analyze and discuss the relationship between Lila environment growing up, her physiology, attitude and behaviors. Full instructions are attached. Please ask any questions if needed.



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Silent Disorders:
Hypertension and Diabetes
Learning Objectives
1. Describe why hypertension and diabetes are called silent diseases
2. Describe how hypertension and diabetes affect different individual, familial, and social domains
3. Explain how self-management and medication can be used to treat hypertension
4. Identify disparities in hypertension awareness, treatment, and control
5. Explain how both lifestyle changes and medication can be used to treat diabetes
6. Identify relationships between diabetes prevalence and larger social issues
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
5.1 Introduction to Hypertension and Diabetes
as Barbara been eating a lot of sweets lately?” the pediatrician asked Barbara’s
mother, Margaret, on the phone. “No, she doesn’t have a sweet tooth and we don’t
keep a lot of sweets in the house,” Margaret replied. Barbara was 11 and had come
down with a particularly nasty stomach ailment. “Why do you ask?” “Well, most of the tests we
did suggest that Barbara has a viral infection, but Barbara’s urine had a very high concentration of
glucose. Let’s just monitor it for a while and see what happens.”
Barbara used urine glucose test strips for several months. At first, her urine glucose went back to
normal, but a few months later it climbed back up and stayed there. She was diagnosed with type
1 diabetes, also known as diabetes mellitus. At the time Barbara was diagnosed, the family was
undergoing quite a bit of stress, because Barbara’s teenaged step-siblings were moving into the
family home.
5.2 D
 efinition and Brief History of Hypertension
and Diabetes
iabetes and hypertension have been called “evil twins” and “bad companions,” because
they are so often found together in the same person. Both are also “silent” disorders, in
that they may cause no early symptoms but create extra work for the heart and blood
vessels. Having hypertension makes it more likely that someone will develop diabetes, and having diabetes makes it more likely that the person will develop hypertension. Both hypertension
and diabetes increase the risk for problems in the small blood vessels, known as microvascular
disease, of the eyes, kidneys, and peripheral nerves, as well as problems in the large blood vessels,
or macrovascular disease, of the heart, peripheral vascular system, and brain. The risk for both
microvascular and macrovascular disease is even higher when a person has both hypertension
and diabetes (see Table 5.1).
Table 5.1: Macrovascular and microvascular complications of hypertension
and diabetes
Macrovascular complications
Disease of the arteries that can result in heart attack
and stroke
Peripheral vascular disease
Narrowing of arteries that can result in ischemia, or
restricted blood supply to tissues, and ulcers
Microvascular complications
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Damage to the retina that can result in loss of vision
Nephropathy and end-stage renal
Disease of the kidney that can result in kidney failure
Disease of the nerves that can result in pain, numbness,
and weakness in the hands and feet
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
Table 5.2 gives a side-by-side comparison of the two disorders and their symptoms. In this section we compare and contrast the history of these two disorders, define them, and examine how
the biology of each affects physical, mental, and social functioning. In the next section we apply
Bronfenbrenner’s system of human ecology to each disorder. We then explore hypertension over
the life span, approaches to its treatment, and its relationship to social issues. Finally, we discuss
diabetes over the life span, its treatments, and related social issues.
Table 5.2: Characteristics of hypertension and diabetes
Type 1 Diabetes
Type 2 Diabetes
Age of onset
Usually older adults
Often in early
childhood, but can be
as late as adulthood
Usually in older
adults, but recently
seen in children and
Early symptoms
Excessive thirst and
urination, weight loss
Later symptoms
Severe headache,
blurred vision,
chest pain, difficulty
Fatigue, blurred vision
Excessive thirst and
urination, weight loss,
slowed healing, fatigue
Hypertension is abnormally high blood pressure. Blood pressure is a measure of the force that the
blood exerts against the walls of the arteries as the heart pumps blood through the body. It is
expressed as two numbers, written as if it were a
fraction, for example, 120/70. The upper number is
the force produced during the time the heart is contracting, called systolic blood pressure, and the
lower number is the force produced when the heart
is relaxing between beats, or diastolic blood pressure. The units for blood pressure measurement are
millimeters of mercury, or mmHg. Watch a short
video from Medline Plus for more detail about blood
Mary Evans Picture Library/Everett Collection
Hypertension, or what was then known as
“hard pulse disease” was originally treated
by bloodletting or applying leeches.
