ENDOCRINOLOGY NURSING

CLASS: September 2022

Mr. Kemboi Denis.
WELCOME.
MAIN OBJECTIVE
By the end of this Course, the learner will be
able to demonstrate the knowledge of
common endocrine disorders and
demonstrate the skills and attitude necessary
for the management of patients with such
disorders.

2
 4 SPECIFIC OBJECTIVES
1. To describe the normal Anatomy and
Physiology of the endocrine organs.

2. To list the common endocrine disorders.

3. To describe the pathophysiology of the common

endocrine disorders.

4. To describe the medical and nursing

management of patients with endocrine
REFERENCES
1. Kathleen J; Waugh A; (2011); Ross and Wilson
Anatomy and Physiology in Health and
Illness; Ed. 12 © Churchill Livingstone.

2. Smeltzer S C, Bare B G, Hinkle J L and Cheever

K H (2010) Brunner & Suddarth’s Textbook of
Medical–Surgical Nursing; Ed.12; © Lippincott
Williams & Wilkins.
INTRODUCTION
The term Endocrinology refers to the science
and the medical specialty concerned with the
study of the structure and the physiology of the
ductless (endocrine) glands whose secretions
(the hormones) are released directly into blood
circulation.

Endocrinopathology or just Endocrinopathy

denotes the study of the disorders in the
structure and/or in the function of such ductless
glands and their ensuing consequences.
 ENDOCRINE SYSTEM

• Endocrine system is a system of ductless glands that secrete

hormones.
• It is a chemical control system.
• It functions in conjunction with the nervous system to control the
internal environment (homeostasis).
• These glands consist of secretory cells which secrete hormones
and dense network of capillaries which carries hormones in blood
 CONT

• The glands are called ductless (do not have ducts to carry
secretions ) because hormones diffuse directly into the blood
stream
• This differentiate them from exocrine glands eg sweat gland
• The major glands are: Pituitary gland , thyroid gland , parathyroid
gland , thymus gland, adrenal gland, testes and ovaries
.
 PRINCIPLE FUNCTIONS OF ENDOCRINE
SYSTEM
1. Growth, metabolism, & tissue maturation by
growth hormone
2. Ion regulation by parathyroid hormone
3. Heart rate & blood pressure regulation
4. Blood glucose control by glucagon and insulin
5. Immune system regulation by thyroid hormone
6. Reproductive functions control by FSH and
testosterone
 HORMONES

• They are chemical released from living cells that travels

some distance to target tissues to have a biological
effect
• They are chemical messengers
• They are secreted in very small amounts and usually
transported in the blood
• They act on distant target cells
• Target cells have specific receptors
• The effects are dependent on the programmed response
of the target cells
 CONT
• When hormones arrive at its target cell, it binds to a specific
area , the receptor ,where it acts to influence a chemical or
metabolic reactions made inside the cell
 3 MECHANISMS OF HORMONE RELEASE
(a) Humoral: in response to changing levels of ions or nutrients
in the blood
(b) Neural: stimulation by nerves
(c) Hormonal: stimulation received from other hormones
(A) HORMONAL MODE OF ACTION
Hormones can act in two ways:
1. Reversing the action of stimulus : negative feedback
mechanism
2. Amplifying the stimulus ; positive feedback mechanism
 1.NEGATIVE FEEDBACK MECHANISM

• Occurs when the action of hormone stops its further

release.
• The stimulus causes a release of hormone which acts
on a target organ or tissue and the resulting action of
hormone tend to suppress its further release
 CONT
• Example of negative feedback mechanism

• Rising blood sugar stimulates pancreatic cells to release

insulin.
• insulin increases uptake of glucose from bloodstream into
body cells hence lowering blood sugar .
• When blood sugar is lowered , the production of insulin
stops this leads rising blood sugar(humoral hormonal
release)
• Hormone released ; insulin
 CONT

• Resulting action of hormone : increase uptake of

glucose
• As a result of glucose uptake ; insulin release stops.
 POSITIVE FEEDBACK MECHANISM

• Occurs when the action of hormone causes additional

secretion of hormone.
• Example : rising levels of Oxytocin stimulates
contractions in the uterus.
• Contractions in the uterus stimulate receptors in the
pelvis which triggers the release of more Oxytocin for
more contractions until child birth
 3 CLASSES OF HORMONES

1. Proteins and polypeptides e.g. hormone secreted by

anterior and posterior pituitary gland , parathyroid
hormone , insulin and glucagon
2. Steroids: hormones secreted by adrenal cortex e.g.
cortisol , aldosterone , hormones secreted by ovaries
e.g. estrogen and progesterone, hormone secreted by
testes e.g. testosterone
3.Amines or amino acids : thyroid hormone, epinephrine
and norepinephrine
ENDOCRINE GLANDS
 GLANDS OF ENDOCRINE SYSTEM

1. 1 Pituitary gland
2. 1 Thyroid gland
3. 4 Parathyroid glands
4. 2 Adrenal (suprarenal)
glands
5. 1 pineal gland or body
6. 1 Thymus gland
7. 2 Ovaries in the female
8. 2 testes in the male
1.PITUITARY GLAND AND HYPOTHALAMUS
 PITUITARY GLAND AND HYPOTHALAMUS
• Location : in Sella Turcica of sphenoid bone Attached to
Hypothalamus by a stalk called Infundibulum
• The pituitary gland and the hypothalamus act as a unit.
 PITUITARY GLAND AND HYPOTHALAMUS

• The hypothalamus has a direct controlling effect on the

pituitary gland and an indirect effect on many others.
• A sort of master gland
• The real boss is the hypothalamus
• It is divided into two;
• Anterior lobe – [glandular part] Adenohypophysis
• Posterior lobe – [neural part] – Neurohypophysis
 1.ANTERIOR PITUITARY GLAND (ADENOHYPOPHYSIS)

It produces six (6) hormones. The hormones are;

I. Growth hormone(GH)

II. Thyroid stimulating hormone(TSH)

III. Adrenocorticotropic hormone-- (ACTH

iv. Prolactin

v. Follicle Stimulating Hormone (FSH)

vi. Luteinizing Hormone.(LH)

 2.POSTERIOR PITUITARY GLAND(NEUROHYPOPHYSIS)

Produces two (2) hormones.

i. Antidiuretic Hormone (ADH) (Vasopressin)
ii. Oxytocin
HYPOTHALAMIC CONTROL OF PITUITARY GLAND
SECRETIONS
• The anterior gland is controlled by hormones released
by hypothalamus
• These hormones are called hypothalamic releasing
and inhibiting hormones
• These hormones are released from hypothalamus and
conducted to anterior pituitary gland through minute
blood vessels called pituitary portal system
 CONT

• Posterior pituitary gland is controlled by nerve signals

that originate from hypothalamus and terminate in
posterior pituitary
• The release of hormones is triggered by excitation of the
gland by nerve impulses
 ANTERIOR PITUITARY GLAND
• There are six hormones secreted by anterior pituitary
gland
• These hormones play role in control of metabolic
functions in the body
• The release of anterior pituitary hormone follows
stimulation of gland by specific releasing hormone
produced by hypothalamus
• The whole system is control by feedback mechanism
 1. GROWTH HORMONE

• Is also called somatotropic hormone

• Its release stimulated by growth releasing hormone and
suppressed by growth hormone releasing inhibiting
hormone
• It is stimulated by hypoglycemia , deep sleep, fasting,
exercise , and anxiety.
• Peak release is reached in adolescence
• It is inhibited by hyperglycemia, glucocorticoids,
dihydrotestosterone,
 CONT

• Inhibition is by negative feedback mechanism

• Major target of the hormone are body cells, bones and
skeletal muscle tissues.
Functions of growth hormone
1.Regulates metabolism-by protein synthesis, use of fats
for fuel and conservation of glucose
2.promote growth of bones and muscles
 2 . THYROID STIMULATING HORMONE
• Is also called thyrotropin
• Its release is stimulated by thyroid releasing hormone from
hypothalamus.
• Its target is thyroid gland
• Function : it stimulate thyroid gland to release thyroxine (T4)
(plays vital role in metabolism,heart & muscle function, brain dev & maintenance of bones)
and Tri-iodothyronine (T3)-(plays vital role in body’s control of metabolism)
• Secretion is regulated by negative feedback mechanism
• When blood levels of thyroid hormones is high, secretion of
TSH is reduced
 3. ADRENOCORTICOTROPIC HORMONE (ACTH)

• Its release is triggered by corticotrophin releasing hormone

from the hypothalamus
• Function : ACTH stimulates adrenal cortex to secrete
glucocorticoid hormones especially cortisol( helps body repond to
stress and danger—increase bodys metabolism of glucose & control BP)
• Secretion is regulated by negative feedback mechanism
• Other factors that stimulate secretion include hypoglycemia,
exercise and stress
 4 . PROLACTIN

• Stimulate lactation (milk production )

immediately after birth.
• Its release is stimulated by Prolactin releasing
hormone from hypothalamus and it is lowered by
Prolactin inhibiting hormone
• After birth, suckling stimulates Prolactin
secretion and lactation
 5.FOLLICLE STIMULATING HORMONE

• Stimulate maturation of ovarian follicles.

• Stimulates secretion of estrogen by ovaries
• Stimulates production of sperm in testes.
• Secreted in puberty

6 . LUTEINISING HORMONE (LH)

• Necessary for final follicular growth and ovulation
• Stimulates secretion of progesterone by corpus
luteum and secretion of testosterone in males testis.
 2.POSTERIOR PITUITARY GLAND

1. OXYTOCIN
• Main targets are breast and uterus.
• Are released during childbirth into the uterus to stimulate
uterine contractions and stretching of uterine cervix as
the baby is expelled
• Its controlled by positive feedback mechanism
• Stimulate glandular cells and ducts of lactating breast to
eject milk.
• The process of milk ejection also involve positive
feedback mechanism.
.
 2. ANTIDIURETIC HORMONE (ADH)

• Also called vassopressin

• It stimulates the distal convoluted
tubules (DCT) of the KIDNEYS nephrone
to reabsorb more water hence leading to
decrease urine output
.
 2.THYROID GLAND
• Highly vascularised gland located infront of larynx at
5th ,6th ,7th cervical and 1st thoracic vertebrae (C5,C6,C7
and T1 vertebrae)
• It’s made up of two lobes
• Blood is supplied through inferior and superior thyroid
arteries.
• Venous return is by thyroid veins
• There are two parathyroid glands laying at posterior
surface of each lobe
.
 CONTD
• It is innervated by recurrent laryngeal nerve
THYROID HORMONES
• There three major thyroid hormones- thyroxine (T4 ) Tri-
iodothyronine (T3) and calcitonin
• T4 and T3 are together called thyroid hormone
• Both hormones profoundly increases the rate of metabolism in the
body.
• Their release into the blood is stimulated by TSH from anterior
pituitary gland
• They are synthesized as large precursor molecules called
thyroglobulin
 CONTD

• Stress , malnutrition , low plasma glucose and exercises

stimulate hypothalamus to release thyroid releasing
Hormone (TRH)
• Once released, the TRH is sent to anterior pituitary gland
which stimulate thyroid stimulating hormone (TSH)
• TSH is sent to Thyroid gland to stimulate production of T3
and T4.
• Iodine react with tyrosine to form thyroid hormone
 CONTD
• When supply of iodine is deficient ,Excess TSH is
secreted and there is proliferation of thyroid gland
cells and enlargement of gland(goitre).
• Thyroxine (T4) is produced in large amounts as
compared to T3 i. e 93% of thyroid hormone is
thyroxine and only 7% is T3
• T3 is more potent than T4.
• 25% of T4 is converted to T3 by deiodination of T4
to T3.
• Hence the hormone derivered to tissues is mainly T3
 FUNCTIONS OF THYROID HORMONE
• They are essential for normal growth and
development
• They regulate metabolism of carbohydrates , fats and
proteins
• Increases basal metabolic rate and heat production
• Regulate expression of genes in the nucleus by
increasing or decreasing synthesis of proteins.
 CALCITONIN
• It is secreted by parafollicular or C-cells of the thyroid
gland when there is increased levels of calcium in the
blood
• It reduces calcium level in the plasma
a) stimulating calcium uptake in the bone matrix
(deposition in the bones)
b) inhibit reabsorption of calcium in the kidney tubules
• The hormone is important during childhood when
bones undergo changes in size
 3.PARATHYROID GLAND

• There are four parathyroid glands , two in each lobe at

posterior surface of the thyroid gland
• They contain chief cells or principal cells which secrete
parathyroid hormone.
• Parathyroid hormone or parathormone is secreted
when the blood calcium levels is low
• Its main function is to increase ionic calcium in the
blood plasma by:
 CONT

1 . Stimulating osteoclast in the bone to digest some of

the bone matrix to release ionic calcium in the blood
2.enhance reabsorption of calcium and excretion of
phosphates by kidneys
3. Increases absorption of calcium by intestinal mucosa
 CONT

• Vit D is required for absorption of ca+ in the instestine.

• For vitamin D to facilitate absorption of Ca2+ ,it must be
converted into Vit D3 form called calcitriol and this
conversion is stimulated by PTH
• Parathormone and Calcitonin act in opposite manner to
regulate normal calcium levels required for muscle
contraction , blood clotting and nerve impulse
transmission.
 4.ADRENAL GLANDS

• Are located at the top of the kidneys.

• Consists of two endocrine glands :

-outer adrenal cortex

-inner adrenal medulla.
• The outer adrenal cortex act more of a gland while
the inner medulla act as part of autonomic nervous
system
 DIVISIONS OF ADRENAL CORTEX

Consists of three distinct layers

1. Zona Glomerulosa –they secretes mineralocorticoids e.g
aldosterone. This is controlled by plasma concentration
of angiotensin II
2. Zona Fasciculata –middle layer and widest. secreats
Glucocorticoids e.g cortisol, corticosterone . Controlled
by hypothalamic-pituitary axis through ACTH
3. Zona Reticularis- the deep layer of the adrenal cortex,
mainly secretes androgens
.
 CONT
ADRENAL CORTEX ;
•produces three steroid hormones
•Glucocorticoids mainly cortisol or hydrocortisone
• Mineralocorticoids mainly aldosterone
• Sex hormones like testosterone (androgen)
 FUNCTIONS OF GLUCOCORTICOIDS
(METABOLIC EFFECTS OF GLUCOCORTICOIDS)
1. Gluconeogenesis – formation of new sugars from non-
sugars e.g proteins
2. Carbohydrate metabolism hence raising blood sugar
( hyperglycemia)
3. Reduced cell utilization of glucose
4. Lipolysis ;breakdown of triglycerides into fatty acids
and glycerol for energy production
5.stimulate breakdown of proteins releasing amino acids
which can be used for synthesis of other proteins
 1.GLUCOCORTICOIDS

• Cortisol or hydrocortisone is the main hormone

• Its release is stimulated by ACTH from anterior
pituitary gland
• Secretion is controlled by negative feedback system
Glucocorticoids .
• Cortisol (very potent, accounts for about 95 percent
of all glucocorticoid activity)
• Corticosterone (provides about 4 per cent of total
glucocorticoid activity)
• Cortisone (synthetic, almost as potent as cortisol)
• Prednisone (synthetic, four times as potent as
cortisol)
• Methylprednisone (synthetic, five times as potent
ascortisol)
• Dexamethasone (synthetic, 30 times as potent as
cortisol)
 PHYSIOLOGICAL AND PHARMACOLOGICAL EFFECTS

1. Anti- inflammatory actions

2. Suppression of immune responses
3.Delayed wound healing.
 MINERALOCORTICOIDS (ALDOSTERONE)

• Secreted in Zona Glomerulosa

• Main function is regulation of electrolytes
concentration in extracellular fluids particularly
sodium and potassium ions
• This is by increasing uptake of sodium from the
kidney nephrone.
 ADRENAL MEDULLA

