ENDOCRINE SYSTEM

Review of Systems

1
 ENDOCRINE SYSTEM
Made of glands in many tissue and
organs in different areas of the body.
Features-secretion of hormones.
HORMONES –are natural chemicals that
exert their effect on specific tissue
known as “TARGET TISSUE”
 Exocrine glands:
–Discharge secretions
with lubricating or
digestive function
through a duct into an
epithelial surface

3
 Endocrine glands:
◆ Discharge hormones.
–Chemical substances
secreted by endocrine
glands directly into the
blood stream to act on
specific target cell.
–So they are called
“ductless” glands
4
 Endocrine glands
1. Pituitary gland
2. Adrenal glands
3.Thyroid gland
4. Islet cells of pancreas
5. Parathyroid glands
6.Gonads

5
Common Features of Hormones
1.All hormones exert their effects at low
blood concentration.
2. Receptors on or within target tissues
are needed for all hormones to exert
an effect.
3. Most hormones are not stored to any
great extent and must be produced
when needed.(except for thyroid and
adrenal medullary hormones)
6
4. Hormones in the blood are bound to
Plasma protein.
5. Only free hormones can bind to their
receptor sites.
6. Most hormones causes target tissue to
increase or decrease their activity.
7. The activity of most hormones is short
duration.
8. Continued hormone activity requires
continued production and secretion.
7
◆ Regulate:

–Growth and development

–Electrolytes and fluids
–Reproduction
–Metabolism
–Stress adaptation

8
◆ Types are:
1. Protein peptides
◆ Insulin
◆ ADH
◆ GH
◆ ACTH
2. Amine & amino acid derivatives
◆ epinephrine
◆ norepinephrine
3. Steroids
◆ Cortisol
◆ Estrogen
◆ Testosterone

9
◆ May or may be controlled
directly or indirectly by
feedback mechanisms:
– Negative
– Positive

10
Negative Feedback Mechanism
When body condition starts to move
away from normal range and a
specific response or action is needed
to correct this change , hormones
secretion capable of correcting action
or response is stimulated until the
demand is meet. Then if needs are
meet hormone secretion is decrease or
halt. This is now the negative feedback
11
12
◆ Some non-endocrine organs
has special endocrine cells:
1.Kidneys
– Renin

2.GI Tract
– gastrin

13
14
GLANDS RELATED TO
ENDOCRINE SYSTEM

15
 PITUITARY GLAND
◆ A small pea-
shaped gland
◆ Connected to the
hypothalamus

◆ 2 lobes – anterior
and posterior
16
Hypothalamus TRH TRF ACTHRF LHRH

APG GH Prolactin TSH ACTH FSH LH

Target All Breast Thyroid Adrenal Reproductive

Tissues Gland Cortex Organs
17
 Anterior
◆ Secretes 6 hormones
1. GH promotes tissue growth
◆ Helps metabolize fats
◆ Promotes protein synthesis.
◆ Enhances fat metabolism of
energy

18
19
2.Prolactin –
stimulates milk
secretion by the
breasts
(prepared by
estrogen &
progesterone)

20
3. TSH – stimulates
thyroid gland to
synthesize and
secrete thyroid
hormones

21
4. ACTH – stimulates
the adrenal cortex
to manufacture and
secrete
adrenocorticol
hormones.
◆ Controls
carbohydrates
metabolism.