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Evidence shows that what was then called “hard
pulse disease” was recognized as long ago as 2600
BCE. Of course, treatment at the time was rather
crude by today’s standards and relied on reducing
the blood volume either by bloodletting or applying leeches (Esunge, 1991). The Reverend Stephen
Hales is recognized as the first to measure intraarterial pressure in a horse in 1733 (Kotchen, 2011).
In the 1800s, Thomas Young and Richard Bright
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
built on Hales’s work and gave us modern descriptions of hypertension (Esunge, 1991). In 1905,
introduction of the blood pressure cuff with mercury columns, or the sphygmomanometer,
together with arterial sounds associated with systolic and diastolic measurement heard via a
stethoscope, allowed objective measurement of blood pressure for the first time (Kotchen, 2011).
The medical community did not think that elevated blood pressure—hypertension—was a problem until well after the insurance industry did. As early as 1918, the insurance industry began
requiring blood pressure measurement for life insurance applicants and gathering actuarial data
that related blood pressure to mortality (Kotchen, 2011). At the same time, the medical community suggested that rising blood pressure was a normal part of aging and that attempts to halt or
reduce the rise were dangerous. Cardiologist J. H. Hay (1931) suggested, “There is some truth in
the saying that the greatest danger to a man with high blood pressure lies in its discovery, because
then some fool is certain to try and reduce it” (p. 26).
We can only wonder what might have happened if President Franklin Roosevelt’s hypertension had
been treated. His blood pressure was recorded as 162/98 mmHg in 1937 at age 54; 180/88 mmHg
in 1940; 188/105 mmHg in 1941; between 180/110 and 230/140 mmHg in 1944, when he had a
series of small strokes at the age of 62; and 260/150 mmHg in early 1945. He died of a stroke later
that year at the age of 63. Just before his death, his blood pressure had been recorded as greater
than 300/190 mm Hg (Moser, 2006).
One reason hypertension was not treated aggressively during the first half of the 20th century
was the lack of treatments. Most of the medications of the time were either ineffective or had
nasty side effects. The first clinical trial demonstrating efficacy and tolerability of a treatment for
hypertension (the diuretic chlorothiazide) was published in 1959 (Moser & Macaulay, 1959). At
first, diuretics were used as adjuncts for hypertension treatment, but later it was recognized that
they could be used effectively alone to reduce the medical problems and death associated with
hypertension (Moser & Hebert, 1996).
At the same time effective treatments were found, the underlying causes of hypertension were
being uncovered, and hypertension was beginning to be understood as the result of multiple
interacting systems, including the heart and the kidneys, and the vasculature, the endocrine, and
the nervous systems. Later, the major proponent of this theory, I. H. Page (1982), added genetic
and environmental aspects, bringing the theory current for the 21th century.
Two large studies published in the 1960s—the Veterans Administration Study (“Effects of Treatment on Morbidity in Hypertension,” 1967) and the Framingham Heart Study (Kannel, Schwartz,
& McNamara, 1969)—finally convinced most medical practitioners that controlling hypertension
reduces the rate of stroke, heart attacks, and kidney damage. At the same time, more medications for treating hypertension were being introduced, including beta blockers and angiotensinconverting enzyme (ACE) inhibitors. Another class of medications, angiotensin receptor blockers
(ARBs), was first introduced in 1995.
The U.S. National Hypertension Program was established in 1972, and the first report of the Joint
National Committee (JNC) on detection, evaluation, and treatment of high blood pressure was
published in 1977. Since then, the JNC has issued updates every few years through publication of
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
the JNC 7 in 2003 (Chobanian et al., 2003). The JNC 7 was the first to describe prehypertension as
blood pressure that is higher than normal but not high enough to be considered hypertension. See
Table 5.3 for blood pressure measurements.
