Transcript Assessment and Management of Patients with Endocrine Disorders

Assessment and Management of
Patients with Endocrine Disorders
Dr Ibraheem Bashayreh
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Location of the major endocrine glands.
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Definition of Hormones
 Chemical messengers of the body
 Act on specific target cells
 Regulated by negative feedback
 Too much hormone, then hormone release reduced
 Too little hormone, then hormone release increased
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Glands of the Endocrine
System
 Hypothalamus
 Posterior Pituitary
 Anterior Pituitary
 Thyroid
 Parathyroids
 Adrenals
 Pancreatic islets
 Ovaries and testes
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Hypothalamus
 Sits between the cerebrum and brainstem
 Houses the pituitary gland and hypothalamus
 Regulates:
 Temperature
 Fluid volume
 Growth
 Pain and pleasure response
 Hunger and thirst
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Hypothalamus Hormones
 Releasing and inhibiting hormones
 Corticotropin-releasing hormone
 Thyrotropin-releasing hormone
 Growth hormone-releasing hormone
 Gonadotropin-releasing hormone
 Somatostatin-=-inhibits GH and TSH
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Pituitary Gland
 Sits beneath the hypothalamus
 Termed the “master gland”
 Divided into:
 Anterior Pituitary Gland
 Posterior Pituitary Gland
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Anterior Pituitary Gland
 Promotes growth
 Stimulates the secretion of six hormones
 Controls pigmentation of the skin
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Anterior Pituitary Gland
Hormones
 Growth Hormone- Adrenocorticotropic hormone
 Thyroid stimulating hormone
 Follicle stimulating hormone—ovary in female,
sperm in males
 Luteinizing hormone—corpus luteum in females,
secretion of testosterone in males
 Prolactin—prepares female breasts for lactation
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Actions of the major hormones of the anterior pituitary.
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Posterior Pituitary Gland
 Stimulates the secretion of two hormones
 Promotes water retention
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Posterior Pituitary Hormones
 Antidiuretic Hormone
 Oxytocin—contraction of uterus, milk ejection
from breasts
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Adrenal Cortex
 Mineralocorticoid—aldosterone. Affects sodium
absorption, loss of potassium by kidney
 Glucocorticoids—cortisol. Affects metabolism,
regulates blood sugar levels, affects growth, antiinflammatory action, decreases effects of stress
 Adrenal androgens—dehydroepiandrosterone and
androstenedione. Converted to testosterone in the
periphery.
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Adrenal Medulla
 Epinephrine and norepinephrine
serve as neurotransmitters for sympathetic system
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Thyroid Gland
 Butterfly shaped
 Sits on either side of the trachea
 Has two lobes connected with an isthmus
 Functions in the presence of iodine
 Stimulates the secretion of three hormones
 Involved with metabolic rate management and
serum calcium levels
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Thyroid
 Follicular cells—excretion of triiodothyronine (T3)
and thyroxine (T4)—Increase BMR, increase bone
and calcium turnover, increase response to
catecholamines, need for fetal G&D
 Thyroid C cells—calcitonin. Lowers blood calcium
and phosphate levels
 BMR: Basal Metabolic Rate
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Parathyroid Glands
 Embedded within the posterior lobes of the thyroid
gland
 Secretion of one hormone
 Maintenance of serum calcium levels
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Parathyroid
 Parathyroid hormone—regulates serum
calcium
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Pancreas
 Located behind the stomach between the spleen and
duodenum
 Has two major functions
 Digestive enzymes
 Releases two hormones: insulin and glucagon
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Pancreatic Hormones
Insulin
Glucagon—stimulates glycogenolysis and
glyconeogenesis
Somatostatin—decreases intestinal absorption of
glucose
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Insulin
 Produced by the Beta cells in the islets of
Langerhans
 Regulates blood glucose levels
 Mechanisms
 Eases the active transport of glucose into muscle and
fat cells
 Facilitates fat formation
 Inhibits the breakdown and movement of stored fat
 Helps with protein synthesis
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Action of insulin and glucagon on blood glucose levels. (A) High blood glucose is lowered by
insulin release.