22
5. FSH and LH – gonadotropic
hormones
◆ Growth and development of
the gonads
◆ Development of secondary
sex characteristics.
◆ LHRH – regulates the 2; from
the hypothalamus

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24
 Posterior
1. Oxytocin
– Contraction of uterus
– Stimulates milk ejection
2. Antidiuretic hormone (ADH,
vasopressin)
– Promotes water retention

25
 THYROID GLAND
◆ 2 lateral
lobes
◆ Fixed to the
anterior
surface of the
upper trachea

26
◆ T3 – Overall body
metabolism
◆ T4 - Overall body heat
production
◆ Thyrocalcitonin – PTH
regulator

27
◆ Other effects of T3 and T4

◆ Normal growth and

development
◆ Maturation of nervous
system

28
 PARATHYROID GLANDS
◆ 4 small structures embedded in
the surface of the thyroid gland
◆ Secrete parathyroid hormone –
principal regulator of calcium
metabolism
◆ Together with Vitamin D – raise
blood calcium level
◆ Thyrocalcitonin – lowers blood
calcium level

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30
 ADRENAL GLANDS
◆ Located on top of the
kidneys

◆ Consistsof an outer cortex

and an inner medulla

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32
 Adrenal cortex
◆ Secretes 3 hormones:
1. Glucocorticoids – cortisol
(major), corticosterone and
cortisone, which acts by:
◆ Raising the blood glucose
through gluconeogenesis
◆ Promoting protein breakdown
into amino acids ! converted
into liver as glucose

33
2. Mineralocorticoid
◆ The major aldosterone
◆ Promotes sodium absorption
and potassium excretion.
3. Sex hormones
◆ Progesterone, estrogen and
testosterone
◆ Small amounts of androgen
appears ! sex drive for
women

34
 Adrenal Medulla
◆ Produces catecholamines
– Norepinephrine - 60%
– Epinephrine - 30%
– Others - 10%

◆ Emotional stress activates

CNS ! release by A.
Medulla
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36
37
38
◆ Liberated catecholamines ! “Fight
or Flight”

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40
41
 ISLETS OF LANGERHANS
◆ Islets are about 1 million cell
clusters throughout the pancreas.
◆ Classified with cells:
1. Alpha
◆ 20% of islet cells
◆ Produces glucagon – raises
blood glucose level by
promoting the conversion of
liver glycogen into glucose

42
2.Beta
◆ 70% of islet cells
◆ Secretes insulin which
lowers blood glucose
level

43
 C

C
G
C
G

44
3.Delta
◆ 10% of islet cells
◆ Secretes somatostatin

45
 NCM 105

DISORDERS OF THE PITUITARY

GLAND

Prepared by:
ROWENA R. TOSOC, RN, MAN, Ph.D
Associate Professor II

46
 Hyperpituitarism
Etiology: due to overactivity of gland or
from adenoma. Characterized by an
excessive concentration of pituitary
hormone (GH,ACTH, PRL) in the
blood, overactivity and changes in
the anterior lobe of the pituitary
gland

47
 Adenoma gets larger they compresses
the brain tissue, causing neurologic
symptoms and endocrine symptoms
like visual changes, headache and
increased ICP.
PRL secreting hormone inhibits the
secretion of gonadotropin and sex
hormone in men and women
resulting in galactorrhea, (production
of breast milk)amenorrhea and
infertility
48
 Two Classification of GH
overproduction
1.Giantism-generalized increase in
size, especially in children, involves
the long bone.(occur before puberty)
2. Acromegaly- occurs after epiphyseal
closing with subsequent enlargement
of cartilage bone and soft tissue of
the body. (occur after puberty)

49
50
Onset is gradual and slow in
progression, changes in the soft
tissue of the face, hands and feet ,
there is rapid proportional growth in
the length of all bones. In
Acromegaly excessive GH causes
increased skeletal thickness,
hypertrophy of the skin and
enlargement of many visceral organs
like the liver and the heart.