Table 5.3: Blood pressure categories
Systolic Pressure
Diastolic Pressure
Less than 120
Hypertension Stage 1
Hypertension Stage 2
160 or higher
100 or higher
Less than 80
Source: Chobanian, A. V., Bakris, G. L., Black, H. R., Cushman, W. C., Green, L. A., Izzo, J. L., . . . National High Blood Pressure Education
Coordinating Committee. (2003). Seventh report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of
High Blood Pressure. Hypertension, 42(6), 1206–1252.
Most hypertension does not have a clear cause—it is classified as essential hypertension. In contrast, secondary hypertension results from an identifiable cause, such as kidney disease or as the
side effect of a medication. We do know that certain traits and categories put people at higher risk
for developing hypertension, such as:

being Black,
having diabetes,
drinking too much alcohol (more than one drink a day for women, more than two
drinks a day for men),
being overweight or obese,
being older,
consuming too much salt,
smoking, and
experiencing frequent stress or anxiety.
The two main approaches to care for hypertension are lifestyle modification and medication.
Although no one can control heritage or age, it is possible to modify many of these risk factors, as
we see in the section on treatment of hypertension. Everyone can benefit from the suggested lifestyle modifications, but some people have to add medication (sometimes two or three) to reach
recommended blood pressure goals.
The usual way to define overweight and obesity is by body mass index (BMI), which is calculated
from weight and height. (The formula is weight in kilograms divided by surface area in square
meters [kg/m2], but most people look it up in a table.) Table 5.4 shows the ranges of BMI that categorize normal weight, overweight, and obesity. You can look up your own BMI by entering your
weight and height on this NHLBI website:
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
Table 5.4: Body mass index (BMI) categories
Extremely obese
≥ 40.0
Diabetes is characterized by high levels of glucose in the blood. Glucose is a simple sugar that
all cells use as an energy source. The two main types of diabetes are type 1 (T1D), which affects
about 5% of people diagnosed with diabetes, and type 2 (T2D), which affects 90% to 95% of people diagnosed with the disorder. When one or another is specified, we use the terms T1D or T2D,
but when we talk about the disorder in general, we use the term diabetes. A third type of diabetes, which may be becoming more common, is gestational diabetes. New diagnostic criteria for
gestational diabetes have increased the number of women diagnosed to 18% of pregnant women
(American Diabetes Association, 2013).
Type 1 diabetes (T1D) is a disorder in which the body’s own immune system attacks and kills beta
cells in the pancreas that produce insulin, a hormone needed for cells to absorb glucose from
the blood and transport it across the cell’s outer surface to the inside, where it can be used for
energy. As a result, the body produces too little insulin. This kind of misdirected attack on the body
is known as autoimmune disease. T1D was previously called insulin-dependent diabetes mellitus
or juvenile diabetes. It is usually first diagnosed in children and young adults. In order to survive,
people with T1D must have insulin delivered to their blood by injection or a pump.
In contrast to T1D, people with type 2 diabetes (T2D) produce enough insulin at first, but their
cells do not respond to it properly, a condition known as insulin resistance, or insensitivity. As a
result, more and more insulin is required, and the beta cells of the pancreas become exhausted
and lose their ability to produce it. T2D was previously called non–insulin-dependent diabetes, or
adult-onset diabetes. It is associated with older age, obesity, a family history of diabetes, physical
inactivity, and certain racial or ethnic groups. As people have become more sedentary and obesity
rates have risen, T2D is being diagnosed in a younger population.
Both T1D and T2D appear to need both an inherited susceptibility and some environmental trigger
to set the disease process in motion. All the environmental triggers have not yet been identified,
although in some cases, it appears that certain viral infections may trigger the body to produce
antibodies to the virus that cross-react with and destroy pancreatic beta cells. This is probably
what happened to 11-year-old Barbara in the case study at the beginning of the chapter.
Gestational diabetes is defined as excess blood glucose that shows up in the later stages of pregnancy in women who did not have diabetes before they became pregnant. It appears to be a form
of insulin resistance that develops perhaps in response to a hormone produced by the placenta.
