THE ENDOCRINE SYSTEM 1.

Change plasma membrane permeability or

membrane potential by opening or closing
• Second controlling system of the body ion channels
• Nervous system is the fast-control 2. Activate or inactivate enzymes
system 3. Stimulate or inhibit cell division
• Uses chemical messengers (hormones) that 4. Promote or inhibit secretion of a product
are released into the blood 5. Turn on or turn off transcription of certain
• Hormones control several major processes genes
• Reproduction • Hormones act by two mechanisms
• Growth and development 1. Direct gene activation
• Mobilization of body defenses • Used by steroid hormones and thyroid
• Maintenance of much of homeostasis hormone
• Regulation of metabolism 2. Second-messenger system
• Hormones are produced by specialized cells • Used by protein and peptide hormones
• Cells secrete hormones into extracellular fluids • Direct gene activation
• Blood transfers hormones to target sites 1. Steroid hormones diffuse through the
• These hormones regulate the activity of other plasma membrane of target cells
cells 2. Once inside the cell, the hormone enters
• Endocrinology is the scientific study of the nucleus
hormones and endocrine organs 3. Then, the hormone binds to a specific
The Chemistry of Hormones protein within the nucleus
4. Hormone-receptor complex binds to specific
• Hormones are classified chemically as: sites on the cell's DNA
• Amino acid-based, which includes: 5. Certain genes are activated to transcribe
• Proteins messenger RNA
• Peptides 6. New proteins are synthesized
• Amines
• Steroids-made from cholesterol
• Prostaglandins-made from highly active lipids
that act as local hormones

Hormone Action

• Hormones affect only certain tissues or organs

(target cells or target organs)
• Target cells must have specific protein
receptors
• Hormone binding alters cellular activity
• Hormones arouse cells or alter cellular activity
• Typically, one or more of the following occurs:

(a) Direct gene activation

• Second-messenger system
1. Hormone (first messenger) binds to a
membrane receptor
2. Activated receptor sets off a series of
reactions that activates an enzyme
3. Enzyme catalyzes a reaction that produces a
3. second-messenger molecule (such as cyclic
AMP, known as cAMP)
4. Oversees additional intracellular changes to
promote a specific response in the target cell

• Hormonal stimuli
• Most common category of stimulus
• Endocrine organs are activated by other
hormones
• Example:
• Hormones of the hypothalamus
stimulate the anterior pituitary to
secrete its hormones
• Humoral stimuli
(b) Second-messenger system
• Changing blood levels of certain ions and
Stimuli for Control of Hormone Release nutrients stimulate hormone release
• Humoral indicates various body fluids,
• Hormone levels in the blood are maintained
such as blood and bile
mostly by negative feedback
• A stimulus or low hormone levels in the blood Examples:
trigger the release of more hormone
• Parathyroid hormone and calcitonin are
• Hormone release stops once an appropriate
produced in response to changing levels of
level in the blood is reached
blood calcium levels
• The stimuli that activate endocrine glands fall • Insulin is produced in response to changing
into three major categories
levels of blood glucose levels
1. Hormonal
2. Humoral
3. Neural
 Location of the major endocrine organs of the body

The Major Endocrine Organs

➢ Hypothalamus
• Neural stimuli ➢ Pituitary gland
• Nerve fibers stimulate hormone release ➢ Pineal gland
• Most are under the control of the ➢ Thyroid gland
sympathetic nervous system ➢ Parathyroid gland
Examples: ➢ Thymus
➢ Adrenal glands
• Sympathetic stimulation of the adrenal ➢ Thymus
medulla to release epinephrine and ➢ Adrenal glands
norepinephrine ➢ Pancreas
➢ Gonads (testes and ovaries)
• Some glands have purely endocrine functions
• Anterior pituitary, thyroid, adrenals,
parathyroids
• Endocrine glands are ductless glands
• Hormones are released directly into blood or
lymph
• Other glands are mixed glands, with both
endocrine and exocrine functions (pancreas,
gonads)

Pituitary Gland and Hypothalamus

• Pituitary gland
• Pea-sized gland that hangs by a stalk from
the hypothalamus in the brain
• Protected by the sella turcica of the sphenoid
bone
• Has two functional lobes
 • Anterior pituitary glandular tissue • Urine volume decreases, blood pressure
• Posterior pituitary-nervous tissue increases
• Often called the "master endocrine gland" • In large amounts, causes constriction of
• Hypothalamus produces releasing hormones arterioles, leading to increased blood
and inhibiting hormones pressure (the reason why ADH is known as
• These hormones are released into portal vasopressin)
circulation, which connects hypothalamus to • Alcohol inhibits ADH secretion
anterior pituitary
• Hypothalamus also makes two hormones:
oxytocin and antidiuretic hormone/vasopressin
• Carried to posterior pituitary via
neurosecretory cells for storage
• Posterior pituitary
• Does not make the hormones it releases
• Stored hormones made by the
hypothalamus
• Two hormones released
• Oxytocin Hypothalamus also secretes somatostatin - pituitary
• Antidiuretic hormone (ADH) gland to stop the release of growth hormone
• Oxytocin
• Stimulates contractions of the uterus during
labor, sexual relations, and breastfeeding
• Causes milk ejection (let-down reflex) in a
breastfeeding woman
• Posterior pituitary
• Inhibits urine production (diuresis) by
promoting water reabsorption by the
kidneys Six anterior pituitary hormones
• Urine volume decreases, blood pressure
• Two hormones affect nonendocrine targets
increases
1. Growth hormone
• In large amounts, causes constriction of
2. Prolactin
arterioles, leading to increased blood
pressure (the reason why ADH is known as Four are tropic hormones
vasopressin) 1. Follicle-stimulating hormone
• Alcohol inhibits ADH secretion 2. Luteinizing hormone
• Antidiuretic hormone (ADH) 3. Thyrotropic hormone
4. Adrenocorticotropic hormone

• Inhibits urine production (diuresis) by

promoting water reabsorption by the
kidneys
 Growth hormone (GH)

• General metabolic hormone

• Major effects are directed to growth of
skeletal muscles and long bones
• Plays a role in determining final body size
• Causes amino acids to be built into proteins
• Causes fats to be broken down for a source
of energy

Gonadotropic hormones
Hormones of the Anterior Pituitary
• Regulate hormonal activity of the gonads
Growth hormone (GH) disorders • Follicle-stimulating hormone (FSH)
• Pituitary dwarfism results from hyposecretion - Stimulates follicle development in
of GH during childhood ovaries
• Gigantism results from hypersecretion of GH - Stimulates sperm development in testes
during childhood • Luteinizing hormone (LH)
• Acromegaly results from hypersecretion of GH - Triggers ovulation of an egg in females
during adulthood - Stimulates testosterone production in
males

Thyrotropic hormone (TH)

• also called thyroid- stimulating hormone

(TSH)
- Influences growth and activity of the
thyroid gland
• Adrenocorticotropic hormone (ACTH)
- Regulates endocrine activity of the
adrenal cortex

Pineal Gland

• Hangs from the roof of the third ventricle of the

Hormones released by the posterior pituitary and their target organs
brain
• All anterior pituitary hormones: • Secretes melatonin
• Are proteins (or peptides) • Believed to trigger the body's sleep/wake
• Act through second-messenger systems cycle
• Are regulated by hormonal stimuli • Believed to coordinate the hormones of
• Are regulated mostly by negative feedback fertility in humans and to inhibit the
• Prolactin (PRL) reproductive system until maturity occurs
• Stimulates and maintains milk production
following childbirth
• Function in males is unknown
 (a) Gross anatomy of the thyroid gland, anterior view (b) Photomicrograph of thyroid gland

Thyroid Gland • Calcitonin

• Decreases blood calcium levels by causing
• Found at the base of the throat, inferior to the
calcium deposition on bone
Adam's apple
• Antagonistic to parathyroid hormone
• Consists of two lobes and a connecting isthmus
• Produced by parafollicular cells found
• Follicles are hollow structures that store between the follicles
colloidal material
• Produces two hormones Thyroid Hormone Disorders
1. Thyroid hormone • Goiters
2. Calcitonin • Thyroid gland enlarges due to lack of iodine
• Thyroid hormone • Salt is iodized to prevent goiters
• Major metabolic hormone • Cretinism
• Controls rate of oxidation of glucose to • Caused by hyposecretion of thyroxine
supply body heat and chemical energy • Results in dwarfism during childhood
• Needed for tissue growth and
development Parathyroid Glands
• Composed of two active iodine-containing • Tiny masses on the posterior of the thyroid
hormones • Secrete parathyroid hormone (PTH)
- Thyroxine (T4)-secreted by thyroid • Most important regulator of calcium ion
follicles (Ca2+) homeostasis of the blood
- Triiodothyronine (T3)-conversion of T4 at • Stimulates osteoclasts to remove calcium
target tissues from bone Hypercalcemic hormone
(increases blood calcium levels)
• Stimulates the kidneys and intestine to
absorb more calcium
 • Aldosterone production is inhibited by atrial
natriuretic peptide (ANP), a hormone
produced by the heart when blood pressure is
too high
• Sex Hormones
- Produced in the inner layer of the
adrenal cortex
- Small amounts are made throughout life
- Most of the hormones produced are
androgens (male sex hormones), but
some estrogens (female sex hormones)
are also formed

Hormonal control of the level of calcium ions in the blood

Thymus

• Located in the upper thorax, posterior to the

sternum
• Largest in infants and children
• Decreases in size throughout adulthood
• Produces a hormone called thymosin
• Matures some types of white blood cells
• Important in developing the immune system

