diabetes) to achieve glycemic control. Weight loss is an effec-
tive strategy to reduce insulin resistance and usually allows patients to reduce the number of medications needed
to achieve and maintain their goal HbA1c.
10. Who develops ketosis-prone diabetes?
A less commonly encountered form of diabetes is characterized by a temporary lack of insulin production by
pancreatic beta cells. Ketosis-prone diabetes disproportionately affects nonwhite individuals. Patients with DKA
require insulin therapy to manage this condition and for a short time after resolution of DKA. However, in most
individuals, beta cell function is eventually recovered, and insulin therapy can be tapered off within a few months.
In fact, patients tend to become hypoglycemic within weeks of hospital discharge if maintained on their original
basal-bolus regimen unless the clinician and patient closely monitor blood glucose values to scale back the insulin
regimen. Once the immediate post-DKA period of glucose toxicity is overcome and beta cell function is regained,
patients can typically be maintained on one or more noninsulin agents. Without lifestyle modifications and medi-
cation adherence, patients are at risk for a repeating cycle of DKA–glucose toxicity–insulin dependence–possible
hypoglycemia–recovery.
11. What is LADA?
LADA is a form of autoimmune diabetes with onset later in life compared with typical type 1 diabetes. This was pre-
viously thought to be a rare cause of diabetes, and individuals were often misdiagnosed as having type 2 diabetes
because of the later age of presentation. However, unlike patients with type 2 diabetes, patients with LADA have pos-
itive antibodies (usually GAD Ab). After their initial presentation, they may go through a “honeymoon phase,” during
which noninsulin agents are sufficient to achieve and maintain glycemic control. However, as beta cell failure pro-
gresses, patients eventually require insulin and ultimately experience a course similar to those with type 1 diabetes.
12. What other causal factors should I be thinking about when I see a patient with high glucose?
When evaluating a patient with high blood glucose, a new diagnosis of diabetes or existing poorly controlled
diabetes should always be at the forefront of consideration. However, there are other causes of hyperglycemia
that ought to be considered. The most common non–diabetes-related cause is glucocorticoid administration.
Although most individuals do not develop hyperglycemia while on steroids, these medications (given via any route)
10 FUEL METABOLISM
may precipitate hyperglycemia in those with underlying glucose intolerance. Critical illnesses and medical condi-
tions, such as infections, may also cause hyperglycemia because of stress-induced increase in cortisol production.
Similarly, hyperglycemia may develop in patients with endogenous hypercortisolism (Cushing syndrome)—either
from overproduction of adrenocorticotropic hormone (ACTH) by a pituitary tumor or ectopic tumor or from overpro-
duction of cortisol by an adrenal tumor. Other rare causes of hyperglycemia include acromegaly resulting from a
growth hormone–secreting pituitary adenoma or a catecholamine-producing tumor, such as a pheochromocytoma
or paraganglioma. In the inpatient setting, patients with glucose intolerance receiving intravenous dextrose as
either maintenance fluid or with IV medications may also develop hyperglycemia. Those receiving enteral nutrition
or total parenteral nutrition are at particularly high risk for developing hyperglycemia when nutrition is delivered
in this nonphysiologic manner.
13. What is type 3c diabetes?
Also known as pancreatogenic or pancreatogenous diabetes, type 3c diabetes is a form of diabetes that develops
when nonautoimmune disorders of the pancreas compromise pancreatic endocrine function, resulting in decreased
insulin production. Patients who have had recurrent acute pancreatitis or chronic pancreatitis; those who have
sustained abdominal trauma, such as from a motor vehicle accident; and those who have undergone partial or
complete pancreatectomy are most likely to develop type 3c diabetes.
14. Who should be screened for diabetes?
The United States Preventive Services Task Force (USPSTF) recommends screening for abnormal fasting plasma
glucose levels in overweight and obese adults ages 40 to 70 years. People who have a family history of diabetes,
those who have a history of gestational diabetes or polycystic ovarian syndrome, and those who are members of
certain racial/ethnic groups (African American, American Indian or Alaskan Native, Asian American, Hispanic or Latino
American, or Native Hawaiian/Pacific Islander in origin) may develop diabetes at a younger age or at a lower BMI
and, therefore, should be screened earlier. The American Diabetes Association (ADA) has made similar recommenda-
tions and suggests screening every 3 years starting at age 45 years with a fasting plasma glucose test.
15. Can diabetes be prevented?
The Diabetes Prevention Program (DPP) has demonstrated the significant beneficial effects of intensive lifestyle mod-
ifications in patients with prediabetes to prevent progression to diabetes. Randomized controlled trials have shown
that pharmacotherapy may also reduce the rates of progression to overt diabetes in individuals at high risk for type
2 diabetes, but the risks of these medications may outweigh their benefits in some patients. The ADA recommends
pharmacotherapy for patients who are at high risk for progression to diabetes because of multiple risk factors at
baseline and for those who have a persistently elevated HbA1c . 6% despite lifestyle modifications.
Although numerous strategies have been evaluated in controlled clinical trials, no therapies have been
demonstrated to effectively prevent the progression of type 1 diabetes.
16. What is monogenic diabetes?
Unlike type 1 and type 2 diabetes, which are multifactorial in etiology, monogenic diabetes results from single
gene mutations causing pancreatic beta cell dysfunction or insulin signaling defects. Patients are typically young
at the time of diagnosis, do not require insulin, and lack autoantibodies. Monogenic diabetes is often inherited in
an autosomal dominant pattern, and it is common to have multiple generations of family members affected. Neo-
natal diabetes and MODY are the two more common forms of monogenic diabetes. Identification of the affected
genes is beneficial from a therapeutic standpoint because the various forms of monogenic diabetes are treated
differently. For example, MODY3 is caused by a mutation in the hepatocyte nuclear factor-1 alpha and is most
effectively treated with sulfonylureas, whereas MODY2 results from a defect in the glucokinase gene and is best
treated with dietary changes alone.
17. How can insulin resistance be assessed clinically?
Insulin resistance has a wide array of clinical manifestations, including acanthosis nigricans, skin tags, hirsutism,
ovarian hyperandrogenism, and androgenic alopecia. Of these, acanthosis nigricans is the most commonly recognized
sign and is described as symmetric, velvety, light brown to black, thickened plaques and accentuated skin marks that
appear on knuckles and in intertriginous areas. The pathophysiology is thought to be stimulation of insulin growth
factor-1 receptors in fibroblasts and keratinocytes by extremely high insulin levels, resulting in proliferation of these
skin cells. Insulin resistance can be estimated in patients without diabetes by using the Homeostatic Model Assessment
of Insulin Resistance (HOMA-IR) score after measuring fasting blood glucose and serum insulin levels. Measurements
of insulin resistance, such as the hyperinsulinemic euglycemic clamp, are used in the research setting but not in the
clinical setting.
18. What is metabolic syndrome?
The diagnosis of metabolic syndrome requires at least 3 out of 5 of the following: hyperglycemia, hypertension,
hypertriglyceridemia, low levels of high-density lipoprotein (HDL), or increased abdominal circumference. When
present, metabolic syndrome is associated with significantly increased risk of heart disease, stroke, and diabetes
(if not already present). Treatment to reduce the risk for cardiovascular events requires intensive lifestyle modifi-
cation with dietary changes, exercise, and weight loss. Often, medications are needed to treat each individual
component of metabolic syndrome.
DIABETES MELLITUS: ETIOLOGY, CLASSIFICATION, AND DIAGNOSIS 11
KE Y P O I N T S
• Diabetes results from absolute or relative insulin deficiency. In type 1 diabetes, beta cells are destroyed, result-
ing in complete insulin deficiency. In type 2 diabetes, beta cells cannot produce enough insulin to compensate
for the underlying insulin resistance.
• Diabetes is diagnosed via blood testing and requires abnormal results on two separate occasions to confirm the
diagnosis. The diagnostic criteria include HbA1c  6.5%, fasting plasma glucose  126 mg/dL, random plasma
glucose  200 mg/dL in addition to the typical symptoms of diabetes, or plasma glucose  200 mg/dL 2
hours after receiving a 75-g glucose load during an oral glucose tolerance test (OGTT).
• There are several ways to classify the types of diabetes. The first method involves classifying diabetes as type 1,
type 2, type 3c, gestational (type 4), and “other.” Diabetes can also be conceptualized as falling on a spectrum
of autoimmunity and beta cell function (A 1/b2). More recently, some investigators have proposed that the
types of diabetes be divided into five distinct groups, which may be more helpful in predicting diabetes-related
outcomes.
• Patients with type 1 diabetes require lifelong insulin therapy, although there is often a short-lived initial “honey-
moon phase” during which pancreatic beta cells are still able to produce a small amount of insulin. In compari-
son, the natural history of type 2 diabetes involves insulin resistance that develops before beta cell dysfunction,
at which stage patients can be managed with noninsulin agents, but progressive insulin deficiency ensues.
Approximately half the patients with type 2 diabetes in the United States are on insulin therapy with or without
noninsulin agent(s).
• When evaluating a patient with hyperglycemia, a new diagnosis of diabetes or preexisting diabetes should be
at the forefront of consideration. However, glucocorticoids, critical illness, or medical therapies, such as enteral
or parenteral nutrition, may cause stress hyperglycemia. Acromegaly and pheochromocytoma are rare causes
of hyperglycemia and diabetes.
Bibliography
Ahlqvist, E., Storm, P., Käräjämäki, A., Martinell, M., Dorkhan, M., Carlsson, A., … Groop, L. (2018). Novel subgroups of adult-onset
diabetes and their association with outcomes: a data-driven cluster analysis of six variables. Lancet Diabetes & Endocrinology, 6,
361–369.
American Diabetes Association. (2018). Classification and diagnosis of diabetes: standards of medical care in diabetes—2018.
Diabetes Care, 41(Suppl. 1), S13–S27.
Balasubramanyam, A., Nalini, R., Hampe, C. S., & Maldonado, M. (2008). Syndromes of ketosis-prone diabetes mellitus. Endocrine
Reviews, 29, 292–302.
Duggan, S. N., & Conlon, K. C. (2017). Pancreatogenic type 3c diabetes: underestimated, underappreciated and poorly managed.
Practical Gastroenterology, 163, 14–23.
Fajans, S. S., & Bell, G. I. (2011). MODY: history, genetics, pathophysiology, and clinical decision making. Diabetes Care, 34(8), 1878–
1884.
González-Saldivar, G., Rodríguez-Gutiérrez, R., Ocampo-Candiani, J., González-González, J. G., & Gómez-Flores, M. (2017). Skin mani-
festations of insulin resistance: from a biochemical stance to a clinical diagnosis and management. Dermatologic Therapy, 7(1),
37–51.
U.S. Preventive Services Task Force. (2018, April). Final recommendation statement: abnormal blood glucose and type 2 diabetes
mellitus: screening. Rockville, MD: U.S. Preventive Services Task Force.
e1
AbstrAct
Diabetes mellitus is a term that encompasses a heterogeneous group of disorders that are all characterized by elevated
blood glucose. The most common type is type 2 diabetes, which has a strong genetic component and environmental
contributors, but there are many other types to be aware of including type 1 diabetes, gestational diabetes, and “secondary”
forms of diabetes. This chapter provides a general overview of diabetes mellitus including the pathophysiology, classifi-
cation, diagnosis, screening, and prevention. It also outlines a few of the key types of diabetes including types 1 and 2,
latent onset autoimmune diabetes of adults and ketosis-prone diabetes, and monogenic diabetes, as well as features of
insulin resistance and metabolic syndrome.
Key Words
diabetes mellitus, beta cell function, autoimmune, diagnosis, insulin resistance, monogenic, metyabolic syndrome
DIABETES MELLITUS: ACUTE
CHAPTER 2
AND CHRONIC COMPLICATIONS