Gestational diabetes must be treated to avoid problems for both the mother and the child.
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
Egyptian texts as old as 1500 BCE have identified diabetes as a rare condition in which people have
excessive volumes of urine and lose weight. Similarly, Indian texts from the fifth century BCE refer
to people with excessive urine production that is sweet, accompanied by emaciation. The term
diabetes mellitus, reflecting the sweet taste of urine from people with the disorder, was used by
the Greek physician Aretaeus, who lived from about 80 to 138 CE and wrote one of the first accurate clinical descriptions of the disorder. Until well into the 18th century, when Matthew Dobson
measured the concentration of sugar in the urine and blood, diabetes was thought to be a disease
of the kidneys (Eknoyan & Nagy, 2005; Polonsky, 2012).
In 1788, Thomas Cawley became the first to suggest that the pancreas played a role in the development of diabetes. His observations were later confirmed in 1889, when Minkowski and Mering
showed that removing the pancreas from dogs caused diabetes that could be reversed by implanting pancreatic fragments. Edward Sharpey-Schafer suggested that diabetes resulted from the lack
of a single product of the pancreatic cells, which he named insulin (Eknoyan & Nagy, 2005; Polonsky, 2012). In 1922, Banting and Best isolated insulin from cows and were the first to use it to treat
patients with diabetes (Banting, Best, Collip, Campbell, & Fletcher, 1922).
The availability of purified insulin turned an inevitably fatal disorder into one that could be
treated—one of the first instances in which scientific investigation was almost immediately translated into clinical treatment. Insulin’s biology and chemistry became an intense area of research.
Insulin is a peptide hormone made up of two linked chains of amino acids. Insulin was the first
hormone whose amino acid sequence (the order that the amino acids appear in the peptide
chain) was determined. It also became the first hormone to be produced by recombinant DNA
techniques, so that fully human insulin could be produced in vast quantities rather than isolating
insulin from pig or cow pancreas, which had been the method until then (Keen et al., 1980).
During the first half of the 20th century, it became evident that not all diabetes was caused by the
lack of insulin. For a long time, people had noted that those who developed diabetes as children
or young adults were usually underweight, while those who developed it when they were mature
adults were usually overweight. Himsworth (1936) first proposed that some patients had diabetes
because they were resistant or insensitive to insulin. Yalow and Berson (1959) devised the first
immunoassay to measure circulating levels of insulin. Subsequently, they found that obese people
with early diabetes actually released more insulin after an oral glucose tolerance test compared
with normal controls—in other words, they didn’t have too little insulin, but they were insensitive
to it, as Himsworth had proposed (Yalow & Berson, 1960).
Insulin resistance is difficult to measure in a clinical setting; therefore, having high blood glucose
levels (higher than normal but not high enough to qualify as diabetes) is used in its place as a
marker. This intermediate level of blood glucose is termed prediabetes, also known as impaired
glucose tolerance or impaired fasting glucose (fasting plasma glucose [FPG] of 100–125 mg/dL).
There are three main ways of determining whether someone has prediabetes or diabetes:

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hemoglobin A1C (HbA1C) test,
FPG test, and
oral glucose tolerance test (OGTT).
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Section 5.2 Definition and Brief History of Hypertension and Diabetes
The HbA1C test (or A1C test for short) reflects average blood glucose levels over the last 3 months.
It is not as sensitive as the other tests, and certain conditions (e.g., abnormal hemoglobin, anything that changes red blood cell survival, possible racial differences) can alter the results. FPG
measures blood glucose after fasting for at least eight hours. It is most reliable when done in the
morning. OGTT measures blood glucose after fasting for at least eight hours, then drinking a liquid
containing glucose, and measuring blood glucose two hours later. For all three tests, within the
prediabetes range, the higher the test result, the greater the risk of diabetes (see Table 5.5).
Table 5.5: Blood test levels for diagnosing diabetes and prediabetes
A1C (%)
Fasting plasma
glucose (mg/dL)
Oral glucose
tolerance test
About 5
99 or below
139 or below
6.5 or above

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