Adrenal Glands

• Sit on top of the kidneys

• Two regions
1. Adrenal cortex-outer glandular region has
three layers that produce corticosteroids
- Mineralocorticoids are secreted by
Major mechanisms controlling aldosterone release from the adrenal cortex
outermost layer
- Glucocorticoids are secreted by middle • Adrenal medulla
layer • Produces two similar hormones
- Sex hormones are secreted by innermost (catecholamines)
layer 1. Epinephrine (adrenaline)
2. Adrenal medulla-inner neural tissue region 2. Norepinephrine (noradrenaline)
• Hormones of the adrenal cortex • These hormones prepare the body to deal with
• Released of aldosterone is stimulated by: short-term stress (fight or flight) by:
- Humoral factors (fewer sodium ions or • Increasing heart rate, blood pressure, blood
too many potassium ions in the blood) glucose levels
- Humoral stimulation (ACTH) • Dilating small passageways of lungs
- Renin and angiotensin II in response to a • Hormones of the adrenal cortex
drop in blood pressure • Mineralocorticoids (mainly aldosterone)
- Produced in outer adrenal cortex
 - Regulate mineral (salt) content in blood, • The pancreatic islets (islets of Langerhans)
particularly sodium and potassium ions produce hormones
- Regulate water and electrolyte balance • Insulin-produced by beta cells
- Target organ is the kidney
• Glucagon-produced by alpha cells
• Hormones of the adrenal cortex • These hormones are antagonists that
• Glucocorticoids (including cortisone and maintain blood sugar homeostasis
cortisol) • Insulin
- Produced by middle layer of adrenal cortex • Released when blood glucose levels are
- Promote normal cell metabolism high
- Help resist long-term stressors by • Increases the rate of glucose uptake and
increasing blood glucose levels metabolism by body cells
(hyperglycemic hormone) • Effects are hypoglycemic
- Anti-inflammatory properties
• Glucagon
- Released in response to increased blood
• Released when blood glucose levels are
levels of ACTH
low
• Stimulates the liver to release glucose to
blood, thus increasing blood glucose levels

Gonads

• Produce sex cells

• Produce sex hormones
• Ovaries
• Female gonads located in the pelvic cavity
• Produce eggs
Pancreatic Islets
• Produce two groups of steroid hormones
• Pancreas 1. Estrogens
• Located in the abdomen, close to stomach 2. Progesterone
• Mixed gland, with both endocrine and
exocrine functions
• Testes Other organs that are generally nonendocrine in
• Male gonads suspended outside the pelvic function also secrete hormones
cavity
• Stomach
• Produce sperm
• Small intestine
• Produce androgens, such as testosterone
• Kidneys
• Estrogens
• Heart
• Stimulate the development of secondary
• Placenta
female characteristics
- Produces hormones that maintain
• Mature the female reproductive organs
pregnancy
• With progesterone, estrogens also:
- Some hormones play a part in the delivery
• Promote breast development
of the baby
• Regulate menstrual cycle
- Produces human chorionic gonadotropin
• Progesterone
(hCG) in addition to estrogen,
• Acts with estrogen to bring about the
progesterone, and other hormones
menstrual cycle
- Human placental lactogen (hPL) prepares
• Helps in the implantation of an embryo
the breasts for lactation
in the uterus
- Relaxin relaxes pelvic ligaments and pubic
• Helps prepare breasts for lactation
symphysis for childbirth
• Testes
• Produce several androgens
• Testosterone is the most important
androgen
• Responsible for adult male secondary
sex characteristics
• Promotes growth and maturation of
male reproductive system
• Required for sperm cell production
Developmental Aspects of the Endocrine System also called cretinism, is a medical condition
present at birth marked by impaired physical and
• In the absence of disease, efficiency of the
mental development due to insufficient thyroid
endocrine system remains high until old age
hormone production (hypothyroidism), often
• Decreasing function of female ovaries at
caused by insufficient dietary iodine during
menopause leads to such symptoms as
pregnancy.
osteoporosis, increased chance of heart
disease, and possible mood changes ❖ Thyroiditis
• Efficiency of all endocrine glands gradually
in a medical context, refers to inflammation of
decreases with aging, which leads to a
the thyroid gland, which can lead to various
generalized increase in incidence of:
thyroid-related issues, including temporary or
• Diabetes mellitus
permanent hyperthyroidism (overactive
• Immune system depression
thyroid) or hypothyroidism (underactive
• Lower metabolic rate
thyroid).
• Cancer rates in some areas
❖ Hashimoto's thyroiditis
ENDOCRINE
also known as Hashimoto's disease or chronic
• A growth hormone. lymphocytic thyroiditis, is a chronic
• Listen to pronunciation. (grothe HOR-mone). autoimmune disorder where the body's immune
• A protein made by the pituitary gland that system attacks the thyroid gland, leading to
helps control body growth and the use of hypothyroidism (underactive thyroid).
glucose and fat in the body.
• Also called somatotropin. ❖ Graves' disease
an autoimmune disorder, the most common
For a 24-hour urine collection, discard the first cause of hyperthyroidism (overactive thyroid),
morning urine, note the start time, and collect all where the body's immune system mistakenly
subsequent urine for 24 hours, including the first attacks the thyroid gland, causing it to produce
urine of the following day, keeping the container too much thyroid hormone
refrigerated and ensuring it's returned to the lab Results in increased metabolism, heat
promptly intolerance, rapid heartbeat, weight loss, and
THYROID GLAND DISORDERS: exophthalmos

❖ CRETINISM ❖ Myxedema

a condition of abnormal mental and physical often used in the context of hypothyroidism,
development resulting from a deficiency of refers to a state of severe thyroid hormone
thyroid hormone in fetal or early life, typically deficiency characterized by skin and soft tissue
characterized by intellectual disability, small swelling, and can lead to the life-threatening
stature, and thickening of the facial features. condition of myxedema coma.

❖ Congenital iodine deficiency syndrome Results in physical and mental sluggishness.

(CIDS)
Dermatological Changes: Radioactive iodine therapy involves using a
radioactive form of iodine (I-131) that the thyroid
Myxedema also refers to the specific
gland readily absorbs.
dermatological changes that can occur in
hypothyroidism, including swelling and How it works:
thickening of the skin particularly in the face line
The thyroid gland takes up the radioactive iodine,
eyelids and tongue.
and the radiation emitted destroys the thyroid cells,
Myxedema coma is characterized by: either to reduce an overactive thyroid or to kill
cancer cells.
Altered Mental Status: This can range from
lethargy and confusion to psychosis and coma. Uses:
Hypothermia: A dangerously low body
Hyperthyroidism: Treating an overactive thyroid
temperature.
gland (hyperthyroidism), which can be caused by
Multiple Organ Dysfunction: As the body's
Graves' disease or nodules within the thyroid.
organs struggle to function with insufficient
Thyroid Cancer: Treating certain types of thyroid
thyroid hormone.
cancer, especially differentiated thyroid cancers
Precipitating Factors: like papillary and follicular thyroid carcinoma,
which are iodine-uptaking.
Myxedema coma is often triggered by:
Infection: Especially pneumonia. Administration:
Medications: Certain drugs, like sedatives and
Radioactive iodine is typically administered
tranquilizers.
orally, either as a capsule or liquid, and is usually
Other Medical Conditions: Heart failure, stroke,
an outpatient procedure.
or gastrointestinal bleeding.
Mechanism of Action:
Treatment:
The radioactive iodine circulates through the
Myxedema coma is a medical emergency that
bloodstream, and the thyroid cells take up the
requires prompt and intensive treatment,
iodine, receiving a high dose of radiation that
including:
destroys the cells.
Thyroid Hormone Replacement: To restore thyroid
Targeted Treatment:
hormone levels.
This is a targeted treatment because the thyroid
Supportive Care: To address hypothermia,
cells are the primary absorbers of iodine,
respiratory failure, and other complications.
minimizing the
Addressing the Precipitating Cause: Treating the
After treatment, it's important to take
underlying infection or other medical condition.
precautions to avoid exposing others to
Radioactive iodine (I-131) therapy is a nuclear radiation, as the body will excrete the
medicine treatment used to target and destroy radioactive iodine through urine and other
overactive thyroid tissue or residual cancer cells, bodily fluids.
leveraging the thyroid's natural iodine uptake,
Subtotal thyroidectomy removes part of the
primarily for hyperthyroidism and certain thyroid
thyroid gland, while total thyroidectomy
cancers.
 removes the entire gland. Total thyroidectomy is • Eliminates the source of thyroid hormone
often used for thyroid cancer or uncontrollable production, which can be beneficial in some
hyperthyroidism, while subtotal thyroidectomy cases.
may be used for benign conditions or to preserve
PARATHYROID GLAND DISORDERS:
some thyroid function.
❖ Tetany
Detailed comparison:
is a condition characterized by involuntary muscle
Subtotal Thyroidectomy:
contractions or spasms, often caused by low blood
Removes a portion of the thyroid gland, leaving calcium levels (hypocalcemia) or other electrolyte
some thyroid tissue behind. imbalances.
Purpose:
Tetany is a symptom, not a disease itself, and refers
• It may be used to treat benign conditions like to a state of hyperexcitability of the nervous system,
goiter or nodules. leading to muscle spasms.
• It can be used for Graves' disease to preserve
Causes:
some thyroid function and avoid the need for
Hypocalcemia: The most common cause is low
lifelong hormone replacement.
calcium levels in the blood, which can be due to
Considerations: various factors like:

• May leave some thyroid tissue, which can Underactive parathyroid glands
lead to the recurrence of the original (hypoparathyroidism)
condition or the development of new
Vitamin D deficiency
problems.
• It may have a lower risk of complications like Kidney problems
nerve damage or hypoparathyroidism
Malabsorption syndromes
compared to total thyroidectomy.
Other electrolyte imbalances, such as low
Total Thyroidectomy:
magnesium (hypomagnesemia) or potassium levels
Removes the entire thyroid gland. or metabolic alkalosis, can also contribute to tetany.
Purpose: Symptoms:

• Often used to treat thyroid cancer. • Muscle spasms: These can be mild, like cramps
• It may be used for uncontrollable in the hands and feet, or more severe,
hyperthyroidism or goiter that causes severe involving the larynx (voice box), leading to
symptoms. difficulty breathing.
• Numbness and tingling, especially around the
Considerations:
mouth, hands, and feet.
• Requires lifelong thyroid hormone • Seizures: In severe cases.
replacement therapy. • Other symptoms: Vomiting, difficulty
• May have a higher risk of complications like breathing, and decreased cardiac function.
nerve damage or hypoparathyroidism
compared to subtotal thyroidectomy.
Diagnosis: People with Addison’s disease can have many skin
Assess for signs of tetany, such as muscle spasms changes, such as darkening of the elbow skin
and tingling sensations. surface, darkening of the creases of the palm,
darkening of the gums, and patchy areas of skin
Blood tests are used to measure calcium,
lightening (vitiligo) mixed with skin darkening.
magnesium, and other electrolytes to confirm the
diagnosis. ❖ Cushing’s Syndrome
Chvostek's and Trousseau's signs are physical exam Is a collection of signs and symptoms due to
signs that can suggest tetany. prolonged exposure to glucocorticoids such as
cortisol.
Chvostek's Sign:
Other names: Hypercortisolism, Itsenko-Cushing
This sign is characterized by a twitching or spasm of
syndrome, hyperadrenocorticism
the facial muscles when the facial nerve (just in front
of the ear) is tapped lightly. Common symptoms of Cushing’s syndrome
Trousseau's Sign: Weight gain in the trunk, with thin arms and legs.
Weight gain in the face. This is sometimes called
This sign is elicited by inflating a blood pressure cuff
moon face. A fatty lump between the shoulders.
on the arm to a level above systolic pressure for 3
minutes causing a hand spasm (carpal spasm). Cushing’s syndrome happens when you have too
many corticosteroids in your body. When the
Treatment:
disorder often starts with the pituitary gland, the
Treatment focuses on correcting the underlying condition is called Cushing’s syndrome. The gland
cause, such as restoring calcium levels with makes too much adrenocorticotropin hormone
intravenous calcium or addressing other electrolyte (ACTH). This causes the adrenal glands to make too
imbalances. many corticosteroids.
❖ Carpopedal spasm What are the warning signs of Cushing’s? Five P’s:
Polyuria and polydipsia (increased urination and
refers to painful, involuntary contractions of the
drinking), polyphagia (excessive hunger), panting
muscles in the hands and feet, often associated with
(breathing with short, quick breath), and a pot belly
conditions like hypocalcemia (low calcium levels) or
appearance.
hyperventilation.
- may notice changes in the skin, such
ADRENAL GLAND DISORDERS:
as symmetrical hair loss on the body
❖ Addison's disease or thinner skin.

also known as primary adrenal insufficiency, is a rare ENDOCRINE DISORDERS

long-term endocrine disorder characterized by
inadequate production of the steroid hormone Endocrine System
cortisol and aldosterone by the two outer layers of • Effects almost every cell, organ, and function
the cell of the adrenal glands, causing adrenal of the body
insufficiency. • The endocrine system is closely linked with
the nervous system and the immune system
• Negative feedback mechanism
 • Hormones
• Chemical messengers of the body
• Act on specific target cells

Actions of the major hormones of the pituitary gland.

Adrenal Glands

• Pyramid-shaped organs that sit on top of the

Location of the major endocrine glands. kidneys
Hypothalamus • Each has two parts:
• Outer Cortex
• Sits between the cerebrum and brainstem • Inner Medulla
• Houses the pituitary gland and
hypothalamus Adrenal Cortex
• Regulates: • Mineralocorticoid—aldosterone. Affects
• Temperature sodium absorption, loss of potassium by
• Fluid volume kidney
• Growth • Glucocorticoids—cortisol. Affects
• Pain and pleasure response metabolism, regulates blood sugar levels,
• Hunger and thirst affects growth, anti-inflammatory action,
Hypothalamus Hormones decreases effects of stress
• Adrenal androgens—
• Releasing and inhibiting hormones dehydroepiandrosterone and
• Corticotropin-releasing hormone androstenedione. Converted to testosterone
• Thyrotropin-releasing hormone in the periphery.
• Growth hormone-releasing hormone
Adrenal Medulla
• Gonadotropin-releasing hormone
• Somatostatin -- inhibits GH and TSH • Secretion of two hormones
• Epinephrine
Pituitary Gland
• Norepinephrine
• Sits beneath the hypothalamus • Serve as neurotransmitters for sympathetic
• Termed the “master gland” system
• Divided into: • Involved with the stress response
• Anterior Pituitary Gland
Thyroid Gland
• Posterior Pituitary Gland
• Butterfly shaped
 • Sits on either side of the trachea • Parathyroid hormone—regulates serum
• Has two lobes connected with an isthmus calcium
• Functions in the presence of iodine
Pancreas
• Stimulates the secretion of three hormones
• Involved with metabolic rate management • Located behind the stomach between the
and serum calcium levels spleen and duodenum
• Has two major functions
• Digestive enzymes
• Releases two hormones: insulin and
glucagon

Kidney

• 1, 25 dihydroxyvitamin D—stimulates
calcium absorption from the intestine
• Renin—activates the Renin-Angiotensin
Thyroid Gland System (RAS)
• Erythropoietin—Increases red blood cell
production

Ovaries

• Estrogen
• Progesterone—important in menstrual
cycle, maintains pregnancy,

Testes

Hypothalamic-Pituitary-Thyroid Axis • Androgens, testosterone—secondary sexual

characteristics, sperm production
Thyroid
Thymus
• Follicular cells—excretion of
triiodothyronine (T3) and thyroxine (T4)— • Releases thymosin and thymopoietin
Increase BMR, increase bone and protien • Affects maturation of T lymphocetes
turnover, increase response to
Pineal
catecholamines, need for infant G&D
• Thyroid C cells—calcitonin. Lowers blood • Melatonin
calcium and phosphate levels • Affects sleep, fertility and aging
• BMR: Basal Metabolic Rate
Past Medical History
Parathyroid Glands
• Hormone replacement therapy
• Embedded within the posterior lobes of the • Surgeries, chemotherapy, radiation
thyroid gland • Family history: diabetes mellitus, diabetes
• Secretion of one hormone insipidus, goiter, obesity, Addison’s disease,
• Maintenance of serum calcium levels infertility
 • Sexual history: changes, characteristics, • Cardiovascular status: blood pressure,
menstruation, menopause heart rate, palpitations, SOB
• Vision: changes, tearing, eye edema
Physical Assessment
• Neurologic: numbness/tingling lips or
• General appearance extremities, nervousness, hand tremors,
• Vital signs, height, weight mood changes, memory changes, sleep
• Integumentary patterns
• Skin color, temperature, texture, • Integumentary: hair changes, skin
moisture changes, nails, bruising, wound healing
• Bruising, lesions, wound healing
Most Common Endocrine Disorders
• Hair and nail texture, hair growth
• Face • Thyroid abnormalities
• Shape, symmetry • Diabetes mellitus
• Eyes, visual acuity
Diagnostic Tests
• Neck
• Extremities • GH: fasting, well rested, not physically
• Hand and feet size stressed
• Trunk • T3/T4, TSH: no specific preparation
• Muscle strength, deep tendon reflexes • Serum calcium/phosphate: fasting may or
• Sensation to hot and cold, vibration may not be required
• Extremity edema • Cortisol/aldosterone level
• Thorax • 24 urine collection to measure the level of
• Lung and heart sounds catecholamines (epinephrine,
norepinephrine, dopamine).
Older Adults and Endocrine Function
THYROID DISORDERS
• Relationship unclear
• Aging causes fibrosis of thyroid gland • Cretinism
• Reduces metabolic rate • Hypothyroidism
• Contributes to weight gain • Hyperthyroidism
• Cortisol level unchanged in aging • Thyroiditis
• Goiter
Abnormal Findings
• Thyroid cancer
• Ask the client: ❖ HYPOTHYRODISM
• Energy level Hypothyroidism is the disease state caused by
• Fatigue insufficient production of thyroid hormone by
• Maintenance of ADL the thyroid gland.
• Sensitivity to heat or cold
INCEDENCE
• Weight level
• Bowel habits • 30-60 yrs of age
• Level of appetite • Mostly women (5 times more than men)
• Urination, thirst, salt craving
Causes:
 • Autoimmune disease (Hashimoto's • Teach about S&S of hyperthyroidism with
thyroiditis, post–Graves' disease) replacement therapy
• Atrophy of thyroid gland with aging
• Therapy for hyperthyroidism ❖ MYXEDEMA DEVELOPS
- Radioactive iodine (131I) • Rare serious complication of untreated
- Thyroidectomy hypothyroidism
• Medications • Decreased metabolism causes the heart
• Radiation to head and neck muscle to become flabby
• Leads to decreased cardiac output Leads to
Clinical Manifestations:
decreased perfusion to brain and other vital
1. Fatigue. organs
2. Constipation. • Leads to tissue and organ failure
3. Apathy. • LIFE THREATENING EMERGENCY WITH HIGH
4. Weight gain. MORTALITY RATE
5. Memory and mental impairment and • Edema changes client’s appearance
decreased concentration. • Nonpitting edema appears everywhere
6. masklike face. especially around the eyes, hands, feet,
7. Menstrual irregularities and loss of libido. between shoulder blades
8. Coarseness or loss of hair. • Tongue thickens, edema forms in larynx,
9. Dry skin and cold intolerance. voice husky
10. Menstrual disturbances
Problems seen with Myxedema Coma
11. Numbness and tingling of fingers.
12. Tongue, hands, and feet may enlarge • Coma
13. Slurred speech • Respiratory failure
14. Hyperlipidemia. • Hypotension
15. Reflex delay. • Hyponatremia
16. Bradycardia. • Hypothermia
17. Hypothermia. • Hypoglycemia
18. Cardiac and respiratory complications.
Treatment of Myxedema Coma
Laboratory Assessment
• Patent airway
 T3 • Replace fluids with IV
• Give levothyroxine sodium IV
 T4
• Give glucose IV
 TSH • Give corticosteroids
• Check temp, BP hourly
Treatment:
• Monitor changes LOC hourly
LIFELONG THYROID HORMONE REPLACEMENT • Aspiration precautions, keep warm
• levothyroxine sodium (Synthroid, T4,
Eltroxin)
• IMPORTANT: start at low does, to avoid
hypertension, heart failure and MI
❖ HYPERTHYROIDISM
Clinical Manifestations (thyrotoxicosis):