Cecilia C. Low Wang and Adnin Zaman
1. What are the acute complications of diabetes?

Diabetic ketoacidosis (DKA), hyperglycemic hyperosmolar state (HHS), and hypoglycemia.
2. What symptoms are characteristic of hyperglycemia?
Patients are often asymptomatic, but when the hyperglycemia is severe, individuals may report the “3 P’s”—
polyuria, polydipsia and polyphagia—along with blurry vision and fatigue. Patients may note more frequent urinary
tract or genitourinary infections and/or delayed healing of skin infections or ulcers. With insulin deficiency, patients
become catabolic and experience weight loss. Some patients report feeling agitated or confused, although this is
not common.
3. What is DKA, and how common is it?
DKA stands for diabetic ketoacidosis. Three elements are required for the diagnosis: uncontrolled hyperglycemia
(blood glucose usually . 250 mg/dL), metabolic acidosis (pH % 7.3), and increased ketone concentrations. It
occurs more often in patients with type 1 diabetes and is the first presentation of type 1 diabetes in about 25%
of patients. DKA accounts for 140,000 hospital admissions in the United States each year. The age-adjusted rate
declined by 1.1% per year from the years 2000 to 2009 but then increased dramatically by 54.9% between
2009 and 2014, from 19.5 to 30.2 per 1000 persons (an increase of 6.3% per year), with the highest rates in
adults , 45 years old. This group of younger adults also had a 27-fold higher rate of hospitalization for DKA
compared with adults  65 years of age. The T1D Exchange Network reports that young adults, ages 18 to
25 years, have the overall highest occurrence of DKA.
4. What is the mortality rate for DKA?
Before the discovery of insulin in 1921, the mortality rate in DKA was . 90%. The mortality rate for DKA in the
United States and in the European countries is currently , 2% but is . 10% in countries with limited resources
for acute care. DKA is the leading cause of death in children and young adults with type 1 diabetes ( 50% of all
deaths in individuals with diabetes , 24 years of age). The case fatality rate for mortality in the hospital de-
creased from 1.1% to 0.4% during the years 2000 to 2014.
5. Do all patients who develop DKA have type 1 diabetes?
No. Patients with type 2 diabetes may also develop DKA if the relative insulin deficiency is severe enough, such
as with severe stress or concurrent illness. Patients with ketosis-prone diabetes (KPD), which is described in
Chapter 1, are diagnosed when they present with DKA.
6. What causes DKA?
The two key factors leading to DKA are insulin deficiency and elevated levels of counterregulatory hormones
(epinephrine, glucagon, cortisol, growth hormone). These factors promote hepatic glycogenolysis and gluconeo-
genesis, resulting in increased hepatic glucose production. Glucose uptake into skeletal muscle is reduced as a
result of insulin deficiency. Catabolism of fat stores increases serum concentrations of free fatty acids, which
are then oxidized to ketone bodies (beta-hydroxybutyrate and acetoacetate) in the liver; this also consumes
bicarbonate, resulting in metabolic acidosis.
7. What are the common precipitating factors for DKA?
A new diagnosis of diabetes, omission of insulin doses, infection, myocardial infarction, pancreatitis, stroke,
alcohol use, and insulin pump malfunction may all precipitate DKA. Risk factors include psychiatric disorders,
eating disorders, substance abuse, and homelessness. In the United States, the most common precipitating
factor is failure to adhere to insulin therapy. Elsewhere in the world, infections are the most common precipitating
factors.
8. What are the symptoms and signs of DKA?
Patients often present with nausea and vomiting, abdominal pain, polyuria, polydipsia, fatigue, and weight loss.
They may have decreased mental status but , 25% present with coma. Signs of volume depletion, such as
hypotension, tachycardia, dry mucous membranes, and decreased skin turgor, are usually apparent. Patients with
severe DKA may have Kussmaul respirations (respiratory compensation for metabolic acidosis) and a “fruity”
breath resulting from acetone production.
12
DIABETES MELLITUS: ACUTE AND CHRONIC COMPLICATIONS 13
9. How is DKA diagnosed?

The following laboratory findings are also needed for the diagnosis of DKA:
• Hyperglycemia (blood glucose usually  250 mg/dL)
• Anion gap metabolic acidosis (pH # 7.3; HCO3 # 18 mEq/L; anion gap . 15)
• Positive serum or urine ketones
Blood glucose levels are usually over 250 mg/dL but may be lower than this (termed “euglycemic DKA”) in the
following situations: pregnancy, starvation, alcohol use, insulin therapy, and use of sodium-glucose cotransporter-2
(SGLT-2) inhibitors. A definitive determination of anion gap metabolic acidosis can only be made with simultane-
ous measurement of blood gases (partial pressure of carbon dioxide [PaCO2] and pH are decreased) and serum
chemistries (basic metabolic panel). Ideally, arterial blood gas measurement is done for the diagnosis, but venous
blood gas measurements may be used to monitor therapy. The anion gap is calculated using the equation: sodium
[Na1] 2 chloride [Cl2] 2 bicarbonate [HCO32]. Ketonemia may be documented by using the serum beta-
hydroxybutyrate method, but it may be underestimated if ketones are measured by using the nitroprusside method.
10. What are the basic principles of DKA management?
Key measures for treating DKA include:
1. Volume repletion
2. Correction of electrolyte abnormalities
3. Insulin therapy to correct hyperglycemia and ketonemia
4. Identification and treatment of the precipitating event(s)
DKA often resolves within 10 to 18 hours if appropriate treatment is instituted promptly. Patients must
be monitored every 1 to 2 hours initially and then every 2 to 4 hours, with assessment of serial vital signs,
physical examination to determine volume status and mental status, urine output, basic metabolic panels
(for bicarbonate, potassium, anion gap) and venous blood gas measurements (pH) to assess the effective-
ness of treatment. Changes in the rate of intravenous fluid administration and insulin doses are often
needed.
11. Should ketones be monitored in the management of DKA?
When point-of-care beta-hydroxybutyrate measurements are available, these can be used to diagnosis ketosis
and to monitor therapy. However, measurement of ketones by using the nitroprusside method helps detect
acetoacetate and acetone but not beta-hydroxybutyrate, which is the main ketone body produced in DKA. Serial
measurement of ketones in DKA, therefore, is not accurate if the nitroprusside method is used.
12. When can patients be transitioned off intravenous insulin infusion after treatment for DKA?
Intravenous insulin can be discontinued when the patient’s acidemia (determined by both the absolute bicarbon-
ate concentration and the elevated anion gap) has resolved, the patient shows clinical improvement (off vasopres-
sors), the patient is able to tolerate oral intake, and the precipitating cause(s) have been addressed. Factors that
predict successful transition from intravenous insulin to a subcutaneous regimen include a stable infusion rate
of , 2.0 to 2.5 units/hr with blood glucose levels consistently , 130 mg/dL.
13. What is HHS?
HHS is an abbreviation for hyperglycemic hyperosmolar state.
14. Who develops HHS?
HHS generally occurs in elderly patients with type 2 diabetes who have an impaired thirst mechanism or are
unable to access free water for any reason.
15. What are symptoms and signs of HHS?
Patients often report typical symptoms of hyperglycemia, including polyuria, polydipsia, blurred vision, and weak-
ness. They may have decreased mental status and often will have signs of dehydration, such as dry mucous
membranes and decreased skin turgor. Patients with HHS are often hemodynamically unstable with significantly
decreased blood pressure and tachycardia.
16. Why do people with HHS generally not have ketoacidosis?
Patients with HHS have sufficient insulin production to suppress lipolysis and subsequent generation of ketones.
In addition, these patients usually have lower circulating levels of the counterregulatory hormones.
17. How does one distinguish between DKA and HHS? (Table 2.1)
Patients with DKA have increased acidemia with ketonemia, whereas patients with HHS have little to no ketones,
normal serum bicarbonate levels, and elevated serum osmolality of . 320 mOsm/kg. Patients with HHS also usu-
ally have more severe hyperglycemia compared with those with DKA (occasionally presenting with blood glucose
levels . 1000 mg/dL) and have a more severe volume deficit.
18. Can a patient present with both DKA and HHS?
Yes. Patients may have features of both ketoacidosis and hyperosmolarity. Patients with HHS may have mild
to moderate ketonemia and may have a concomitant metabolic acidosis caused by lactic acidosis, uremia, or
alcoholic ketoacidosis.
14 FUEL METABOLISM
Table 2.1. Diagnostic Criteria for DKA and HHS.