51
 Clinical Findings
1.Increased soft tissue & bone
thickness
2. Facial features become coarse and
heavy, with enlargement of lower
jaw, lips and tongue
3. Enlarge hands and feet.
4. Increased GH, corticotrophic
hormone(ACTH) or prolactin (PRL)
52
5. Amenorrhea
6. Signs of increase ICP like vomiting,
papilledema, focal neurologic deficit.
7. DM and hyperthyroidism may occur
8. Arthralgia (bone pain)
9. X-ray of long bones and jaw will
demonstrates changes in the
structure.(Prognathism-projection of
the jaw)

53
 Diagnostic Test
◆ Level of hormone in the blood
◆ Skull X-ray –to determine the size of
the pituitary gland
◆ Computed Tomography
◆ MRI- to determine a masds

54
 Intervention
Medication :
1. Somatostatin-reduce plasma GH
2. Dopamine agonist bromocriptine
mesylate (Parlodel) Cabergoline
(Dostinex)-lower growth hormone
This drug stimulates dopamine
receptors in the brain & inhibit
release of the many pituitary
hormone
55
3. Radiation therapy-4-6 weeks
4. Surgical Intervention –removal of
pituitary gland and tumor
HYPOPHYSECTOMY
Pre-op Care
1. Explain that decrease hormone will
relieve headache and reverse sexual
function.
2. Nasal packing for 2-3 days, teach to
breath through the mouth
56
3. Instruct not to brush teeth, cough,
sneeze, blow nose or bend forward
after surgery.
Post-op care
1. Monitor client’s neurologic response,
changes in vision, mental status,
altered level of consciousness or
decreased strength of extremities
2. Monitor intake and output and daily
weight of client.
3. Assess nasal drip for leakage of CSF
57
4. Encourage client to do pulmonary
hygiene by doing deep breathing
exercises
5. Instruct client to avoid bending,
sneezing and blowing of nose.
6. Monitor bowel movement to prevent
constipation.
7. Teach client the use of life long
hormonal replacement.

58
 General Nursing care
1. Help client accept the altered body
image is irreversible.
2. Assist the family to understand what
the client is experiencing.
3. Help client understand the basis for
the change in sexual functioning.
4. Help client recognize that medical
supervision will be required for life.
59
5. Protect from stress situation
6. Protect from infection
7. Follow and maintain an established
schedule for hormone replacement.
8. Care of client who undergone
intracranial surgery
a. Perform neurologic assessment
b. Measure specific gravity of urine ,
monitor I&O
c. Check daily weight to identify
complication of DM insipidus
60
d. Check clear nasal drainage for
glucose to determine presence of
CSF.
e. Encourage deep breathing but not
coughing.
f. Institute measure to prevent
constipation because straining will
increase ICP.

61
 Complication
◆ Increased ICP
◆ Compression of optic chiasma-visual
loss
◆ After Surgery CSF leak, meningitis,
neurologic deficit
◆ Pituitary apoplexy syndrome there is
sudden enlargement of tumor causing
hemorrhagic necrosis there is vascular
damage
62
 Hypopituitarism
Deficiency of one or more anterior
pituitary hormone. Total absence of
pituitary hormones referred to as
panhypopituitarism (Simmonds’
disease)
Occurs when there is destruction of the
anterior lobe of the gland by trauma,
tumor or hemorrhage.

63
 Pathophysiology
◆ Deficiencies of ACTH and TSH- life
threatening because of decrease
secretion of vital hormones from
adrenal and thyroid gland
◆ Deficiency of the gonadotropin LH and
FSH causes problem in sexual function
◆ GH deficiency has little effect on tissue
and cells

64
65
 Clinical Findings
Subjective: lethargy, loss of strength
and libido, decreased tolerance for
cold.
Objective
1.Decreased temperature
2. Postural hypotension
3. Hypoglycemia
4. Decreased level of GH,ACTH, FSH
and LH. 66
5. Sterility, infertility, dyspareunia, loss
of secondary sexual characteristics
6. Visual disturbance if tumor impinges
on optic nerve like diplopia (double
vision), ocular muscle paralysis

67
68
 Intervention
Hormone replacement, like androgen for
men
For women a combination of estrogen
and progesterone
For those who want to be pregnant
Clomiphene (Clomid)citrate may be
given
Surgical intervention if tumor is present.