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(continued)
Action of insulin and glucagon on blood glucose levels. (B) Low
blood glucose is raised by glucagon release.
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Glucagon
 Produced by the alpha cells in the islets of Langerhans
 Glucagon released when blood glucose falls below 70
mg/dL
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Glucagon
 Prevents blood glucose from decreasing below a
certain level
 Functions:
 Makes new glucose
 Converts glycogen into glucose in the liver and
muscles
 Prevents excess glucose breakdown
 Decreases glucose oxidation and increases blood
glucose
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Kidney
 1, 25 dihydroxyvitamin D—stimulates calcium
absorption from the intestine
 Renin—activates the RAS
 Erythropoietin—Increases red blood cell
production
 RAS: Renin-Angiotensin System
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Adrenal Glands
 Pyramid-shaped organs that sit on top of the
kidneys
 Each has two parts:
 Outer Cortex
 Inner Medulla
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Adrenal Cortex
 Secretion of two hormones
 Glucocorticoids: cortisol
 Mineralocortocoids: aldosterone
 Involved with blood glucose level, anti-
inflammatory response, blood volume, and
electrolyte maintenance
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Adrenal Medulla
 Secretion of two hormones
 Epinephrine
 Norepinephrine
 Involved with the stress response
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Ovaries
 Estrogen
 Progesterone—inportant in menstrual
cycle,*maintains pregnancy,
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Testes
 Androgens, testosterone—secondary sexual
characteristics, sperm production
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Thymus
 Releases thymosin and thymopoietin
 Affects maturation of T lymphocetes
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Pineal
 Melatonin
 Affects sleep, fertility and aging
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Prostaglandins
 Work locally
 Released by plasma cells
 Affect fertility, blood clotting, body temperature
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Past Medical History
 Hormone replacement therapy
 Surgeries, chemotherapy, radiation
 Family history: diabetes mellitus, diabetes insipidus,
goiter, obesity, Addison’s disease, infertility
 Sexual history: changes, characteristics, menstruation,
menopause
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Physical Assessment
 General appearance
 Vital signs, height, weight
 Integumentary
 Skin color, temperature, texture, moisture
 Bruising, lesions, wound healing
 Hair and nail texture, hair growth
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Physical Assessment
 Face
 Shape, symmetry
 Eyes, visual acuity
 Neck
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Palpating the thyroid gland from behind the client. (Source: Lester V.
Bergman/Corbis)
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Physical Assessment
 Extremities
 Hand and feet size
 Trunk
 Muscle strength, deep tendon reflexes
 Sensation to hot and cold, vibration
 Thorax
 Lung and heart sounds
 Extremity edema
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Older Adults and Endocrine
Function
 Relationship unclear
 Aging causes fibrosis of thyroid gland
 Reduces metabolic rate
 Contributes to weight gain
 Cortisol level unchanged in aging
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Abnormal Findings
 Ask the client:
 Energy level
 Fatigue
 Maintenance of ADL
 Sensitivity to heat or cold
 Weight level
 Bowel habits
 Level of appetite
 Urination, thirst, salt craving
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Abnormal Findings (continued)
 Ask the client:
 Cardiovascular status: blood pressure, heart rate,
palpitations, SOB
 Vision: changes, tearing, eye edema
 Neurologic: numbness/tingling lips or extremities,
nervousness, hand tremors, mood changes, memory
changes, sleep patterns
 Integumentary: hair changes, skin changes, nails,
bruising, wound healing
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Most Common Endocrine
Disorders
 Thyroid abnormalities
 Diabetes mellitus
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Diagnostic Tests
 GH: fasting, well rested, not physically stressed
 Water deprivation: fasting for 12 hours, no fluids/smoking
after midnight
 T3/T4: no specific preparation
 Serum calcium/phosphate: fasting may or may not be
required
 Collection that needs to be iced or refrigerated
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Diagnostic Tests
 Cortisol/aldosterone level: two blood samples, client to
be up for at least 2 hours before test is drawn
 Urine 17-ketosteroids: 24-hour urine collection that
needs to be iced or refrigerated
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Diagnostic Tests
 FBS: fast before the test
 HbA1c: No fasting required
 2-hour OGTT: drink 75 g of glucose and do not eat
anything until blood is drawn
 Urine glucose/ketones: fresh urine specimen
 Urine microalbumin: fresh urine specimen
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Imaging Studies
 MRI: metallic implants, lie motionless during test;
remove all metal objects
 CT scan: assess for allergies to iodine and seafood; lie
immobile during the test
 Thyroid scan: allergies to iodine and seafood; hold
thyroid drugs containing iodine for weeks before the
study
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Imaging Studies
 RAI: fast for 8 hours before; can eat 1 hour after
radioiodine capsule/liquid taken; hold thyroid drugs
with iodine for weeks before the study
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THYROID
DISORDERS
Dr Ibraheem Bashayreh, RN, PhD
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Thyroid Anatomy
1-The gland as seen from the front is
more nearly the shape of a
butterfly.