• Produces catecholamines: epinephrine and

norepinephrine
• Epinephrine is also called Adrenaline

Its functions include;

 it increases contraction of the heart
 causes bronchodilation of bronchial muscles
 causes vasocontriction of the blood vessels
 GENERAL FUNCTIONS OF CATECHOLAMINES

• Stimulate the fight or fight reaction

• Increased plasma glucoses levels
• Increased cardiovascular function
• Increased metabolic function
• Decreased gastrointestinal and genitourinary function.
 PANCREASE

• There are three main types of cells found in

pancreatic islet
• Alpha cells : secrete glucagon
• Beta cells : secrete insulin
• Delta cells : secrete somatostatin.
• Normal blood glucose levels is 5.5 -8.5 mmol/l
• Blood glucose levels are control by opposing actions
of insulin and glucagon
 INSULIN
• Its main function is to lower raised blood glucose levels
• It lowers blood glucose levels by :
i. Acting on cell membrane and stimulating uptake and
use of glucose by muscle and connective tissue cells
ii. Increasing conversion of glucose to glycogen
(glycogenesis) for storage
iii.Signals the liver to stop releasing glucose
iv. Enhances storage of dietary fats in the adipose tissue
• Secretion of insulin is stimulated by increased blood
glucose levels e. g after eating a meal.
• It also inhibits glycogenolysis and gluconeogenesis
 CONT

GLUCAGON
• Secretion is stimulated by low blood glucose levels
and exercise
• It promote conversion of glycogen to glucose in liver
and skeletal muscle (glycogenolysis)
 PHYSICAL EXAMINATION

And
History taking
 ASSESSMENT OF ENDOCRINE DYSFUNCTION.
• Consist of Health History , Physical Examination and
lab and diagnostic studies
1.Health History.
a) Elicit a description of client's present illness and chief
complain including onset ,course ,location,
precipitating and alleviating factors.
• Cardinal signs and symptoms indicating altered
endocrine and metabolic function include :
• unexplained weight loss or gain
 CONT
• Alteration in metabolic rate e.g Tachycardia or
bradycardia , diarrhoea or constipation.
• Sleep pattern disturbances
• Labile mood swings and change in mental status
• Alteration in sexual performance.
b) Explore the client’s health history for risk factors
associated with endocrine and metabolic disorders
including family history of endocrine disorders , radiation
therapy and trauma
 CONT
2. Physical examination
a) Assess vital signs and measure body weight
b) Inspection
• Observe stature , fat distribution and shape of the face
• Assess for the presence of goitre (enlarged thyroid
gland)
• Note protruding or sunken eyes and lid or retraction.
 CONT

• Note the color ,texture and turgor of the skin,

surgical scars and unusual bruising.
c) Palpation ; palpate the thyroid for size ,
shape ,symmetry and tenderness
d) Auscultation
• Auscultate heart , lung and bowel sounds
 3.LABORATORY AND DIAGNOSTIC STUDIES

• Measurement of hormones in the blood and urine ,

reflects production and activity of hormones related
to specific endocrine and metabolic disorders.
 3.LABORATORY AND DIAGNOSTIC STUDIES
1.Thyroid function tests (TFTs)
• Measurements of TSH ,T3 and T4.
• Normal serum levels of T3 70-220ng/dl..
• Usually done to diagnose hypothyroidism and
hyperthyroidism
• Elevated T3 and T4 with depressed TSH reflect primary
hyperthyroidism.
• Reduced T3 and T4 with depressed TSH reflect primary
hypothyroidism.
 CONT
2.Radioactive iodine uptake test
• A client take an oral dose of a small amount
radioiodine and over time ,the iodine collects in the
thyroid because thyroid uses iodine
• It will be checked after 2, 6 or 24 hrs to determine
how much iodine has been absorbed by thyroid
• Increased uptake may indicate hyperfunctioning of
thyroid gland
• Decreased uptake may indicate hypofunctioning of
the gland
 CONT
3.Thyroid scan
• Performed to identify nodules or growth in the thyroid
gland ,tumors and growths in the brain.
Before thyroid scan is taken :
• Client is put on NPO
• Thyroid medications are temporarily withheld
• After the test has been done ,ensure proper disposal of
waste.
 CONT
4. Glucose Tolerance Test (GTT);
• Sometimes it is called Oral Glucose Tolerance Tests
(OGTT)
• Glucose is given to patient and after 2 hrs ,samples of
blood are taken to determine how quickly it is cleared
from the blood.
• It is used to test for type 2 diabetes , insulin resistance
and disorders of carbohydrate metabolism.
 CONT

Before test:
• Provide high carbohydrate food for 3 days
• Instruct client to avoid alcohol , smoking and caffeine.
• Put the client on NPO for 10 hrs before the test.
• After test, instruct the client to avoid any strenuous
activity for 8 hrs.
 5.GLYCOSYLATED HEMOGLOBIN A-1C (HBAIC)
• Refers to blood glucose bound to RBC hemoglobin.
• Used to gauge how one is managing the Diabetes
and to diagnose type one and type 2 DM.
• It reflect average blood sugars for the last 2-3
months.
• HBA1C measures percentage of hemoglobin coated
with sugar
• Normal HBA1C is 4%-5.6% for non-diabetic patient
• Levels at 5.7%- 6.4% indicate high risk for diabetes
• Levels above 6.4% indicate diabetes
Common Endocrine disorders
Pituitary disorders
(i) Diabetes Insipidus
(ii) Pituitary Gigantism /Acromegaly
(iii)Precocious Puberty
(iv) Hypopituitarism

Thyroid disorders
(v) Hypothyroidism
(vi)Hyperthyroidism
(vii)Thyroiditis
(viii)Endemic (Iodine Deficient) Goitre
Common Endocrine disorders cont’d

Parathyroid disorders
• Hyperparathyroidism
• Hypoparathyroidism

Pancreatic disorders
• Diabetes Mellitus (DM)

Adrenal disorders
• Pheochromocytoma
• Cushing Syndrome
PITUITARY DISORDERS
PITUITARY GLAND DISORDERS
1. DIABETES INSIPIDUS

This is a condition characterized by

excretion of large amounts of severely
diluted urine.

It’s the commonest abnormality associated

with the dysfunction of the posterior
pituitary gland .

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TYPES OF DIs
(i) Neurogenic DI which results from hypo
secretion of ADH.
It may be caused by brain tumor, head
trauma or brain surgery that damages the
posterior pituitary.
DI Cont’d
(ii) Nephrogenic DI which occurs because of lack
of renal response to ADH. The ADH receptors
may be non functional or the kidneys may be
damaged.

It may also occur as a side effect to some

medications like lithium citrate and Amphotericin-
B, Polycystic kidney disease and Sickle cell and
also in hyperkalaemia and hypercalcemia
conditions.

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DI Cont’d
(iii) Dipsogenic DI which is a defect or
damage to the thirst perception mechanism
in the hypothalamus.

This defect results in an abnormal increase

in thirst and fluid intake that suppresses
ADH secretion and increases the urine
output.

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DI Cont’d
(iv) Gestational DI which occurs during
pregnancy. All pregnant women produce
vasopressinase enzyme in the placenta
which breaks down ADH.

This form can be managed by

desmopressin.
Pathophysiology of DI
ADH is the primary determinant of free water excretion
in the body. Regulation of urine production occurs in
the hypothalamus which produces ADH (vasopressin)
in the supraoptic and Para ventricular nuclei.

After synthesis the hormone is transported to the

posterior lobe for release. The main effector organ for
fluid homeostasis is the kidney.

ADH increases water permeability in the collecting

tubules by acting on proteins called aquaporins which
open to allow water into collecting tubules
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Pathophysiology of DI Cont’d
This permeability allows re-absorption of water into
the blood stream thus concentrating the urine. When
there is hypo-secretion of ADH or the kidney
receptors fail to respond to ADH this mechanism
fails and Diabetes insipidus occurs.

When there is excessive urination, dehydration

occurs resulting to increased serum osmolality, this
causes the hypothalamus to regulate the sensation of
thirst in the ventromedial nucleus by relaying the
information to the cortex. This in turn causes
polydipsia.
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Clinical features of DI
1.Polyuria (excessive urination) up to 20 liters of dilute urine.

2.Polydipsia (excessive water intake) due to increased thirst.

3. Sleep disturbance due to polyuria.

4. Elevated serum osmolality.

5. In infant, crying, irritability, growth retardation,

hyperthermia and weight loss may occur.

6. In children, enuresis, anorexia, linear growth defects and

fatigability are predominant.

7. Azotemia
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and potential circulatory collapse. 83
Diagnosis of DI
Can be done clinically but laboratory confirmation is
important.

(i) Serum electrolytes reveals hypernatremia.

(ii) Urinalysis shows a specific gravity of 1.005 or less

and a urine osmolality of less than 200 mOsm/kg.

(iii) The water deprivation test (Miller Moses test) is

done to determine whether the DI is caused by a defect
in ADH production or in the kidneys’ response to ADH.
06/18/2024 84
Diagnosis of DI Cont’d
Fluid deprivation test measures body weight, urine
output and composition when fluids are withheld and as
dehydration occurs.

The body’s normal response to dehydration is to

concentrate urine and conserve water, yet those with DI
continue to urinate large amounts of dilute urine in spite
of fluid deprivation.

A weight loss between 3%-5% indicates significant

dehydration and requires termination of the test

06/18/2024 85
Diagnosis of DI Cont’d
When positive, the patient is given a test dose of
aqueous vasopressin (pitressin) which alleviates
polyuria and polydipsia.

Unresponsiveness to exogenous vasopressin indicates

nephrogenic DI.

(iv) Pituitary MRI can be done to rule out Neurogenic DI.

(v) CT scan of the brain to detect tumors
(vi) Kidney function tests and blood electrolyte levels to
assess renal failure.
(vii)Specific endocrine studies.
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MANAGEMENT OF DI
Objectives of management
a. To replace ADH as a long term therapeutic
regime.
b. To ensure adequate fluid replacement.
c. To identify & correct the underlying pathology
1.MEDICAL/ SURGICAL MANAGEMENT
- In emergencies patients can drink enough fluid
to replace urine losses with dextrose or IV fluid
that is hyposmolar to the patient’s serum

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MANAGEMENT OF DI Cont’d
Patients with hypernatremia should have fluid
replacement over 48 hours to avoid cerebral
edema
a. The drug of choice is desmopressin because of its
prolonged action: It can be given 5-30mcg bd
intranasally. The patient sprays the solution into
the nose through a flexible calibrated tube OD or
BD.
b. Vasopressin (pitressin).
IM Vasopressin in oil is used when the intranasal
route is not possible given 24 hrs to 96 hrs in the
evening.

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 MANAGEMENT OF DI Cont’d
It promotes smooth muscle contraction through out
the renal tubular epithelium: Give 5-10 IU SC -6
hourly or 2.5-10IU sc bid in children.

Rotation of injection sites is necessary to prevent

lipodystrophy.
• Chlorpropamide (Diabenes)- promotes renal
response to ADH: Give 125-250 mg BD
• Clofibrate a hypolipidemic agent also gives an
antidiuretic effect together with Carbamazipine in
patients with residual hypothalamic vasopressin

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MANAGEMENT OF DI Cont’d
• If the DI is nephrogenic in origin, Thiazide
diuretics, mild salt depletion and prostaglandin
inhibitors (ibuprofen, aspirin) are used
• Ibuprofen 600-800mg PO: Inhibition of
prostaglandin synthesis reduces delivery of solute
to distal tubules reducing urine volume and
increasing urine osmolarity
• Thiazide diuretics like HCT
(hydrochrolorothiazide) or HCTZ or
indomethacin can improve Nephrogenic DI

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 MANAGEMENT OF DI Cont’d
• Indomethacin (Indocin) 25-50mg PO bid acts
like brufen
• HCT is sometimes combined with amiloride to
prevent hypokalemia
• If there is renal pathology requiring surgery, it
may be done and monitored closely

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NURSING MANAGEMENT OF DI
• Maintaining fluid and electrolyte balance-
Monitor fluid retention and hyponatremia during
initial therapy.
-weigh daily and maintain I & O chart, monitor
serum sodium and urinalysis for specific gravity
• Monitoring neurological status- Check for change
in mental state which indicates hypernatremia or
cerebral edema. Also take vital signs frequently.

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 Nuring Management of DI Cont’d
• Diet: Advocate for low sodium diet which together
with thiazides induce mild volume depletion that
enhance reabsorption at the tubules. Low protein
diet decreases water loss by reducing solutes to be
excreted from the body
• Encourage adequate rest during the day since
nocturia disrupts sleep cycles
• Monitor side effects of the drugs being
administered and report
• Request for post hospitalization follow up visits
with the patient every 6-12 months

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Nursing Management of DI Cont’d
• Patient education:
- On simple principles of water balance to avoid
dehydration and water intoxication
- The importance of medications
- Frequent monitoring of weight
- Advice pt to carry an identification bracelet always
- That signs like polyuria and thirst will still occur
even after commencement of treatment
- That prognosis is usually excellent depending on
underlying illness

06/18/2024 94
Complications of DI
• Hydronephrosis

• Hypernatremia

• Increased bladder capacity

• Hypovolemia

06/18/2024 95
2.PITUITARY GIGANTISM /ACROMEGALY

• This a condition characterized by extreme

physical size and stature
• It refers to growth hormone excess and it
originates during infancy, childhood or
adolescence before the closure of the epiphyses. A
person with this condition is unusually tall but
has approximately normal body proportions
• Hyper secretion of hGH during adulthood causes
Acromegaly since further lengthening of the long
bone cannot occur as the epiphyseal plates are
closed.