69
 DISORDER OF THE
POSTERIOR PITUITARY GLAND
Diabetes Insipidus
- is a water metabolism problem
caused by an ADH deficiency( either
a decrease in ADH synthesis or
inability of the kidney to respond to
ADH)

70
 Pathophysiology
ADH deficiency result in excretion of
large volume of diluted urine. In the
absent of ADH, distal kidney tubules
and collecting duct remains
impermeable to water. Water is
excreted as urine= POLYURIA.
Then dehydration increases plasma
osmolarity that will stimulates the
osmoreceptors to relay sensation of
thirst to cerebral cortex. 71
Thirst promote increased fluid intake to
maintain water homeostasis. If thirst
mechanism is poor or absent
dehydration become severe since
person is unable to obtain water.

72
Classification of ADH Deficiency
1. Nephrogenic diabetes insipidus- it is
an inherited disorder. The renal
tubules does not respond to action of
ADH, the actual hormone produced is
not deficient.
2. Primary diabetes insipidus- caused by
a defect in the hypothalamus or
pituitary gland, resulting in lack of
ADH production or release. Secondary
is caused by tumor adjacent to
hypothalamus 73
3. Drug related diabetes insipidus- is
caused by lithium carbonate and
demeclocycline. This drug interferes
with the response of the kidneys to
ADH.

74
 Clinical Manifestation
Hypotension
Decreased pulse pressure
Tachycardia
Weak peripheral pulses
Hemoconcentration
increased hemoglobin,hematocrit and
increase BUN

75
Increased urine output
Diluted, low specific gravity urine.
Hypo-osmolar
Poor skin turgor
Dry mucous membrane
Increased thirst sensation
Irritability
Hyperthermia
Decreased cognition
Ataxia
76
 Laboratory test
24 hour urine collection
Dehydration test
deprived client of fluid and observe
client for adherence to fluid restriction,
then measure urine output, specific
gravity and osmolarity hourly. Give 5
units of aqueous vasopressin and
continue hourly urine measurement

77
Hypertonic Saline test-used to
stimulate release of ADH
administer normal water load to the
client, followed by infusion of
hypertonic saline. Then measure
urine output hourly.

78
 Medical Management
Partial ADH deficit- oral chlorpropamide
(Diabinese , Novo-Propamide) This
drug increases the acting of existing
ADH
Severe ADH deficiency- Desmopressin
acetate-this drug is a synthetic
vasopressin given intranasally. In
severe dehydration IM /IV given

79
 Nursing management
Early detection of dehydration and
maintaining adequate hydration
a. Accurate I&O monitoring

b. Check urine specific gravity

c. Weight client daily

d. Urge client to drink fluid equal to

urine output
e. Ensure IV fluid patency and
regulation 80
2. Teach client that life long vasopressin
therapy
a. Teach client that polyuria and polydipsia
are signal for another dose of vasopressin
b. B. Wear a medical alert bracelet

3. Facilitate learning
a. Instruct client to blow nose gently prior
to administration of nasal medication
unless contraindicated.
b. Instruct client to remain upright and not
to tilt head backward.....

81
d. Insert nozzle into nostril and
squeeze bottle quickly and firmly
when nasal spray is administered
e. Instruct client not to blow nose for
several minutes after administration
f. Monitor client to determine response
to medication
g. Weight in the same weighing scale
with the same weight of clothing
82
 Nursing Intervention
1. Monitor effect of hormone therapy.
2. Discuss the importance of adhering
to medical regimen on a long term
basis.
3. Allow client to verbalize feeling.
4. Provide adequate rest.