1. Heat intolerance.
2. Palpitations, tachycardia, elevated systolic
BP.
3. Increased appetite but with weight loss.
4. Menstrual irregularities and decreased
libido.
5. Increased serum T4, T3.
6. Exophthalmos (bulging eyes) ❖ THYROIDITIS
7. Perspiration, skin moist and flushed; • Inflammation of the thyroid gland.
however, elders’ skin may be dry and pruritic • Can be acute, subacute, or chronic
8. Insomnia. (Hashimoto's Disease)
9. Fatigue and muscle weakness • Each type of thyroiditis is characterized by
10. Nervousness, irritability, can’t sit quietly. inflammation, fibrosis, or lymphocytic
11. Diarrhea. infiltration of the thyroid gland.
• Characterized by autoimmune damage to the
• Hyperthyroidism is the second most prevalent thyroid.
endocrine disorder, after diabetes mellitus. • May cause thyrotoxicosis, hypothyroidism, or
• Graves' disease: the most common type of both
hyperthyroidism, results from an excessive ❖ THYROID TUMORS
output of thyroid hormones. • Can be being benign or malignant.
• May appear after an emotional shock, stress, or • If the enlargement is sufficient to cause a
an infection visible swelling in the neck, referred to as a
• Other causes: thyroiditis and excessive goiter.
ingestion of thyroid hormone • Some goiters are accompanied by
• Affects women 8X more frequently than men hyperthyroidism, in which case they are
(appears between second and fourth decade) described as toxic; others are associated with
a euthyroid state and are called nontoxic
Medical Management of Hyperthyroidism goiters.

• Radioactive 131I therapy ❖ THYROID CANCER

• Medications
• Much less prevalent than other forms of
• Propylthiouracil and methimazole
cancer; however, it accounts for 90% of
• Sodium or potassium iodine solutions
endocrine malignancies.
• Dexamethasone
• Diagnosis: thyroid hormone, biobsy
• Beta-blockers
• Management
• Surgery; subtotal thyroidectomy
• The treatment of choice surgical
• Relapse of disorder is common
removal. Total or near-total
• Disease or treatment may result in thyroidectomy is performed if possible.
hypothyroidism
 Modified neck dissection or more 5. Pain meds, analgesic lozengers
extensive radical neck dissection is 6. Humidified oxygen, suction
performed if there is lymph node 7. First fluids: cold/ice, tolerated best, then soft
involvement. diet
• After surgery, radioactive iodine. 8. Limited talking, hoarseness common
• Thyroid hormone supplement to replace 9. Assess for voice changes: injury to the
the hormone. recurrent laryngeal nerve

THYROIDECTOMY CHECK FOR HEMORRHAGE 1st 24 hours:

• Treatment of choice for thyroid cancer • Look behind neck and sides of neck Check for
• Preoperative goals include the reduction of c/o pressure or fullness at incision site Check
stress and anxiety to avoid precipitation of drain
thyroid storm (euothyroid)
REPORT TO MD CHECK FOR RESPIRATORY DISTRESS
• Iodine prep (Lugols or K iodide solution) to
decrease size and vascularity of gland to • Laryngeal stridor (harsh hi pitched resp
minimize risk of hemorrhage, reduces risk of sounds)
thyroid storm during surgery • Result of edema of glottis, hematoma, or
• Preoperative teaching includes dietary tetany
guidance to meet patient metabolic needs • Tracheostomy set/airway/ O2, suction
and avoidance of caffeinated beverages and • CALL MD for extreme hoarseness
other stimulants, explanation of tests and Complication of operation:
procedures, and demonstration of support
of head to be used postoperatively • Hemorrhage
• Laryngeal nerve damage.
POSTOPERATIVE CARE • Hypoparathyrodism
• Monitor dressing for potential bleeding and • Hypothyroidism
hematoma formation; check posterior • Septesis
dressing • Postoperative infection
• Monitor respirations; potential airway PARATHYROID
impairment
• Assess pain and provide pain relief measures • Four glands on the posterior thyroid gland
• Semi-Fowler’s position, support head • Parathormone regulates calcium and
phosphorus balance
• Assess voice but discourage talking
• Increased parathormone elevates blood
• Potential hypocalcemia related to injury or
calcium by increasing calcium absorption
removal of parathyroid glands; monitor for
from the kidney, intestine, and bone.
hypocalcemia.
• Parathormone lowers phosphorus level.
Post-Op Thyroidectomy Nursing Care

1. VS, I&O, IV
2. Semifowlers
3. Support head
4. Avoid tension on sutures
 Management of Hypoparathyroidism

• Increase serum calcium level to 9—10 mg/dL

• Calcium gluconate IV
• May also use sedatives such as pentobarbital
to decrease neuromuscular irritability
• Parathormone may be administered;
potential allergic reactions • Environment
free of noise, drafts, bright lights, sudden
movement
• Diet high in calcium and low in phosphorus
Parathyroid Glands
• Vitamin D
❖ HYPERPARATHYROIDISM • Aluminum hydroxide is administered after
• Primary hyperparathyroidism is 2–4 X more meals to bind with phosphate and promote
frequent in women. its excretion through the gastrointestinal
• Manifestations include elevated serum tract.
calcium, bone decalcification, renal calculi, ADRENAL GLANDS
apathy, fatigue, muscle weakness, nausea,
vomiting, constipation, hypertension, • Adrenal medulla
cardiac dysrhythmias, psychological • Functions as part of the autonomic nervous
manifestations system
• Treatment • Catecholamines; epinephrine and
• Parathyroidectomy norepinephrine
• Hydration therapy • Adrenal cortex
• Encourage mobility reduce calcium • Glucocorticoids
excretion • Mineralocorticoids
• Diet: encourage fluid, avoid excess or • Androgens
restricted calcium
❖ ADRENAL INSUFFICIENCY
• Adrenal cortex function is inadequate to
❖ HYPOPARATHRYOIDISM meet the needs for cortical hormones
• Deficiency of parathormone usually due to • Primary: Addison’s Disease
surgery • Secondary
• Results in hypocalcemia and • May be the result of adrenal suppression by
hyperphosphatemia exogenous steroid use
• Manifestations include tetany, numbness
and tingling in extremities, stiffness of hands
and feet, bronchospasm, laryngeal spasm,
carpopedal spasm, anxiety, irritability,
depression, delirium, ECG changes
• Trousseau’s sign and Chvostek’s sign
 Nursing Process: The Care of the Patient with
Adrenocortical Insufficiency

Assessment

• Level of stress; note any illness or stressors

that may precipitate problems
• Fluid and electrolyte status
• VS and postural blood pressures
• Note signs and symptoms related to
adrenocortical insufficiency such as weight
Adrenal Crisis
changes, muscle weakness, and fatigue
Manifestations: • Medications
• Monitor for signs and symptoms of
• Muscle weakness, anorexia, GI symptoms,
Addisonian crisis
fatigue, dark pigmentation of skin and
mucosa, hypotension, low blood glucose, Diagnoses
low serum sodium, high serum potassium,
• Risk for fluid volume deficit
mental changes, apathy, emotional lability,
• Activity intolerance and fatigue
confusion
• Knowledge deficit
• Addisonian crisis: circulatory collapse
• Diagnostic tests; adrenocortical hormone Interventions
levels, ACTH levels, ACTH stimulation test
• Risk for fluid deficit; monitor for signs and
Adrenal Crisis symptoms of fluid volume deficit, encourage
fluids and foods, select foods high in sodium,
Medical Management:
administer hormone replacement as
• Immediate prescribed
• Reverse shock • Activity intolerance; avoid stress and activity
• Restore blood circulation until stable, perform all activities for patient
• Antibiotics if infection when in crisis, maintain a quiet nonstressful
• Identify cause environment, measures to reduce anxiety
• Supplement glucocorticoids during stressful ❖ CUSHING’S SYNDROME
procedures or significant illness • Due to excessive adrenocortical activity or
corticosteroid medications
Nursing Management:
• Women between the ages of 20 and 40 years
• Assess fluid balance are five times more likely than men to
• Monitor VS closely develop Cushing's syndrome.
• Good skin assessment
Manifestations
• Limit activity
• Provide quiet, non-stressful environment • Hyperglycemia which may develop into
diabetes, weight gain, central type obesity
with “buffalo hump,” heavy trunk and thin
extremities, fragile thin skin, ecchymosis,
 striae, weakness, lassitude, sleep • Activity level and ability to carry out self-care
disturbances, osteoporosis, muscle wasting, • Skin assessment
hypertension, “moon-face”, acne, increased • Changes in physical appearance and patient
susceptibility to infection, slow healing, responses to these changes
virilization in women, loss of libido, mood • Mental function
changes, increased serum sodium, • Emotional status
decreased serum potassium • Medications
• Diagnosis: Dexamethasone suppression test,
↑ Na+ ↑ glucose, ↓ K+, metabolic alkalosis Diagnoses

