Screening for endocrine and

metabolic disease
a. ASSOCIATED NEUROMUSCULAR AND MUSCULOSKELETAL SIGNS
AND SYMPTOMS
b. ENDOCRINE PATHOPHYSIOLOGY
c. INTRODUCTION TO METABOLISM

SUBMITTED BY
ARPITA BISOTIYA
BPT FINAL YEAR
2015 BATCH
Screening for Endocrine and Metabolic
Disease

 Endocrinology is the study of ductless (endocrine) glands

that produce hormones.
 A hormone acts as a chemical agent that is transported by the
bloodstream to target tissues, where it regulates or modifies
the activity of the target cell.
 The endocrine system cannot be understood fully without
consideration of the effects of the nervous system on the
endocrine system.
 The endocrine system works with the nervous system to
regulate metabolism, water and salt balance, blood pressure,
response to stress, and sexual reproduction.
 The endocrine system is slower in response and takes longer to act than
the nervous system in transferring biochemical information.
 The pituitary (hypophysis), thyroid, parathyroids, adrenals, and pineal
are glands of the endocrine system whose functions are solely endocrine
related and have no other metabolic functions.
 The hypothalamus controls pituitary function and thus has an important
indirect influence on the other glands of the endocrine system.
 Feedback mechanisms exist to keep hormones at normal levels.
 The endocrine system meets the nervous system in a complex series
of interactions that link behavioral-neural-endocrine-immunologic
responses.
 The hypothalamus and the pituitary form an integrated axis that
maintains control over much of the endocrine system.
 The discovery and study of this complex interface axis is called
psychoneuroimmunology (PNI) and has provided a new
understanding of interactive biologic signaling.
 The hypothalamus exerts direct control over both the anterior and posterior
portions of the pituitary gland and can synthesize and release hormones from
its axon terminals directly into the blood circulation.
 These neurons can have a hormone-secreting function, the opposite pathway is
also present.
 Hormones that can stimulate the neural mechanism (e.g., acetylcholine) are
called neurohormones. 
 Acetylcholine is a neurotransmitter and a neurohormone. It is released at
synapses to allow messages to pass along a nerve network, resulting in the
release of both hormones and chemicals.
Associated Neuromuscular And
Musculoskeletal Signs And Symptoms

 The musculoskeletal system is composed of a variety of

connective tissue structures in which normal growth and
development are influenced strongly and sometimes
controlled by various hormones and metabolic processes.
 Alterations in these control systems can result in structural
changes and altered function of various connective tissues,
producing systemic and musculoskeletal signs and
symptoms.
Signs and Symptoms of Endocrine
Dysfunction
 Muscle Weakness, Myalgia, And
Fatigue

 Muscle weakness, myalgia, and fatigue may be early manifestations

of thyroid or parathyroid disease, acromegaly, diabetes, Cushing’s
syndrome, and osteomalacia.
 Proximal muscle weakness associated with endocrine disease is
usually painless and unrelated to either the severity or the duration
of the underlying disease.
 The muscular system is sometimes but not always restored with
effective treatment of the underlying condition.
Bilateral Carpal Tunnel Syndrome

 Bilateral carpal tunnel syndrome (CTS), resulting from

median nerve compression at the wrist, is a common
finding in a variety of systemic and neuromusculoskeletal
conditions
  The fact that the majority of persons with CTS are women at
or near menopause suggests that the soft tissues about the
wrist could be affected in some way by hormones.
Causes of Carpal Tunnel Syndrome

 IDIOPATHIC
• cause unknown
 ANATOMICAL
(Compression)
•
 The signs and symptoms often associated with CTS include
paresthesia, tingling, and numbness and/or pain (or burning pain)
with cutaneous distribution of the median nerve to the thumb,
index, middle, and radial half of the ring finger.
 Nocturnal paresthesia is a common complaint, and this discomfort
causes sleep disruption.
 It can be partially relieved by shaking of the hand or changing wrist
and hand position.
 Pain may radiate into the palm and up the forearm and arm
Periarthritis And Calcific Tendinitis

 Periarthritis (inflammation of periarticular structures,

including the tendons, ligaments, and joint capsule) and
calcific tendinitis occur most often in the shoulders of people
who have endocrine disease.
 Treatment of the underlying endocrine impairment often
improves the clinical picture; physical therapy intervention
may have a temporary palliative effect.
Chondrocalcinosis

 Chondrocalcinosis is the deposition of calcium salts in the cartilage

of joints.
 When accompanied by attacks of gout-like symptoms, it is
called pseudogout.
  Chondrocalcinosis is commonly seen on x-ray films as calcified
hyaline or fibrous cartilage.
 There is an associated underlying endocrine or metabolic disease
in approximately 5% to 10% of individuals with chondrocalcinosis.
Endocrine and Metabolic Disorders
Associated with Chondrocalcinosis