83
 SIADH
SIADH or syndrome of inappropriate
antidiuretic hormone-occurs when
vasopressin(ADH) is secreted even
when plasma osmolarity is low or
normal
Also known as SCHWARTZ-BARTTER
SYNDROME

84
 Pathophysiology
SIADH total body water increases
because water is retained because ADH
do not function properly
Hypoosmolar state result due to
hyponatremia(decrease serum sodium)
Expansion of the extracellular fluid
volume, this increases the plasma
volume causes increase in glomerular
filtration rate.
85
There will be inhibition in the release of
renin and aldosterone that will further
cause hyponatremia due to
loss of urine.
The hyponatremia causes
hypoosmolarity and thus creates an
osmolar gradient across the blood
brain barrier, that will cause the
movement of water in the brain and
other cell causing cellular
overhydration.
86
 Clinical Manifestation
Loss of appetite, nausea & vomiting
Increased weight, absence of edema
Lethargy, headache, hostility
Disorientation and changes in the level
of consciousness
Tachycardia and hypothermia
Seizure and coma occur if serum
sodium falls below 110 to 115mEq/L
87
 Goal of Intervention
1. Restrict fluid intake.
2. Promoting the excretion of water
3. Replacement of loss sodium
4.Interfering the action of ADH
5. Preventing injury

88
 Medical Intervention
◆ Fluid Restriction- 500ml-600ml/24hr.
◆ Sodium restriction
◆ Drug therapy, includes diuretic,
Lithium carbonate and
demeclocycline
◆ Provide safe environment

89
 Nursing Care
1. Limit fluid intake at 500ml-600ml/24
hr.
2. Dilute tube feeding with solution
other than plain water
3. 3. Use saline to irrigate GI tubes
4. Mix drugs to be given by GI tube
with saline.
5. Measure I&O,weight
90
 6. Keep mucous membrane moist.
7. Monitor sodium loss
8. Give saline cautiously
9. If need IV fluid saline is used rather
than water.
10. Observe for changes in the client’s
neurologic status
11. Check orientation to 3 spheres.
12. Reduce environmental noise and
lighting to prevent overstimulation.
13. Provide a safe environment.
91
 Hyperthyroidism/Graves’
Disease(thyrotoxicosis)
Excessive concentration of thyroid
hormones in the blood as a result of
thyroid disease or increase TSH that
leads to hypermetabolic state.
Etiology : Autoimmune process of
impaired regulation secondary to other
autoimmune disorders.
The gland may also enlarge(goiter) as
result of decreased iodine intake.
92
 Etiology

1.Autoimmune disorder
2.Graves disease a toxic diffuse goiter
3. Hyperthyroidism cause by multiple
thyroid nodules.
4. Hyperthyroidism cause by thyroid
replacement hormone

93
 Clinical Findings
Subjective: polyphagia, emotional
lability, apprehension ,heat
intolerance.
Objective:
1. Weight loss, loose stool, tremors,
hyperactive reflexes, diaphoresis,
insomnia, exophthalmos, corneal
ulceration, increase systolic BP,
temperature, pulse and RR.
94
2. Decreased TSH level if thyroid
disorder increased TSH levels if
secondary to pituitary disorder.
3. Increased T3, T4, protein bound
iodine, and radioactive iodine uptake.
4. Thyrotoxic crisis (thyroid storm) –a
state of hyper metabolism that may
lead to heart failure, usually
precipitated by period of severe
physiologic or psychological stress,
surgery or radio iodine therapy
95
 Other Features
◆ 1. Diaphoresis, heat intolerance
◆ 2Fine, soft, silky hair (body)
◆ 3.Smooth,warm, moist skin
◆ 4.Thinning of scalp hair
◆ 5. Shortness of breath,rapid shallow
respiration and decreased vital
capacity.
◆ 6. Palpitation
96
◆ 7. Chest pain
◆ 8. Increased systolic BP
◆ 9. Widened pulse pressure
◆ 10. Tachycardia, dysrhythmias
◆ 11. Weight loss
◆ 12. increased appetite, increased
stool
◆ 13. Hypoproteinemia
◆ 14. muscle weakness & wasting
◆ 15. Increased metabolic rate
97
◆ 16. Heat intolerance, low grade fever
◆ 17. fatigue
◆ 18. Decreased attention span
◆ 19. Restlessness, irritability
◆ 20. Emotional lability
◆ 21. Manic behavior
◆ 22. Blurred or double vision
◆ 23.Increased tears, photophobia
◆ 24.Tremors, insomnia
◆ 24. Corneal infection, eye lid
retraction 98
 Pathophysiology
◆ Hyperthyroidism due to excessive
thyroid secretion affects metabolism
in all body organs.
◆ The normal feedback control over
thyroid hormone secretion fails,
causing hypermetabolism and
increased sympathetic nervous
system activity