• Risk for injury

• Risk for infection
• Self-care deficit
• Impaired skin integrity
• Disturbed body image
• Disturbed thought processes

Collaborative Problems/Potential Complications

• Addisonian crisis
• Adverse effects of adrenocortical activity

Planning
Cushing’s Syndrome
Goals may include
Medical Management
1. Decreased risk of injury,
• Pituitary tumor 2. Decreased risk of infection,
• Surgical removal 3. Increased ability to carry out self-care
• radiation activities,
• Adrenalectomy 4. Improved skin integrity,
• Adrenal enzyme inhibitors 5. Improved body image,
• Attempt to reduce or taper corticosteroid 6. Improved mental function, and
dose 7. Absence of complications

Interventions
Nursing Management
• Decrease risk of injury; establish a protective
• Prevent injury Increased protein, calcium environment; assist as needed; encourage
and vitamin D in diet diet high in protein, calcium, and vitamin D.
• Medical asepsis • Decrease risk of infection; avoid exposure to
• Monitor blood glucose infections, assess patient carefully as
• Moderate activity with rest periods corticosteroids mask signs of infection.
• Provide restful environment • Plan and space rest and activity.
• Meticulous skin care and frequent, careful
Assessment
skin assessment.
 • Explanation to the patient and family about • History of gestational diabetes or delivery of
causes of emotional instability. babies over 9 pounds
• Patient teaching.
INSULIN

❖ DIABETES INSIPIDUS • A hormone secreted by beta cells.