Endocrine Metabolic
 Hypothyroidism  Hemochromatosis

 Hyperparathyroidism  Hypomagnesemia
 Acromegaly  Hypophospatasia
 Ochronosis
 Oxalosis
 Wilson’s diseases
Spondyloarthropathy And
Osteoarthritis

 Spondyloarthropathy (disease of joints of the spine) and

osteoarthritis occur in individuals with various metabolic or
endocrine diseases, including hemochromatosis (disorder of
iron metabolism with excess deposition of iron in the tissues;
also known as bronze diabetes and iron storage disease),
ochronosis (metabolic disorder resulting in discoloration of
body tissues caused by deposits of alkapton bodies),
acromegaly, and diabetes mellitus.
Hand Stiffness And Hand Pain

 Hand stiffness and hand pain, as well as arthralgias of the

small joints of the hand, can occur with endocrine and
metabolic diseases.
 Hypothyroidism is often accompanied by CTS; flexor
tenosynovitis with stiffness is another common finding.
Endocrine Pathophysiology

 Disorders of the endocrine glands can be classified as

primary (dysfunction of the gland itself) or secondary
(dysfunction of an outside stimulus to the gland) and are a
result of either an excess or an insufficiency of hormonal
secretions.
 Secondary dysfunction may also occur (iatrogenically) as a
result of chemotherapy, surgical removal of the glands,
therapy for a nonendocrine disorder (e.g., the use of large
doses of corticosteroids resulting in Cushing’s syndrome), or
excessive therapy for an endocrine disorder.
 Pituitary Gland
Diabetes Insipidus

 Diabetes insipidus (DI) is caused by a lack of secretion or

action of vasopressin (antidiuretic hormone [ADH]).
 This hormone normally stimulates the distal tubules of the
kidneys to reabsorb water.
 Without ADH, water moving through the kidney is not
reabsorbed but is lost in the urine, resulting in severe water
loss and dehydration through diuresis.
 There are two main types of DI: central DI and nephrogenic DI.
 Central DI, which is the most common type, can be idiopathic (primary) or
related to other causes (secondary), such as pituitary trauma, head injury
(including neurosurgery), infections such as meningitis or encephalitis,
pituitary neoplasm, anorexia, and vascular lesions such as aneurysms.
 Nephrogenic DI occurs as a result of some medications (e.g., lithium,
phenytoin, corticosteroids, anticholinergics), alcohol, electrolyte
imbalances such as hypercalcemia and hypokalemia, and diseases
affecting the renal system (e.g., sarcoidosis, multiple myeloma,
pyelonephritis, systemic lupus erythematosus).
 Clinical Signs And Symptoms
Diabetes Insipidus

  Polyuria (increased urination more than 3 L/day in adults)

 Polydipsia (increased thirst, which occurs subsequent to polyuria in response
to the loss of fluid)
 Dehydration (dry, cracked lips/skin; fever; orthostatic hypotension; weakness;
dizziness; fatigue)
 Decreased urine specific gravity (1.001 to 1.005)
 Nocturia, fatigue, irritability
 Increased serum sodium (more than 145 mEq/dL; resulting from
concentration of serum from water loss)
Syndrome of Inappropriate Secretion
of Antidiuretic Hormone

 Syndrome of inappropriate secretion of ADH (SIADH) is an

excess or inappropriate secretion of vasopressin that results
in marked retention of water in excess of sodium in the body.
 Urine output decreases dramatically as the body retains large
amounts of water.
 Almost all the excess water is distributed within body cells,
causing intracellular water gain and cellular swelling (water
intoxication).
Risk Factors: Risk factors for the development of SIADH include pituitary damage
caused by infection, trauma, or neoplasm; secretion of vasopressin-like substances
from some types of malignant tumors (particularly pulmonary malignancies); and
thoracic pressure changes from compression of pulmonary or cardiac pressure
receptors, or both.
Clinical Presentation:
 They are the result of water retention and the subsequent dilution of sodium in
the blood serum and body cells.
 Neurologic and neuromuscular signs and symptoms predominate and are
directly related to the swelling of brain tissue and sodium changes within
neuromuscular tissues.
 Clinical Signs And Symptoms
Syndrome of Inappropriate Secretion of
Antidiuretic Hormone
• Headache, confusion, lethargy (most significant early indicators)
• Decreased urine output
• Weight gain without visible edema
• Seizures
• Muscle cramps
• Vomiting, diarrhea
• Increased urine specific gravity (greater than 1.03)
• Decreased serum sodium (less than 135 mEq/dL; caused by dilution of
serum from water)
 Acromegaly