2-composed of 2 encapsulated lobes, one
on either side of the trachea,
connected by a thin isthmus.
3-The thyroid extending from the level of
the fifth cervical vertebra down to
the first thoracic. The gland varies
from an H to a U shape, overlying
the second to fourth tracheal rings.
4-The pyramidal lobe is a narrow
projection of thyroid tissue
extending upward from the
isthmus and lying on the surface
of the thyroid cartilage.
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Thyroid Anatomy
5-The thyroid is enveloped by a thin, fibrous,
nonstripping capsule that sends septa into
the gland substance to produce an
irregular, incomplete lobulation. No true
lobulation exists.
6-The weight of the thyroid of the normal
nongoitrous adult is: 10-20 g depending
on body size and iodine supply.
7-The width and length of the isthmus
average; 20 mm,
and its thickness is ;2-6 mm.
8-The lateral lobes from superior to inferior
poles usually measure 4 cm. and their
thickness is 20-39 mm.
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Relations of the Lobes
1-Anterolaterally:
*The sternothyroid
*The superior belly of the
omohyoid
*The sternohyoid
*The anterior border of the
sternocleidomastoid
2-Medially:
*The larynx & the trachea.
*The pharynx & the oesophagus.
*Associated with these
structures are the
cricothyroid muscle & its
nerve supply, the external
laryngeal nerve.
*In the groove between the
esophagus and the trachea is
the recurrent laryngeal
nerve.
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Relations of the Lobes
3-Posterolaterally:
The carotid sheath with: The common carotid artery, the internal jugular vein, and the
vagus nerve.
Relations of the Isthmus
1-Anteriorly:
The sternothyroids
The sternohyoids
The anterior jugular veins
Fascia & skin.
2-Posteriorly:
The second, third, & fourth rings of the trachea.
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Venous Drainage
1-The superior thyroid vein:
ascends along the superior thyroid
artery and becomes a tributary of the
internal jugular vein.
2- The middle thyroid vein:
follows a direct course laterally to the
internal jugular vein.
3- The inferior thyroid veins :
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follow different paths on each side. The
right passes anterior to the innominate
artery to the right brachiocephalic vein or
anterior to the trachea to the left
brachiocephalic vein. On the left side,
drainage is to the left brachiocephalic vein.
Occasionally, both inferior veins form a
common trunk called the thyroid ima vein,
which empties into the left brachiocephalic
vein.
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Physiology
The thyroid follicles secretes tri-iodothyronine(T3)and thyroxin(T4)synthesis involves combination
of iodine with tyrosine group to form mono and di-iodotyrosine which are coupled to form T3
andT4.
The hormones are stored in follicles bound to thyrogobulin .
When hormones released in the blood they are bound to plasma proteins and small amount remain
free in the plasma .
The metabolic effect of thyroid hormones are due to free (unbound)T3 and T4.
90%of secreted hormones is T4 but T3is the active hormone so, T4is converted to T3 peripherally.
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Physiological control of
secretion
Synthesis and libration of T3 and T4 is controlled by thyroid stimulating
hormone(TSH)secreted by anterior pituitary gland.