06/18/2024 96
Acromegaly Cont’d
• In Acromegaly hyper secretion after the
closure of the epiphysis results in
overgrowth of the head, lips, nose, tongue,
jaw and Para nasal and mastoid sinuses:
separation and malocclusion of the teeth in
the enlarged jaw, disproportion of the face,
increased facial hair, thickened, deeply
creased skin and tendency to have
hyperglycemia and DM
06/18/2024 97
Pathophysiology of Acromegaly
• The growth hormone is a protein that increases
the protein synthesis in many tissues, increases
breakdown of fatty acids in adipose tissue and
increases glucose level in the blood.
• When there is hyper function of the eosinophilic
cells of the anterior pituitary there is excess
production of the growth hormone that result in
enlargement of all tissues and organs of the body.
Eosinophilic tumors early in life result in
gigantism and when the disorder begins in adult
life it results in acromegally
06/18/2024 98
Signs and symptoms of Acromegaly
1. Gradual onset in the enlargement of facial
features: mandible, molar bones and protrusion
of the orbital ridges
2. Teeth become widely separated, hands and feet
become gradually enlarged
3. Hyperglycemia resulting in DM
4. Hypercalcemia leading to renal stones
5. Hypertrophy of sweat glands leading to profuse
diaphoresis (odor due to increased secretions of
sebum and sweat glands
6. Hypertension, muscular weakness & pains

06/18/2024 99
Clinical Manifestations of Acromegaly Cont’d

• Exaggerated facial wrinkles

• Thick oily and rubbery skin
• Enlarged viscera (lungs, brain, thyroid,
kidneys, salivary glands )
• Visual impairment: loss of color
discrimination, diplopia (double vision) or
blindness of a field of vision
• Decalcification of the skeleton
• Endocrine disturbances
06/18/2024 100
Diagnostic evaluation of Acromegaly
• History of excessive growth
• Physical exam
• Increased GH levels in the blood
• Radiographic studies that may reveal
tumors
• Endocrine studies to confirm excess of other
hormones (thyroid, cortisol and sex
hormones)
• CT scan and MRI
06/18/2024 101
Medical / Surgical management
• Surgical removal of the pituitary tumor through a
trans sphenoidal approach is the treatment of
choice
• X-ray therapy or radiation of the gland can be
done (stereotactic radiation which requires
neurosurgery-type frame that delivers external
beam radiation to the pituitary tumor)
• The patient can also be managed by drugs like
bromocriptine (dopamine antagonist) and
octreotide (synthetic analog of GH) which inhibit
the production or release of GH and bring about
marked improvement of symptoms

06/18/2024 102
Med/Surg Management Cont’d
• Octreotide (sandostatin) may also be used
preoperatively to improve the patient’s clinical
condition and to shrink the tumor
• Hypophysectomy (removal of the pituitary gland)
ma be done to treat primary tumors
NB The absence of the pituitary gland alters the
functions of many body systems hence
replacement therapy with corticosteroids and
thyroid hormones is necessary together with other
measures

06/18/2024 103
Nursing Management of Acromegaly
• Pre and post op care like for any other
patient undergoing head surgery
• Taking patient’s body measurements and
instructing the patient to keep periodic
body measurement records
• Patient teaching on long term management
of condition is given
• Advice on complications that can occur and
how to recognize them

06/18/2024 104
 GIGANTISM
• This is a condition in which there is hypersecretion of
growth hormone in childhood.
• Before closure of epiphyses of long bones i.e. before
ossification of bones is complete.
• Occurs mainly in childhood and adolescents.
• Usually caused by tumors especially adenomas of the
pituitary gland. Diagnosis is made when the blood
growth hormone level is high

•
 pathophysiology
• There is excessive production of growth hormone
leading to delayed epiphyseal closure with extended
growth period.
• There is tremendous increase in size of bones that
lead to formation of giants whose height is 8 feet or
more
• These giants tend to have short lifespan, die early life
• They develop signs of increased intracranial pressure
from the tumor and are also subjected to infection
 CT
• There is excessive production of growth hormone
leading to protein synthesis in many tissues ,increase
the breakdown of fatty acids in adipose tissue ,increase
in glucose level and delayed epiphyseal closure with
extended growth period.
• There is tremendous increase in size of bones that lead
to formation of giants whose height is 8 feet or more
• These giants tend to have short lifespan, die in early life
• They develop signs of increased intracranial pressure
from the tumor and are also subjected to infection
 diagnosis
• Exams and tests
• CT scan or MRI scan of the head
showing pituitary tumor
• High prolactin levels
• Damage of pituitary may lead to low
levels of other hormones e.g.
• Cortisol, estradiol(girls),testorone
(boys) ,thyroid hormone
 Medical management
• Medications to reduce growth hormone
release ,block the effects of growth hormone or
prevent growth in stature e .g
• Dopamine agonist like bromocriptine mesylate,
carbagoline(dostinex)
• They reduce growth hormone release
• GH antagonist ,pegvisomant (somavet) –blocks effect
of GH
• Sex hormones therapy e.g. estrogen and
testosterone may inhibit growth of long bones
• Somatostatin analogs e.g. octreotide ,somatuline
which reduce GH release
 management

• Prepare and assist in investigations e.g. blood for GH ,

scan of the skull.
• Administer drugs as prescribed e.g. dopamine
antagonists e.g. Bromocryptine inhibit the release of
GH
• Closely monitor vital signs
• Reassure the patient and relatives
• Surgical management involves resection or removal of
pituitary gland and is indicated if;
– There is no improvement in medical treatment
– Intracranial pressure is causing blindness
 Conti…
• Prepare the patient for theatre
Provide post- operative care to include;
– When receiving the patient from theatre , check pulse respiratory,
level of consciousness and bleeding from the operated site.
– Put the patient in bed and observe ¼ hourly till fully awake
– Maintain IV fluids and keep accurate input output charts
– If BP is low, give the patient hydrocortisone IV
– Observe the limbs and pupils for movement
– Observe for any fits and report to the doctor
– Provide care of pressure areas
– Encourage early ambulation
– Start the patient on oral feeding once able to swallow
 Conti…
• Give medication as prescribed
• Remove alternate sutures and all by 7th day
• If the patient is in a radiotherapy, observe for side effects
• Provide adequate diet , fluids and rest
• Provide health education to include compliance with
treatment since it is for lifetime.
• other treatment include radiation of the pituitary gland-
less recommended due to side effects e.g. obesity,
emotional impairment, and learning disabilities
 complications
• Delayed puberty
• Difficulty functioning in every day due to large
size and un usual features
• Diminished vision or blindness
• Embarassment,isolation,difficulties with
relationship and other social problem
• Hypothyroidism
• Severe chronic headache
• Sleep apnea
 PRECOCIOUS PUBERTY
• This is a condition in which manifestations of sexual
development occur before age 9 in boys and age 8
in girls

CAUSES
1. Idiopathic
2. Secondary:
- Congenital anomalies
- Post inflammatory; encephalitis, meningitis
- Radiation therapy

06/18/2024 114
 Pathophysiology
• Normally the hypothalamic releasing factors
stimulate secretion of gonadotropic hormones at
the time of puberty
If for some reason there is premature activation in
males and females, then the child displays signs of
puberty
MX
1. Monthly injections of a synthetic analog of
luteinizing hormone releasing hormone which
regulates pituitary secretions

06/18/2024 115
 Cont;
The available preparation, leuprolide acetate (lupron
Depot) is given in a dose of 0.2- 0.3mg/kg IM every 4
weeks
Treatment is discontinued when need to allow
pubertal changes is felt
2. Psychological care is very important for both parents
and the child
3. No form of contraception is needed unless the child
is sexually active
NB hormonal birth control pills will initiate epiphyseal
closure resulting in stunted linear growth

06/18/2024 116
 SIADH-Syndrome of Inappropriate Anti-Diuretic Hormone

• Too much ADH produced or secreted.

• SIADH commonly results from malignancies, CHF, & CVA - resulting in
damage to the hypothalamus or pituitary which causes failure of the
feedback loop that regulates ADH.
• Client retains water causing dilutional hyponaetremia & decreased
osmolality.
• Decreased serum osmolality cause water to move into cells
• Excessive production of ADH secreted from posterior pituitary
or an ectopic source.
• Often the result of a carcinoma (i.e. lung oat cell ca), also
infections, trauma, drugs.
• Key features are water retention, hyponatremia and hypo-
osmolality
 SIGNS AND SYMPTOMS
• Lethargy & weakness
• Confusion or changes in neurological status
• Cerebral edema
• Muscle cramps
• Decreased urine output
• Weight gain without edema
• Hypertension
 ASSESSMENT
• Serum sodium low
• Serum osmolality low
• Urine osmolality disproportionately elevated
in relation to the serum osmolality
• Urine specific gravity elevated
• Plasma ADH elevated
!!!!!!
Treatment of SIADH
Treat underlying cause
Hypertonic or isotonic IV solution
Monitor for signs of fluid and electrolyte
imbalance
Monitor for neurological effects
Monitor in and out
Monitor Weight
Restrict fluid intake
Medic Alert
Lithium inhibits action of ADH to promote
water excretion.
 HYPOPITUITARISM
• This is diminished or deficient secretion of pituitary
hormones
• It may result from disease of the pituitary gland itself
or the hypothalamus
• Panhypopituitarism (simmond’s disease) is the total
absence of all pituitary functions
• Post partum pituitary necrosis (Sheehan’s syndrome)
is a failure of the anterior pituitary in women with
severe blood loss, hypovolemia and hypotension at
the time of delivery

06/18/2024 122
 CAUSES
• Tumors in the pituitary e.g. pituitary adenomas or
hypothalamic region (craniopharyngiomas)
• Idiopathic
• Congenital due to developmental defects, mutations,
birth complications
• Irradiation of the CNS, eye, middle ear
• Infection e.g. meningitis ,inflammation; Auto
immune hypophysitis, empty sella syndrome and
infiltration e.g. hemochromatosis
06/18/2024 123
 Causes cont’
• Surgery to remove pharyngeal pituitary
• Functional deficiency- psychosocial dwarfism,
anorexia nervosa
• Growth hormone deficiency
• Vascular causes as in Sheehan's syndrome

06/18/2024 124
 Dwarfism
• Pituitary disorder in children characterized by
stunted growth
 Cause of
Dwarfism
• Reduction in the GH in infancy or early childhood
• Occurs because of following reasons:
 Deficiency of GH releasing hormone from
hypothalamus

 Deficiency of Somatomedin – C

 Atrophy of acidophilic cells in the adenohypophysis

Tumor of chromophobes : nonfunctioning

tumor , compresses and destroys the normal
cells

 Panhypopituitarism
Signs and Symptoms
• Stunted skeletal growth

• Maximum height approximately 3 feet

• Head becomes slightly larger in relation of body

• Mental activity is normal without any deformity

• Reproductive system is not affected due to lack of

GH but in Panhypopituitarism puberty is not
obtained due to lack of gonadotropic hormone
 Types of
Dwarfism
• Laron dwarfism
• Psychogenic dwarfism
• Dwarfism in dystrophia adiposogenitalis
 Laron
Dwarfism
• Genetical disorder

• Caused by GH insensitivity

• Occurs due to presence of abnormal GH secretagogue

receptors in liver

• GHS becomes abnormal due to mutation in genes

responsible for receptor

• Doesn’t depend on amount of GH secretion , hormone

can’t stimulate the growth due to abnormal GHS
Psychogenic Dwarfism
• Due to extreme emotional deprivation or stress

• Deficiency of GH

• Also called as psychosocial dwarfism or Stress

dwarfism
 Dwarfism in Dystrophia adiposogenitalis
• Called as Frohlich syndrome
• Rare childhood disorder
• Characterized by :
oObesity
oGrowth retardation
oRetarded development of genital organs
oAssociated with tumors of hypothalamus –
increased appetite and decrease in
gonadotropin hormone
 Disorders of Pituitary
Gland
Parts involved Hyperactivity Hypoactivity
Anterior Pituitary 1. Gigantism 1. Dwarfism
2. Acromegaly 2. Acromicria
3. Acromegalic 3. Simmond’s disease
gigantism
4. Cushing’s
disease
Posterior Pituitary Syndrome of Diabetes insipidus
inappropriate
hypersecretion of
ADH (SIADH)
Anterior and Posterior ……. Dystrophia
Pituitary adiposogenitalis
 Acromicria
• Rare disease in adults characterized by the atrophy of the
extremities of the body
Causes of Acromicria
• Deficiency of GH in adults
• Secretion of GH decreases in the
following conditions:
 Deficiencyof GH releasing hormone
Atrophy of acidophilic cells in the anterior
pituitary
 Tumor of chromophobes
 Panhypopituitarism
Signs and Symptoms
• Atrophy and thinning of extremities ( major
symptoms )

• Associated with hypothyroidism

• Hyposecretion of adrenocortical hormone

• Person becomes lethargic and obese

• Loss of sexual function

Simmond’s Disease
• Rare pituitary disease
• Also called as cachexia
• Occurs mostly in panhypopituitarism
Signs and Symptoms
• Developing senile decay
• Senile decay is due to deficiency of hormone
from target glands of anterior pituitary e.g. thyroid
gland, adrenal cortex and the gonads

• The condition is characterized by various signs

and symptoms related to the hormones lacking
as discussed below
 S &S of Panhypopituitarism (Simmond’s
disease)
1. Growth hormone
a. Short stature but proportional height and
weight
b. Delayed epiphyseal closure
c. Retarded bone age proportional to height
d. Premature aging later in life
e. Increased insulin sensitivity & central obesity
f. impaired attention and memory .

06/18/2024 138
 2. TSH
a. Dry, coarse skin, yellow discoloration,
pallor
b. Cold intolerance
c. Constipation, bradycardia delayed
dentition
d. Weight gain & hair loss.
e. In children cretinism
06/18/2024 139
 Cont’
3. Gonadotrophins
a. Absence of sexual maturation
b. Atrophy of genitalia, prostate gland and breasts
c. Amenorrhea
d. Decreased spermatogenesis
4. ACTH
a. Severe anorexia, fatigue & weight loss; failure to
thrive in children.
b. Hypotension, hypoglycemia, hyponatremia
c. Hyperkalemia
06/18/2024 140
 Cont’
d. Circulatory collapse, shock & vomiting in
abrupt onset
e. highly similar to Addison’s disease though
hyper pigmentation does not occur in ACTH
deficiency
5. ADH
f. Polyuria
g. Polydipsia
h. Dehydration
i. Hypernatremia
6. Melanocyte stimulating hormone
- Decreased pigmentation
06/18/2024 141
 Diagnostic evaluation
• Family history
• Child’s growth history
• Physical exam
• Radiographic surveys for centres of
ossification (bone age)
• Endocrine studies

06/18/2024 142
 MANAGEMENT
• Treatment of GH deficiency caused by organic lesions
is directed towards correction of the underlying
diseases process e.g. surgical removal or irradiation
of a tumor
• Replacement with GH offers 80% success
• Daily administration of GH at a dose of 25-50ug/kg to
short prepubertal children that increases growth
velocity
• Children with other hormone deficiencies require
replacement therapies to correct specific disorders

06/18/2024 143
 Cont’
• For children to achieve their genetic growth
potential, early diagnosis and intervention is
essential
NURSING CONSIDERATIONS
• Identification children with growth problems
• Assisting with diagnostic tests
• Child and family support
• Children undergoing hormone replacement require
additional support, education of self management is
important

06/18/2024 144
 Cont’
• Educate concerning medication preparation and
storage, injection sites, timing and syringe disposal
• Even with hormone replacement these children
attain adult height at a slower rate than their peers
hence the nurse should help them set realistic goals
regarding improvement
• They should be advised to wear medical
identification at all times

06/18/2024 145
THYROID DISORDERS
THYROID DISORDERS
The thyroid gland secretes T3, T4 and thyrocalcitonin.

Secretion is controlled by TSH.

Hypothyroidism or hyperthyroidism may result from

a defect in the target gland or from a disturbance in
the secretion of TSH.

Synthesis of TH depends on the available sources of

dietary iodine and tyrosine.

The thyroid is the only endocrine gland capable of

storing excess amounts of hormone for release as
needed.
18/06/2024 147
 Physiologic effects of Thyroid hormone

1. Regulation of metabolic rate of all cells: proteins, fat,

carbohydrate and nitrogen excretion.

2. Regulation of body heat production and heat

dissipating mechanism.

3. Regulation of protein synthesis and transcription of

messenger RNA.

4. Increases gluconeogenesis and peripheral utilization

of glucose.

5. Maintains appetite and secretion of GIT substances.

18/06/2024 148
 Effects of Thyroid hormone Cont’d
6. Maintain calcium mobilization.

7. Stimulates cholesterol synthesis and hepatic mechanisms

that remove cholesterol from the circulation.

8. Maintains growth hormone secretion, skeletal

maturation and tissue differentiation.

9. It is necessary for muscle tone and vigor of normal skin

constituents.