 Acromegaly is an abnormal enlargement of the extremities of the skeleton resulting

from hypersecretion of growth hormone (GH) from the pituitary gland.
 This condition is relatively rare and occurs in adults, most often owing to a tumor of
the pituitary gland.
 In children, overproduction of GH stimulates growth of long bones and results in
gigantism, in which the child grows to exaggerated heights.
 With adults, growth of the long bones has already stopped, so the bones most
affected are those of the face, jaw, hands, and feet.
 Other signs and symptoms include amenorrhea (in women), diabetes mellitus,
profuse sweating, and hypertension.
 Clinical Presentation: Degenerative arthropathy may be seen in
the peripheral joints of a client with acromegaly, most frequently
attacking the large joints.
 On x-ray studies, osteophyte formation may be seen, along with
widening of the joint space because of increased cartilage
thickness.
 In late-stage disease, joint spaces become narrowed, and
occasionally chondrocalcinosis may be present.
 Stiffness of the hand, typically of both hands, is associated
with a broad enlargement of the fingers from bony
overgrowth and with thickening of the soft tissue.
 Thickening and widening of the phalangeal tufts are typical
x-ray findings in soft tissue.
 In patient with these x-ray findings, much of the pain and
stiffness is believed to be due to premature osteoarthritis.
 Clinical Signs And Symptoms
Acromegaly

• Bony enlargement (face, jaw, hands, feet)

• Amenorrhea
• Diabetes mellitus
• Profuse sweating (diaphoresis)
• Hypertension
• Carpal tunnel syndrome (CTS)
• Hand pain and stiffness
• Back pain (thoracic and/or lumbar)
• Myopathy and poor exercise tolerance
 Adrenal Glands

 The adrenals are two small glands located on the upper part of each
kidney.
 Each adrenal gland consists of two relatively discrete parts: an outer
cortex and an inner medulla.
 The outer cortex is responsible for the secretion of mineralocorticoids
(steroid hormones that regulate fluid and mineral balance),
glucocorticoids (steroid hormones responsible for controlling the
metabolism of glucose), and androgens (sex hormones).
 The centrally located adrenal medulla is derived from neural tissue and
secretes epinephrine and norepinephrine. Together, the adrenal cortex
and medulla are major factors in the body’s response to stress.
Adrenal Insufficiency

 Primary Adrenal Insufficiency: Chronic adrenocortical

insufficiency (hyposecretion by the adrenal glands) may be
primary or secondary.
 Primary adrenal insufficiency is also referred to as Addison’s
disease (hypofunction), named after the physician who first
studied and described the associated symptoms.
 It can be treated by the administration of exogenous cortisol
(one of the adrenocortical hormones).
 Primary adrenal insufficiency occurs when a disorder exists
within the adrenal gland itself.
 This adrenal gland disorder results in decreased production
of cortisol and aldosterone, two of the primary adrenocortical
hormones.
 The most common cause of primary adrenal insufficiency is
an autoimmune process that causes destruction of the
adrenal cortex.
 The most striking physical finding in the person with primary
adrenal insufficiency is the increased pigmentation of the skin and
mucous membranes.
 In primary adrenal insufficiency, the increase in pigmentation is
initiated by the excessive secretion of melanocyte-stimulating
hormone (MSH) that occurs in association with increased secretion of
adrenocorticotropic hormone (ACTH).
 ACTH is increased in an attempt to stimulate the diseased adrenal
glands to produce and release more cortisol.
 Most commonly, pigmentation is visible over extensor surfaces such
as the backs of the hands; elbows; knees; and creases of the hands,
lips, and mouth.
 Increased pigmentation of scars formed after the onset of the disease
is common.
 However, it is possible for a person with primary adrenal
insufficiency to demonstrate no significant increase in pigmentation.
Secondary Adrenal Insufficiency: Secondary adrenal insufficiency
refers to a dysfunction of the gland because of insufficient stimulation
of the cortex owing to a lack of pituitary ACTH.
 Causes of secondary disease include tumors of the hypothalamus or
pituitary, removal of the pituitary, or rapid withdrawal of
corticosteroid drugs.
 Clinical manifestations of secondary disease do not occur until the
adrenals are almost completely nonfunctional and are primarily
related to cortisol deficiency only.
 Clinical Signs And Symptoms
Adrenal Insufficiency

• Dark pigmentation of the skin,

especially mouth and scars • Gastrointestinal (GI)
(occurs only with primary disturbances
disease; Addison’s disease) • Anorexia and weight loss
• Hypotension (low blood • Nausea and vomiting
pressure causing orthostatic
symptoms) • Arthralgias, myalgias
(secondary only)
• Progressive fatigue (improves
with rest) • Tendon calcification