TSH release is in turn controlled by thyrotropin releasing hormone (TRH)from
hypothalamus .
Circulating T3and T4 exert –ve feedback mechanism on hypothalamus and anterior
pituitary gland .
So, in hyperthyroidism where hormone level in blood is high ,TSH production is
suppressed and vice versa.
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Thyroid Hormones
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Stimulated by
Hormone
Function
T3/T4
h metabolic rate
i metabolic rate
h protein synthesis
i T3/T4
h energy production
h TSH
Most important hormone in day
today regulation of metabolic rate
Calcitonin
i blood calcium concentration
i the reabsorption of Ca and Ph
from bones to blood
Calcitonin “tones” down serum
Ca levels
h blood Ca levels
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HYPOTHYRODISM
Hypothyroidism is the disease state in humans and animals caused by insufficient
production of thyroid hormone by the thyroid gland.
INCEDENCE
•
30-60 yrs of age
•
Mostly women
 Clinical Manifestations:
1. Goiter.
2. Fatigue.
3. Constipation.
4. Weight gain.
5. Memory and mental impairment and decreased
concentration.
6. Depression.
7. Menstrual irregularities and loss of libido.
8. Coarseness or loss of hair.
9. Dry skin and cold intolerance.
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Clinical Manifestations:
10. Irregular or heavy menses.
11. Infertility.
12. Hoarseness.
13. Myalgias.
14. Hyperlipidemia.
15. Reflex delay.
16. Bradycardia, elevated diastolic BP.
17. Hypothermia.
18. Ataxia.
19. Decreased serum T4,T3 levels.
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LABORATORY ASSESSMENT
 T3
 T4
 TSH
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TREATMENT
LIFELONG THYROID HORMONE REPLACEMENT
 levothyroxine sodium (Synthroid, T4, Eltroxin)
 IMPORTANT: start at low does, to avoid hypertension, heart
failure and MI
 Teach about S&S of hyperthyroidism with replacement therapy
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MYXEDEMA DEVELOPS
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Rare serious complication of untreated hypothyroidism
Decreased metabolism causes the heart muscle to become flabby
Leads to decreased cardiac output
Leads to decreased perfusion to brain and other vital organs
Leads to tissue and organ failure
LIFE THREATENING EMERGENCY WITH HIGH
MORTALITY RATE
With low metabolism metabolites build up inside the cells which
increases mucous and water leading to cellular edema
Edema changes client’s appearance
Nonpitting edema appears everywhere especially around the
eyes, hands, feet, between shoulder blades
Tongue thickens, edema forms in larynx, voice husky
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PROBLEMS SEEN WITH MYXEDEMA
COMA
 Coma
 Respiratory failure
 Hypotension
 Hyponatremia
 Hypothermia
 hypoglycemia
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TREATMENT OF MYEXEDEMA COMA
 Patent airway
 Replace fluids with IV.
 Give levothyroxine sodium IV
 Give glucose IV
 Give corticosteroids
 Check temp, BP hourly
 Monitor changes LOC hourly
 Aspiration precautions, keep warm
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Hyperthyroidism
Hyperthyroidism is a condition caused by the effects of too much thyroid hormone on
tissues of the body. Although there are several different causes of hyperthyroidism, most
of the symptoms that patients experience are the same regardless of the cause.
Clinical Manifestations:
1. Heat intolerance.
2. Palpitations, elevated systolic BP.
3. Weight changes.
4. Menstrual irregularities and decreased libido.
5. Increased serum T4, T3.
6. Exophthalmos (bulging eyes)
7. Goiter.
8. Insomnia.
9. Muscle weakness.
10. Heat intolerance.
11. Diarrhea.
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Clinical presentation of specific
condition
THYROIDITIS:
Thyroiditis is an inflammation (not an infection) of the thyroid gland. Several types of
thyroiditis exist .
1-Hashimoto's Thyroiditis. Hashimoto's Thyroiditis (also called autoimmune or chronic
lymphocytic thyroiditis) is the most common type of thyroiditis.