10. Maintains cardiac rate, force and output.

11. Affects milk production during lactation and menstrual

cycle fertility.
18/06/2024 149
DISORDERS OF THYROID GLAND
 HYPERTHYROIDISM
• Def: Hyperthyroid state characterized by increased
circulating T3 and T4
• There is oversecretion of thyroid hormones by the
thyroid gland.
PREVALENCE
• It affects women eight times more frequently than
men, with onset usually between the second and
fourth decades
 CAUSES
• Overstimulation of thyroid gland by
immunoglobulins(Graves disease)
• Thyroiditis -Sub acute thyroiditis/ post partum thyroiditis
• Excessive ingestion of thyroid hormone.
• Tumors of thyroid gland or pituitary gland
• Multinodular goiter
• Solitary active nodule (toxic adenoma)
• Excess stimulation of thyroid gland by TSH
• Hydatiform mole choriocarcinoma –HCG from the placenta
stimulates thyroid gland.
• Metastasis/ cancer of thyroid tissue
FORMS OF HYPERTHYROIDISM
1.Graves disease :the most common type of
hyperthyroidism, results from an excessive
output of thyroid hormones caused by
abnormal stimulation of the thyroid gland by
circulating immunoglobulins.
• Also called Toxic goiters : causes
overstimulation of thyroid gland.
 GRAVES DISEASE
• This is diffuse enlargement of thyroid gland mainly due to
TSH receptor antibody.
• There is overproduction of thyroid hormone due to
production of antibodies(thyroid s.immunoglobulin) which
will act as TSH binding with thyroid gland and make the
gland enlarged with increase of T3 and T4 production.
• The TSI recognize &bind to the thyrotropin receptor
Which stimulates the secretion of T4 and T3.T4 receptors in
the pituitary gland are activated by the surplus
hormone,suppressing additional release of TSH in a –ve
feedback loop.result is high levels of circul thyroid hormones
and low TSH level
 Clinical features

• GIT – anorexia, vomiting, diarrhea, stearrtorrhoea

• Cardiac- palpitations, tachycardia, angina, cardiac
failure.
• Respiratory – dyspnea on exertion, exacerbation of
asthma
• Skin- purititis, alopecia , pretibial myoedema .
• Eyes- diplopia, retraction of eyelids, excessive
lacrimation, exophthalmos.
• Neuromuscular- emotional irritability, psychosis,
aggitiation muscle weakness, increase tender reflex
 Conti…

• Reproductive- impotence, libido,

spontaneous abortion, oligo- menorrhea,
amenorrhea, infertility.
• Heat intolerance
• Osteoporosis
• Weight loss
 PATHOPHYSIOLOGY OF HYPERTHYROIDISM
• Hyperthyroidism may occur with the release of
excessive amounts of thyroid hormone as a result of
inflammation after irradiation of the thyroid or
destruction of thyroid tissue by tumor.
• Excessive hormones leads to increased hormone
activity which leads to increased Basal Metabolism
and cardiac activity
• Increased metabolism is characterised by increased
appetite and dietary intake, progressive weight loss,
abnormal muscular fatigability and weakness
• The patients exhibits a group of sign and symptoms
( sometimes called thyrotoxicosis
 CLINICAL MANIFESTATIONS
8.Oligomenorrhea to
1.Weight loss amenorrhea
2.HEAT intolerance
9.Fine tremors and
3. Hypertension
nervousness and
4. Tachycardia and palpitations
and increased pulse pressure clubbing
• Fast Pulse rate btw 90-160 10. Irritability, mood
5. Exopthalmos (bulging eyes) swings, personality
with startled facial expression changes and agitation
6. Diarrhea 11. Enlarged thyroid
7.flushed skin : warm, soft, and 12. Osteoporosis and
moist
fractures
.
.
.
 ASSESSMENT FINDINGS
• Client has heat intolerance and may have diaphoresis
(increased sweating) even when environmental
temperatures are comfortable for others.
• Client report palpitations or chest pain
• Client experiences emotional lability ( mood instability)
,irritability, decreased attention span and manic
behaviour.
• Fatigue, weakness and insomnia
• The thyroid gland invariably is enlarged to some
extent. It is soft and may pulsate
• Increased serum levels of T4 and iodine intake by the
thyroid gland
 MEDICAL MANAGEMENT
Can be managed by:
1. Pharmacological therapy
2.Surgical therapy
PHARMACOLOGICAL THERAPY
(1) use of irradiation by administration of the radioisotope
121I or 131I for destructive effects on the thyroid gland
(2) antithyroid medications that interfere with the
synthesis of thyroid hormones
 ANTITHYROID MEDICATIONS

Include ; propylthiouracil , carbimazole.

1.PROPYLTHIOURACIL propacil( PTU)
(A) Mechanism of action : inhibit thyroid hormone
synthesis by inhibiting incorporation of iodine into
tyrosine. It also suppress conversion of T4 into T3 the
more active form of thyroid hormone.
(B) Pharmacokinetics
-is rapidly absorbed following oral administration
-Therapeutic effects begin after 30 mins
-The plasma half-life is short(2hrs).
As a result ,it is administered three times a day
 CONT
( c) therapeutic uses /indications
• Hyperthyroidism
• Adjunct to radiation therapy. Used to control
hyperthyroidism until effects of radiation become
manifest.
• Thyrotoxic crisis, (thyroid storm)
(d)ADVERSE EFFECTS
1.hypothyroidism ; excessive dosing with PTU may lead to
hypothyroidism
 CONT

2. agranulocytosis ; severe bone marrow depression.

Resulting in failure to produce neutrophils.Usually
occurs during the first 2 months of life. sore throat
and fever are the earliest indications. Patients are
instructed to report these immediately. The drug is
stoped immediately if the symptom S/E develops.
3. skin rashes , headaches , nausea and joint pains
 CONT

DOSAGE : Propylthiouracil-100-150mg every 6 or 8 hrs

DURATION :18-24 months
PTU AND PREGNANCY
-PTU crosses placenta
• Propylthiouracil is preferred over carbimazole in
pregnant women because its rapid action reduces
transfer across the placental barrier and it doesn’t
cause aplasia cutis (a severe skin disorder) in the
fetus
 CONT

• Mothers taking these drugs shouldn’t breast-feed.

• If a breast-feeding woman must take one of these
drugs, propylthiouracil is the preferred drug.
CARBIMAZOLE
• Mechanism of action : decreases uptake iodine
needed in formation of thyroxine and incorporation
of iodine into tyrosine to form thyroxine
 DOSAGE

• The initial dose is 15-40 mg daily given for 4 to 8 weeks

until euthyroid status is achieved .
• The dose is gradually reduced to a maintenance of 5-15
mg daily.
• Treatment is usually required for 12-18 months
• Patients should have their T4 levels checked every 4-6
weeks
 CONT

• Once maintenance dose has been established , T4 and

TSH should be checked every 3 months.
• Patients should be regularly reviewed during the first
year after discontinuing carbimazole because there is
high rate of relapse during this period.
• Carbimazole is used at the lowest dose possible in
pregnancy however PTU is preferred over carbimazole
 RADIOACTIVE IODINE THERAPY

• Is used as a radiation therapy

• Used to destroy thyroid tissue in patients with
hyperthyroidism
• Mechanism of action: produce emission of
beta particles that destroy thyroid tissue.
• Reduction of thyroid tissue is gradual and
effects takes weeks to become apparent
• A single oral dose of the agent is administered
 .
• Is used as a radiation therapy
• Used to destroy thyroid tissue in patients with
hyperthyroidism
• Mechanism of action: produce emission of
beta particles that destroy thyroid tissue.
• Reduction of thyroid tissue is gradual and
effects takes weeks to become apparent
 CONT

• Almost all the iodine that enters and is retained in the

body becomes concentrated in the thyroid gland.
• Radioactive isotope of iodine is concentrated in the
thyroid gland, where it destroys thyroid cells without
jeopardizing other radiosensitive tissues.
NB: Antithyroid medications are contraindicated in late
pregnancy because they may produce goiter and
cretinism in the fetus
 ADJUNCTIVE THERAPY
• Beta-adrenergic blocking agents are important in
controlling the sympathetic nervous system effects of
hyperthyroidism.
• Propranolol (Inderal) is used to control nervousness,
tachycardia, tremor, anxiety and heat intolerance.
 NURSING MANAGEMENT
1. Provide adequate rest periods in a quiet room because
fatigue is common
2. Administer anti-thyroid medications that block hormone
synthesis- carbimazole and PTU and monitor for side
effects
3. Provide a high-calorie diet, high protein to provide
energy and build the body
4.Provide a cool and quiet environment to reduce
irritability . Noises, such as loud music, conversation,
and equipment alarms, are minimized .
 CONT

5.Maintain the environment at a cool, comfortable

temperature and change beddings and clothing as
needed. Cool baths and cool or cold fluids may provide
relief.
6.Assesses and monitor the patient’s cardiac status,
including heart rate, blood pressure, heart sounds, and
peripheral pulses
7. To reduce diarrhea, highly seasoned foods and
stimulants such as coffee, tea, cola, and alcohol are
discouraged. In additions, fluids are added as needed
 THYROID STORM (THYROTOXIC CRISIS,
THYROTOXICOSIS)
• An acute LIFE-threatening condition characterized by
excessive thyroid hormone
• Is the most severe form of hyperthyroidism with
acute onset.
 CLINICAL MANIFESTATIONS

Thyroid storm is characterized by:

1.High fever (hyperpyrexia) above 38.5°C (101.3°F)
2.Extreme tachycardia (more than 130 beats/min)
3.Severe weight loss, diarrhea, abdominal pain
4.dyspnea
5.Altered neurologic or mental state, which frequently
appears as delirium, psychosis, or coma
6.Restlessness, Agitation, confusion and Seizures
 PRECIPITATING FACTORS
• Injury on the body
• Systemic infection
• Thyroid and non thyroid surgery
• Tooth extraction
• Insulin reaction
• Diabetic acidosis
• Pregnancy
• Digitalis intoxication,
• abrupt withdrawal of antithyroid medications,
• Extreme emotional stress
• Vigorous palpation of the thyroid.
 EMERGENCY MANAGEMENT

• Humidified oxygen is administered to improve tissue

oxygenation and meet the high metabolic demands
• Arterial blood gas levels or pulse oximetry may be used to
monitor respiratory status.
• Intravenous fluids containing dextrose are administered to
replace liver glycogen stores that have been decreased in
the hyperthyroid patient.
• PTU or Carbimazole is administered to impede formation
of thyroid hormone and block conversion of T4 to T3, the
more active form of thyroid hormone.
• Hydrocortisone is prescribed to treat shock or adrenal
insufficiency.
 CONT

• Cool environment and acetaminophen (Tylenol) to

reduce fever. Salicylates (eg, aspirin) are not used
because they displace thyroid hormone from binding
proteins and worsen the hypermetabolism
• Propranolol, combined with digitalis, are
administered to reduce severe cardiac symptoms
• Iodine is administered to decrease output of T4 from
the thyroid gland
 NURSING INTERVENTIONS

1. Maintain PATENT airway and adequate ventilation. Oxygen

is needed to meet metabolic demands
2. Administer anti-thyroid drugs with medications such as
(a) Lugol’s solution : consist of 5% Iodide and 10%
potassium… blocks peripheral conversion of T4 to T3
hence inhibiting hormone release .
b) Propranolol : is a beta blockers to reduce cardiac heart
rate.
c) Glucocorticoids :inhibit hormone production and decrease
peripheral conversion from T4 to T3.
 CONT

3.Monitor VS including pulse rate and temperature

4. Monitor Cardiac rhythms
5.Provide a quiet environment
6.Administer antipyretics like paracetamol
7.Administer IV fluids to correct dehydration
 GOITRE
• Abnormal enlargement of thyroid gland due to
inflammation or tumor that become visible
Mortality and Morbidity
• Most goitres are benign , causing only cosmetic
disfigurement
• Morbidity or mortality may result from compression of
sorrounding structures , thyroid cancer ,
hyperthyroidism or hypothyroidism
Causes
• Deficiency of iodine in the diet
• Lack of TSH in pituitary gland
• Over production of T4 caused by toxic /malignant goitre
 .

• Female to male ratio : 4 : 1

• They are common in women than men
Classification of goiters
1.Toxic goiter : a goiter that is associated with
hyperthyroidism
Examples include : a. diffuse toxic goiter (graves disease)
b. toxic multinodular goiter and toxic adenoma
2.Non toxic goiter: a goiter without hyperthyroidism or
hypothyroidism. Examples are congenital goitre and
physiologic goiter that occurs during puberty
3. Malignant goiter
 1.NON – TOXIC GOITERS

There are four types of Non Toxic goiters

a. Diffuse non-toxic goiter
b.Multinodular non-toxic goiter
c. simple goiter
d. uninodular goitre
A. Diffuse non – toxic goiter
• Develops during early stage of disease
• The thyroid gland is diffusely enlarged
• There is hypertrophy and hyperplasia of follicular
cells.
 CONT

B. Multinodular non-toxic goiter

• Evolves as the disease becomes chronic
• The gland develops nodules that vary in shape
• Is the most common especially in older patients.
• It's the most common cause of tracheal and
oesophageal compression and may cause laryngeal
nerve palsy..
 CONT

C. simple goiter - There is no clear cause for

enlargement of the thyroid which is usually smooth
and soft.

d. Solitary nodular goiter (Plummers syndrome) - They

are usually cystic or benign with a history of pain,
rapid enlargement or associated lymph nodes.
 CLINICAL FEATURES OF NON-TOXIC GOITERS

• Patients are asymptomatic presenting with

a mass in the neck
• If goiter is large ,there will be compressive
symptoms such as dysphagia (difficulty in
swallowing)
 CAUSES OF GOITRES

• Hypertrophy caused by excess stimulation

• Iodine deficiency
• Hashimoto's thyroiditis
• Goitrogens : are substances that suppress the
function of thyroid gland by interfering with iodine
uptake e. g cassava and sweet potatoes
 PATHOPHYSIOLOGY OF SIMPLE GOITRE
• This is the most common type of goitre, also called
ENDEMIC/colloid goitre/IODINE defiency, and is
encountered in regions where natural supply of iodine is
deficient.
• simple goiter may be caused by lack of iodine and intake of
large quantities of goitrogenic substances
• The pituitary gland produces thyrotropin or TSH, a hormone
that controls the release of thyroid hormone from the
thyroid gland.
• Its production increases if there is subnormal thyroid
activity, as when insufficient iodine is available for
production of the thyroid hormone..
• Increase in TSH courses overstimulation of thyroid gland
leading to compensatory hypertrophy or enlargement
 INVESTIGATIONS

• Thyroid function tests of thyroid stimulating

hormone, thyroxine and triodothyronine to
determine whether a goitre is associated with
hyperthyroidism, hypothyroidism or normal thyroid
function
• Chest and thoracic inlet x-rays to detect tracheal
compression.
 CONT
• Measurement of thyroid antibodies to assess for
thyroiditis.
• Ultrasound to demonstrate whether the nodules are
cystic or solid.
• Thyroid scan to determine whether the nodule is
malignant.
 TREATMENT

• Goitres of this type recede after iodine imbalance

has been corrected
• Supplementary iodine is prescribed to suppress
the pituitary thyroid activity

• A goitre associated with normal thyroid function in

pregnancy and puberty rarely requires intervention
and patient needs to be reassured
• Surgery if there is obstructive symptoms
• In older patients Radioactive iodine therapy
 INDICATIONS FOR SURGERY

• The possibility of malignancy where there is a history

of rapid growth, pain, cervical lymphadenopathy or
previous irradiation.
• Pressure symptoms on the trachea.
• Cosmetic reasons.
 THYROIDECTOMY
• Refers to surgical removal of the thyroid gland
Indications for thyroidectomy
Increase in size of the gland
Substantial malignancy
Increase pressure symptoms
Thyrotoxicosis patients not responding to medical
treatment
Patients’ choice.
NB-Operation done may be partial or total
thyroidectomy
 PRECAUTIONS DURING THE SURGERY

• Identification and preservation of recurrent

laryngeal nerve , superior laryngeal nerve and
parathyroid gland.
• Unilateral damage to recurrent laryngeal nerve will
result in post-operative hoarseness due to paralysis
of one vocal cord.
 CONT

• Bilateral damage to both recurrent laryngeal will

result in paralysis of both vocal cords, and it may
cause acute airway obstruction.
• Damage to superior laryngeal nerve is less noticeable
because mobility of vocal cords is maintained
• Removal of parathyroid gland will result in post
operative hypoparathyroidism.
 PRE-OPERATIVE PREPARATION

• Provide a restful, quiet environment.

• Regulate nutritional intake, that is, food should be
high in carbohydrate and protein.
• Pre-operative investigations.
• Prepare the patient for surgery by sharing
information, giving instructions on what to expect
and the informed consent
 CONT

• Patient must be restored to euthyroid state.