• Hyperkalemia (generalized • Hypoglycemia

weakness and muscle flaccidity)
 Cushing’s Syndrome

 Cushing’s syndrome (hyperfunction of the adrenal gland) is a general

term for increased secretion of cortisol by the adrenal cortex.
 When corticosteroids are administered externally, a condition of
hypercortisolism called iatrogenic Cushing’s syndrome occurs,
producing a group of associated signs and symptoms.
 Hypercortisolism caused by excess secretion of ACTH (e.g., from
pituitary stimulation) is called ACTH-dependent Cushing’s syndrome.14
 Whenever corticosteroids are administered externally, the increase in serum
cortisol levels triggers a negative feedback signal to the anterior pituitary
gland to stop adrenal stimulation.
 Adrenal atrophy occurs during this time, and adrenal insufficiency will result
if external corticosteroids are abruptly withdrawn.
 Corticosteroid medications must be reduced gradually so that normal adrenal
function can return.
 Because cortisol suppresses the inflammatory response of the body, it can
mask early signs of infection. Any unexplained fever without other symptoms
should be a warning to the therapist of the need for medical follow-up.
 Clinical Signs And Symptoms
Cushing’s Syndrome
 Moonface” appearance (very
• Kyphosis and back pain (secondary to bone
round face;
loss)
 Buffalo hump at the neck (fatty
• Easy bruising
deposits)
• Psychiatric or emotional disturbances
 Protuberant abdomen with
accumulation of fatty tissue and • Impaired reproductive function (e.g.,
stretch marks decreased libido and changes in menstrual cycle)
 Muscle wasting and weakness • Diabetes mellitus
 Decreased density of bones • Slow wound healing
(especially spine) • For women: Masculinizing effects (e.g., hair
 Hypertension growth, breast atrophy, voice changes)
 Effects of Cortisol on Connective Tissue: Overproduction of cortisol or
closely related glucocorticoids by abnormal adrenocortical tissue leads to a
protein catabolic state.
 This overproduction causes liberation of amino acids from muscle tissue.
 The resultant weakened protein structures (muscle and elastic tissue) cause
a protuberant abdomen, poor wound healing, generalized muscle weakness,
and marked osteoporosis (demineralization of bone causing reduced bone
mass), which is made worse by an excessive loss of calcium in the urine.
 The effect of increased circulating levels of cortisol on the muscles of clients
may be so much muscle wasting that the condition simulates muscular
dystrophy.
 Marked weakness of the quadriceps muscle often prevents affected clients
from rising out of a chair unassisted.
 Those with Cushing’s syndrome of long duration almost always
demonstrate demineralization of bone.
 In severe cases, this condition may lead to pathologic fractures, but it results
more commonly in wedging of the vertebrae, kyphosis, bone pain, and back
pain
 Obesity, diabetes, polycystic ovarian syndrome, and other
metabolic/endocrine problems can resemble Cushing’s syndrome.
 It is important to recognize critical indicators of this particular disorder,
such as excessive hair growth, moonface, mood disorders, and increased
muscle weakness, as indicators for further endocrine diagnostic testing.
 The poor wound healing that is characteristic of this syndrome becomes a
problem when any surgical procedures are required.
 Inhibition of collagen formation with corticosteroid therapy is responsible
for the frequency of wound breakdown in postsurgical clients.
 Thyroid Gland

 The thyroid gland is located in the anterior portion of the lower neck
below the larynx, on both sides of and anterior to the trachea.
 The chief hormones produced by the thyroid are thyroxine (T 4),
triiodothyronine (T3), and calcitonin.
 Both T3and T4 regulate the metabolic rate of the body and increase
protein synthesis.
 Calcitonin has a weak physiologic effect on calcium and phosphorus
balance in the body.
 Genetics plays a role in thyroid disease. A family history of thyroid disease is a
risk factor.
 Age and gender are also factors; most cases occur after age 50. Women are more
likely than men to develop thyroid dysfunction.
 Thyroid function is regulated by the hypothalamus and pituitary feedback
controls, as well as by an intrinsic regulator mechanism within the gland itself.
 Basic thyroid disorders of significance to physical therapy practice include goiter,
hyperthyroidism, hypothyroidism, and cancer.
 Alterations in thyroid function produce changes in hair, nails, skin, eyes,
gastrointestinal (GI) tract, respiratory tract, heart and blood vessels, nervous
tissue, bone, and muscle.
 Goiter