Fatigue-Depression-Modest weight gain--Cold intolerance-Excessive sleepiness-Dry, coarse
hair-Constipation-Dry skin-Muscle cramps-Increased cholesterol levels-Decreased
concentration-Vague aches and pains-Swelling of the legs
2-De Quervain's Thyroiditis. (also called subacute or granulomatous thyroiditis). The
thyroid gland generally swells rapidly and is very painful and tender.]
Patients will experience a hyperthyroid period as the cellular lining of colloid spaces fails,
allowing abundant colloid into the circulation, with neck pain and fever. Patients typically
then become hypothyroid as the pituitary reduces TSH production and the inappropriately
released colloid is depleted before resolving to euthyroid. The symptoms are those of
hyperthyroidism and hypothyroidism. In addition, patients may suffer from painful
dysphagia. There are multi-nucleated giant cells on histology.Thyroid antibodies can be
present in some cases.There is decreased uptake on isotope scan.
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Clinical presentation of
specific condition
3-Silent Thyroiditis. Silent Thyroiditis is the third and least common type of
thyroiditis..
Silent thyroiditis features a small goiter without tenderness and, like the other
types of resolving thyroiditis, tends to have a phase of hyperthyroidism followed
by a phase of hypothyroidism then a return to euthyroidism. The time span of each
phase is not concrete, but the hypo- phase usually lasts 2-3 months.
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Pressure effect:
Dysphagia.
breathlesness & orthopnoea.
Hoarseness.
Facial congestion.
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Goitre
Enlargement of thyroid gland.
Classification:
Simple (non-toxic) goitre.
Toxic goitre.
Neoplastic goitre.
Inflammatory goitre.
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Simple (non-toxic) goitre
include:
simple hyperplastic goitre (colloid goiter)
Cause: -physiological in pregnancy, puberty
-iodine definiecy.
Appearance: Large, smooth firm, non-tendern goitre
Effect: euythyroid & pressure effect.
Multinodular goitre.
Cause: presence of areas of hyperplasia & areas of
hypoplasia in gland.
Appearance: Large, irregular, nodular goiter
Effect: euythyroid & pressure effect.
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Toxic goitre
Grave’s disease
Cause: Autoimmune disease characterizeby
presence of antibodies stimulate TSH receptors
in gland.
Appearance: Diffuce, nodular, hyperemic gland.
Effect: hyperthyroidism.
Toxic Multinodular goiter (plummer’s
disease)
Cause: Toxic effect of MNG
Appearance: Large, irregular, nodular goiter.
Effect: hyperthyroidism
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Neoplastic goitre
Include:
-benign: adenoma
-malignant: papillary, follicular, anaplastic, medullary and
lymphoma
Cause: -complication of MNG.
-radiation
Appearance: Enlarged goiter associated with lymphadenopathy
Effect: -pressure effect.
-euthyroid.
-invasive effect
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Inflammatory goitre
Rediel’s thyroditis
Cause: Fibrosis of thyroid
Appearance: Enlarged stony hard thyroid
Effect: Pressure effect
De quervain’s thyroiditis
Cause: Viral infection
Appearance: Diffuse, firm, tender swelling
Effect: Mild hyperthyroidism
Hashimoto’s thyroiditis
Cause: Autoantibody against thyroid gland.
Appearance: Diffuse, enlarged, non-tender goitre
Effect: Hypothyroidism
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Investigation:
Laboratory investigation:
-serum T3, T4.
-serum TSH.
-serum LATS: (Long Acting Thyroid Stimulator)
in grave’s disease
-thyroid antibodies:
in hashimoto’s disease.
-serum cholesterol
increase cholesterol level in hypothyroidism
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LABORATORY ASSESSMENT
IN HYPERTHYROIDISM:
 T3
 T4
 TSH in Graves disease

Radioactive Thyroid Scan
 Ultrasonography: used to determine goiter or nodules
 EKG: note tachycardia
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Radiological Investigation:
-chest and neck x-ray:
Show descend of thyroid gland to thorax and
mediastanal shifting in retrosternal goitre.