• Pre-operative teaching should include comfort and
safety measures.
• Coughing and deep breathing exercises should be
practiced including how to support the neck
manually while turning in bed because this minimises
stress on the suture line after surgery and exercises
of the neck
 CONT

• Medications that are used to restore euthyroid state

are ;
 propylthiouracil is administered until signs of
hyperthyroidism have disappeared.
 A beta-adrenergic blocking agent (propranolol) may
be used to reduce the heart rate and other signs and
symptoms of hyperthyroidism
 Iodine (Lugol’s solution or potassium iodide)
is administered to reduce blood loss;
 CT
• Carbimazole is given for several weeks and
stopped 10 days before surgery
• Administer the following pre-operatively
Glucose iodine 0.3-0.9ml p.o tab*10 14/7
Propranolol 120-160mg od
Valium 5mg note to quieten patient and ensure
sleep
Digoxin 0.25mg if there are trial fibrillations
 POST OPERATIVE MANAGEMENT
1. Set Oxygen, suction equipment and a tracheostomy
tray at the bed side to be readily available in case
airway obstruction occurs.
2. Position patient: Semi-Fowler’s, neck on neutral
position to avoid tension on the neck sutures.
3.Assess patient every two hours for 24 hours for signs
of haemorrhage or tracheal compression e.g.
irregular breathing, neck swelling, blood on the
anterior and posterior dressing.
4. Check for signs of tetany secondary to
hypoparathyroidism e.g. tingling in toes, fingers or
around mouth, muscular twitching.
 CONT

5.Monitor vital signs temperature, pulse, respiration

and blood pressure.
6. Assess frequently for frequent airway obstruction.
Significant irritation of or injury to both recurrent
laryngeal nerve may result to bilateral vocal cord
paralysis with airway obstruction.
7.Observe for signs of thyrotoxic crisis which include
tachycardia ,diaphoresis , increased blood pressure
and anxiety
8. Administer prescribed analgesics to control pain
9. Administer IV fluids
 COMPLICATIONS OF THYROIDECTOMY
• Thyrotoxicosis crisis (thyroid storm) which is an acute
but rare condition in which all the hyperthyroid
manifestation are worsened and may include severe
tachycardia, heart failure, hyperthermia,
restlessness.
• Recurrent laryngeal nerve damage which may lead to
vocal cord paralysis.
• Difficulty in breathing due to swelling of neck tissues,
haemorrhage, haematoma formation.
 CONT

• Laryngeal stridor (harsh vibratory sound) may occur

during respiration due to tetany from damaged or
removal of parathyroid.
• Early post-operative bleeding
• Recurrent hyperthyroidism occurs in 1-3% within one
year and then 1% per year
• Hypothyroidism occurs in about 10% of patients
within one year.
 RECURRENT HYPERTHYROIDISM
• All three treatments (radioactive iodine therapy,
antithyroid medications, and surgery) share the same
complications: relapse or recurrent hyperthyroidism and
permanent hypothyroidism.
• The rate of relapse increases in patients who had very
severe disease, a long history of dysfunction, ocular and
cardiac symptoms, large goiter, and relapse after
previous treatment.
• The relapse rate after radioactive iodine therapy depends
on the dose used in treatment.
• Hypothyroidism occurs in almost 80% of patients
at 1 year and in 90% to 100% by 5 years for both the
multiple low-dose and single high-dose methods.
 SUMMARY OF COMPLICATIONS
• Hemorrhage
• Laryngeal paralysis
• Voice coarseness
• Myxedema
• Thyroid storm or crisis
• Infection
• Keloids
 HYPOTHYROIDISM
• Def : refers to hyposecretion of thyroid hormones
specifically T3 and T4.
• It is also referred to as thyroid deficiency. Thyroid
deficiency affect all body functions
• When thyroid deficiency is present at birth, the
condition is known as cretinism.
CAUSES
1.Autoimmune thyroiditis (Hashimoto’s disease), in
which the immune system attacks the thyroid gland.
• It is the most common cause.
 CONT

2. Atrophy of thyroid gland with aging

3. Radioactive iodine
4. Thyroidectomy
5. Medications like Lithium and Antithyroid medications
6. Radiation to head and neck for treatment of head and
neck
7. cancers, lymphoma
8. Infiltrative diseases of the thyroid (amyloidosis,
scleroderma)
9. Iodine deficiency and iodine excess
 PREDISPOSING FACTORS

• Previous treatment with antithyroid

medications and radioactive iodine
• Thyroidectomy
• Advance age ; common in older women
• Radiation therapy for head and neck for
cancer
 PATHOPHYSIOLOGY

• Hypothyroidism can be caused by thyroid

dysfunction itself or pituitary gland and
hypothalamus.
• In both, there is hyposecretion of T3 and
T4 hormones which leads to decreased
basal metabolic rate characterized by
lethargy , fatigue , cold intolerance , weight
gain and constipation.
 CLINICAL MANIFESTATIONS
• Extreme fatigue • Forgetfullness
• hair loss, brittle • Menstrual
nails, and dry skin disturbances
• numbness and such as menorrhagia or
tingling of the Fingers amenorrhea
• Cold intolerance • Slowness of
• Weight gain movement
• constipation • Bradycardia
• irritability
 MEDICAL MANAGEMENT
• Hormone replacement therapy : synthetic
levothyroxine is administered.
• BRAND NAME : Synthroid , levoxyl , levothroid and
unithroid
• Is a drug of choice for most patients who need
thyroid hormone replacement.
MODE OF ACTION : It increases metabolic rate of all
cells of all tissues in the body
 CONT
PHARMACOKINETICS
-Most of it converted into T3 in the body
hence can produce both T3 and T4
-highly bound to proteins and has a half life
of 7 days hence it therapeutic effects are
delayed for 2 weeks
-The long half life facilitate once a day
dosing
 CONT

THERAPEUTIC USES (INDICATIONS)

• Indicated in hypothyroidism in adult and
children
• Maintenance of thyroid hormones
following surgery
• Myxedema coma
• Simple goiter.
 DOSAGE AND ADMINISTRATION

• Starting dosage is 12.5mcg/day orally.

• Dosage changes may differ with individual patients
based upon age, the presence of cardiovascular
disease and development of tolerance or reduced
effectiveness of drug
• The drug is available in tablet forms, capsules and IV.
 DRUG INTERACTIONS

• Increases the need of insulin in diabetic patients

• Increases the effects of warfarin therefore
monitoring of blood clotting is necessary
• Increases cardiac response to catecholamines
(epinephrine) thereby increasing the risk of
catecholamine induced dysrhythmias.
• Caution must be exercised when administering
catecholamines to patients using the drug
 DURATION OF THERAPY

• Replacement therapy must be continued for life.

• The patient must be made fully aware of the chronic
nature of the condition
 NURSING MANAGEMENT OF HYPOTHYROIDISM

1. Promote independence in self-care

Activities by:
a. Spacing activities to promote rest and
exercise as tolerated.
b. Assisting with self-care activities when
patient is fatigued.
c. Monitor patient’s response to increasing
activities.
 CONT

2.Provide extra layer of clothing or extra blanket to

minimize heat loss
3.Avoid and discourage use of external heat
source (eg, heating pads, electric or warming
blankets).it reduces the risk of peripheral
vasodilation and vascular collapse
4.Encourage increased fluid intake within limits of fluid
restriction. It promotes passage of soft stool
 CONT

5.Administer hormone replacement: usually

Levothyroxine( Synthroid)-should be taken on an empty
stomach 30-60 min before eating…in the morning… food,
iron and calcium..may reduce its absorption in the gut.
6.Provide foods with low calories and high in fiber It
increases bulk of stools and more frequent bowel
movements.
7.Monitor patient’s vitals signs esp body temperature and
report decreases from patient’s baseline value.
Monitoring detects decreased body temperature and
onset of myxedema coma baseline value.
 CONT

8.Health education : Explain rationale for thyroid

hormone replacement
9.Advise to report palpitation, tachycardia, and chest
pain when using levothyroxine
 MYXEDEMA

• Def : myxedema refers to the accumulation of

mucopolysaccharides in subcutaneous and other
interstitial tissues. There is thickening of skin with non
pitting edema
• This is a condition resulting from insufficient thyroid
activities in adults due to the loss or destruction of
thyroid gland tissues
• It is a complication of hypothyroidism.
• It presents with symptoms of hypothyroidism plus
extreme hypothermia with personality and cognitive
changes characteristic of dementia.
 CAUSES
• Surgical removal of thyroid gland in thyrotoxic and
malignant goitre
• Primary atrophy of thyroid gland ( autoimmune
process)
• Radioactive iodine in therapy of exophthalmic goitre
• Severe and prolonged iodine deficiency
• Chronic thyroiditis
• Anti thyroid drugs and those containing iodine, e.g.
lithium carbonate
• Failure of primary pituitary glands to secrete TSH
• Hypothermic effect of production of TSHRF
 Conti…
Pathophysiology
• Deficiency in thyroid hormone leads to
decrease in basal metabolic rate. Fat
mobilization from the tissues is impaired
and cholesterol level is high.
• Vasodilation of peripheral vessels occurs
and this lowers cardiac output leading to
cardiomegaly.
• Metabolism of carbohydrates, fat and
proteins are affected.
 Conti…
Signs and symptoms
• Anemia
• Constipation
• Chronic headache
• Hypersomnia
• Decreased libido
• Wrinkled scalp
• Deep hoarse voice
• Swelling of the face puffy eyelids and thick nostrils
• Dull and sluggish mentally
 Conti…
• Slurred speech
• Bradycardia
• Slow movement
• Cardiomegaly
• Slow relaxation of tendon reflexes
• Increased sensitivity to cold
• Amenorrhea or menorrhagia
• Weight gain with low appetite
• Muscle pain
• Dry coarse thickened skin
 Conti…
• Non-pitting oedema
• Dry coarse hair that tends to fall
• Irritability
• Low temperature
• Loss of memory (confusion)
• Numbness and tingling of arms and legs
 Conti…