 Goiter, an enlargement of the thyroid gland, occurs in areas of the

world where iodine (necessary for the production of thyroid hormone)
is deficient in the diet.
 It is believed that when factors (e.g., a lack of iodine) inhibit normal
thyroid hormone production, hypersecretion of TSH occurs because of
a lack of a negative feedback loop.
 The TSH increase results in an increase in thyroid mass.
 Pressure on the trachea and esophagus causes difficulty in breathing,
dysphagia, and hoarseness.
Clinical Signs And Symptoms
Goiter

• Increased neck size

• Pressure on adjacent tissue (e.g., trachea and esophagus)
• Difficulty in breathing
• Dysphagia
• Hoarseness
 Thyroiditis

 Thyroiditis is an inflammation of the thyroid gland. Causes can include infection

and autoimmune processes.
 The most common form of this problem is a chronic thyroiditis called Hashimoto’s
thyroiditis. This condition affects women more frequently than men and is most
often seen in the 30- to 50-year-old age group.
 Destruction of the thyroid gland from this condition can cause eventual
hypothyroidism.
 Other symptoms are related to the functional state of the gland itself. Early
involvement may cause mild symptoms of hyperthyroidism, whereas later
symptoms cause hypothyroidism.
Clinical Signs And Symptoms
Thyroiditis

• Painless thyroid enlargement

• Dysphagia, “tight” sensation when swallowing, or choking
• Anterior neck, shoulder, or rib cage pain without biomechanical
changes
• Gland sometimes easily palpable over anterior neck (warm,
tender, swollen)
• Fatigue, weight gain, dry hair and skin, constipation (these are
later symptoms associated with hypothyroidism)
 Hyperthyroidism

 Hyperthyroidism (hyperfunction), or thyrotoxicosis, refers to those

disorders in which the thyroid gland secretes excessive amounts of thyroid
hormone.
 Graves’ disease is a common type of excessive thyroid activity characterized
by a generalized enlargement of the gland (or goiter leading to a swollen
neck) and often, protruding eyes caused by retraction of the eyelids and
inflammation of the ocular muscles.
 Clinical Presentation: Excessive thyroid hormone creates a generalized
elevation in body metabolism. The effects of thyrotoxicosis occur gradually
and are manifested in almost every system.
Systemic Manifestations of
Hyperthyroidism
 In more than 50% of adults older than
70, three common signs are tachycardia,
fatigue, and weight loss. In clients
younger than 50, clinical signs and
symptoms found most often include
tachycardia, hyperactive reflexes,
increased sweating, heat intolerance,
fatigue, tremor, nervousness,
polydipsia, weakness, increased
appetite, dyspnea, and weight loss.

FIG.  Comparison of
hyperthyroidism and
hypothyroidism.
 Chronic periarthritis is also associated with hyperthyroidism.
 Inflammation that involves the periarticular structures, including the
tendons, ligaments, and joint capsule, is termed periarthritis.
  The syndrome is associated with pain and reduced range of motion.
Calcification, whether periarticular or tendinous, may be seen on x-ray
studies.
 Both periarthritis and calcific tendinitis occur most often in the shoulder,
and both are common findings in clients who have endocrine disease
 Painful restriction of shoulder motion associated with periarthritis has been
widely described among patients of all ages with hyperthyroidism.
 The involvement can be unilateral or bilateral and can worsen progressively to
become adhesive capsulitis (frozen shoulder).
 Acute calcific tendinitis of the wrist also has been described in such patient.
Although antiinflammatory agents may be needed for the acute symptoms,
chronic periarthritis usually responds to treatment of the underlying
hyperthyroidism.
 The incidence of myasthenia gravis is increased in clients with
hyperthyroidism, which in turn can aggravate muscle weakness.
 Thyroid Storm: Life-threatening complications with
hyperthyroidism are rare but still important for the therapist to
recognize. Unrecognized disease, untreated disease, or incorrect
treatment can result in a condition called thyroid storm. In
addition, precipitating factors, such as trauma, infection, or
surgery, can turn well-controlled hyperthyroidism into a thyroid
storm.
 Thyroid storm is characterized by signs and symptoms of
hypermetabolism including severe tachycardia with heart failure,
shock, and hyperthermia (up to 105.3° F [40.7° C]).
 Restlessness, agitation, chest pain, abdominal pain, nausea and
vomiting, and coma can occur.
 Immediate medical referral is required to return the patient to a
normal thyroid state and prevent cardiovascular or hyperthermic
collapse.
 Hypothyroidism