• A disorder of the posterior lobe of the • Insulin is an anabolic, or storage, hormone.
pituitary gland that is characterized by a Has the following actions:
deficiency of ADH (vasopressin). Excessive
thirst (polydipsia) and large volumes of dilute 1. Transports and metabolizes glucose for energy
urine. 2. Stimulates storage of glucose in the liver and
• It may occur secondary to head trauma, muscle (in the form of glycogen)
brain tumor, or surgical ablation or 3. Signals the liver to stop the release of glucose
irradiation of the pituitary gland, infections 4. Enhances storage of dietary fat in adipose
of the central nervous system or with tumors tissue
• Another cause of diabetes insipidus is failure 5. Accelerates transport of amino acids (derived
of the renal tubules to respond to ADH from dietary protein) into cells
6. Inhibits the breakdown of stored glucose,
Medical Management protein, and fat
The objectives of therapy are 7. Initially, the liver produces glucose through the
breakdown of glycogen (glycogenolysis).
1. to replace ADH (which is usually a long-term 8. After 8 to 12 hours without food, the liver
therapeutic program), forms glucose from the breakdown of
2. to ensure adequate fluid replacement, and noncarbohydrate substances, including amino
3. to identify and correct the underlying acids (gluconeogenesis).
intracranial pathology.
❖ TYPE 1 DIABETES
DIABETES • Characterized by the destruction of the
pancreatic beta cells.
Risk Factors:
• Combined genetic, immunologic, and
• Family history of diabetes (parents or siblings possibly environmental factors are thought
with diabetes) to contribute to beta-cell destruction.
• Obesity (>20% over desired body weight or • Destruction of the beta cells results in
BMI>27 kg/m2) decreased insulin production, increased
• Race/ethnicity (eg, African Americans, glucose production by the liver, and fasting
Hispanic Americans, Native Americans, Asian hyperglycemia.
Americans, Pacific Islanders) • Glucose from food cannot be stored in the
• Age > 45 y liver but instead remains in the bloodstream
• Previously identified impaired fasting and contributes to postprandial (after meals)
glucose or impaired glucose tolerance hyperglycemia.
• Hypertension (>140/90 mm Hg) • If the concentration of glucose in the blood
• HDL cholesterol level <35 mg/dL (0.90 exceeds 180 to 200 mg/dL, glucose appears
mmol/L) and/or triglyceride level >250 in the urine (glycosuria).
mg/dL (2.8 mmol/L)
 • When excess glucose is excreted in the urine, • Decreased insulin-stimulated glucose uptake
it is accompanied by excessive loss of fluids by the muscles.
and electrolytes (osmotic diuresis). • Glucose remains in the bloodstream
• Insulin normally inhibits glycogenolysis and • Increased amounts of insulin must be
gluconeogenesis, causing the opposite in secreted
type 1 diabetes. • Metabolic syndrome (hypertension,
• Fat breakdown results in an increased hypercholesterolemia, and abdominal
production of ketone bodies (a highly acidic obesity)
substance). • Type 2 diabetes
• Hyperglycemic Hyperosmolar Nonketotic
DIABETIC KETOACIDOSIS (DKA)
Syndrome
• a metabolic derangement that occurs most ➢ To overcome insulin resistance and to prevent
commonly in persons with type 1 diabetes. the buildup of glucose in the blood, increased
• Results from a deficiency of insulin; amounts of insulin must be secreted to maintain
formation of highly acidic ketone bodies the glucose level at a normal or slightly elevated
causing metabolic acidosis. level. This is called metabolic syndrome, which
• The breath has a characteristic fruity odor includes hypertension, hypercholesterolemia,
due to the presence of ketoacids. and abdominal obesity.
❖ TYPE 2 DIABETES ➢ There is enough insulin present to prevent the
• Affects approximately 95% of adults with the breakdown of fat and the accompanying
disease. production of ketone bodies. Therefore, DKA
does not typically occur in type 2 diabetes.
The two main problems are: However, uncontrolled type 2 diabetes may lead
1. Insulin resistance - decreased tissue to another acute problem—hyperglycemic
sensitivity to insulin. hyperosmolar nonketotic syndrome
• may also lead to metabolic syndrome Common symptoms
(hypertension, hypercholesterolemia,
abdominal obesity, and other • Fatigue, irritability, polyuria, polydipsia,
abnormities. poorly healing skin wounds, vaginal
2. Impaired insulin secretion infections, or blurred vision.
• DKA does not typically occur in type 2 • Long-term diabetes complications include
diabetes. eye disease, peripheral neuropathy,
• If uncontrolled, may lead to peripheral vascular disease.
hyperglycemic hyperosmolar syndrome ❖ GESTATIONAL DIABETES
(HHS). • any degree of glucose intolerance with its
onset during pregnancy.
PATHOPHYSIOLOGY
• Hyperglycemia develops because of the
• Insulin resistance and Impaired insulin secretion of placental hormones, which
secretion. causes insulin resistance.
• Intracellular reactions are diminished • Women considered to be at high risk or
• Increased glucose production by the liver, average risk should have either an oral
glucose tolerance test (OGTT) or a glucose
 challenge test (GCT) followed by OGTT in • a slow-progressing form of autoimmune
women who exceed the glucose threshold diabetes.
value of 140 mg/d. • Patients with LADA are not insulin-
• OGTT - blood sample will be taken from a dependent in the initial 6 months of disease
vein in the arm to test the starting blood onset.
sugar level. • Clinical manifestation of LADA shares the
• The client will then drink a mixture of features of types 1 and 2 diabetes.
glucose dissolved in water.
Prevention
• The client will get another blood glucose
test 2 hours later (1 hour for pregnant • Type 2 diabetes can be prevented with
women). appropriate changes in lifestyle.
• Below 140 mg/dL: normal blood sugar
Clinical Manifestations in General
• Between 140 and 199: impaired glucose
tolerance, or prediabetes • Clinical manifestations depend on the
• 200 or higher: diabetes patient’s level of hyperglycemia.
• GCT - measures the body's response to • Classic clinical manifestations include the
glucose. “three Ps”: polyuria, polydipsia, and
• The client drinks a sugary solution. polyphagia.
• One hour later, the client’s blood sugar - Polyuria (increased urination) and
level is measured. polydipsia (increased thirst) occur as
• A blood sugar level below 140 mg/dL (7.8 a result of the excess loss of fluid
mmol/L) is considered normal. associated with osmotic diuresis.
• A blood sugar level of 140 mg/dL (7.8 Patients also experience polyphagia
mmol/L) or higher might indicate (increased appetite)
gestational diabetes. • Other symptoms include fatigue and
• Initial management includes dietary weakness, sudden vision changes, tingling or
modification and blood glucose numbness in hands or feet, dry skin, skin
monitoring. lesions or wounds that are slow to heal, and
• If hyperglycemia persists, insulin is recurrent infections.
prescribed. • The onset of type 1 diabetes may also be
• Goals for blood glucose levels during associated with sudden weight loss or
pregnancy are 95 mg/dL or less before nausea, vomiting, or abdominal pains, if DKA
meals and 120 mg/dL or less 2 hours has developed.
after meals.
Assessment and Diagnostic Findings
• After delivery, blood glucose levels in
women with gestational diabetes usually • An abnormally high blood glucose level is the
return to normal. basic criterion for the diagnosis of diabetes.
• However, many women who have had • Fasting plasma glucose (FPG)
gestational diabetes develop type 2 • Random plasma glucose
diabetes later in life (35% to 60%).
Criteria for the Diagnosis of Diabetes Mellitus
❖ LATENT AUTOIMMUNE DIABETES OF
ADULTS (LADA)
 1. Symptoms of diabetes plus casual plasma a. Blood glucose levels in the normal range or
glucose concentration equal to or greater than as close to normal as is safely possible
200 mg/dL (11.1mmol/L). Casual is defined as b. A lipid and lipoprotein profile that reduces
any time of day without regard to time since the risk for vascular disease
last meal. The classic symptoms of diabetes c. Blood pressure levels in the normal range or
include polyuria, polydipsia, and unexplained as close to normal as is safely possible
weight loss. II. To prevent, or at least slow, the rate of
2. Fasting plasma glucose greater than or equal development of the chronic complications of
to 126 mg/dL (7.0 mmol/L). Fasting is defined diabetes by modifying nutrient intake and
as no caloric intake for at least 8 hours. lifestyle
3. Two-hour postload glucose equal to or greater III. To address individual nutrition needs, taking
than 200 mg/dL (11.1 mmol/L) during an oral into account personal and cultural
glucose tolerance test. The test should be preferences and willingness to change
performed as described by the World Health IV. To maintain the pleasure of eating by only
Organization, using a glucose load containing limiting food choices when indicated by
the equivalent of 75 g anhydrous glucose scientific evidence
dissolved in water. In the absence of
unequivocal hyperglycemia with acute
metabolic decompensation, these criteria a) Meal Planning and Related Education
should be confirmed by repeat testing on a • must consider the patient’s food
different day. The third measure is not preferences, lifestyle, usual eating times, and
recommended for routine clinical use. ethnic and cultural background.
• helps prevent hypoglycemic reactions and
Medical Management
maintain overall blood glucose control.
• The main goal of diabetes treatment is to • Initial education addresses the importance
normalize insulin activity and blood glucose of consistent eating habits, the relationship
levels to reduce the development of of food and insulin, and the provision of an
complications. individualized meal plan.
• The therapeutic goal for diabetes • In-depth follow-up education then focuses
management is to achieve normal blood on management skills, such as eating at
glucose levels (euglycemia) without restaurants; reading food labels; and
hypoglycemia while maintaining a high adjusting the meal plan for exercise, illness,
quality of life. and special occasions.
• Diabetes management has five components: b) Caloric Requirements
nutritional therapy, exercise, monitoring, • Calorie-controlled diets are planned by first
pharmacologic therapy, and education. calculating a person’s energy needs and
1. NUTRITIONAL THERAPY caloric requirements based on age, gender,
Nutritional management includes the following height, and weight.
goals: • An activity element is then factored in to
provide the actual number of calories
I. To achieve and maintain: required for weight maintenance.
 • To promote a 1- to 2-lb weight loss per week, • Glycemic Index - used to describe how much
500 to 1000 calories are subtracted from the a given food increases the blood glucose
daily total. level compared with an equivalent amount
• The calories are distributed into of glucose.
carbohydrates, proteins, and fats, and a meal 1) [Link] starchy foods with protein-
plan is then developed, taking into account and fat-containing foods tends to slow
the patient’s lifestyle and food preferences. their absorption and lower the glycemic
c) Caloric Distribution index.
• Carbohydrates - recommended is higher in 2) [Link] general, eating foods that are raw
carbohydrates (50-60%) than in fat (20% to and whole results in a lower glycemic
30% and protein (10% to 20%). index than eating chopped, puréed, or
• Fats - reducing the total percentage of cooked foods (except meat).
calories from fat sources to less than 30% of 3) [Link] whole fruit instead of drinking
total calories and limiting the amount of juice decreases the glycemic index,
saturated fats to 10% of total calories. because fiber in the fruit slows
• Protein - The meal plan may include the use absorption.
of some nonanimal sources of protein (e.g., 4) [Link] foods with sugars to the diet
legumes, whole grains) to help reduce may result in a lower glycemic index if
saturated fat and cholesterol intake. these foods are eaten with foods that are
• Fiber – Soluble fiber—in foods such as more slowly absorbed.
legumes, oats, and some fruits. Insoluble e) Other Dietary Concerns
fiber is found in whole-grain breads and 1) Alcohol Consumption - Alcohol is absorbed
cereals and in some vegetables. before other nutrients and does not require
d) Food Classification Systems insulin for absorption.
• Exchange Lists - There are six main exchange - Large amounts can be converted to
lists: bread/starch, vegetable, milk, meat, fats, increasing the risk for DKA.
fruit, and fat. Foods within one group (in the - Alcohol may decrease the normal
portion amounts specified) contain equal physiologic reactions in the body that
numbers of calories and are approximately produce glucose.
equal in grams of protein, fat, and 2) Sweeteners - The use of artificial sweeteners
carbohydrate. is acceptable, especially if it assists in overall
• Nutrition Labels - Food manufacturers are dietary adherence.
required to have the nutrition content of - There are two main types of
foods listed on their packaging. The label sweeteners: nutritive and
includes information about how many grams nonnutritive. The nutritive
of carbohydrate are in a serving of food. sweeteners contain calories, and the
• Healthy Food Choices - An alternative to nonnutritive sweeteners have few or
counting grams of carbohydrate is measuring no calories in the amounts normally
servings or choices. It is similar to the food used.
exchange list and emphasizes portion control - Misleading Food Labels - Foods
of total servings of carbohydrate at meals labeled “sugarless” or “sugar-free”
and snacks. may still provide calories equal to
 those of the equivalent sugar- caused by heat or humidity, the use of
containing products if they are made outdated strips, and improper meter
with nutritive sweeteners. cleaning and maintenance.
- Foods labeled “dietetic” are not • Nurses play an important role in providing
necessarily reduced-calorie foods. initial education about SMBG techniques.
2. EXERCISE • For most patients who require insulin,
• Extremely important in diabetes SMBG is recommended two to four times
management because of its effects on daily (usually before meals and at
lowering blood glucose and reducing bedtime).
cardiovascular risk factors. • For patients who take insulin before each
• The nurse instructs the patient to: meal, SMBG is required at least three times
a. Exercise three times each week with no daily before meals to determine each dose.
more than 2 consecutive days without • Patients are asked to keep a record or
exercise. logbook of blood glucose levels so that
b. Perform resistance training twice a week if they can detect patterns.
you have type 2 diabetes. • Testing is done at the peak action time of
c. Exercise at the same time of day (preferably the medication to evaluate the need for
when blood glucose levels are at their peak) dosage adjustments.
and for the same duration each session. b. Testing for Glycated Hemoglobin - also
d. Use proper footwear and, if appropriate, referred to as glycosylated hemoglobin,
other protective equipment (i.e., helmets HgbA1C, or A1C.
for cycling). • a measure of glucose control for the past 3
e. Avoid trauma to the lower extremities, months.
especially if you have numbness due to • When blood glucose levels are elevated,