Investigations
• Protein bound iodine is low
• Blood analysis- low thyroxine level, high
cholesterol, low BMR
• LCG- enlarged heart with bradycardia
 Conti…
Management
• Give thyroid hormones e.g. sodium levothyroxine
0.05mg p.o then increase gradually to reach
maintenance dose of 0.2-0.3mg daily after 2 weeks
• Give triiodothyronine (Cytomol) 0.05mg p.o then
increase gradually to 0.2mg
• Observe for side effects of drugs such as
tachycardia, dyspnea, sweating, skin rash,
palpitations, dizziness, weight loss , pericardial pain,
diarrhea
• Nurse the patient in a warm room and add him live
because he has poor tolerance to cold.
 Conti…
• Take vital signs and report any abnormality e.g. low
temperature
• Patient to massage the skin with lotion or cream that
will prevent it from being dry and course
• Give diet low in cholesterol
• To prevent constipation, give diet rich in roughage and
have adequate fluid intake.
• Give antibiotics to treat any infection.
• Advise the patient to avoid factors that make the
condition worse e.g. cold, stress, trauma, infection
• Give health education to the patient about the
condition.
• Discharge home through MOPC
 Conti…
Complications
• Hypothermia
• Anemia
• Myxedema coma
• Arteriosclerosis
• cardiomegaly
 MYXEDEMA COMA
• Myxedema coma describes the most extreme, severe
stage of hypothyroidism, in which the patient is
hypothermic and unconscious.
• It is a life threatening condition and it is regarded as a
medical emergency.
PRESENTING FEATURES
• Severe hypothermia
• Depressed respirations
• Coma
• Cool clummy skin
 EMERGENCY MANAGEMENT
• Admit the patient into the ICU
• IV levothyroxine is administered until consciousness
is restored. The patient is then continued on oral
thyroid hormone therapy
• Arterial blood gases are measured to determine CO2
retention and to guide the use of assisted ventilation
to combat hypoventilation
• Provide warmth to the patient by covering with
enough blankets
• Fluids are administered cautiously because of the
danger of water intoxication
 CAUTION WHEN ADMINISTERING IV LEVOTHYROXINE
IN MYXEDEMA COMA
• monitor for myocardial ischemia or infarction, which
may occur in response to therapy
• The nurse must also be alert for signs of angina,
especially during the early phase of treatment; if
detected, it must be reported and treated at once to
avoid a fatal myocardial infarction
 NURSING MANAGEMENT
• Administer prescribed medications(eg, levothyroxine)
with extreme caution because the slow metabolism
and atherosclerosis of Myxedema may result in
angina with administration of levothyroxine
• Assist in Ventilatory support : is necessary to
maintain adequate oxygenation and maintenance of
an airway.
• Turn and reposition patient at interval. Minimizes
risks associated with immobility
• Monitor patients respiratory status.
• Apply other nursing interventions of hypothyroidism
 CRETINISM
This is a condition in which there is lack of thyroid activity from
childhood resulting into lack of physical growth and mental
development.
Clinical features
• May present with congenital absence of thyroid gland
• Retarded physical growth and mental development
• Disproportionally short limbs
• Large protruding tongue
• Coarse dry skin
• Poor abdominal muscle tone
• Umbilical hernia
• Early RX can lead to complete cure
.
PARATHYROID DISORDERS
 PARATHYROID DISORDERS
• The parathyroid glands(4 in number) are situated in
the neck and embedded in the posterior aspect of the
thyroid gland
• Parathormone, the protein hormone from the
parathyroid regulates calcium and phosphorus
metabolism
• Increased secretion of this hormone results in
increased calcium absorption from the kidneys,
intestines and bones thereby raising the blood calcium
levels (life threatening condition)
• It also lowers the blood phosphorus level
 HYPER PARATHYROIDISM
• This is caused by overproduction of parathyroid
hormone
• Its characterized by bone decalcification and
development of renal calculi containing calcium
• Occurs in more women than men and in patients
between 60-70years of age
• It is rare in children younger than 15 years
• Secondary hyperparathyroidism occurs in patients
with chronic renal failure and renal rickets as a result
of phosphorus retention and increased stimulation of
the glands
 Clinical manifestations
• Apathy, fatigue muscle weakness
• Nausea, Vomiting, constipation
• Hypertension and cardiac dysrhythmias because of
increased calcium concentration in the blood
• Psychological manifestations vary from irritability,
neurosis and psychoses caused by the direct effect of
calcium on the brain and nervous system
• Renal damage due to precipitation of calcium
phosphate in the renal pelvis and parenchyma hence
renal calculi
 Cont’
• Musculoskeletal symptoms resulting from
demineralization of the bones or bone tumors
composed of benign giant cells resulting from
overgrowth of osteoclasts
• There is skeletal pain on weight bearing, pathological
fractures, deformities and shortening of body stature
Assessment and diagnostic findings
• Elevated serum calcium levels
• Elevated level of Parathormone-
 Cont’
• Radioimmunoassay which differentiates
hyperparathyroidism from other causes of
hypercalcemia in 90% of patients
• Bone changes on X rays or bone scans
• Double antibody parathyroid hormone test which
differentiates between primary hyperparathyroidism
and malignancy as a cause of hypercalcemia
• U/S/ MRI. Thallium scan and fine needle biopsy
 MEDICAL MANAGEMENT /NURSING
MANAGEMENT
• The recommended treatment of primary
hyperparathyroidism is surgical removal of the
parathyroid tissue
• Hydration therapy: because of the risk of renal calculi
initiation of fluids (2000ml or more) is important
• Cranberry juice is suggested because it may lower
the urinary PH
• Thiazide diuretics are avoided as they decrease renal
excretion of calcium
Avoid hypercalcemic crisis: monitor for dehydration
 Cont’
• Encourage mobility since bed rest increases calcium
excretion and the risk of renal calculi
• Oral phosphates lower the serum calcium levels in
some patients
• Nutritional needs are met but the patient is advised
to avoid a diet with excess calcium
• If the patient has a coexisting peptic ulcer,
prescribed anti acids and protein feeding are
necessary
• Offset constipation by giving stool softeners, fluid
intake and encouraging physical activity
 Cont’
• Parathyroidectomy is done and the nurse must
observe for symptoms of tetany (an early post
operative complication
• Health education is also important
• Follow up is encouraged
• Prognosis is good
 Hypercalcemic crisis
• This occurs with extreme elevation of calcium levels
higher than 15mg/dl (3.7mmol/L
• It presents with neurologic, cardiovascular and renal
symptoms which may be life threatening
• Treatment includes rehydration with large volumes of
IV fluids, diuretic agents to promote renal excretion
of excess calcium and phosphate therapy to correct
hypophosphatemia
• Cytotoxic agents (mithramycin), calcitonin and
dialysis may be used in emergencies to decrease
serum calcium levels quickly
 Cont’
• A combination of calcitonin and corticosteroids has
been administered in emergencies to reduce serum
calcium levels by increasing calcium deposition in the
bone
• The patient requires expert assessment and care to
minimize complications and reverse life threatening
hypercalcemia
• Medications are administered with care and
attention is given to fluid balance to promote return
of normal fluid and electrolyte balance
 HYPOPARATHYROIDISM
• This is caused by inadequate secretion of parathyroid
hormone after interruption of the blood supply or
surgical removal of the parathyroid tissue during
thyroidectomy, Parathyroidectomy or radical neck
resection.
• It may also be caused by atrophy of the glands
• Congenital Hypoparathyroidism may be caused by a
specific defect in the synthesis or cellular processing
of the parathyroid hormone or from aplasia or
hypoplasia of the gland.
 Pathophysiology
• The condition is caused by a deficiency of
Parathormone that results in elevated blood
phosphate and decreased blood calcium levels
• In the absence of this hormone there is decreased
intestinal absorption of dietary calcium and
decreased resorption of calcium from the bone and
through the renal tubules
• Decreased excretion of phosphate causes
hypophosphaturia, and hypocalcuria
 Clinical manifestations
Hypocalcemia causes
1. Irritability of the neuromuscular system
2. Tetany-general muscle spasms with tremor and spasmodic or
uncoordinated contractions occurring without effort
3. Latent tetany- numbness, tingling and cramps in the extremities
and stiffness in the hands and feet
others
• Brittle nails
• Bone weakness
• Paresthesia
• Development of cataracts
 Cont’
4. In overt tetany there may be
Bronchospasms, laryngeal spasm, dysphagia,
carpopedal spasm, photophobia, cardiac
dysrhythmias and seizures
4. Anxiety, irritability, depression-Psychiatric
disturbances
5. Delirium
6. ECG changes and hypotension
 Assessment and diagnostic findings
• A positive Trousseau’s sign- carpopedal (flexion of the
elbows and wrists and extension of the
carpophalangeal joints) spasm is induced by
occluding the blood flow to the arm for 3 minutes
with a blood pressure cuff
• A positive Chvostek’s sign- occurs when a sharp
tapping over the facial nerve just in front of the
parotid gland and anterior to the ear causes spasm
or twitching of the mouth, nose and eye
• Low serum calcium levels of 5-6mg/dl
• Increased phosphate levels
 Cont’
• Xrays show increased bone density and calcification
of subcutaneous or Para spinal basal ganglia of the
brain
MEDICAL MANAGEMENT
-The goal is to raise the serum calcium levels to 9-
10mg/dl (2.2-2.5mmol/L and to eliminate symptoms
-When there is tetany, administer calcium gluconate
IV, if this does not decrease neuromuscular irritability
and seizure activity immediately, sedative agents like
Phenobarbital may be given
 Cont’
- Parenteral Parathormone can be administered
(watch for allergic reactions)
- A diet high in calcium and low in phosphates is
prescribed in chronic cases
- Oral tablets of calcium salts like calcium gluconate
may be used to supplement the diet
- Aluminium hydroxide gel or aluminium carbonate
(gelusil, Amphojel) is administered after meals to
bind phosphate and promote its excretion though
the GIT
 Cont’
- Variable dosages of vitamin D preparation-
dihydrotachysterol (AT10 or hytakerol) ergocalciferol
(Vit D, cholecalciferol (Vit D) are required to enhance
calcium absorption through the GIT
NURSING MANAGEMENT
- Care of post op patients in detecting early signs of
hypocalcaemia and anticipated signs of tetany,
seizures and respiratory difficulties
- Calcium gluconate is kept at the bedside with
equipment necessary for IV administration
 Cont’
• Calcium and digitalis increase systolic contraction
and also potentiate each other producing fatal
dysrhythmias hence continuous monitoring is
important
• Patient teaching about medications and diet
therapy is very important
• He should also be taught to contact the physician
immediately when he notices symptoms
 TETANY
• This is a condition characterized by high
neuromuscular excitation and a great
irritability due to reduced serum Ca2+
levels (hypocalcaemia). There are very
strong painful spasms of skeletal causing
characteristic bending inwards of the
hands, fore arm and feet.
• In children it may present as laryngeal
spasms and convulsions.
 Predisposing factors
• Hyperparathyroidism
• Inadequate dietary calcium intake
• Chronic renal failure with excessive secretion of Ca2+
• Removal or injury of parathyroid gland
• Lack of vitamin D necessary for absorption of Ca2+ in
the gut
• Alkalosis- e.g. metabolic due to vomiting , ingestion
of excess alkalis or respiratory alkalosis due to
hyperventilation alter calcium.
• Lack of Na+ absorption like malabsorption syndrome
• Idiopathic autoimmune response by antibodies
against PTH
 Pathophysiology
• Deficiency of PTH causes a fall in serum Ca2+
with a great irritability of nerves which is
manifested by spasms and twitching of muscles.
Signs and symptoms
– Dysphagia
– Nausea and vomiting
– Photophobia due to cataracts
– Stiffness of hands and feet
– Numbness and tingling sensation in extremities or around the
lips ( paresthesia)
– Trousseau's sign – when blood supply in the arms if secluded
for 3 minutes, there will be carpal pedal spasm which may
cause inward bending of arms and feet
• Chvostek’s sign- quick touch of facial nerve
near the ear produces twitching of facial
muscles.
• Anxiety and irritability
• Convulsions
• Bronchospasms with dyspnea
• Laryngeal spasms leading to stridor and
cyanosis
• Patchy alopecia and loss of eyebrows
• Nails become brittle and break easily
• Rickets and osteomalicia
• Cardiac arrhythmias
 CT
• Psychosis due to deposition of calcium
basal ganglia depression and delirium
• Coarse dry skin with brown pigment
• Anxiety and irritability
Diagnosis
• Clinical features
• Low serum calcium
• Raised serum potassium
• Positive chvostek’s sign
• Low PTH levels
 ASSESSMENT

• if the facial nerve ( immediately in front of the ear) is

tapped, the client’s mouth twitches and the jaw
tightens. This is called positive chvostek’s sign.
• A positive trousseau's sign may be elicited by placing
a blood pressure cuff on the upper arm inflating it
and waiting for 3 minutes.
• The client is observed for spasm of the hand
( carpopedal spasm) which is evidenced by hand
flexing inward
 MANAGEMENT
• Admit and nurse the patient in a warm room quiet
with dim light and with limited movement to
minimize neuromuscular excitation and photophobia.
• Prepare and assist in investigations e.g. blood for
Ca2+, BP level X ray to rule out rickets and
osteomalicia, administer medication as prescribed
e.g. IV calcium gluconate , vitamin D e.g. calciferol 1-
5mg daily, parenteral parathormone is given in acute
hypoparathyroidism
• Give sedative e.g. valium to control convulsions /
spasm
• If the patient develops respiratory distress , do
tracheostomy or give mechanical ventilation in
• Give diet high in calcium and low potassium
• Closely observe the patient’s vital signs and for
convulsions ¼ hourly and report any
abnormality.
• Reassure the patient and relatives to allay
anxiety
• Give health education once the patient
stabilizes and discharge him home.
• Take medication as prescribed and complete the dose
• How to recognize the side effects of drugs
• Importance of taking diet with high calcium and low
potassium
 NURSING INTERVENTIONS

1. Monitor VS and signs of HYPOcalcemia

2. Initiate seizure precautions and management
3. Place a tracheostomy set. O2 tank and suction at the
bedside
4. Prepare CALCIUM gluconate
5. Provide a HIGH-calcium and LOW phosphate diet
6. Advise client to eat Vitamin D rich foods
DIABETES MELLITUS
 DIABETES MELLITUS
 This is a group of metabolic diseases
characterized by elevated levels of glucose in
the blood
 It results from defects in insulin secretion,
insulin action or both
 Major sources of glucose in the body are:
ingested food in the GIT and formation of
glucose by the liver
 Insulin is a hormone produced by the
pancreas
 Cont’
It acts by: controlling the level of glucose in
the blood by regulating the blood
production and storage of glucose
• In diabetic state the cells may stop
responding to insulin or the pancreas may
stop producing insulin entirely
• DM affects about 17 million people, 5.9 of
whom are undiagnosed
• It is usually prevalent in the elderly with up
to 50% of people older than 65 suffering
some degree of glucose intolerance
 RISK FACTORS FOR DM
• Genetic predisposition: human leukocyte antigen
(DR3, DR4 and DQ8) effect on chromosome 6
• Autoimmune mechanisms: pancreatic islet
antibodies are found in 70%-85% of patients with
newly diagnosed type 1 DM
• Obesity (>20% of desired body wt)/sedentary life
style
• Race/ethnicity (Common in African Americans,
Hispanics, Native Americans, pacific Islanders)
• Age- >45 years & HPTN
 Cont’
• Previously identified impaired fasting
glucose or impaired glucose tolerance
• HDL cholesterol level < 35mg.dl or
triglyceride level >250mg/dl
• History of gestational DM
• Viruses: mumps, coxsackie B and congenital
rubella have been implicated as prime
environmental factor in the etiology of DM.
This damages the beta cells by inducing an
immune response
 Genetic Marker
– HLA –DR4 and HLA – DR3
– 20 to 40 % more susceptible
Natural History;
• Exposure of genetically predisposed
individuals to environmental triggers
• Leads to inflammation of beta cells of the
pancreatic islets (islitis) and subsequent beta-
cell injury.
 Pre-clinical Period
• Hyperglycemia
– 80 to 90% of beta cell function must be lost
before hyperglycemia develops
 CLASSIFICATION OF DM
• Type 1 DM – previously called insulin
dependent DM
• Type 2 DM (previously NIDDM)
• Gestational DM
 CLASSIFICATION OF DM CONT’
• Maturity onset diabetes of the young
(MODY) associated with monogenic defects
in beta cell function and is characterized by
impaired insulin secretion with minimal or
no defects in insulin action. It is inherited as
an autosomal dominant pattern
• DM associated with other conditions or
syndromes
NB- Approximately 5-10% of patients have
type 1 DM while 90-95% have type 2
Hormones involved in glucose metabolism
1. Insulin and glucagon
2. Growth hormone and Adrenocorticotropic
3. Cortisol
4. Adrenaline and Noradrenaline