 Hypothyroidism (hypofunction) is more common than hyperthyroidism, results

from insufficient thyroid hormone, and creates a generalized depression of body
metabolism.
 Hypothyroidism in fetal development and infants is usually a result of absent
thyroid tissue and hereditary defects in thyroid hormone synthesis. Untreated
congenital hypothyroidism is referred to as cretinism.
The condition may be classified as either primary or secondary. Primary
hypothyroidism results from reduced functional thyroid tissue mass or impaired
hormonal synthesis or release (e.g., iodine deficiency, loss of thyroid tissue,
autoimmune thyroiditis). Secondary hypothyroidism occurs as a result of inadequate
stimulation of the gland because of anterior pituitary gland dysfunction
 Risk Factors: Women are 10 times more likely than men to have
hypothyroidism. More than 10% of women over age 65 and 15%
over age 70 are diagnosed with this disorder. Risk factors include
surgical removal of the thyroid gland, external irradiation, and some
medications (e.g., lithium, amiodarone).
Systemic Manifestations of
Hypothyroidism
  Ichthyosis, or dry scaly skin (resembling fish scales;
the word ichthyosis is derived from the Latin
word ichthus, which means “fish”), may be an
inherited dermatologic condition (Fig. 11-4). It may
also be the result of a thyroid condition. It must not be
assumed that clients who present with this condition
are merely in need of better hydration or regular use
of skin lotion. A medical referral is needed to rule out
underlying pathology.

FIG. Ichthyosis of the legs in a woman

with severe hypothyroidism. 
 Myxedema: A characteristic sign of hypothyroidism and more
rarely associated with hyperthyroidism (Graves’ disease)
is myxedema (often used synonymously with hypothyroidism).
 Myxedema is a result of an alteration in the composition of the
dermis and other tissues, causing connective tissues to be
separated by increased amounts of mucopolysaccharides and
proteins.
 This mucopolysaccharide-protein complex binds with water,
causing a nonpitting, boggy edema, especially around the eyes,
hands, and feet and in the supraclavicular fossae
 The binding of this protein-mucopolysaccharide complex causes
thickening of the tongue and the laryngeal and pharyngeal mucous
membranes.
 This results in hoarseness and thick, slurred speech, which are also
characteristic of untreated hypothyroidism.
Neuromuscular Symptoms:
  Neuromuscular symptoms are among the most common manifestations of
hypothyroidism.
 Flexor tenosynovitis with stiffness often accompanies CTS in people with
hypothyroidism.
 CTS can develop before other signs of hypothyroidism. CTS arises from
deposition of myxedematous tissue in the carpal tunnel area.
 Acroparesthesias may occur as a result of median nerve compression at the
wrist.
 The paresthesias are almost always located bilaterally in the hands.
Neoplasms

 Cancer of the thyroid is a relatively uncommon, slow-growing

neoplasm that rarely metastasizes.
 It is often the incidental finding in persons being treated for other
disorders (e.g., musculoskeletal disorders involving the head and
neck).
 Primary cancers of other endocrine organs are rare and are not
encountered by the clinical therapist very often.
 Risk factors for thyroid cancer include female gender, age
over 40 years, Caucasian race, iodine deficiency, family
history of thyroid cancer, and being exposed to
radioactive iodine (I-131), especially as children. In
addition, nuclear power plant fallout could expose large
numbers of people to I-131 and subsequent thyroid cancer.
The use of potassium iodide (KI) can protect the thyroid
from the adverse effects of I-131 and is recommended to be
made available in areas of the country near nuclear power
plants in case of nuclear fallout. The initial
manifestation in adults and especially in children is a
palpable lymph node or nodule in the neck lateral to the
sternocleidomastoid muscle in the lower portion of the
posterior triangle overlying the scalene muscles.
FIG. 11-5 Lymph node regions of the head and neck. Palpable nodal disease associated with thyroid carcinoma is
commonly located lateral to the sternocleidomastoid muscle in the lower portion of the posterior triangle overlying
the scalene muscles (dark red triangle).
Clinical Signs And Symptoms
Thyroid Carcinoma

• Presence of asymptomatic nodule or mass in thyroid tissue

• Nodule is firm, irregular, painless
• Hoarseness
• Hemoptysis
• Dyspnea
• Elevated blood pressure
 Parathyroid Glands

 Two parathyroid glands are located on the posterior surface of each lobe of
the thyroid gland.
 These glands secrete parathyroid hormone (PTH), which regulates calcium
and phosphorus metabolism.
 Parathyroid disorders include hyperparathyroidism and
hypoparathyroidism.
 Disorders of the parathyroid glands may produce periarthritis and tendinitis.
 Both types of inflammation may be crystal induced and can be associated
with periarticular or tendinous calcification.
 Hyperparathyroidism