MEASURE MILD MODERATE SEVERE HHS DKA
Plasma glucose (mg/dL) . 250 . 250 . 250 . 600
Arterial pH 7.25–7.30 7.00 to , 7.24 , 7.00 . 7.30
Serum bicarbonate (mEq/L) 15–18 10–15 , 10 . 18
a
Urine to serum ketones Positive Positive Positive Small
Urine or serum b-hydroxybutyrate (mmol/L) . 3.0 . 3.0 . 3.0 , 3.0
Effective serum osmolalityb Variable Variable Variable . 320 mOsm/kg
Anion gap . 10 . 12 . 12 Variable
Mental status Alert Alert/drowsy Stupor/coma Stupor/coma
a
Nitroprusside reaction.
b
Effective serum osmolality: 2[measured Na1(mEq/L) 1 glucose (mg/dL)/18.
DKA, Diabetic ketoacidosis; HHS, hyperglycemic hyperosmolar state.
Adapted from Kitabchi, A. E., Umpierrez, G. E., Miles, J. M., & Fisher, J. N. (2009). Hyperglycemic crises in adult patients with diabetes.
Diabetes Care, 32(7), 1335–1343. With permission.
19. What is needed for the diagnosis of HHS?

The diagnosis of HHS is made by the following findings:
• Serum glucose of . 600 mg/dL
• Serum osmolality . 320 mOsm/kg
• Ketones absent
Effective osmolality [ sodium ion (mEq/L) 3 2 1 glucose (mg/dL)/18 1 blood urea nitrogen (BUN) (mg/dL) 4 2.8
20. What is key to the treatment of HHS?

Patients with HHS are extremely volume depleted; therefore, the key to treatment is adequate volume repletion.
21. What role does insulin play in the treatment of HHS?
Insulin therapy is important but is secondary. Unlike the treatment for DKA, in which insulin deficiency is the most
important driving factor, correction of volume loss is the critical element in the management of HHS.
22. Describe the signs and symptoms of hypoglycemia
Common symptoms of hypoglycemia include shakiness, diaphoresis, irritability, hunger, and fatigue. Neuroglyco-
penic symptoms, such as confusion, unusual behavior, visual disturbances, and loss of consciousness, may also
occur. Patients with severe hypoglycemia may appear to be intoxicated, with slurred speech and clumsiness, and
seizures can develop. Hypoglycemia can be fatal, with recent reports indicating that 4% to 10% of deaths in type
1 diabetes were caused by hypoglycemia.
23. What are common reasons patients with diabetes become hypoglycemic?
Hypoglycemia in patients with diabetes most often results from missed or delayed meals after taking rapid-
acting insulin, a sulfonylurea, or a meglitinide; excessive prandial and/or correctional insulin; too much basal
insulin; physical activity without medication or nutritional adjustments; and renal disease resulting in decreased
insulin clearance and loss of renal gluconeogenesis. Other causes are similar to those in patients with diabetes
and in those without diabetes: liver failure, cardiac failure, sepsis, critical illness, untreated adrenal insufficiency,
untreated hypothyroidism, and starvation or malnutrition. Patients with diabetes rarely have insulinomas, but this
is still in the differential diagnosis for hypoglycemia.
24. Which diabetes medications are most commonly associated with hypoglycemia?
Insulins, sulfonylureas, and meglitinides (repaglinide, nateglinide) account for the vast majority of cases of hypo-
glycemia in patients with diabetes.
25. What diabetes medications are associated with a low risk of hypoglycemia?
Metformin, acarbose, thiazolidinediones, dipeptidyl peptidase-4 inhibitors, glucagon-like peptide-1 receptor ago-
nists, and SGLT-2 inhibitors rarely cause hypoglycemia, unless used in combination with one of the medications
listed in question 24. Two of the more recently approved, but less often used, “old drugs for a new indication”
(bromocriptine and colesevelam) may occasionally lead to mild hypoglycemia.
26. Do patients with type 1 diabetes and type 2 diabetes have the same risk of hypoglycemia?
Patients with type 1 diabetes are two to three times more likely to develop hypoglycemia compared with patients
with type 2 diabetes, and the risk increases with increasing duration of diabetes. Other risk factors for hypoglyce-
mia include advancing age, intensive glycemic control, renal disease, and decreased cognitive function.
27. What is “hypoglycemia unawareness”?

Patients with diabetes typically develop adrenergic symptoms of hypoglycemia when blood glucose levels drop
below 70 mg/dL; lower glucose levels may also be associated with neuroglycopenic symptoms. “Hypoglycemia
unawareness” (absence of hypoglycemic symptoms when blood glucose levels decrease into the hypoglycemic
range) typically occurs when a patient has had multiple, recurrent episodes of hypoglycemia, resulting in low-
ering of the glucose threshold that triggers counterregulatory hormone release. Affected patients often need
assistance from others to recognize and treat hypoglycemia. Hypoglycemia-associated autonomic failure
(HAAF) is a term that is used to describe hypoglycemia unawareness and impaired counterregulatory hormone
responses.
28. Is hypoglycemia unawareness reversible?
Yes. With strict avoidance of hypoglycemia for a certain period (weeks to months), patients often regain hypogly-
cemia awareness.
29. How is hypoglycemia treated in a conscious patient?
Hypoglycemia in a conscious patient should be treated with 15 g of oral carbohydrates (glucose tablets or gel;
half cup, or 4 ounces, of juice or regular soda; 1 cup, or 8 ounces, of milk; 1 tablespoon of honey; three 3-packs
of SweeTARTS; or  3 rolls of Smarties).
30. What should be done if a patient is unconscious and severe hypoglycemia is suspected?
For severe hypoglycemia, when a patient is unconscious or otherwise unable to take anything by mouth, glucagon
(available as a glucagon kit) should be injected subcutaneously or intramuscularly to stimulate immediate glyco-
genolysis in the liver. Because glucagon is injected in these situations by a family member, friend or coworker,
individuals who may potentially need to administer glucagon should be trained on when and how to inject this
hormone. An emergency 911 call should also be made.
31. What are the key elements of education needed to prevent and avoid hypoglycemia?
Patient education is essential to decrease the risk of iatrogenic hypoglycemia. Key elements of patient education
include recognizing the symptoms of hypoglycemia, proper treatment of hypoglycemia, and being familiar with
situations in which one might anticipate a higher risk for hypoglycemia. These elements need to be reviewed
at every visit. In addition, patients may require guidance on dietary and exercise modifications, medication
adjustments, and sensible glucose monitoring methods. Meticulous surveillance by the health care provider is
imperative.
32. What are the common long-term complications of diabetes mellitus?
The long-term complications of diabetes are often divided into microvascular and macrovascular types; the
former include retinopathy, diabetic kidney disease (DKD), and neuropathy, whereas the latter includes athero-
sclerotic cardiovascular disease (coronary heart disease, cerebrovascular disease, and peripheral arterial
disease presumed to be of atherosclerotic origin). Macrovascular disease is the leading cause of morbidity
and mortality among individuals with diabetes and is the largest contributor to the direct and indirect costs
of diabetes, but microvascular disease also causes significant morbidity and decreased quality of life. Diabetic
foot ulcers are multifactorial and cannot be classified neatly into a “microvascular versus macrovascular”
complication.
Diabetes is associated with a number of comorbid conditions, including obesity, obstructive sleep apnea,
fatty liver disease, fractures, pancreatitis, hearing loss, certain cancers (liver, pancreas, endometrium, colon/
rectum, breast, bladder), depression, anxiety, cognitive impairment and dementia, eating disorders, and periodontal
disease; these will not be discussed in this section.
33. Why do these complications develop in individuals with diabetes?
The basic mechanisms underlying the development of microvascular and macrovascular complications are
complex and are under intensive investigation by researchers around the world. Uncontrolled hyperglycemia,
insulin resistance, and hyperinsulinemia, as well as associated conditions, such as dyslipidemia, hypertension,
and obesity, conspire to create a “perfect storm” leading to increased oxidative stress and inflammation and
promoting the development of these complications. With microvascular complications, hyperglycemia leads to
activation of protein kinase C and reactive oxygen species and to the generation of toxic products of abnormal
glucose metabolism (e.g., advanced glycation end-products and methylglyoxal).
34. What fundamental factors need to be managed to prevent microvascular complications?
Hyperglycemia, hypertension, and dyslipidemia must all be well controlled to prevent the development and/or
progression of these conditions.
35. How common is diabetic retinopathy?
Diabetic retinopathy is the most common microvascular complication of diabetes. Globally, diabetic retinopathy
affects almost 100 million people. In developed countries, it is the most common cause of new cases of blindness
among adults 20 to 74 years of age. Glaucoma and cataracts also occur earlier and at a higher frequency in
patients with diabetes.
16 FUEL METABOLISM
36. How does diabetic retinopathy manifest?