99
 Cont.
◆ Thyroid hormone stimulate the heart
-increased heart stroke volume
=increase CO and blood flow.
◆ Thyroid hormone level affect protein,
lipid and carbohydrate metabolism
Protein synthesis (build up) and
degradation (breakdown) are
increased. Breakdown exceeds build
up= loss of protein (Negative
Nitrogen Balance)
100
◆ Glucose tolerance decreased=
hyperglycemia. Fat metabolism
increased so decreased body fat.
◆ Oversecretion of thyroid hormones
changes the secretion of hormones
from hypothalamus and anterior
pituitary gland. It also influence sex
hormone production.

101
 Diagnostic procedure
◆ Laboratory T3 and T4 level, TSH
level, antibodies to TSH
◆ Thyroid Scan to evaluate position
size and function
◆ Ultrasound of the thyroid gland
◆ 12 leads ECG

102
 Medical Intervention
◆ Nonsurgical
a. Drug therapy-antithyroid
thioamides like PTU(propylthiouracil,
Methimazole (Tapazole)
Iodine preparations
Lithium carbonated.
Beta-adrenergic blocking drugs like
propanolol
103
. Radioactive Iodine therapy
Surgical management
a. Total thyroidectomy-removal of all
thyroid tissue.
b. Subtotal thyroidectomy- removal of
part of the thyroid tissue

104
 Nursing Intervention
1.Use measure such as decreased
stimulation, medications and back
rub or provide uninterrupted rest.
2. Protect client from stress producing
situations.
3. Keep room cool.
4. Provide diet high in calories,
proteins and carbohydrates with
supplemental feeding between meal
and at bedtime 105
5. Discuss disease process involved like
patient’s lability of mood and
exaggerated response to environment.
6. Provide eye patches when needed.
7. Care of client prior to surgery:
a. Administer antithyroid medication to
achieve euthyroid state .
b. . Teach deep breathing exercises and
use of hands to support neck and to
avoid strain on suture line.

106
 Post Op Thyroidectomy Care
1. Observe for signs of respiratory
distress and laryngeal stridor caused
by tracheal edema (keep
tracheotomy set available)
2. Provide humidity with cold steam
nebulizer to keep secretion moist.
3. Keep bed in semi-Fowler’s position.
4. Observe for signs of thyroid storm ,
like high fever, tachycardia etc.
107
4. Notify physician immediately for
signs of thyroid storm, administer
Propanolol, iodides, PTU and steroid
as order.
5. Observe for sign of tetany such as
numbness or twitching of extremities,
spasm of glottis, hypocalcemia (this
can occur after accidental trauma or
removal of the parathyroid gland) If
tetany occur give Calcium gluconate
or calcium chloride
108
6. Assess for hoarseness of voice , this
may result from ET intubation or
laryngeal damage.
7. Teach client for sign and symptoms
of:
Hypothyroidism as a result of
treatment.
Hyperthyroidism as a result of
thyroid storm or over medication
8. Teach client importance of taking
antithyroid medication regularly
109
Use of sandbag to support the head or
neck.
When awake place client in semi-
Fowler’s position.
Decreased tension on suture lines,
avoid neck distention

110
 Complication after surgery
◆ Hemorrhage- Inspect the neck
dressing and behind client’s neck
◆ Respiratory distress may be due to
swelling or tetany, have an
emergency and suction apparatus
◆ Hypocalcemia and Tetany due to
decrease parathyroid hormone-give
calcium gluconate or chloride IV.