-iodine isotopes
By i.v injection of I131. Then, use gama rays to
show hot and cold nodules.
-CT scan
Show thyroid size and if there is compression to
trachea
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Endoscopic investigation:
-bronchoscopy: show compression and infiltration of
trachea by tumer
Biopsy:
-fine needle aspiration biopsy.
-true-cut biopsy.
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DRUG THERAPY
 Antithyroid drugs:
 Thioamides: blocks thyroid hormone production; takes time
 propylthiouracil (PTU)
 methimazole (Tapazole)
 carbimazole (Neo-Mercazole)
 Need to control cardiac manifestations (tachycardia,
palpitations, diaphoresis, anxiety) until hormone production
reduced: use Beta-adrenergic blocking drugs: propranolol
(Inderal, Detensol)
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DRUG THERAPY
Iodine preparations:
 Lugol’s Solution
 SSKI (saturated solution of potassium iodide)
 Potassium iodide tablets, solution, and syrup
ACTION:
 decreases blood flow through the thyroid gland
 This reduces the production and release of thyroid hormone
 Takes about 2 wks for improvement
 Leads to hypothyroidism
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DRUG THERAPY
 Lithium Carbonate
 ACTION: inhibits thyroid hormone release
 NOT USED OFTEN BECAUSE OF SIDE EFFECTS:
depressions, diabetes insipidus, tremors, N&V
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DRUG THERAPY
RADIOACTIVE IODINE THERAPY:
 Receives RAI in form of oral iodine
 Takes 6-8 Weeks for symptomatic relief
 Additional drug therapy used during this type of
treatment
 Not used on pregnant women
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SURGICAL MANAGEMENT
Why use surgery?

Used to remove large goiter causing tracheal or esophageal
compression

Used for pts who do not have good response to antithyroid
drugs
TWO TYPES OF SURGERIES:
1.
Total thyroidectomy (must take lifelong thyroid hormone
replacement)
2.
Subtotal thyroidectomy
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PREOPERATIVE CARE
Patient should become euthyroid before surgery to
prevent thyroid crisis.
Assessmment vocal cord condition
Low weight:
 Hi protein, hi CHO diet for days/weeks before surgery
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PRE-OPERATIVE CARE
1.
2.
3.
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Antithyroid drugs to suppress function of the thyroid
Iodine prep (Lugols or K iodide solution) to
decrease size and vascularity of gland to minimize
risk of hemorrhage, reduces risk of thyroid storm
during surgery
Tachycardia, BP, dysrhythmias must be controlled
preop
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PREOPERATIVE TEACHING
 Teach C&DB
 Teach support neck when C&DB
 Support neck when moving reduces strain on suture
line
 Expect hoarseness for few days (endotracheal tube)
 C&DB: cough & deep breathing
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POST-OP THYROIDECTOMY NURSING
CARE
1.
2.
3.
4.
5.
6.
7.
8.
9.
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VS, I&O, IV
Semifowlers
Support head
Avoid tension on sutures
Pain meds, analgesic lozengers
Humidified oxygen, suction
First fluids: cold/ice, tolerated best, then soft diet
Limited talking , hoarseness common
Assess for voice changes: injury to the recurrent
laryngeal nerve
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POSTOP THYROIDECTOMY NURSING
CARE
 CHECK FOR
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HEMORRHAGE 1st 24 hrs:
Look behind neck and sides of
neck
Check for c/o pressure or
fullness at incision site
Check drain
REPORT TO MD
 CHECK FOR

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
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RESPIRATORY DISTRESS
Laryngeal stridor (harsh hi
pitched resp sounds)
Result of edema of glottis,
hematoma,or tetany
Trach set/airway/ O2, suction
CALL MD for extreme
hoarseness
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Complication of operation:
Hemorrhage
Recurrent laryngeal nerve damage.
Superior laryngeal nerve damage
Hypoparathyrodism
Hypothyroidism
Septesis
Postoperative infection
Hypertrofic scaring (keloid)
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Thank You !!
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29/11/2010