Patients are asymptomatic in the earlier stages, and therefore, without routine ophthalmologic screening, retinop-
athy can be missed. The different types include nonproliferative diabetic retinopathy (NPDR), proliferative diabetic
retinopathy (PDR), and diabetic macular edema (DME). NPDR is the earliest detectable stage and includes a num-
ber of findings on retinal examination, such as microaneurysms, retinal hemorrhages, intraretinal microvascular
abnormalities (IRMAs), and venous caliber changes. PDR, which indicates a more advanced stage, is characterized
by preretinal neovascularization. Evolving technologies are allowing for the detection of more subtle abnormalities,
such as alterations of retinal function and of the neural layer. DME can occur at any stage of diabetic retinopathy
and is the most common cause of visual loss in this disorder. In DME, the blood–retina barrier breaks down with
leakage of circulating fluid and proteins into the neural retina, leading to abnormal retinal thickening and cystoid
macular edema.
37. How is diabetic retinopathy managed?
Treatment options include focal and panretinal laser photocoagulation, intravitreal injections of anti–vascular
endothelial growth factor (VEGF), intravitreal steroids, and vitreoretinal surgery. The eye-specific therapeutic
paradigm is designed to treat advanced disease (PDR and/or DME).
38. How common is DKD?
Approximately 35% of adults with diabetes develop chronic kidney disease. DKD disproportionately affects
middle-aged African Americans, Native Americans, and Hispanic Americans; these groups also have significantly
higher rates of progression to end-stage renal disease (ESRD).
39. Is there more than one manifestation of DKD?
Yes. Albuminuria, decreased glomerular filtration rate (GFR), glomerular hematuria, other abnormalities of the
urinary sediment, and abnormalities on imaging studies are all manifestations of DKD. Not all individuals with DKD
and reduced estimated GFR (eGFR) have increased albuminuria. The United Kingdom Prospective Diabetes Study
(UKPDS) reported that only about 50% of people who developed an estimated creatinine clearance of , 60 mL/
min/1.73 m2 ever tested positive for albuminuria.
40. What is the treatment for DKD?
Good control of blood glucose and blood pressure, especially with an angiotensin-converting enzyme (ACE)
inhibitor or an angiotensin receptor blocker (ARB) can prevent or slow the progression of established DKD.
When DKD progresses to ESRD despite these measures, dialysis or kidney transplantation becomes necessary.
41. What types of diabetic neuropathies are there?
Multiple types of neuropathies occur in people with diabetes; these include distal symmetric sensorimotor poly-
neuropathy (the most common); autonomic neuropathy; focal limb neuropathies; mononeuropathies; entrapment
syndromes, such as carpal tunnel syndrome; diabetic amyotrophy (proximal motor neuropathy); diabetic truncal
radiculopathy; and acute sensory neuropathy. Diabetic neuropathies have two distinct patterns of progression:
sensory and autonomic neuropathies generally progress gradually with increasing duration of diabetes, whereas
mononeuropathies, radiculopathies, and acute painful neuropathies may be quite severe at onset but are short-
lived and often resolve completely. Diabetic neuropathies encompass heterogeneous clinical presentations, and
the incidence, prevalence; however, the natural histories of diabetic neuropathies have not been well defined.
This can be attributed to variable diagnostic criteria, lack of standardized methods for evaluation, and lack of
recognition by clinicians.
42. What is the pathogenesis of the diabetic neuropathies?
Metabolic abnormalities within the nerves and/or Schwann cells, as well as microvascular injuries contribute to
diabetic neuropathies. In distal symmetric polyneuropathy, progressive axonal degeneration occurs in different
fiber types, usually preceded by segmental demyelination.
43. What are the symptoms of distal symmetric polyneuropathy, and what is the usual pattern of progression?
Numbness, the sensation of a toe or part of the foot “falling asleep,” prickling, tingling, stabbing, burning, electrical-
like shocks, or aching pains may all occur. Symptoms start in the toes or the plantar surface of the foot in a sym-
metric pattern and travel proximally. Patients usually do not develop symptoms in the upper extremities until lower
extremity symptoms have reached the knees (“stocking–glove distribution”). Distal symmetric polyneuropathy is
a diagnosis of exclusion; other causes that must be considered include chronic inflammatory demyelinating
polyneuropathy, vitamin B12 deficiency (particularly in patients on metformin therapy for longer than a year),
hypothyroidism, and uremia.
44. How is diabetic neuropathy treated?
Tight glycemic control prevents progression of neuropathy but does not reduce the pain in distal symmetric poly-
neuropathy. Therapies for painful diabetic neuropathy approved by the U.S. Food and Drug Administration (FDA)
are pregabalin and duloxetine, which are also recommended by the American Diabetes Association (ADA) as
first-line therapies. Other potentially beneficial treatments include gabapentin, sodium valproate, venlafaxine,
amitriptyline, dextromethorphan, topical capsaicin, isosorbide dinitrate spray, and typical opioids. Nonpharmaco-
logic therapies, other than percutaneous electrical nerve stimulation (PENS), lack data to support their use. These
therapies all target the symptoms, and not the underlying mechanisms.
45. What foot problems can patients with diabetes experience?
Diabetic foot ulcers; insensate feet; foot infections; foot deformities, including Charcot foot; peripheral artery
disease; and amputations can all occur in patients with diabetes.
46. What are the important strategies for preventing diabetic foot ulcers?
Patients should be aware of the risk factors for diabetic foot ulcers and amputations; these include poor glycemic
control, peripheral neuropathy with loss of protective sensation, cigarette smoking, foot deformity, preulcerative
callouses and corns, peripheral artery disease, history of previous foot ulcers, prior amputations, visual impair-
ment, and DKD (particularly ESRD on dialysis). Proper foot care includes daily assessment of skin and nails, palpa-
tion or visual surveillance (including use of an unbreakable mirror, if needed) to monitor the condition of the feet,
use of well-fitting shoes (custom-fitted in select circumstances), and proper wound care if an ulcer develops.
47. What are the clinical features of diabetic autonomic neuropathy?
Autonomic neuropathy can cause a variety of clinical manifestations, including hypoglycemia unawareness,
resting tachycardia, orthostatic hypotension, gastroparesis, constipation, diarrhea, fecal incontinence, erectile
dysfunction, neurogenic bladder, and sudomotor dysfunction with either increased or decreased sweating.
48. How do you detect cardiac autonomic neuropathy?
Early cardiac autonomic neuropathy is usually asymptomatic and only manifests as decreased heart rate variabil-
ity with deep breathing. Later, it causes resting tachycardia and orthostatic hypotension. Cardiac autonomic
neuropathy is independently associated with mortality.
49. When do patients with diabetes develop gastroparesis, and when should it be suspected?
Patients with type 1 diabetes generally do not develop gastroparesis until 10 to 15 years after diabetes is diag-
nosed; the condition takes even longer to develop in those with type 2 diabetes. Gastrointestinal neuropathies can
manifest along any portion of the gastrointestinal tract, resulting in esophageal dysmotility, gastroparesis, diarrhea
with or without fecal incontinence, and constipation. Patients who have poorly controlled blood glucose (especially
a pattern of frequent postprandial hypoglycemia, followed by prolonged hyperglycemia) and unexplained gastric or
esophageal symptoms should be suspected of having gastroparesis.
50. How is gastroparesis diagnosed?
Gastric-emptying scintigraphy is the gold standard for diagnosis but mechanical obstruction, and gastric or peptic
ulcer must first be excluded. Patients must discontinue any drugs that might affect gastric emptying, fast overnight,
and then consume a standard low-fat radiolabeled meal within 10 minutes. Imaging is performed at baseline and
then 1, 2, and 4 hours later with the patient in the standing position. Glucose values should be , 275 mg/dL for a
valid result because hyperglycemia itself acutely inhibits gastric emptying. Delayed gastric emptying is defined as
. 60% retention at 2 hours or . 10% retention at 4 hours. Limitations include low sensitivity for detecting mild or
moderate gastroparesis, potential for overdiagnosis in women who have a physiologic delay of gastric emptying,
and intraindividual variation of up to 24%. Furthermore, the low-fat, low-fiber test meal used to standardize testing
conditions may not be similar to actual meals that patients normally consume and may, therefore, lead to underdi-
agnosis of gastroparesis. An alternative is a gastric emptying breath test with use of a radiolabeled carbon-
containing test meal (carbon13–labeled Spirulina platensis or octanoic acid). After consuming this meal, radiola-
beled carbon is released during digestion and is detected as exhaled radiolabeled carbon dioxide 4 to 6 hours later.
Comparative studies suggest that the breath test may be as accurate as scintigraphy. Another approach is a wire-
less motility capsule (a “smart pill”), but evidence supporting its use is of low quality.
51. What is diabetes-related distress?
This is relatively new term for an increasingly recognized affective state resulting from constant worry about ad-
herence to a strict regimen of diet, exercise, and frequent blood glucose monitoring, while feeling afraid, anxious,
overwhelmed, at times angry, and eventually burned out. There is no standard definition for this condition, but it
may be defined simply as “decreased quality of life resulting from a combination of the medical and psychological
burden of diabetes as a complex and chronic condition creating emotional distress often hidden from providers
and sometimes from the sufferer.” Diabetes-related distress can negatively impact diabetes management and
outcomes. The level of diabetes-related distress does not appear to be associated with the duration of diabetes
but has been noted to be much higher in younger patients, females, nonwhite patients, those with a higher body
mass index (BMI), and patients treated with insulin compared with those not treated with insulin.
52. How common is depression in people with diabetes?
Depression is two to three times more common in people with diabetes than in the general population. There is now
emerging evidence that depression may actually be a risk factor for the development of diabetes (up to 60% increased
risk). Conversely, the pooled relative risk (RR) for developing depression in individuals with preexisting diabetes is 1.15.
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Marks of taboo to protect property, 25 sqq., 38 sq., 41 sqq.
Marquesas Islands, taboo in the, 23 sq.
Marrah, in Darfur, 39
Marriage, superstition in relation to, 44 sqq.
—— of cousins, different customs as to the, 88 sq., 91; forbidden,
89, 90, 91, 92, supposed to be unfruitful, 92; expiation for the,
92 sq.
—— laws, their origin unknown, 102
Marriages, consanguineous, question as to the results of, 95 sq.
Masai, the, of British East Africa, 81; of German East Africa, 105
Medicine-man, respect for, 14
Melanesia, taboo as a preserver of property in, 26 sq.
Melanesians, authority of chiefs among the, 6 sq.; rules of
ceremonial avoidance amongst the, 86 sq.; of the Bismarck
Archipelago, 131
Men Aziottenos, 37
Men naturally unequal, 166 sq.
Mental evolution, a scale of, 172
Meteors, superstition as to, 141
Milky Way, 141
Mimic warfare, 129
Mimicry in magic, 100
Minority, mankind dominated by an enlightened, 167 sq.
Montenegrin peasantry, their strict views of sexual immorality, 97
Moral theory, hypothetical development of, 102
Morality, sexual, enforced by superstition, 44 sqq.; change in the
theoretical basis of, 101 sq.; basis of, shifted from supernatural
to natural, 153
Morocco, superstitions concerning granaries in, 56 sq.
Mosaic law, punishments for sexual offences under the, 64
Mother, incest with a, 51, 61; and son, ceremonial avoidance
between, 85, 86, 87
Mother-in-law, ceremonial avoidance of, 75 sqq., 86 sq., 90 sq.
Mount Elgon, 123
Mourning customs of widows and widowers, 142 sqq.
Moxos Indians of Bolivia, 106
Mukjarawaint tribe of Victoria, 74
Murderer, rules observed by pardoned, 126
Murderers, their precautions against the ghosts of their victims, 117
sqq.
Mutilation of corpses in order to disable the ghosts, 132 sq., 134,
136, 137; of the dying or dead, 141
Nails used to prevent ghosts from walking, 133