111
◆ Laryngeal Nerve damage-assess
client for hoarseness and weak voice
◆ Thyroid Storm or thyroid crisis- key
manifestation are fever, tachycardia
and systolic hypertension, Anxiety
and has tremor, restless, seizures and
then coma.

112
 Hypothyroidism
Absence or decreased production of
thyroid hormone because of primary
thyroid disease. A response to
decreased TSH or effect of thyroid
surgery or radioactive iodine
treatment; most common cause is
Hashimoto’s thyroiditis an
autoimmune disorder.

113
 Classification
1. Cretinism-hypothyroidism in infants
and young children.
2. Lymphocytic thyroiditis- frequently
appears after 6 years of age and
peaks during adolescence, generally
self limiting.
3. Hypothyroidism without Myxedema-
mild degree of thyroid failure in older
children and adults.
114
◆ 4. Hypothyroidism with Myxedema-
severe degree of thyroid failure in older
individuals
Decreased thyroid level may interfere with
erythrophesis and lipid metabolism.
◆ Myxedema Coma is the most severe
degree of hypothyroidism a fatal
endocrine emergency precipitated by a
severe physiologic stress, symptoms
include hypothermia, bradycardia,
hypoventilation and progressive loss of
consciousness.
115
 Pathophysiology
◆ When the production of thyroid
hormones are too low or absent , the
blood level of TH are very low or absent
decrease so metabolism is decreased,
this causes the hypothalamus and the
anterior pituitary gland to stimulate
hormones TSH as a compensation.
◆ The TSH binds to thyroid cells and
causes thyroid gland to enlarge
116
◆ Decreased metabolism causes a
decreased cellular energy and
metabolites build up. The build up of
compounds of protein and sugar
(Glycosaminoglycans) increases the
mucous and water forms edema and
changes organ texture. The edema is
non pitting, changing the appearance
of the client. The edema is forms
everywhere, especially around the
eyes, in hands and feet and shoulder
blades
117
 Clinical Findings
Subjective: dull mental processes
apathy, lethargy, loss of libido,
intolerance to cold.
Objective:
Lack of facial expression, increase in
weight, constipation, subnormal
temperature & pulse, dry, brittle hairs
& nails, pale, dry coarse skin, enlarged
tongue, thinning of lateral eyebrows,
118
 scalp, axilla and pubic hair loss,
diminished hearing and periorbital
edema.
2. Decreased basal metabolism
Decreased T4 (triiodothyronine) and
radioactive iodine uptake delayed or
poor response to TSH stimulating test
in secondary hypothyroidism.
Increased TSH in primary.

119
 Laboratory Assessment

◆ T3 and T4 level
◆ TSH blood level
◆ 12 leads ECG

120
 Medical Management
Administer thyroid hormone- synthetic
hormone Levothyroxine sodium-
therapy is started with low doses and
gradually increased over a period of
two weeks
Monitor for chest pain
Maintain vital function

121
 Nursing Care
1. Increased cardiac output
a. Monitor BP, heart rate, rhythm

b. Observe for signs of shock like

decreased urine output, changes in
mental status
c. Assess for chest pain

2. Maintain respiratory function

a. Observe and record rate and depth
of respiration
122
3. Explain the importance of hormone
therapy throughout life.
4. Explain that increased sensitivity to
narcotics, analgesic and tranquilizer
necessitates dosage adjustment.
5. Avoid giving IM & subq injection
during hypothermic state.
6. Additional protection from cold and
modification of outdoor activity in cold
weather.
7. Increase fluid and roughage in the
diet. 123
 cont

8. Apply moisturizer to the skin and

skin care should be done.
9. Teach the need to restrict calories,
cholesterol and fats in the diet.