• Among all these hormones only insulin lowers

blood glucose, all the others raise it
• The tissues that are sensitive to insulin are; The
skeletal muscle, the liver and the adipose tissue
 Pathophysiology
• Insulin deficiency causes physiologic and metabolic
changes in the body.
• Glucose from dietary sources cannot be utilized by the
cells.
• Renal tubules have difficulty reabsorbing the glucose.
• If the blood glucose level exceeds the renal threshold
for glucose osmotic diuresis ensues (an osmotic
gradient that causes movement of body fluid from
intracellular space into the glomerular filtrate in order
to ‘dilute’ the hyper osmolar filtrate).
 Pathophysiology cont’
• Renal threshold: when serum glucose levels
approach 200mg/dl the renal tubules have
difficulty re-absorbing the glucose, glycosuria
ensues along the osmotic diversion of water
(polyuria)
• Urinary losses causes excessive thirst
(polydipsia) along with potassium depletion
• Hyperglycemia impairs leukocyte function.
 Cont’
• When the glucose is unable to enter the cell,
protein is broken down and converted to
glucose (gluconeogenesis) further
complicating the hyperglycemia
• Without the use of CHO for energy, fat and
protein stores are depleted as the body
attempts to meet its energy needs triggering
Polyphagia which enhances the problem by
elevating the glucose levels
 TYPE 1 DM
• Characterized by destruction (auto immune process)
of beta cells either by genetic, immunologic or
environmental (viral) factors
• From a genetic predisposition, people with type 1 DM
have a certain human leukocyte antigen types
( especially HLA DR3 & DR4) which is a cluster of
genes responsible for transplantation and other auto
immune processes
• Immune mediated DM commonly develops during
childhood and adolescence (juvenile onset) though it
can occur at any age
 Cont’
• When there is an abnormal auto immune
response, antibodies are directed against normal
tissues of the body, dealing with them as if these
tissues were foreign
• Destruction of beta cells results in decreased
insulin production, unchecked glucose production
in the liver and fasting hyperglycemia
• In addition glucose derived from food fails to be
stored in the liver, instead stays in the blood
stream and contributes to postprandial (after
meals) hyperglycemia
 Cont’
• If the concentration of glucose in the blood exceeds
the renal threshold for glucose(9.9-11.l mmol/L), the
kidneys may fail to reabsorb all of the filtered
glucose and this leads to glucosuria
• When excess glucose is excreted in the urine it is
accompanied by excessive loss of fluids and
electrolytes (osmotic diuresis)
• Since insulin inhibits glycogenolysis and
gluconeogenesis, pts with insulin insufficiency have
these processes unrestrained worsening
hyperglycemia. In addition fat breakdown occurs
resulting in production of ketone bodies
 TYPE 2 DM
• These occurs due to: Impaired insulin secretion
and Insulin resistance
 Insulin resistance refers to decreased tissue
sensitivity to insulin.
 Normally insulin binds to special receptors on
cell surfaces and initiates a series of reactions
involved in glucose metabolism. In this
condition these intracellular reactions are
diminished thus rendering insulin less effective
at stimulating glucose uptake by tissues and at
regulating glucose release by the liver
 Cont’
• To overcome insulin resistance and to prevent the
build up of glucose in the blood, increased
amounts of insulin are secreted to maintain
normalcy
• If beta cells fail o keep up with the increased
demand for insulin, the glucose level rises and
type 2 DM develops
• In type 2 DM there is enough insulin present to
prevent the breakdown of fats hence ketone
bodies are not present
• Uncontrolled type 2 DM leads to Hyperglycemic
hyper osmolar non ketotic syndrome
 GESTATIONAL DIABETES
• This is any degree of glucose intolerance with its
onset in pregnancy
• Hyperglycemia develops in pregnancy because of
secretion of placental hormones which causes
insulin resistance
• All pregnant women who meet the following
criteria should be screened for DM: Obese, age 25
years or older, age 25 year or younger and a
history of DM in first degree relatives
• It occurs in up to 14% of pregnant women and
increases the risk for hypertensive disorders
 CLINICAL MANIFESTATIONS OF DM
• 3 P’S: Polyuria, Polydipsia due to excess loss of fluid
associated with osmotic diuresis
• Polyphagia due to the catabolic state induced by
insulin deficiency and the breakdown of fats and
proteins
• Fatigue and weakness
• Sudden vision changes
• Tingling or numbness in hands or feet
• Skin lesions or wounds that are slow to heal
• Recurrent infections
• Sudden wt loss, nausea, vomiting In early DKA
 Clinical Manifestations
• Elevated blood glucose leads to osmotic
diuresis. (polyuria and thirst)
• Protein and fat breakdown lead to weight
loss.
• Accumulation of ketones causes a drop in
pH. (metabolic acidosis)
• Acetone is blown off giving breath a fruity
odor.
 Presenting Symptoms
• Hyperglycemia / glucose in blood stream
• Glycosuria / sugar in urine
• Polyuria / increased urine output
• Electrolyte imbalance from dehydration
• Polydipsia / attempt to relieve dehydration
• Polyphagia / attempt to compensate for lost
calories
 Assessment and diagnostic findings
1. History taking
2. Physical examination: BP, BMI, neurologic
exam etc
Lab findings
3. Fasting lipid profile
4. High fasting plasma glucose (7.0 mmol/L or
more
5. RBS of 11.1 mmol/L or more
 Criteria for the diagnosis of DM
1. Symptoms of DM plus casual plasma glucose
concentration equal or greater than 11.1
mmol/L
2. Fating plasma glucose levels greater than 7.0
mmol/L (f0r at least 8 hrs)
3. 2 hour post load glucose equal or greater than
11.1 mmol during an oral glucose tolerance
test (according to WHO requirements using a
glucose load containing the equivalent of 75g
anhydrous glucose dissolved in water)
 MANAGEMENT
• Aim: To normalize insulin activity and
blood glucose levels without
hypoglycemia and without seriously
disrupting the patient’s usual lifestyle
and activity
To reduce development of vascular
and neuropathic complications
 COMPONENTS OF DM MX
1. Nutritional mx
2. Exercise
3. Monitoring
4. Pharmacologic therapy
5. Education
 1. Nutritional management
• Nutrition, diet and weight control are the
foundation of DM management
• The aim is to control the total caloric intake, to
attain or maintain a reasonable body weight and
control blood glucose levels (Greatly helps manage
type 2 DM)
GOALS:
1. To provide all the essential food constituents
necessary for optimal nutrition
2. To meet energy needs and maintain reasonable
weight.
 Cont’
3. Prevent wide fluctuations in blood glucose
levels
4. To decrease serum lipid levels, if elevated and to
reduce the risk of macro vascular disease
Caloric requirements
 Calorie controlled diets are planned by first
calculating the individual energy needs and
caloric requirements based on the patient’s
age, gender, height and weight
 An activity element is factored in to provide the
actual number of calories required
 Cont’
 To promote a 1-2 pound weight loss per
week, 500- 1000 calories are subtracted
from the daily total and the calories
distributed into carbohydrates, proteins
and fats through a meal plan
 Currently caloric requirements are that the
patients should take 0-60% carbohydrates,
20-30% from fat and 10-20% from protein
(ADA, Evidence Based Nutrition principles
and recommendations for the treatment
and prevention of DM and related
complications, 2003)
 Cont’
• There should be moderation in carbohydrate intake
to prevent postprandial blood glucose though
counting from a variety of food choices containing
CHO rather than the diabetic food exchange list.
Measuring of servings and choices can also help to
moderate CHO intake
• Recommendations regarding fat content is to
reduce amount of saturated fats to 10% of total
calories, limiting the total intake of cholesterol to
less than 300mg/day
 Cont’
• The meal plan may include the use of some non
animal sources of protein to help reduce saturated
fat and cholesterol
• The amount of protein intake may be reduced in
patients with early signs of renal disease
• High carbohydrate high fibre diet also plays a role
in lowering total cholesterol and low density
lipoprotein cholesterol in the blood. Fibre also
improves blood glucose levels and decreases the
need for exogenous insulin
• Patients taking insulin and are alcoholics need to
be watchful for the risk of hypoglycemia
 Cont’
• Alcohol may lead to excessive weight gain (high
caloric content of alcohol), hyperlipedemia and
elevated glucose levels
• Using sweeteners is acceptable for DM patients
especially if it assists with overall dietary
adherence
• Nutritive sweeteners include fructose, sorbitol
and xylitol cause less elevation in blood sugar
levels than sucrose
• Non nutritive sweeteners have minimal or no
calories and include baked goods, non alcoholic
beverages and frozen dairy products
 2. Exercise
• This is extremely important in managing DM
because of its effects in lowering blood glucose
and reducing cardiovascular risk factors
• Exercise lowers the blood glucose level by
increasing the uptake of glucose by body muscles
and by improving insulin utilization
• It also improves circulation and muscle tone
• Resistance or strength training such as weight
lifting can increase lean muscle mass there by
increasing the resting metabolic rate
 Cont’
• These effects are useful in DM in relation
to loosing weight, easing stress and
maintaining a feeling of well being
• It also alters blood lipid levels, increasing
the levels of high density lipoproteins and
decreasing total cholesterol and triglyceride
levels
General recommendations for exercise in DM
1. Exercise at the same time, preferably when
blood glucose levels are at their peak and
the same amount each day
 Cont’
2. Regular exercise, rather than sporadic
exercise should be encouraged
3. Use proper footwear and if appropriate
other protective equipment
4. Avoid exercise in extreme heat or cold
5. Inspect feet daily after exercise
6. For patients older than 30 years and who
have two or more risk factors for heart
disease, an exercise stress test is essential
 Cont’
7. Patients participating in extended periods of
exercise should test their blood glucose,
before, during and after the exercise. They
should snack on CHO as needed to maintain
blood glucose
8. A patient with type 2 DM who is not taking
insulin or an oral agent may not need extra
food before exercise
3. Monitoring glucose levels and ketones
• Important through self monitoring of blood glucose
(SMBG)
• Candidates include those with unstable DM, those
with tendency for severe ketosis or hypoglycemia
and those with hypoglycemia without warning
signs.
• It is also important in monitoring the effectiveness if
exercise, diet and oral antidiabetic agents for those
not on insulin.
• Patients are instructed to keep a record or logbook
of blood glucose levels so that they can detect
patterns
 Cont’
• Testing is done at the peak action time of
medication to evaluate the need for dosage
adjustments.
• For basal insulin testing is done before meals
1. Glycosylated hemoglobin (HbA1c or AIC) is a blood
test that reflects the average blood glucose levels
over a period of 2-3 months
2. Urine testing for glucose- limited to patients who
cannot perform SMBG. It involves applying urine
to a reagent strip or tablet and matching colors on
a color chart
 Cont’
3. Testing for ketones
• A signal that control type 1 DM, deterioration and
increased risk for DKA.
• Most commonly patients use a dipstick (ketostix or
chemostrip uK) to determine ketonuria
• The reagent pad on the strip turns purplish when
ketones are present
• Urine ketone testing should be performed
whenever patients with type 1 DM have glucosuria
or persistently elevated blood glucose levels.
 Pharmacologic therapy
Insulin therapy and insulin preparations
• In type 1 the body loses its ability to produce
insulin therefore exogenous insulin must be
administered for life.
• In many cases insulin injections are
administered 2 or more times a day to control
the blood glucose levels.
• Adequate monitoring of blood glucose is
essential
• Depending on the course of action,
manufacturer and source there are a number
 Cont’
Time course of action
1. Rapid acting e.g. lispro for rapid reduction of
blood glucose, treat postprandial hyperglycemia
and prevent nocturnal hypoglycemia.
2. Short acting e.g. regular insulin takes 4-6 hrs
usually administered 20-30 min before a meal.
Taken alone or in combination
3. Intermediate acting e.g. Lente takes 16-20 hrs
and is taken after food.
4. Long acting e.g. Ultra lente duration 20-30 hrs
primarily for control of fasting glucose levels.
 Cont’
5. Very long acting e.g. glagine duration 24 hrs
and used for basal doses.
 Hypoglycemia
Symptoms: Lab Values:
• Rapid onset • Glucose = low, below
• Shaky feeling, hunger
60
• Headache
• Dizziness • Ketones = negative
• Vital signs • Urine output
– Shallow respirations
– Normal
– tachycardia
• Tremors
– sugar negative
– negative ketones
 Treatment of Hypoglycemia
• Simple concentrated sugars such as honey by mouth,
hard candy, sugar cubes, or glucose tablets will
elevate the blood sugar immediately. Orange juice or
sugar containing soda or fruit drink.
• Follow by complex carbohydrate such a slice of
bread, or cracker with peanut butter.
• Glucagon in a pre-mixed syringe. IM or sub-q
administration can take 15 to 20 minutes.
• Identify reason for hypoglycemia. In children it is
often increase in activity without increase in food
intake.
 Hyperglycemia
Symptoms:
Onset = gradual
Lethargic, confused, weak
Thirsty
Abdominal pain often with nausea and vomiting
Signs of dehydration
Vital signs: deep, rapid respirations, fruity
acetone breath, and weak pulses
 DKA
• Presenting symptoms may include:
– Altered level of consciousness
– Dehydration
– Electrolyte disturbances
– Dysrhythmias
– Shock
– Complete vascular collapse
 Diabetic Ketoacidosis
• Mild
• Moderate
• Severe
 Mild DKA
• Hyperglycemia and ketonuria with a preserved
ability to take in and retain oral fluids.
• Management: increased fluid intake
• Diet drinks when blood glucose > / = 240 and
supplemental insulin administration
 Moderate DKA
• Hyperglycemia, ketonuria, and acidosis (ph
between 7.25 and 7.4) associated with an
impaired ability to retain oral fluids.
• Need emergency care: IV fluids,
supplementary insulin
• Management of underlying medical condition:
infections, trauma
 Severe DKA
• Characterized by severe acidosis (ph > 7.25),
dehydration, hyperglycemia, ketosis and a
variety of other symptoms including Kussmaul
respirations, alteration in mental status, and
unconsciousness. Severe dehydration may led
to shock.
 Management of severe DKA
• 3 phases of management
• Resuscitation
• Correction of acid-base, glucose and
electrolyte abnormalities
• Transition to daily routine
 Resuscitation
• ABC’s: securing an airway, ensuring adequate
ventilation, and correcting shock with IV
volume expanders.
 Phase 2 & 3
• Correct acid-base:
– Intravenous fluids and insulin
– Administration of bicarbonate if acidosis is
severe
– Slowly bring down BGL to avoid cerebral
edema
• Restart child on regular routine with emphasis
on teaching and review of routine
 Life Management
• Management by endocrinologist
• Insulin
• Blood sugar monitoring
• Diet
• Exercise
• Screen for retinopathy: ophthalmologic exam
annually
 Long term complications of DM
• Both macro and micro vascular are seen in
both type 1 and 2 but usually do not occur the
first 5-10 years after diagnosis;
• However at diagnosis of type 2 there may be
evidence of these complications due to
undiagnosed DM for many years.
• Renal disease (micro) more prevalent in type 1
whereas CVS complications (macro ) in type 2.
 1. Macro vascular complications
• Atherosclerotic changes (blood vessel walls thicken,
sclerose, and become occluded by plaques that
adhere to blood vessel wall) occur more often and
at an earlier age in diabetic patients and are
unstable.
• Three main types include;
1. Coronary artery disease; account for 50-60% of
deaths, typical ischemic symptoms may be absent
secondary to autonomic neuropathy, may have
silent MI
2. Cerebrovascular disease due to emboli or occlusive
change in cerebral blood vessels lead to transient
ischemic attacks and stroke.
 Cont’
3. Peripheral vascular disease; due to
atherosclerotic changes in lower extremities
twice or thrice as high in diabetic pts. S & S
diminished peripheral pulses, and
intermittent claudication. Increases risk for
gangrene.
 2. Micro vascular complications
• Characterized by thickening of the capillary
basement membrane due to a series of
biochemical responses to increased blood
glucose.
• Affected areas are the kidneys and the retina
thus complications are;
1. Diabetic retinopathy has three main stages
nonproliferative, preproliferative and
proliferative. Occurs in both type 1 and 2.
2. Nephropathy; almost 50% new cases of end
stage renal disease in the US every year are
 Long term complications cont’
3. Diabetic neuropathies
4. Foot and leg problems.
Complications leading to increased foot and leg
problems are;
• Neuropathy; sensory lead to loss of pain &
pressure sensation, autonomic increased
dryness and fissuring of the skin and motor to
muscular atrophy which may cause changes in
the shape of the foot.
• Peripheral vascular disease; poor circulation lead
to poor wound healing and development of
 Neuropathic ulcers occur on pressure points in areas with
diminished sensation in diabetic polyneuropathy. Pain is absent
(and therefore
the ulcer may go unnoticed).
 Cont’
• Immunocompromise; hyperglycemia impairs
ability of specialized leucocytes to destroy
bacteria.
 instrument—a monofilament—is gently applied to about five pressure
points on the foot (as shown in image on left).
(A) This is an example of a monofilament used for advanced quantitative
assessment; (B) Sennes-Weinstein monofilament
used by clinicians; (C) disposable monofilament used by patients. The
examiner applies the monofilament to the test
area to determine if the patient feels the device. Adapted with permission
from Cameron, B. L. (2002). Making diabetes
management routine. American Journal of Nursing, 102 (2); 26–32.
 Assignment
• Find out
1. Definition, presentation and management of
HHNS (Hyperglycemic Hyperosmolar
Nonketotic Syndrome)
2. Differences between DKA and HHNS

Reference
Brunner’s and Saddarth’s Textbook of medical
surgical nursing
ADRENAL DISORDERS
 ADRENAL DISORDERS
• The adrenal medulla at the centre of the gland
secretes catecholamines (Adrenaline,
Noradrenaline) and the outer portion of the gland,
the adrenal cortex, secretes steroid hormones
(glucocorticoids like hydrocortisone, Mineral
corticoids mainly Aldosterone and sex hormones
mainly androgens)
• The adrenal medulla functions as part of the ANS
• The Adrenal cortical secretions make it possible
for the body to adapt to stress of all kinds

336
 PHEOCHROMOCYTOMA
• This is a tumor that is usually benign and originates
from the chromaffin cells of the adrenal medulla.

• In 80-90% of patients the tumor arises in the medulla

while the remaining 10-20% it occurs in extra-adrenal
chromaffin tissue in or near the aorta, ovaries, spleen or
other organs.

• It may occur at any age but its peak is at 40-50yrs

• Affects men and women equally
• 10% of the tumor is bilateral and 10% malignant

337
PHEOCHROMOCYTOMA Cont’
• It is the cause of high BP in 0.2% of pts with
new onset of HTN
• Without treatment it is usually fatal
• It may occur in the familial form as part of
multiple endocrine neoplasia type 2, hence
it should be considered a possibility in
patients with medullary thyroid carcinoma
and parathyroid hyperplasia or tumor.

338
 Clinical manifestations of
Pheochromocytoma
• Depends largely on the relative proportions of
epinephrine and norepinephrine secretion.
• Headache, diaphoresis, palpitations.
• HTN (intermittent or persistent) and other
cardiovascular disorders
• Tremors, flushing and anxiety.
• Hyperglycemia that results from conversion of liver
and muscle glucose by epinephrine secretion.
• In the paroxysmal form it is characterized by acute,
unpredictable attacks lasting seconds/hrs.

339
 Clinical manifestations of
Pheochromocytoma Cont’d
• There is extreme anxiety, tremors, vertigo, blurring of
vision, tinnitus, air hunger and dyspnoea.

• Hyperventilation, nervousness, heat intolerance.

• Polyuria, nausea, vomiting, diarrhoea.

• Abdominal pains and a feeling of impending doom.

• The BP may rise to as high as 250/150mmHg and this

may cause severe complications: cardiac
dysrhythmias, dissecting aneurism, stroke and acute
renal failure
340
 Assessment and diagnostic findings
in Pheochromocytoma
• Suspected in patients with SNS hyperactivity and
marked elevation of BP.

• These signs associated with the 5 H’S: HTN, headache,

hyperhydrosis, hyper metabolism and hyperglycemia.

• Measurements of urine for catecholamine metabolites

(metanephrines -MN and vanyllymandelic acid-VMA)
of free catecholamines is very diagnostic.

• Total plasma catecholamine concentration when the

patient is at rest for 30 minutes using a scalp vein or
venous catheter.
341
Assessment of Pheochromocytoma Cont’d

• Normal epinephrine values are 100pg/Ml (590pmol/L

while those of norepinephrine are less than 100-
550pg/mL.

• A clonidine suppression test may be done if the

results of plasma and urine tests are inconclusive.

• Clonidine is centrally acting anti adrenergic

medication that suppress the release of neurogenically
mediated catecholamines. In pts with
pheochromocytoma, clonidine is not effective after 2-3
hrs following administration. 342
Assessment of Pheochromocytoma Cont’d

• Imaging studies: CT scans, MRI, U/S done to

localize the pheochromocytoma and to determine
whether more than one tumor is present.