peripheral neuropathy. glucose molecules attach to hemoglobin in
f. Inspect feet daily after exercise. red blood cells.
g. Avoid exercise in extreme heat or cold. • The longer the amount of glucose in the
h. Avoid exercise during periods of poor blood remains above normal, the more
metabolic control. glucose binds to hemoglobin and the
i. Stretch for 10 to 15 minutes before higher the glycated hemoglobin level
exercising. becomes.
• This complex (hemoglobin attached to the
3. MONITORING GLUCOSE LEVELS AND KETONES glucose) is permanent and lasts for the life
a. SMBG - a method of capillary blood glucose of an individual red blood cell,
testing in which the patient pricks their approximately 120 days.
finger and applies a drop of blood to a test c. Testing for Ketones - Ketones (or ketone
strip that is read by a meter. bodies) accumulate in the blood and urine.
• It is recommended that SMBG occurs when • Ketones in the urine signal that there is a
circumstances call for it. deficiency of insulin and control of type 1
• Some common sources of error include diabetes is deteriorating.
improper application of blood (e.g., drop • The patient may use a urine dipstick to
too small), damage to the reagent strips detect ketonuria. The reagent pad on the
 strip turns purple when ketones are - The risk of severe hypoglycemia
present. increases threefold in patients receiving
4. PHARMACOLOGIC THERAPY intensive treatment.
c. Complications of Insulin Therapy
In the absence of adequate insulin, pharmacologic
• Systemic Allergic Reactions – the treatment
therapy is essential.
is desensitization.
I. [Link] Therapy - In type 1 diabetes, • Insulin Lipodystrophy - a localized reaction,
exogenous insulin must be given for life. in the form of either lipoatrophy or
• In type 2 diabetes, insulin may be necessary lipohypertrophy, occurring at the site of
on a long-term basis to control glucose insulin injections.
levels. • Resistance to Injected Insulin - Patients may
• Insulin injections are given two or more develop insulin resistance and require large
times daily to control the blood glucose level. insulin doses. Immune antibodies develop
• SMBG is a cornerstone of insulin therapy. and bind the insulin.
Insulin dose required is determined by the • Morning Hyperglycemia - caused by several
level of glucose in the blood. factors: the dawn phenomenon, the Somogyi
a. Preparations - vary according to three main effect, or insulin waning.
characteristics: time course of action, species - The dawn phenomenon - thought to
(source), and manufacturer. result from nocturnal surges in growth
b. Insulin Regimens - vary from 1 to 4 injections hormone secretion.
per day. - Somogyi effect – nocturnal hypoglycemia
- Usually, there is a combination of a short- followed by rebound hyperglycemia.
acting insulin and a longer-acting insulin. d. Methods of Insulin Delivery
- There are two general approaches to • Insulin Pens - Insulin is delivered by dialing in
insulin therapy: conventional and a dose or pushing a button for every 1- or 2-
intensive. unit increment given.
- There are no set guidelines as to which • Jet Injectors - deliver insulin through the skin
insulin regimen should be used for which under pressure in an extremely fine stream.
patient. • Insulin Pumps - involves the use of small,
• Conventional Regimen – simplified insulin externally worn devices that closely mimic
regimen. the functioning of the normal pancreas.
- The simplified regimen would be 2. Oral Antidiabetic Agents - for patients who have
appropriate for the terminally ill, the type 2 diabetes that cannot be treated
older adult who is frail and has limited effectively with MNT and exercise alone.
self-care abilities. 3. Other Pharmacologic Therapy
• Intensive Regimen - complex insulin • Pramlintide (Symlin) - a synthetic analogue of
regimen. human amylin. It acts to slow the rate at
- allows the patient more flexibility to which food leaves the stomach and reduces
change the insulin doses from day to day appetite.
in accordance with changes in eating and • Exenatide (Byetta, Byduron) - derived from a
activity patterns. hormone that is produced in the small
 intestine and has been found to be deficient • Recognition, treatment, and prevention of
in type 2 diabetes. acute complications
- It is normally released after food is a. Hypoglycemia
ingested to delay gastric emptying and b. Hyperglycemia
enhance insulin secretion. • Pragmatic information
a. Where to buy and store insulin, syringes, and
Nursing Management
glucose monitoring supplies
1. Managing Glucose Control in the Hospital b. When and how to contact the primary
Setting provider
• Blood glucose targets are 140 to 180 mg/dL. 3. Storing Insulin - should be refrigerated.
• Insulin (subcutaneous or IV) is preferred to • Extremes of temperature should be avoided;
oral antidiabetic agents to manage insulin should not be allowed to freeze and
hyperglycemia. should not be kept in direct sunlight or in a
• Hospital insulin protocols or order sets hot car.
should minimize complexity, ensure • The insulin vial in use should be kept at room
adequate staff training, include standardized temperature to reduce local irritation at the
hypoglycemic treatment, and make injection site.
guidelines available for glycemic goals and • Cloudy insulins should be thoroughly mixed.
insulin dosing. • Bottles of intermediate-acting insulin should
• Appropriate timing of blood glucose checks, also be inspected for flocculation (frosted,
meal consumption, and insulin dose are all whitish coating inside the bottle).
crucial for glucose control and to avoid 4. Selecting Syringes - currently, three sizes of U-
hypoglycemia. 100 insulin syringes are available:
2. Providing Patient Education • 1-mL syringe, 100-unit capacity
Pathophysiology • 0.5-mL syringe, 50-unit capacity
• 0.3-mL syringe, 30-unit capacity
a. Basic definition of diabetes (having a high • Most insulin syringes have a disposable 27-
blood glucose level) to 29-gauge needle that is approximately 0.5
b. Normal blood glucose ranges and target in long.
blood glucose levels 5. Mixing Insulins
c. Effect of insulin and exercise (decrease
• When rapid- or short-acting insulins are to be
glucose)
given simultaneously with longer-acting
d. Effect of food and stress, including illness and
insulins, they are usually mixed together in
infections (increase glucose)
the same syringe.
e. Basic treatment approaches
• the ADA recommends that the regular insulin
• Treatment modalities
be drawn up first.
a. Administration of insulin and oral anti-
6. Withdrawing Insulin
diabetes medications
• instruct patients to inject air into the bottle
b. Meal planning (food groups, timing of meals)
of insulin equivalent to the number of units
c. Monitoring of blood glucose and urine
of insulin to be withdrawn.
ketones
7. Selecting and Rotating the Injection Site
 ••The four main areas for injection are the Clinical Manifestations
abdomen, upper arms (posterior surface),
• may be grouped into two categories:
thighs (anterior surface), and hips.
adrenergic symptoms and central nervous
• The speed of absorption is greatest in the
system (CNS) symptoms.
abdomen and decreases progressively in the
• In mild hypoglycemia, the sympathetic
arm, thigh, and hip, respectively.
nervous system is stimulated, resulting in a
• Systematic rotation of injection sites within
surge of epinephrine and norepinephrine.
an anatomic area is recommended to
This causes symptoms such as sweating,
prevent localized changes in fatty tissue
tremor, tachycardia, palpitation,
(lipodystrophy).
nervousness, and hunger.
• The patient should be encouraged to use all
• In moderate hypoglycemia, the drop in blood
available injection sites within one area
glucose level deprives the brain cells of
rather than randomly rotating sites from
needed fuel for functioning. Signs of
area to area.
impaired function of the CNS may include
• The patient should try not to use the exact
inability to concentrate, headache,
same site more than once in 2 to 3 weeks.
lightheadedness, confusion, memory lapses,
• If the patient is planning to exercise, insulin numbness of the lips and tongue, slurred
should not be injected into the limb that will speech, impaired coordination, emotional
be exercised.
changes, irrational or combative behavior,
8. Preparing the Skin - allow the skin to dry after
double vision, and drowsiness.
cleansing with alcohol before injection.
• In severe hypoglycemia, CNS function is so
9. Inserting the Needle - for a normal or
impaired that the patient needs the
overweight person, a 90-degree angle is the
assistance of another person for treatment
best insertion angle.
of hypoglycemia. Symptoms may include
• Aspiration is not necessary.
disoriented behavior, seizures, difficulty
ACUTE COMPLICATIONS OF DIABETES arousing from sleep, or loss of
consciousness.
[Link] (INSULIN REACTIONS)
Assessment and Diagnostic Findings
• Occurs when the blood glucose falls to less
than 70 mg/dL. • The hypoglycemia may not be detected until
• Severe hypoglycemia is when glucose levels moderate or severe CNS impairment occurs.
are less the 40 mg/dL. • Affected patients must perform SMBG on a
• It can occur when there is too much insulin or frequent regular basis, especially before
oral hypoglycemic agents, too little food, or driving or engaging in other potentially
excessive physical activity. dangerous activities.
• It often occurs before meals, especially if meals Management
are delayed or snacks are omitted.
1. Treating With Carbohydrates - Immediate
treatment must be given when hypoglycemia
occurs.
 • The usual recommendation is for 15 g of a • Patients with marked intravascular volume
fast-acting concentrated source of depletion may have orthostatic hypotension.
carbohydrate. • Volume depletion may also lead to frank
• It is not necessary to add sugar to juice, even hypotension with a weak, rapid pulse.
if it is labeled as unsweetened juice. • The ketosis and acidosis of DKA lead to
2. Initiating Emergency Measures - In emergency gastrointestinal symptoms, such as anorexia,
situations, for adults who are unconscious and nausea, vomiting, and abdominal pain.
cannot swallow, an injection of glucagon 1 mg • The patient may have acetone breath (a
can be given either subcutaneously or fruity odor).
intramuscularly. • In addition, hyperventilation (with very
• After injection of glucagon, the patient may deep, but not labored, respirations) may
take as long as 20 minutes to regain occur.
consciousness.
Pathophysiology
• A concentrated source of carbohydrate
followed by a snack should be given to the 1. Without insulin, the amount of glucose entering
patient on awakening to prevent recurrence the cells is reduced, and the production and
of hypoglycemia (glucagon onset is 8 to 10 release of glucose by the liver are increased.
minutes, and its action lasts 12 to 27 • In an attempt to rid the body of the excess
minutes). glucose, the kidneys excrete the glucose
• The patient should be turned to the side to along with water and electrolytes (e.g.,
prevent aspiration in case the patient vomits. sodium, potassium).
• For patients who are unconscious or cannot • This osmotic diuresis, which is characterized
swallow, 25 to 50 mL of dextrose 50% in by excessive urination (polyuria), leads to
water (D50W) may be administered IV. dehydration and marked electrolyte loss.
• Providing Patient Education 2. Another effect of insulin deficiency or deficit is
❖ DIABETIC KETOACIDOSIS the breakdown of fat (lipolysis) into free fatty
• Caused by an absence or markedly acids and glycerol.
inadequate amount of insulin. • The free fatty acids are converted into ketone
bodies by the liver.
The three main clinical features of DKA are as
• Ketone bodies are acids; their accumulation
follows:
in the circulation due to lack of insulin leads
1. [Link] to metabolic acidosis.
2. [Link] and electrolyte loss
Assessment and Diagnostic Findings
3. [Link]
• Blood glucose levels may vary between 300
Clinical Manifestations
and 800 mg/dL.
• The hyperglycemia of DKA leads to polyuria, • Some patients have lower glucose values,
polydipsia (increased thirst), and marked and others have values of 1000 mg/dL or
fatigue. higher (usually depending on the degree of
• In addition, the patient may experience dehydration).
blurred vision, weakness, and headache.
 • Evidence of ketoacidosis is reflected in low • Insulin administration enhances the
serum bicarbonate (0 to 15 mEq/L) and low movement of potassium from the
pH (6.8 to 7.3) values. extracellular fluid into the cells.
• A low partial pressure of carbon dioxide • Potassium replacement - 40 mEq per hour
(PCO2 10 to 30 mm Hg) reflects respiratory may be needed for several hours.
compensation (Kussmaul respirations) for • Frequent (every 2 to 4 hours initially) ECGs
the metabolic acidosis. and laboratory measurements of potassium
• Accumulation of ketone bodies is reflected in are necessary during the first 8 hours of
blood and urine ketone measurements. treatment.
• Increased levels of creatinine, blood urea 3. Reversing Acidosis
nitrogen (BUN), and hematocrit may also be • Insulin - inhibits fat breakdown, thereby
seen with dehydration. ending ketone production.
• Regular insulin, the only type of insulin
Management
approved for IV use, may be added to IV
1. Rehydration solutions.
• The patient may need as much as 6 to 10 L of • Insulin must be infused continuously until
IV fluid to replace fluid losses caused by subcutaneous administration of insulin can
polyuria, hyperventilation, diarrhea, and be resumed.
vomiting. • Bicarbonate infusion to correct severe
• Initially, 0.9% sodium chloride (normal saline acidosis is avoided during treatment of DKA
[NS]) solution is given at a rapid rate, usually because it precipitates further, sudden (and
0.5 to 1 L per hour for 2 to 3 hours. potentially fatal) decreases in serum
• After the first few hours, half-strength NS potassium levels.
solution is the fluid of choice for continued ❖ HYPERGLYCEMIC HYPEROSMOLAR SYNDROME
rehydration, provided the blood pressure is • a metabolic disorder of type 2 diabetes
stable and the sodium level is not low. resulting from a relative insulin deficiency
• Plasma expanders may be necessary to initiated by an illness that raises the demand
correct severe hypotension that does not for insulin.
respond to IV fluid treatment. • This is a serious condition in which
hyperosmolarity and hyperglycemia
[Link] Electrolytes - major concern during
predominate, with alterations of the
treatment of DKA is potassium.
sensorium (sense of awareness).
• The plasma concentration of potassium • ketosis is usually minimal or absent.
tends to be high (hyperkalemia) from • The basic biochemical defect is the lack of
disruption of the cellular sodium-potassium effective insulin.
pump (in the face of acidosis). • Persistent hyperglycemia causes osmotic
• Rehydration leads to increased plasma diuresis, which results in losses of water and
volume and subsequent decreases in the electrolytes. To maintain osmotic
concentration of serum potassium. equilibrium, water shifts from the
• Rehydration also leads to increased urinary intracellular fluid space to the extracellular
excretion of potassium. fluid space.
 • With glycosuria and dehydration, 4. Monitoring and Managing Potential
hypernatremia and increased osmolarity Complications (Fluid Overload, Hypokalemia,
occur. 5. Cerebral Edema)