Names of kings sacred, 10
Nandi, the, of British East Africa, 14, 56, 66, 118; curses among the,
40 sq.
Natchez Indians of North America, 124
Natural inequality of men, 166 sq.
Nature, why illicit relations between the sexes are thought to disturb
the balance of, 99 sqq.
—— the Sphinx, 102
Nebuchadnezzar, the king, quoted, 37 sq.
Nepal, 138
Nets to catch ghosts, 139
New Britain, 109; taboo in, 26 sq.
—— Guinea, British, 125, 147; Dutch, 131; German, 82, 124, 127,
131
—— Hebrides, 86
—— Ireland, 89, 90
—— Mecklenburg, 89
—— South Wales, 74
—— Zealand, authority of chiefs in, 7 sqq. Nias, the island of, 46 sq.;
curses in, 34
Niece, incest with, 51, 53
Niger, tribes of the Lower, 119
Nile, the Upper, 57
Ninib, Babylonian god, 38
Nuru, the spirit of the slain, 121
Nusku, Babylonian god, 38
Oaths and imprecations as preservers of property, 24 sqq. See also

Curses
Obeah man, magician, 42
Obi, magic, 42
Oedipus, the incest of, 61
Ojèbways, their modes of keeping off ghosts, 139 sq.
Omaha Indians, 132 sq.; their customs as to pardoned murderers,
126
Opinion and action, their relative values for society, 155
Orang Glai, the, savages of Annam, 46
Oraons of Bengal, their fear of the ghosts of women dying in
childbed or pregnancy, 134
Oregon, Chinook Indians of, 126
Orestes, the matricide, 114, 115, 117, 118, 119, 126
Orinoco, the, 112
Ottawa Indians, 131
Ovakumbi, a tribe of Angola, 108
Ovambo, a Bantu people of South-West Africa, 80 sq.
Pacific, first exploration of the, 173

Paestum, the temples at, 170
Paint-house, the, 55
Pamali, taboo, 27
Papuans of New Guinea, 131; of Issoudun, 147
Parents-in-law, ceremonial avoidance by man of his future, 81, 83
Parricide, Roman punishment of, 52; guilt of, 61
Pasemhers, a tribe of Sumatra, 69
Pasir, a district of Borneo, 51
Patagonians, their fear of the dead, 111 sqq.
Peasantry of Europe, their intellectual savagery, 170
Pemali, taboo, 27
Pepper put in eyes of corpse to blind ghost, 133
Perham, J., 47
Persephone, 36
Peru, the Yncas of, 15 sq., 173
Petara, Dyak name for deity, 47
Pig’s blood used in ceremonies of purification, 116 sq.
Pigs used in expiatory ceremonies, 44 sqq.
Physical causation, false notions of, 100
—— infection supposed to be spread by unchaste persons, 109
—— relationship supposed to exist between adulterer and injured
husband, 104 sq.
Plato on sanctity of landmarks, 37
Pollution, ceremonial, 93, 105; incurred by homicide, 115 sqq., 128
——, dangerous, supposed to be incurred by unchastity, 109
Polynesia, authority of chiefs in, 7 sqq.; taboo in, 20 sqq.
Pomali, taboo, 27
Pontianak, ghost of woman who died in childbed, 137 n.
Precautions taken by homicides against the ghosts of their victims,
117 sqq., 123 sqq.; against the ghosts of bad people, 132 sq.;
against ghosts of women dying in pregnancy or childbed, 133
sqq.; taken by widows and widowers against the ghosts of their
spouses, 142 sqq.
Prehistoric ages, imperfections in the records of, 171 sq.
Primæval man unknown, 163 sq.
Primitive, relative sense in which the word is applied to existing
savages, 163 sq.
Private property, superstition as a prop of, 20 sqq.
Propagation of animals and plants supposed to be affected by the
relations of the human sexes, 99 sqq.
Property, superstition as a support of private, 20 sqq.; of the dead
destroyed, 111 sq., 135
Psanyi, 122
Punans, the, of Borneo, 50
Punishments, severe, for sexual offences, 63 sqq., 96 sqq.
Punjaub, the, 133
Purification for unchastity by means of blood, 44 sqq.; for unchastity
by means of water, 109; for homicide, 114, 115 sqq., 120 sqq.,
123 sqq.; and capital punishment, 151 sq.
Queen Anne, 18
Queen Charlotte Islands, 107
Queen Draga of Servia, 97
Queensland, native tribes of, 72 sqq.; their mutilation of the dead,
137
Rain, kings expected to give, 13 sq.; failure or excess of, supposed
to be caused by sexual immorality, 44, 46, 47, 48, 54, 55, 56
Rajah Brooke, 12
Rajamahal in Bengal, 45
Ramanandroany, a Malagasy deity, 31
Rape, punishment of, 66
Red paint put on homicides, 118, 124, 127
Regalia, sanctity of, 11
Relations by marriage, ceremonial avoidance of, 75 sqq.
Religion supplies the new theoretical basis of sexual morality, 101; of
one generation the superstition of the next, 170 sq.
—— and magic, their relations, 100
Renan, Ernest, on the menace to civilization, 170
Reproduction of men, animals, and plants, analogy between the, 99
sq.
Rhodesia, Northern, 66, 79, 103, 120
Rhys, Sir John, quoted, 54 n. 2, 62 sq.
Rio de Janeiro, 96
Risley, Sir Herbert H., quoted, 138
Road from the grave barred against the ghost, 138 sq.
Robert the Pious, 18
Roman custom as to incest, 61 sq.
—— punishment of parricide, 52
Roscoe, Rev. J., quoted, 64 sq., 90 sq., 102 sq.
Ruanda, a district of Central Africa, 96
Sacred chiefs, 7 sqq.