 Hyperparathyroidism (hyperfunction), or the excessive secretion of PTH,

disrupts calcium, phosphate, and bone metabolism.
 The primary function of PTH is to maintain a normal serum calcium level.
Elevated PTH causes release of calcium by the bone and accumulation of
calcium in the bloodstream.
 Symptoms of hyperparathyroidism are related to this release of bone calcium
into the bloodstream.
 This causes demineralization of bone and subsequent loss of bone strength
and density. At the same time, the increase of calcium in the bloodstream can
cause many other problems within the body, such as renal stones.
 The major cause of primary hyperparathyroidism is a tumor of a parathyroid
gland, which results in the autonomous secretion of PTH.
 Renal failure, another common cause of hyperparathyroidism, causes
hypocalcemia and stimulates PTH production.
 Hyperplasia of the gland occurs as it attempts to raise the blood serum
calcium levels.
 Thiazide diuretics (used for hypertension) and lithium carbonate (used for
some psychiatric problems) can exacerbate or even cause hyperparathyroid
disorders.
Clinical Presentation: 
 Proximal muscle weakness and fatigability are common findings and may be
secondary to a peripheral neuropathic process.
 Myopathy of respiratory muscles with associated respiratory involvement.
 Other symptoms associated with hyperparathyroidism are muscle weakness,
loss of appetite, weight loss, nausea and vomiting, depression, and increased
thirst and urination.
 Hyperparathyroidism can also cause GI problems, pancreatitis, bone
decalcification, and psychotic paranoia.
Systemic Manifestations of
Hyperparathyroidism
FIG.  The pathologic processes of body structures as a result of
excess parathyroid hormone. 
 Bone erosion, bone resorption, and subsequent bone destruction from
hypercalcemia associated with hyperparathyroidism.
 In most cases, hypercalcemia is mild and detected before any
significant skeletal disease develops.
 The classic bone disease osteitis fibrosa cystica affects persons with
primary or renal hyperparathyroidism.
 Bone lesions called Brown tumorsappear at the end stages of the cystic
osteitis fibrosa.
 Hypoparathyroidism

 Hypoparathyroidism (hypofunction), or insufficient secretion of PTH,

most commonly results from accidental removal or injury of the
parathyroid gland during thyroid or anterior neck surgery.
 A less common form of the disease can occur from a genetic
autoimmune destruction of the gland.
 Hypofunction of the parathyroid gland results in insufficient secretion
of PTH and subsequent hypocalcemia, hyperphosphatemia, and
pronounced neuromuscular and cardiac irritability.
Clinical Presentation: 
 Hypocalcemia occurs when the parathyroids become
inactive. The resultant deficiency of calcium in the blood
alters the function of many tissues in the body.
 These altered functions are described by the systemic
manifestations of signs and symptoms associated with
hypoparathyroidism 
Systemic Manifestations of
Hypoparathyroidism
 The most significant clinical consequence of hypocalcemia is neuromuscular
irritability. This irritability results in muscle spasms, paresthesias, tetany,
and life-threatening cardiac arrhythmias.
 Muscle weakness and pain have been reported along with hypocalcemia in
patient with hypoparathyroidism.
 Hypoparathyroidism is primarily treated through pharmacologic
management with intravenous calcium gluconate, oral calcium salts, and
vitamin D.
 Acute hypoparathyroidism is a life-threatening emergency and is treated
rapidly with calcium replacement, anticonvulsants, and prevention of
airway obstruction.
Pancreas

 The pancreas is a fish-shaped organ that lies behind the stomach.

 Its head and neck are located in the curve of the duodenum, and its
body extends horizontally across the posterior abdominal wall.
 The pancreas has dual functions. It acts as both an endocrine
gland, secreting the hormones insulin and glucagon, and an exocrine
gland, producing digestive enzymes.
 Disorders of endocrine function affecting digestion
 Diabetes Mellitus

 Diabetes mellitus (DM) is a chronic disorder caused by deficient insulin or

defective insulin action in the body.
 It is characterized by hyperglycemia (excess glucose in the blood) and
disruption of the metabolism of carbohydrates, fats, and proteins.
 Over time, it results in serious small vessel and large vessel vascular
complications and neuropathies.
 Diabetes is the leading cause of end-stage renal disease (ESRD) [kidney
failure requiring dialysis or transplantation], nontraumatic lower extremity
amputations, and a major cause of heart disease and stroke.
 Primary Differences Between Type 1
and Type 2 Diabetes
Factor Type I Type II

Age of onset Usually younger than 30 Usually older than 35 (can be younger
if history of child hood obesity)

Type of onset Abrupt Gradual

Endogenous (own) insulin production Little or none Below normal or above normal

Incidence 5% - 10% 90% - 95%

Ketoacidosis May occur Unlikely

Insulin injections Required Needed in 20% to 30% of patients

Factor Type I Type II

Body wieght at onset Normal or thin 80% are obese

Management Diet, insulin, and exercise Diet, exercise, oral hypoglycemic agents
or insuline