Clinical Manifestations LONG-TERM COMPLICATIONS OF DIABETES

• Hypotension 1. Macrovascular Complications

• Profound dehydration (dry mucous 2. Microvascular Complications
membranes, poor skin turgor) • Retinopathy
• Tachycardia • Nephropathy
• Variable neurologic signs (e.g., alteration of 3. Peripheral Neuropathy
consciousness, seizures, hemiparesis) 4. Foot and Leg Problems

Assessment and Diagnostic Findings Macrovascular Complications

• Blood glucose (usually 600 to 1200 mg/dL) • Result from changes in the medium to large
• Electrolytes blood vessels.
• BUN • Blood vessel walls thicken, sclerose, and
• Complete blood count become occluded by plaque that adheres to
• Serum osmolality (exceeds 320 mOsm/kg) the vessel walls.
• Arterial blood gas analysis • Coronary artery disease, cerebrovascular
disease, and peripheral vascular disease are
Management the three main types of macrovascular
• The overall approach to the treatment of complications in diabetes.
HHS is similar to that of DKA: fluid • MI is twice as common in men with diabetes
replacement, correction of electrolyte and three times as common in women with
imbalances, and insulin administration. diabetes.
• Other therapeutic modalities are • People with diabetes have twice the risk of
determined by the underlying illness and the developing cerebrovascular disease and an
results of continuing clinical and laboratory increased risk of death from stroke.
evaluation. • Signs and symptoms of peripheral vascular
• After recovery from HHS, many patients can disease include diminished peripheral pulses
control their diabetes with MNT alone or and intermittent claudication (pain in the
with MNT and oral antidiabetic medications. buttock, thigh, or calf during walking).
• Insulin may not be needed once the acute Management
hyperglycemic complication is resolved.
• Frequent SBGM is important in prevention of • The focus of management is an aggressive
recurrence of HHS. modification and reduction of risk factors.
• This involves prevention and treatment of
Nursing Interventions the commonly accepted risk factors for
1. Maintaining Fluid and Electrolyte Balance atherosclerosis.
2. Increasing Knowledge about Diabetes • MNT and exercise are important in managing
Management obesity, hypertension, and hyperlipidemia.
3. Decreasing Anxiety
 • The use of medications to control • For advanced cases of diabetic retinopathy,
hypertension and hyperlipidemia is the main treatment is argon laser
indicated. photocoagulation. The laser treatment
• Smoking cessation is essential. destroys leaking blood vessels and areas of
neovascularization.
Microvascular Complications
• Vitrectomy - a surgical procedure in which
• Diabetic microvascular disease (or vitreous humor filled with blood or fibrous
microangiopathy) is characterized by tissue is removed with a special drill-like
capillary basement membrane thickening. instrument and replaced with saline or
• Two areas affected by these changes are the another liquid.
retina and the kidneys. ❖ NEPHROPATHY
❖ DIABETIC RETINOPATHY • kidney disease secondary to diabetic
• occurs in both type 1 and type 2 diabetes. microvascular changes in the kidney.
• caused by changes in the small blood vessels • If blood glucose levels are elevated
in the retina. consistently for a significant period of time,
• Retinopathy has three main stages: the kidney’s
nonproliferative (background), • filtration mechanism is stressed, allowing
preproliferative, and proliferative. blood proteins to leak into the urine.
• As a result, the pressure in the blood vessels
Clinical Manifestations
of the kidney increases. Clinical
• Retinopathy is a painless process. Manifestations
• Blurry vision secondary to macular edema
Signs and symptoms of kidney dysfunction
occurs in some patients.
• Symptoms indicative of hemorrhaging • Frequent hypoglycemic episodes (decreased
includes, floaters or cobwebs in the visual catabolism of insulin) Assessment and
field, sudden visual changes including spotty Diagnostic Findings
or hazy vision, or complete loss of vision. • The urine should be checked annually for the
• Assessment and Diagnostic Findings presence of microalbumin.
• Diagnosis is by direct visualization of the • If the microalbuminuria exceeds 30 mg/24
retina through dilated pupils with an hours on two consecutive random urine
ophthalmoscope or with a technique known tests, a 24- hour urine sample should be
as fluorescein angiography. obtained and tested.
• Tests for serum creatinine and BUN levels
Medical Management
should be conducted annually. Management
• The first focus of management of • Control of hypertension (the use of
retinopathy is on primary and secondary angiotensin-converting enzyme [ACE]
prevention. inhibitors, such as captopril [Capoten]),
• Other strategies that may slow the because control of hypertension may also
progression of diabetic retinopathy include decrease or delay the onset of early
control of hypertension, control of blood proteinuria
glucose, and cessation of smoking. • Prevention or vigorous treatment of urinary
tract infections
 • Avoidance of nephrotoxic medications and • Intensive insulin therapy
contrast dye • Pain management
• Adjustment of medications as kidney ❖ AUTONOMIC NEUROPATHIES
function changes • Neuropathy of the autonomic nervous
• Low-sodium diet system results in a broad range of
• Low-protein diet dysfunctions affecting almost every organ
• In chronic or ESKD, two types of treatment system of the body.
are available: dialysis (hemodialysis or • Clinical Manifestations
peritoneal dialysis) and transplantation from • Three manifestations of autonomic
a relative or a cadaver. neuropathy are related to the cardiac,
gastrointestinal, and renal systems.
❖ PERIPHERAL NEUROPATHY • Cardiovascular symptoms range from a fixed,
• Diabetic neuropathy refers to a group of slightly tachycardic heart rate and
diseases that affect all types of nerves, orthostatic hypotension to silent, or painless,
including peripheral (sensorimotor), myocardial ischemia and infarction.
autonomic, and spinal nerves. • Delayed gastric emptying may occur with
• Peripheral neuropathy most commonly typical GI symptoms of early satiety,
affects the distal portions of the nerves, bloating, nausea, and vomiting (“Diabetic”
especially the nerves of the lower constipation or diarrhea).
extremities. • Urinary retention, a decreased sensation of
• It affects both sides of the body bladder fullness, and other urinary
symmetrically and may spread in a proximal symptoms of neurogenic bladder result from
direction. Clinical Manifestations autonomic neuropathy.
• Initial symptoms may include paresthesia
(prickling, tingling, or heightened sensation) 1. Hypoglycemic Unawareness - Autonomic
and burning sensations (especially at night). neuropathy affecting the adrenal medulla is
• As the neuropathy progresses, the feet responsible for diminished or absent
become numb. adrenergic symptoms of hypoglycemia.
• A decrease in proprioception and a 2. [Link] Neuropathy – a decrease or
decreased sensation of light touch may lead absence of sweating (anhidrosis) of the
to an unsteady gait. extremities, with a compensatory increase in
• Decreased sensations of pain and upper body sweating.
temperature place patients with neuropathy 3. [Link] Dysfunction - erectile dysfunction,
at increased risk for injury and undetected decreased libido and lack of orgasm.
foot infections. ❖ FOOT AND LEG PROBLEMS
• Deformities of the foot may also occur; • Between 50% and 75% of lower extremity
neuropathy-related joint changes are amputations are performed on people with
sometimes referred to as Charcot joints. diabetes.
• On physical examination, a decrease in deep • Complications of diabetes that contribute to
tendon reflexes and vibratory sensation is the increased risk of foot problems and
found. Management infections include the following:
1. Neuropathy - Sensory neuropathy leads to
loss of pain and pressure sensation, and
autonomic neuropathy leads to increased
dryness and fissuring of the skin.
2. Peripheral vascular disease - Poor circulation
of the lower extremities contributes to poor
wound healing and the development of
gangrene.
3. Immunocompromise: Hyperglycemia impairs
the ability of specialized leukocytes to destroy
bacteria.