• Use of I-metaiodobenzylguanide (MIBG)

scintigraphy may e required to determine the
location of the tumor and to locate metastatic sites
outside the adrenal gland.

• MIBG is a specific Isotope for catecholamine

producing tissues.

343
 MANAGEMENT of Pheochromocytoma
1. Pharmacotherapy

Patient may be nursed in ICU in severe cases for

close monitoring of ECG changes and careful
administration of α-adrenergic blocking agents
like Phentolamine or Smooth muscle relaxants
like sodium nitoprusside to lower BP quickly.

Phenoxybenzamine, a long acting α-blocker

may be used when the BP is stable to prepare the
patient for surgery.
344
Pharmacotherapy Cont’d
• β-adrenergic blocking agents like propranolol may
be used in patients with cardiac dysrhythmias or those
not responsive to alpha blockers.

• Be careful about these drugs’ sensitivity.

• Catecholamine synthesis inhibitors e.g. alpha-

methyl-p-tyrosine (metyrosine) are occasionally used
when adrenergic blocking agents fail to reduce the
effects of catecholamines.
345
 Management of Pheochromocytoma
cont’d
2. Surgical management

• This is the most definitive treatment

• Bilateral or unilateral adrenalectomy may be
performed.
• Patient preparation includes control of BP and blood
volumes over a 7 – 10 day period
• Phentolamine or Phenoxybenzamine may be used
during the preparation.
• The patient needs to be well hydrated before, during
346
and after surgery to prevent hypotension.
2. Surgical management cont’d

• Care during surgery is important as excessive

manipulation during surgical excision may cause release
of more catecholamines with marked increases in BP
and change in HR.

• In this cases Na+-Nitroprusside and an α-adrenergic

agent may be required during and after surgery.

• Corticosteroid replacement is required if bilateral

adrenalectomy has been done: i.v Methyl-
predinsolone, Sodium succinate immediately and
oral prednisone after the acute stress diminishes
347
 2. Surgical management cont’d

• Hypotension and hypoglycemia may occur in the in the

post operative period because of withdrawal of excessive
amounts of catecholamines hence close monitoring is
necessary.

• One third of patients may continue to be hypertensive

even after surgery.

• Several weeks after surgery, urine and plasma levels of

catecholamines and their metabolites are measured to
determine whether the surgery was successful. 348
 Nursing Management of Pheochromocytoma

• During an episode or attack of HTN, tachycardia and

anxiety, the patient is placed on bed rest with the head
of the bed elevated to promote an orthostatic decrease
in BP.

• Monitor the patient for several days in ICU with special

attention to ECG changes, arterial pressures, fluid and
electrolyte balance and blood glucose levels.

• Several iv catheters are inserted for the administration

of fluids and medications.
349
 Nursing Management cont’d
• Giving medications as prescribed is very
paramount.

• Health education on the medication schedule

and adherence is given.

• The patient is taught how to measure BP and

when to notify the physician of any changes.

• Follow up and home care is an important aspect

350
 CUSHING’S SYNDROME
• Cushing’s syndrome results from excessive,
rather than deficient, adrenocortical activity.

• The syndrome may result from excessive

administration of corticosteroids or ACTH or
from hyperplasia of the adrenal cortex.

351
Etiology of Cushing’s Syndrome
1. Pituitary- adrenal hyperplasia due to excess of ACTH.

2. Adrenal- Hypersecretion of glucocorticoids due to

neoplasms.

3. Ectopic autonomous secretion of ACTH due to extra

pituitary neoplasms e.g. bronchogenic carcinoma.

4. Iatrogenic due to administration of large amounts of

exogenous corticosteroids.

5. Food dependant- inappropriate sensitivity of adrenal

glands to normal postprandial increases in secretion
352 of
 Clinical Manifestations of Cushing’s
Syndrome
1. Centripetal fat distribution resulting in truncal
obesity and buffalo hump due to increased appetite
and deposition of fat.

2. Rounded or moon- like face

3. Muscular wasting (thin extremities, pendulous

abdomen and weakness) due to increased protein
catabolism resulting in negative nitrogen balance.

4. Thin skin and subcutaneous tissue with poor wound

healing.
353
Buffalo hump in Cushing’s Syndrome
 Clinical Manifestations of Cushing’s
Syndrome Cont’d
5. Increased frequency of infection with decreased
inflammatory response due to production and
circulating levels of antibodies caused by lysis of fixed
plasma cells and lymphocytes.

6. Excessive bruising and petechial hemorrhages due to

capillary weakness (loss of protein).

7. Reddish purple abdominal striae and red cheeks due

to the thin skin that allows capillary blood to be seen.

8. Hypertension due to increased salt and water

retention. 355
 Clinical Manifestations of Cushing’s Syndrome
Cont’d
9. Hypokalemia and alkalosis due to increased excretion
of potassium and hydrogen ions.
10. Hypercalciuria and osteoporosis due to increased
glomerular filtration rate and excretion of calcium.
11. Retarded linear growth with delayed bone age since
increased levels of cortisol interferes with the action of
growth hormone.
12. Peptic ulcers due to increased production of HCl and
pepsin and decreased gastric mucus production
13. Hyperglycemiadue to increased gluconeogenesis
14. Hirsutism (excessive body hair), acne, and increased
male characteristics in female due to overproduction
of androgens
356
 Diagnostic evaluation in Cushing’s Syndrome

1. Increased sodium levels.

2. Fasting blood sugars for hyperglycemia.

3. Decreased serum potassium concentration.

4. 24-hour urinary levels that show elevated 17-

hydroxycorticoids and 17- ketosteroids.

5. Radiographic studies CT scan and MRI.

6. Dexamethasone (cortisone) suppression test

Dexa 1mg PO is given at 11pm and plasma levels obtained
at 8 a.m the next day. Suppression to less than 5mg/dl
357
 MANAGEMENT of Cushing’s Syndrome
• Treatment depends on cause
• Surgical intervention involves bilateral
adrenalectomy and post operative replacement of
cortical hormones
• Irradiation may be indicated incase there is a a
pituitary tumor
• Following surgery, replacement of GH, thyroid
extract, ADH, gonadotropins and steroids may be
necessary for indefinite period
• Administer adrenal enzyme inhibitors(metyrapone,
aminogluglutethimide, ketoconazole) to reduce
hyper adrenalism if the symptoms are caused by
ectopic ACTH secretion
358
Nursing considerations in Cushing’s Syndrome
• When the cushingoid features are caused by steroid
therapy, the effects may be lessened with
administration of drug early in the morning and on an
alternate basis (this maintains the normal diurnal
pattern or cortisol secretion).

• Explain the possible complications that may occur

following surgery (signs of Addison's 24 hours after
surgery).

• Decrease risk of injury and infection by providing a

protective environment, high protein diet
359
Nursing Considerations Cont’d
• Since anorexia and nausea are very common it is
important for the nurse to use nasogastric
decompression.

• Promote skin integrity and improve body image.

• Monitoring and manage complications.

• Patient support, education and follow up.

360
 ADRENOCORTICAL INSUFFICIENCY
(ADDISON’s DISEASE)
• This is rare in children and occurs when adrenal
cortex function is inadequate to meet the
patients need for cortical hormones.

• In 80-90% of cases autoimmune or idiopathic

atrophy of the adrenal gland is responsible.

361
Causes of Addison’s Disease
1. Surgical removal of both adrenal glands
2. Infections of the adrenals by tuberculosis or
histoplamosis destroying adrenal gland tissue.
3. Inadequate secretion of ACTH from the pituitary
4. Therapeutic use of corticosteroids
5. Sudden cessation of exogenous adrenocortical
hormone therapy.
6. Autoimmune/ idiopathic

362
 Clinical manifestations of Addison’s
Disease
1. Muscle weakness and Fatigue

2. Anorexia

3. Gastrointestinal symptoms

4. Emaciation

5. Dark pigmentation of the mucous membrane and the

skin esp. knuckles, knees and elbows.

363
Addison’s Symptoms Cont’d
6. Hypotension.

7. Low blood glucose

8. Low serum sodium and high serum potassium. May

be marked by sodium depletion and severe chronic
dehydration.

9. Mental status changes e.g. depression, emotional

lability, apathy and confusion in 60-80% of pts.

10. With disease progression and acute hypotension

364
addisonian crisis develops.
Addisonian crisis
A condition characterized by cyanosis and the classic
signs for circulatory shock ;
 pallor,
 apprehension,
 rapid and weak pulse,
 rapid respirations and
 low blood pressure.

In addition the pt may complain of ;

• Headache
• Nausea
• Abdominal pain and diarrhea
• May show signs of restlessness and confusion

365
Addisonian crisis cont’
Slight overexertion, exposure to cold, acute
infection or decrease in salt intake may lead to
circulatory collapse, shock and death if
untreated.

Stress of surgery or dehydration from

preparations for diagnostic tests or surgery may
precipitate an addisonian/hypotensive crisis.

366
 Assessment & diagnostic findings in
Addison’s Disease
• Lab studies in which combined early morning
serum cortisol and plasma ACTH to differentiate
primary adrenal insufficiency from secondary and
healthy persons.
• In primary plasma ACTH is increased >22.0pmol/L
and low serum cortisol <165 nmol/L
• Other lab findings; hypoglycemia, hyponatremia,
hyperkalemia and leukocytosis.
• Confirmation of the DX is by low serum levels of
adrenocortical hormones in the blood or urine and
decreased serum cortisol levels. Administration of
ACTH fails to cause normal increase in plasma
cortisol and urinary 17 hydroxycorticosteroids if
cortex is destroyed.
367
 Assessment Cont’d
• If the adrenal gland is not properly
stimulated by the pituitary a normal
response to repeated doses of exogenous
ACTH is seen. But after administration of
metyrapone which stimulates endogenous
ACTH, no response is seen.

368
 Medical management of Addison’s
• Immediate treatment is directed toward combating
circulatory shock: restoring blood circulation,
administering fluids and corticosteroids, monitoring
vital signs, and placing the patient in a recumbent
position with the legs elevated.
• Hydrocortisone is administered intravenously,
followed with 5% dextrose in normal saline.
Vasopressor amines may be required if hypotension
persists.
• Antibiotics may be administered if infection has
precipitated adrenal crisis in a patient with chronic
adrenal insufficiency

369
 Medical Management Cont’ d
• The patient is assessed closely to identify other
factors,stressors, or illnesses that led to the acute
episode.
• Oral intake may be initiated as soon as tolerated.
Gradually,intravenous fluids are decreased when oral
fluid intake is adequate to prevent hypovolemia.
• If the adrenal gland does not regain function, the
patient needs lifelong replacement of corticosteroids
and mineralocorticoids to prevent recurrence of
adrenal insufficiency.

370
 Medical Management Cont’ d
• The patient will require additional
supplementary therapy with glucocorticoids
during stressful procedures or significant
illnesses to prevent addisonian crisis.

• Additionally, the patient may need to

supplement dietary intake with added salt
during times of gastrointestinal losses of fluids
through vomiting and diarrhea.

371
NURSING MANAGEMENT OF ADDISON’S
DISEASE
 Nursing management of Addison’s Disease

1. ASSESSING THE PATIENT

• The health history and examination focus on the
presence of symptoms of fluid imbalance and on
the patient’s level of stress.
• To detect inadequate fluid volume, the nurse
monitors the blood pressure and pulse rate as the
patient moves from a lying to a standing position.
• The nurse assesses the skin color and turgor for
changes related to chronic adrenal insufficiency and
hypovolemia.
• Other key assessments include checking for weight
changes, muscle weakness, and fatigue and
investigating any illness or stress that may have
precipitated the acute crisis.
373
2. Monitoring and Managing Addisonian
Crisis
• The patient at risk is monitored for signs and
symptoms indicative of addisonian crisis. These
symptoms are often the manifestations of shock:
hypotension; rapid, weak pulse; rapid respiratory rate;
pallor; and extreme weakness.
• The patient with addisonian crisis is at risk for
circulatory collapse and shock therefore, physical and
psychological stressors must be avoided. These include
exposure to cold, overexertion, infection, and
emotional distress.
• The patient with addisonian crisis requires immediate
treatment .

374
2. Addisonian Crisis Management Cont’d
• During acute addisonian crisis, the patient must avoid
exertion; therefore, the nurse anticipates the patient’s
needs and takes measures to meet them.

• Careful monitoring of symptoms, vital signs, weight,

and fluid and electrolyte status is essential to monitor
the patient’s progress and return to a precrisis state.

• To reduce the risk of future episodes of addisonian

crisis, efforts are made to identify and reduce the factors
that may have led to the crisis.

375
3. Restoring Fluid Balance
• The nurse assesses the patient’s skin turgor,
mucous membranes, and weight while
instructing the patient to report increased
thirst, which may indicate impending fluid
imbalance.

• Lying, sitting, and standing blood pressures

also provide information about fluid status.

• A decrease in systolic pressure (20 mm Hg or

more) may indicate depletion of fluid volume,
especially if accompanied by symptoms. 376
 3. Fluid Balance Maintenance Cont’d
• The nurse encourages the patient to consume foods
and fluids that will assist in restoring and
maintaining fluid and electrolyte balance; along
with the dietitian, the nurse assists the patient to
select foods high in sodium during gastrointestinal
disturbances and very hot weather.
• The nurse instructs the patient and family to
administer hormone replacement as prescribed and
to modify the dosage during illness and other
stressful occasions.
• Written and verbal instructions are provided about
the administration of mineralocorticoid (Florinef )
or corticosteroid (prednisone) as prescribed.
377
 4. Improving Activity Tolerance
• Until the patient’s condition is stabilized, the nurse
takes precautions to avoid unnecessary activity and
stress that could precipitate another hypotensive
episode.
• Efforts are made to detect signs of infection or the
presence of other stressors. Even minor events or
stressors may be excessive in patients with adrenal
insufficiency.
• During the acute crisis, the nurse maintains a quiet,
nonstressful environment and performs all activities
(eg, bathing, turning) for the patient.
• Explaining all procedures to the patient and family
will reduce their anxiety. Explaining the rationale for
minimizing stress during the acute crisis assists the
patient to increase activity gradually. 378
 5. Promoting Home And
Community-based Care
Teaching Patients Self-Care.
• Because of the need for lifelong replacement of
adrenal cortex hormones to prevent addisonian
crises, the patient and family members receive
explicit verbal and written instructions about the
rationale for replacement therapy and proper
dosage.
• instructed about how to modify the medication
dosage and increase salt intake in times of illness,
very hot weather, and other stressful situations.
• The patient also learns how to modify diet and fluid
intake to help maintain fluid and electrolyte
balance.
379
 5. Home Based Care Cont’d
• The patient and family are frequently prescribed
preloaded,single-injection syringes of corticosteroid
for use in emergencies with Careful instructions
about how and when to use.
• instruct the patient to inform other health care
providers, such as dentists, about the use of
corticosteroids, to wear a medical alert bracelet, and
to carry information at all times about the need for
corticosteroids.
• The patient and family need to know the signs of
excessive or insufficient hormone replacement. The
development of edema or weight gain may signify too
high a dose of hormone; postural hypotension
(decrease in systolic blood pressure, lightheadedness,
380
 6. Continuing Care.
• Although most patients can return to their job and
family responsibilities soon after hospital discharge,
others cannot do so because of concurrent illnesses
or incomplete recovery from the episode of adrenal
insufficiency.
• In these circumstances, a referral for home care
enables the home care nurse to assess the patient’s
recovery, monitor hormone replacement, and
evaluate stress in the home.
• The nurse assesses the patient’s and family’s
knowledge about medication therapy and dietary
modifications.
381
 6. Continuing Care Cont’d
• A home visit also allows the nurse to assess the
patient’s plans for follow-up visits to the clinic or
physician’s office.

• The nurse reminds the patient and family about

the importance of participating in health
promotion activities and health screening.

382
THANKS AND GOD BLESS