Etiology Possible viral/ autoimmune, resulting in Obesity-associated insulin receptor

destruction of islet cell resistance

Hereditory Yes Yes

Risk factor May be Insulin resistance syndrome/metabolic

Autoimmune, syndrome
Environmental, Ethnicity
genetic • Native American
• Hispanic/Latin
• Pacific Islanders
Clinical Presentation: 
 Specific physiologic changes occur when insulin is lacking or ineffective.
 Normally, the blood glucose level rises after a meal. A large amount of this
glucose is taken up by the liver for storage or for use by other tissues such as
skeletal muscle and fat.
 When insulin function is impaired, the glucose in the general circulation is not
taken up or removed by these tissues; thus it continues to accumulate in the
blood.
 Because new glucose has not been “deposited” into the liver, the liver
synthesizes more glucose and releases it into the general circulation, which
increases the already elevated blood glucose level.
 The accumulation of high levels of glucose in the blood creates a
hyperosmotic condition in the blood serum.
 This highly concentrated blood serum then “pulls” fluid from the
interstitial areas, and fluid is lost through the kidneys (osmotic diuresis).
 Because large quantities of urine are excreted (polyuria), serious fluid
losses occur, and the conscious individual becomes extremely thirsty and
drinks large amounts of water (polydipsia).
 The kidney is unable to resorb all the glucose, so glucose begins to be
excreted in the urine (glycosuria).
 Clinical Signs And Symptoms
Untreated or Uncontrolled Diabetes
Mellitus
• Polyuria • Ketonuria
• Polydipsia • Fatigue and weakness
• Polyphagia • Blurred vision
• Weight loss in the presence of • Irritability
polyphagia: weight loss caused by • Recurring skin, gum, bladder,
improper fat metabolism and vaginal, or other infections
breakdown of fat stores (usually
only in type 1) • Numbness/tingling in hands
and feet
• Hyperglycemia
• Cuts/bruises that are difficult
• Glycosuria and slow to heal
 Physical Complications:  Infection and atherosclerosis are the two primary
long-term complications of this disease and are the usual causes of severe
illness and death in the person with diabetes.
 Blood vessels and nerves sustain major pathologic changes in the person
affected by DM.
 Atherosclerosis in both large vessels (macrovascular changes) and small
vessels (microvascular changes) develops at a much earlier age and progresses
much faster in the individual with DM.
 The blood vessel changes result in decreased blood vessel lumen size,
compromised blood flow, and resultant tissue ischemia.
 The pathologic end-products are cerebrovascular disease (CVD), coronary
artery disease (CAD), renal artery stenosis, and peripheral vascular disease
(PVD).
 Microvascular changes, characterized by the thickening of capillaries and
damage to the basement membrane, result in diabetic nephropathy (kidney
disease) and diabetic retinopathy (disease of the retina).
 Diabetes is the leading cause of kidney failure.
 Poorly controlled DM can lead to various tissue changes
that result in impaired wound healing. Decreased
circulation to the skin can further delay or diminish
healing. Skin eruptions called xanthomas (Fig.) may
appear when high lipid levels (e.g., cholesterol and
triglycerides) in the blood cause fat deposits in the skin
over extensor surfaces such as the elbows, knees, back of
the head and neck, and heels. Yellow patches on the
eyelids are another sign of hyperlipidemia. Medical
referral is required to normalize lipid levels.

FIG. Multiple eruptive xanthomas over the extensor surface of the elbow in a client with poorly controlled diabetes.
These lipid-filled nodules characterized by an intracellular accumulation of cholesterol develop in the skin, often
around the extensor tendons. Medical referral is required; xanthomas in this population are a sign that the health-care
team, including the therapist, must work with the client to provide further education about diabetes, gain better control
of glucose levels, and prevent avoidable complications. These skin lesions will go away when the diabetes is under
control. Xanthomas can occur in any condition with disturbances of lipoprotein metabolism (not just diabetes).
 Introduction of Metabolism

 Metabolism is the sum of all of the chemical reactions that

occur in the living organism.
 These chemical reactions are necessary to sustain life

Metabolism is a requirement for life. It is the means by which all life forms,
including microorganisms, obtain and use energy. This energy is required for
growth, repair, and maintenance of the chemical and physiological processes of
the cell. Energy is also needed to maintain the structural integrity of the cell by
repairing or replacing damaged components.
 Metabolism is a general term for all of the biochemical
reactions taking place within an organism.
 The biochemical reactions of metabolism fall into 2 broad
categories
1) anabolism
2) catabolism.
Thank you