—— fig-tree among the Akikuyu, 128 sq.
—— fish, 36
Sacredness of chiefs in Polynesia, 7 sqq.
Sahagun on the natives of Mexico, 173
St. Patrick, canon of, 17
Samoa, superstition as a preserver of property in, 24 sqq.
Samoan taboos, 25 sq.
Sarah and Abraham, 60 sq.
Sarawak, Hill Dyaks of, 11 sq., 48
Savage, the, a human document, 172 sq.; the passing of the, 174
sq.
Savage horror of sexual irregularities, suggested reason for, 101
Savagery, civilization evolved out of, 162; importance of the study of,
162 sq., 172 sqq.; intellectual, of European peasantry, 170
Savages of to-day primitive only in a relative sense, 163 sq.
Saxons, their punishment of sexual offences, 97
Scapegoat for ghosts, 141 sq.
Scarecrows for ghosts, 139
Scepticism, religious, undermines foundations of society, 7
Science of man, 159 sq.
——, the temple of, 161
Scrofula, touching for, 17 sq.
Scythians drank the blood of friends and foes, 118
Sea-pike taboo, 25
Seclusion of homicides, 114 sq., 120, 121 sq., 124, 125 sqq.
Semendo, a district of Sumatra, 68
Servius Tullius, King, 61
Sexual communism, era of, 164 sq.
—— immorality supposed to be injurious to the culprits themselves
and to their relations, 102 sqq.; superstitions as to, 110
—— morality enforced by superstition, 44 sqq.; change in the
theoretical basis of, 101
—— offences punished severely, 63 sqq., 96 sqq.; reason why
savages punish these offences severely, 99 sqq.
“Shaking tubercule,” 32
Shans, the, of Burma, 119, 134
Sheep, expiatory sacrifice of, 92, 93
Shushwap Indians of British Columbia, mourning customs of the,
142 sq.
Siam, 32
Sibuyaus, the, of Sarawak, 48
Sibylline Books, 173
Sickness caused by evil spirits or sorcerers, 141
“Sickness of relationship,” 76 sq.
Sierra Leone, 42
Similarity of the human mind in all races, 172
Sister, incest with a, 51, 54, 59, 60 n. 1, 62, 67, 68, 105
Sisters and brothers, mutual avoidance of, 77
Slave Coast, the, 41
Slavery in England, 169
Slavs, punishment of sexual offences among the Southern, 97 sq.
Slayers fear the ghosts of their victims, 113 sqq.
Sle, pollution incurred by unchastity, 109
Smyrna, 36
Social anthropology, the scope of, 157 sqq.
Society, concerned with conduct, not opinion, 155; ultimately
controlled by knowledge, 167; sapped by superstition, 170; its
surface in perpetual motion, 171
Sociology, 160
Sofala, the king of, 13, 14
Son-in-law, ceremonial avoidance of, 79 sq.
Sophocles on Oedipus, 61
Sphinx, riddles of the, 102
State, duty of the, in regard to anthropology, 175 sq.
Stinks to keep off ghosts, 139
Stoning as a punishment of sexual offences, 64, 97 sq.
Sulka, the, of New Britain, 109
Sumatra, 46, 67, 68, 69, 82, 109
Sun, Yncas descended from the, 15
Supernatural powers attributed to chiefs, 6 sqq.
Superstition, baneful effects of, 3; a plea for, 3 sq., 154 sq.; as a prop
of government, 6 sqq.; as a prop of private property, 20 sqq.; as
a prop of marriage, 44 sqq.; as a prop to the security of human
life, 111 sqq.; heavy toll paid to, 113; services which superstition
has rendered to humanity, 154 sq.; at the bar, 155 sq.; the creed
of the laggards in the march of intellect, 168 sq.; a danger to
society, 170; the religion of a past generation, 170 sq.
Superstitions either public or private, 169; the crudest, survive
longest, 170 sq.
Superstitious fear of contact with Maori chiefs, 9 sq.
Surface of society in perpetual motion, 171
Survivals of savagery in civilization, 166
Swedes, the ancient, 16
Taboo as a support of chiefs, 7 sqq.; as a prop of private property, 20
sqq.; (tambu) in Melanesia, 26 sq.
Tabooed, homicides, 121
Tahiti, sacredness of kings of, 10 sq.
Tamanaques, the, of the Orinoco, 112
Tambu (taboo) in Melanesia, 26 sq.
Tapu (taboo) among the Maoris, 20 sqq.
Tattooing of homicides, 121
Taylor, Rev. Richard, 8
Ternate, 54
Thahu, ceremonial pollution, 93, 105, 115, 128
Theal, G. McCall, quoted, 91
Theoretical basis of sexual morality, 101
Thieves cursed, 34 sqq.
Thompson Indians of British Columbia, mourning customs of the,
144 sq.
Thomson, Basil, quoted, 7
Thomson, J. Arthur, quoted, 95 sq.
Thonga tribe of South-East Africa, 57, 80, 92, 104; their purification
of homicides, 121 sq.
Thorn bushes to keep off ghosts, 142 sq., 144, 145
Thunder taboo, 26
Tigers, plague of, a punishment for sexual offences, 45, 46
Timor, taboo in, 27
Togoland, 142
Tololaki, the, of Central Celebes, 53
Tomori, the, of Central Celebes, 52
Tonga, sacredness of chiefs in, 10; taboo in, 26
Tonquin, 33
Toradjas of Central Celebes, 12, 29, 30, 122; their fear of the ghosts
of the slain, 129
Torture to extract confession, 64 sq.
Touched, chiefs and kings not to be, 9, 11
Touching for scrofula, 17 sq.
Traitors disembowelled in England, 169
Travail pangs supposed to be aggravated by adultery, 104
Travancore, 132
Trembling thought to be caused by contact with certain relations, 77,
90
Troezen, purification of Orestes at, 115
Tsetsaut Indians of British Columbia, mourning customs of the, 143
Tubercule, the shaking, 32
Tunguses, their burial customs, 137, 138
Turner, Dr. George, quoted, 24 sq., 26
Tylor, Sir E. B., 159
Ulcer taboo, 25 sq.

Unchastity, supposed physical infection of, 109
United States of America, their Bureau of Ethnology, 175
Universities, the function of the, 175
Unmarried persons, disastrous effects supposed to flow from sexual
intercourse between, 44, 46, 47, 48, 50, 51, 55, 57, 63, 65, 96
Vancouver Island, 143

Victoria, aborigines of, 71 sq.
—— Nyanza, Lake, 78
Voyages to the South Seas, 173
Wagogo, the, of German East Africa, 92, 106

Wakelbura tribe of Queensland, 72
Wallace, A. R., quoted, 27, 70
Wanigela River, 125
Wanika, the, of East Africa, 38
War, a sacred duty, 129; wives expected to be faithful during their
husbands’ absence at the, 106 sq.
Warfare, mimic, conducted by women and children at home, 129
Washamba, the, of German East Africa, 106
Water ordeal, 107
Wawanga, the, of British East Africa, 123
Weeks, Rev. John H., 85 n. 1; quoted, 75 sq., 128
Welsh saying as to rain, 54 n. 2
West Indies, charms to protect property in the, 42 sq.
Westermarck, Dr. Edward, 32, 56
White-shark taboo, 25
Widows and widowers, precautions taken by them against the
ghosts of their spouses, 142 sqq.
Wife of wife’s brother, ceremonial avoidance of, 80
Wife’s mother, ceremonial avoidance of, 75 sqq., 86 sq., 90 sq.
Witches burned in England, 169
Women dying in pregnancy or childbed, fear of their ghosts, 133 sqq.
Wotjobaluk tribe of Victoria, 74
Yabim, the, of German New Guinea, 127, 131

Yncas of Peru, superstitious veneration for the, 15 sq.
Yucatan, Indians of, 83
Yuin tribe of New South Wales, 74
Zanzibar, 78
Zeus as guardian of landmarks, 37
Zulus, their ideas as to injurious effects of adultery, 107 sq.
ENDNOTES
Chapter I Notes
6.1 R. H. Codrington, D.D., The Melanesians (Oxford, 1891), p. 46.
Chapter II Notes
7.1 R. H. Codrington, op. cit. p. 52.
7.2 Basil Thomson, The Fijians, a Study of the Decay of Custom
(London, 1908), pp. 57-59, 64, 158.
8.1 Rev. Richard Taylor, Te Ika A Maui, or New Zealand and its
Inhabitants, Second Edition (London, 1870), pp. 352 sq.; as to the
atuas or gods, see ib. pp. 134 sqq.
9.1 A. S. Thomson, M.D., The Story of New Zealand (London,
1859), i. 95 sq.
9.2 Rev. W. Yate, An Account of New Zealand (London, 1835), pp.
104 sq., note.

9.3 W. Brown, New Zealand and its Aborigines (London, 1845), p.
76. Compare Old New Zealand, by a Pakeha Maori (London, 1884),

pp. 96 sq.
10.1 Rev. R. Taylor, op. cit. p. 164.
10.2 Rev. R. Taylor, op. cit. pp. 164, 165.
10.3 W. Mariner, Account of the Natives of the Tonga Islands,
Second Edition (London, 1818), i. 141 sq. note, 434, note, ii. 82 sq.,
222 sq.
10.4 W. Ellis, Polynesian Researches, Second Edition (London,
1832-1836), iii. 108.
11.1 W. Ellis, op. cit. iii. 101 sq.; J. Wilson, Missionary Voyage to
the Southern Pacific Ocean (London, 1799), pp. 329 sq.
11.2 Zeitschrift für allgemeine Erdkunde (Berlin), vi. (1856) pp. 398
sq.; F. T. Valdez, Six Years of a Traveller’s Life in Western Africa
(London, 1861), ii. 251 sq.
11.3 W. W. Skeat, Malay Magic (London, 1900), pp. 23 sq.
11.4 W. W. Skeat, op. cit. p. 36.
12.1 Hugh Low, Sarawak (London, 1848), pp. 259 sq.
12.2 N. Adriani en Alb. C. Kruijt, De Bare’e-sprekende Toradja’s van
Midden-Celebes, i. (Batavia, 1912) pp. 130 sq.
12.3 For evidence see The Magic Art and the Evolution of Kings, i.
342 sqq., 392 sqq.
13.1 Proyart’s “History of Loango, Kakongo, and other Kingdoms in
Africa,” in John Pinkerton’s Voyages and Travels (London, 1808-

1814), xvi. 577. Compare O. Dapper, Description de l’Afrique
(Amsterdam, 1686), pp. 335 sq.
13.2 “The Strange Adventures of Andrew Battel,” in J. Pinkerton’s
Voyages and Travels, xvi. 330.
14.1 J. Dos Santos, “Eastern Ethiopia,” chapters v. and ix., in G.
McCall Theal’s Records of South-Eastern Africa, vii. (1901) pp. 190

sq., 199.
14.2 J. Dos Santos, op. cit. pp. 194 sq.
14.3 A. C. Hollis, The Nandi, their Language and Folk-lore (Oxford,
1909), pp. 49 sq.

15.1 C. P. Tiele, History of the Egyptian Religion (London, 1882),
pp. 103 sq. For fuller details see A. Moret, Du caractère religieux de
la royauté pharaonique (Paris, 1902); The Magic Art and the
Evolution of Kings, i. 418 sq.
15.2 Ammianus Marcellinus, xxviii. 5. 14.
16.1 Garcilasso de la Vega, First Part of the Royal Commentaries
of the Yncas, translated by C. R. Markham (London, 1869-1871), i.
154 sq.
16.2 The Laws of Manu, vii. 5-8, translated by G. Bühler (Oxford,
1886), p. 217 (Sacred Books of the East, vol. xxv.).

16.3 The Laws of Manu, ix. 246 sq., translated by G. Bühler, p. 385.
16.4 Homer, Odyssey, ii. 409, iv. 43, 691, vii. 167, viii. 2, xviii. 405;
Iliad, ii. 335, xvii. 464, etc.
16.5 Homer, Odyssey, xix. 109-114.
16.6 Ammianus Marcellinus, xxviii. 5. 14.
17.1 Snorro Sturleson, The Heimskringla, or Chronicle of the Kings
of Norway, translated by S. Laing (London, 1844), saga i. chapters

18 and 47, vol. i. pp. 230, 256.
17.2 P. W. Joyce, Social History of Ancient Ireland (London, 1903),
i. 56 sq.; J. O’Donovan, The Book of Rights (Dublin, 1847), p. 8,
note.
17.3 S. Johnson, Journey to the Western Islands, pp. 65 sq. (The
Works of Samuel Johnson, LL.D., London, 1825, vol. vi.).
17.4 J. G. Campbell, Superstitions of the Highlands and Islands of
Scotland (Glasgow, 1900), p. 5.
17.5 W. G. Black, Folk-Medicine (London, 1883), pp. 140 sqq. See
further The Magic Art and the Evolution of Kings, i. 368 sqq.; and
especially Raymond Crawfurd, The King’s Evil (Oxford, 1911), which
contains a full history of the superstition from the eleventh century
onwards, authenticated by documentary evidence.
18.1 W. Mariner, An Account of the Natives of the Tonga Islands,
Second Edition (London, 1818), i. 434, note.
Africa,” in J. Pinkerton’s Voyages and Travels, xvi. 573.
18.3 Raymond Crawfurd, The King’s Evil, pp. 11 sqq., 18 sqq.
18.4 J. Boswell, Life of Samuel Johnson, Ninth Edition (London,
1822), i. 18 sq.
18.5 Raymond Crawfurd, The King’s Evil, pp. 144 sqq., 159 sqq.
Chapter III Notes
21.1 Old New Zealand, by a Pakeha Maori (London, 1884), pp. 94-
97, compare id. p. 83.
21.2 A. S. Thomson, The Story of New Zealand (London, 1859), i.
103. Compare E. Dieffenbach, Travels in New Zealand (London,
1843), ii. 105: “The breaking of the tapu, if the crime does not
become known, is, they believe, punished by the atua, who inflicts
disease upon the criminal; if discovered, it is punished by him whom
it regards, and often becomes the cause of war.”
22.1 W. Brown, New Zealand and its Aborigines (London, 1845).
pp. 12 sq.
22.2 Old New Zealand, by a Pakeha Maori (London, 1884), p. 97.
23.1 Rev. R. Taylor, Te Ika A Maui, or New Zealand and its
Inhabitants, Second Edition (London, 1870), pp. 167, 171.

23.2 A. S. Thomson, The Story of New Zealand (London, 1859), i.
105.
23.3 Rev. R. Taylor, op. cit. pp. 172 sq.
24.1 Vincendon-Dumoulin et C. Desgraz, Iles Marquises ou Nouk-
hiva (Paris, 1843), pp. 258-260. For details of the taboo system in
the Marquesas Islands, see G. H. von Langsdorff, Reise um die Welt
(Francfort, 1812), i. 114-119; Le P. Matthias G * * * Lettres sur les
Isles Marquises (Paris, 1843), pp. 47 sqq. This last writer, who was a
missionary to the Marquesas, observes that while taboo was both a
political and a religious institution, he preferred to class it under the
head of religion because it rested on the authority of the gods and
formed the highest sanction of the whole religious system.
25.1 G. Turner, Samoa (London, 1884), pp. 183-184.
26.1 G. Turner, Samoa, pp. 185-188.
26.2 W. Mariner, An Account of the Natives of the Tonga Islands,
Second Edition (London, 1818), ii. 221.
26.3 R. H. Codrington, D.D., The Melanesians (Oxford, 1891), pp.
215 sq.
27.1 R. Parkinson, Im Bismarck-Archipel (Leipsic, 1887), p. 144; id.,
Dreissig Jahre in der Südsee (Stuttgart, 1907), pp. 193 sq.
27.2 Thomas Williams, Fiji and the Fijians, Second Edition (London,
1860), i. 234.
27.3 G. A. Wilken, Handleiding voor de vergelijkende Volkenkunde
van Nederlandsch Indië (Leyden, 1893), pp. 596-603; G. W. W. C.
Baron van Hoëvell, Ambon en meer bepaaldelijk de Oeliasers
(Dordrecht, 1875), pp. 148-152.
27.4 A. R. Wallace, The Malay Archipelago, Sixth Edition (London,
1877), p. 196.
28.1 J. G. F. Riedel, De sluik- en kroesharige rassen tusschen
Selebes en Papua (The Hague, 1886), pp. 61 sq.
28.2 J. G. F. Riedel, op. cit. pp. 114 sq.
28.3 Van Schmidt, “Aanteekeningen nopens de zeden, gewoonten
en gebruiken, benevens de vooroordeelen en bijgeloovigheden der
bevolking van de eilanden Saparoea, Haroekoe, Noessa Laut, en
van een gedeelte van de zuidkust van Ceram, in vroegeren en
lateren tijd,” Tijdschrift voor Neêrlands Indie, v. Tweede deel
(Batavia, 1843), pp. 499-502.
29.1 J. G. F. Riedel, op. cit. pp. 167 sq.
31.1 N. Adriani en Alb. C. Kruijt, De Bare’e-sprekende Toradja’s van
Midden-Celebes, i. (Batavia, 1912) pp. 399-401.
31.2 H. F. Standing, “Malagasy fady,” The Antananarivo Annual and
Madagascar Magazine, vol. ii. (Antananarivo, 1896) pp. 252-265
(Reprint of the second Four Numbers).
31.3 A. van Gennep, Tabou et Totémisme à Madagascar (Paris,
1904).
31.4 A. van Gennep, op. cit. pp. 183 sqq.
31.5 A. van Gennep, Tabou et Totémisme à Madagascar, p. 184.
The writer has devoted a chapter (xi. pp. 183-193) to taboos of
property.
31.6 H. F. Standing, “Malagasy fady,” Antananarivo Annual and
Madagascar Magazine, vol. ii. (Antananarivo, 1896) p. 256.
32.1 W. Ellis, History of Madagascar (London, preface dated 1838),
i. 414.
32.2 E. Westermarck, The Origin and Development of the Moral
Ideas, ii. (London, 1908) pp. 59-69. In an article on taboo published
many years ago (Encyclopaedia Britannica, Ninth Edition, xxiii.
(1888) pp. 15 sqq.) I briefly pointed out the part which the system of
taboo has played in the evolution of law and morality. I may be
allowed to quote a passage from the article: “The original character
of the taboo must be looked for not in its civil but in its religious
element. It was not the creation of a legislator, but the gradual
outgrowth of animistic beliefs, to which the ambition and avarice of
chiefs and priests afterwards gave an artificial extension. But in
serving the cause of avarice and ambition it subserved the progress
of civilization, by fostering conceptions of the rights of property and
the sanctity of the marriage tie,—conceptions which in time grew
strong enough to stand by themselves and to fling away the crutch of
superstition which in earlier days had been their sole support. For we
shall scarcely err in believing that even in advanced societies the
moral sentiments, in so far as they are merely sentiments and are
not based on an induction from experience, derive much of their
force from an original system of taboo. Thus on the taboo were
grafted the golden fruits of law and morality, while the parent stem
dwindled slowly into the sour crabs and empty husks of popular
superstition on which the swine of modern society are still content to
feed.”
33.1 É. Aymonier, Notes sur le Laos (Saigon, 1885), p. 233.
33.2 Central Provinces, Ethnographic Survey, vii., Draft Articles on
Forest Tribes, Third Series (Allahabad, 1911), p. 45.
33.3 R. Percival, Account of the Island of Ceylon (London, 1803), p.
198.
33.4 C. F. Ph. v. Martius, Zur Ethnographie Amerikas, zumal
Brasiliens (Leipsic, 1867), p. 86.
33.5 P. Giran, Magie et Religion Annamites (Paris, 1912), p. 186.
34.1 P. Giran, op. cit., pp. 190 sq.
34.2 H. Sundermann, Die Insel Nias und die Mission daselbst
(Barmen, 1905), p. 34.

36.1 Edwin H. Gomes, Seventeen Years among the Sea Dyaks of
Borneo (London, 1911), pp. 64-66.

36.2 (Sir) Charles Thomas Newton, Essays on Art and Archaeology
(London, 1880), pp. 193 sq.
36.3 G. Dittenberger, Sylloge Inscriptionum Graecarum2 (Leipsic,
1898-1901), vol. ii. pp. 284 sq., No. 584; Ch. Michel, Recueil
d’Inscriptions Grecques (Brussels, 1900), p. 624, No. 728. The
goddess was probably the Syrian Atargatis or Derceto, to whom fish
were sacred (Xenophon, Anabasis, i. 4. 9). For more examples of
these ancient Greek curses, see Ch. Michel, op. cit., pp. 877-880,
Nos. 1318-1329. Compare W. H. D. Rouse, Greek Votive Offerings
(Cambridge, 1902), pp. 337 sqq.
37.1 (Sir) C. T. Newton, Essays on Art and Archaeology, p. 195.
37.2 Demosthenes, De Halonneso, 40.
37.3 Plato, Laws, viii. 9, pp. 842 sq.
37.4 Festus, s.v. “Termino,” p. 368, ed. C. O. Müller (Leipsic, 1839);
Varro, De lingua latina, v. 74; Dionysius Halicarnasensis, Antiquitates
Romanae, ii. 74. As to Terminus, the Roman god of boundaries, and
his annual festival the Terminalia, see L. Preller, Römische
Mythologie3 (Berlin, 1881-1883), i. 254 sqq.; G. Wissowa, Religion
und Kultus der Römer2 (Munich, 1912), pp. 136 sq.
37.5 Deuteronomy, xxviii. 17.
37.6 C. H. W. Johns, Babylonian and Assyrian Laws, Contracts and
Letters (Edinburgh, 1904), p. 191.
38.1 R. W. Rogers, Cuneiform Parallels to the Old Testament
(Oxford, preface dated 1911), pp. 390-392.
38.2 David Livingstone, Missionary Travels and Researches in
South Africa (London, 1857), p. 285.
39.1 Charles New, Life, Wanderings, and Labours in Eastern Africa
(London, 1873), p. 106.
39.2 John H. Weeks, Among Congo Cannibals (London, 1913), pp.
310 sq.
39.3 P. Amaury Talbot, In the Shadow of the Bush (London, 1912),
p. 296.
40.1 Travels of an Arab Merchant [Mohammed Ibn-Omar El Tounsy]
in Soudan, abridged from the French by Bayle St. John (London,
1854), pp. 69-73.
41.1 A. C. Hollis, The Nandi, their Language and Folk-lore (Oxford,
1909), pp. 36, 37.
Africa,” in J. Pinkerton’s Voyages and Travels (London, 1808-1814),
xvi. 595.
41.3 Rev. J. Leighton Wilson, Western Africa (London, 1856), pp.
275 sq.
42.1 A. B. Ellis, The Ewe-speaking Peoples of the Slave Coast of
West Africa (London, 1890), pp. 91 sq. Compare id., The Yoruba-
speaking Peoples of the Slave Coast of West Africa (London, 1894),
p. 118.
42.2 Thomas Winterbottom, An Account of the Native Africans in
the Neighbourhood of Sierra Leone (London, 1803), pp. 261 sq.
43.1 Bryan Edwards, History, Civil and Commercial, of the British
West Indies, Fifth Edition (London, 1819), ii. 107-111.
Chapter IV Notes
45.1 Rev. F. Mason, D.D., “On Dwellings, Works of Art, Laws, etc.,
of the Karens,” Journal of the Asiatic Society of Bengal, New Series,
xxxvii. (1868) part ii. No. 3, pp. 147 sq. Compare A. R. McMahon,
The Karens of the Golden Chersonese (London, 1876), pp. 334 sq.
45.2 T. C. Hodson, “The Genna amongst the Tribes of Assam,”
Journal of the Anthropological Institute, xxxvi. (1906) p. 94.
45.3 Lieutenant Thomas Shaw, “On the Inhabitants of the Hills near
Rajamahall,” Asiatic Researches, Fourth Edition, iv. (1807) pp. 60-
62.
46.1 Major P. R. T. Gurdon, The Khasis (London, 1907), pp. 94,
123.
46.2 É. Aymonier, “Notes sur l’Annam,” Excursions et
Reconnaissances, x. No. 24 (Saigon, 1885), pp. 308 sq.
46.3 J. B. Neumann, “Het Pane en Bilastroomgebied op het eiland
Sumatra,” Tijdschrift van het Nederlandsch Aardrijkskundig
Genootschap, Tweede Serie, dl. iii., afdeeling, meer uitgebreide
artikelen, No. 3 (Amsterdam, 1886), pp. 514 sq.; M. Joustra, “Het
leven, de zeden en gewoonten der Bataks,” Mededeelingen van
wege het Nederlandsche Zendelinggenootschap, xlvi. (1902) p. 411.
47.1 H. Sundermann, Die Insel Nias und die Mission daselbst
(Barmen, 1905), pp. 34 sq., 37, 84. Compare A. Fehr, Der Niasser
im Leben und Sterben (Barmen, 1901), pp. 34-36; Th. C. Rappard,
“Het eiland Nias en zijne bewoners,” Bijdragen tot de Taal- Land- en
Volkenkunde van Nederlandsch-Indië, lxii. (1909) pp. 594, 596. The
death penalty for these offences has been abolished by the Dutch
Government, so far as it can make its arm felt in the island.
47.2 Rev. J. Perham, “Petara, or Sea Dyak Gods,” Journal of the
Straits Branch of the Royal Asiatic Society, No. 8, December 1881,
p. 150; H. Ling Roth, The Natives of Sarawak and British North
Borneo (London, 1896), i. 180. Petara is the general Dyak name for
deity. The common idea is that there are many petaras, indeed that

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CLASSIFICATION, AND DIAGNOSIS

1. What is diabetes mellitus?

AND CHRONIC COMPLICATIONS

1. What are the acute complications of diabetes?

9. How is DKA diagnosed?

Table 2.1. Diagnostic Criteria for DKA and HHS.

19. What is needed for the diagnosis of HHS?

20. What is key to the treatment of HHS?

27. What is “hypoglycemia unawareness”?

36. How does diabetic retinopathy manifest?

Nails used to prevent ghosts from walking, 133

Oaths and imprecations as preservers of property, 24 sqq. See also

Pacific, first exploration of the, 173

Sacred chiefs, 7 sqq.

Ulcer taboo, 25 sq.

Vancouver Island, 143

Wagogo, the, of German East Africa, 92, 106

Yabim, the, of German New Guinea, 127, 131

104 sq., note.

76. Compare Old New Zealand, by a Pakeha Maori (London, 1884),

Africa,” in John Pinkerton’s Voyages and Travels (London, 1808-

McCall Theal’s Records of South-Eastern Africa, vii. (1901) pp. 190

1909), pp. 49 sq.

1886), p. 217 (Sacred Books of the East, vol. xxv.).

of Norway, translated by S. Laing (London, 1844), saga i. chapters

Inhabitants, Second Edition (London, 1870), pp. 167, 171.

(Barmen, 1905), p. 34.

Borneo (London, 1911), pp. 64-66.

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