124
 Complication
◆ Myxedema coma
◆ Hypotension
◆ Hyponatremia
◆ Hypothermia
◆ Hypoglycemia

125
 Hyperparathyroidism
Hyperfunction of the parathyroid glands,
usually cause by adenoma,
hyperthrophy and hyperplasia of the
glands.
As a result the absorption of calcium
and excretion of phosphorus by the
kidney
If dietary intake is not enough to meet
calcium need by high level of
parathormone, demineralization of
bones occur. 126
 Pathophysiology
◆ The parathyroid glands maintain
calcium and phosphate balance.
◆ Increased level of PTH act directly on
the kidney causing HYPERCALCEMIA
kidney reabsorption of calcium and
increased phosphate excretion .
◆ In the bone excessive PTH level
increase bone resorption(bone lost of
Calcium)
127
◆PTH level increase bone resorption by
decreasing osteoblastic decreasing
bone production activity and
increasing bone destruction This
process release calcium and
phosphate in to the blood and
reduce bone density.
With chronic calcium excess
calcium is deposited in the soft tissue

128
 Clinical Findings
Subjective: apathy, fatigue, muscular
weakness, anorexia, emotional
irritability, deep bone pain.
Objective: Bone pathologic fracture
Renal calculi composed of calcium,
polyuria
Vomiting, constipation
Elevated serum calcium level and
parathormone, decreased serum
phosphorus, cardiac arrhythmias 129
 Management
Surgical excision of a parathyroid
tumor
Calcium intake restriction
Administer Furosemide to increase
renal excretion of calcium.
Administer gallium nitrate, calcitonin or
plicamycin with glucocorticoid to
lower calcium level.
130
 Nursing care
1. Strain the urine to detect for calculi.
2. Encourage fluid intake
3. Assist in ambulating to help prevent
demineralization .
4. Avoid high impact activities.
5. Encourage high fiber diet
6. Instruct to limit intake of foods rich
in calcium
131
 Hypoparathyroidism
Parathyroid glands may not secrete
sufficient amount of parathormone
after thyroid surgery, parathyroid
surgery or radiation therapy.
As the level of parathormone drops the
serum calcium also drop, causing
signs of tetany and a rise of serum
phosphate occur.

132
 Clinical Findings
Subjective: Photophobia, muscle
cramps, irritability, tingling of
extremities.
Objective:
Trousseau’s sign (carpopedal spasm)
Chvostek’s sign (contraction of facial
muscle in response to tapping near
the angle of the jaw)
133
Decreased serum calcium and
parathormone , elevated serum
phosphate.
Stridor, wheezing from laryngeal
spasm, tremors and convulsion.
X-ray show increased bone density
cardiac arrthymias, alkalosis

134
 Management
1.Calcium chloride or calcium
gluconate given IV in emergency for
tetany.
2.Calcium salts orally.
3. Vitamin D to increase absorption of
calcium from GI tract.
4. Parathormone injection
5. High calcium low phosphate diet.
6. Aluminum hydroxide to decrease
absorption of phosphorus in GIT 135
 Nursing care
1. Observe for respiratory distress and E
cart available for tracheostomy and
mechanical ventilation.
2. Observe seizure precaution.
3. Reduce environmental stimuli
4. Provide drug and dietary instruction
including avoidance of milk, cheese,
egg yolk
5. Teach symptoms of hypocalcemia,
hypercalcemia. 136
Cushing Syndrome/Hypercortisolism
Re s u l t f r o m e x c e s s s e c r e t i o n o f
adrenocortical hormones, caused by
hyperplasia or by tumor of the adrenal
cortex, however the primary lesion
may occur in the pituitary gland
causing excess production of ACTH.
Administration of excess glucocorticoid
or ACTH.

137
 Pathophysiology
Excessive stimulation of ACTH either
pituitary or ectopic in origin causes
hyperplasia which result in the loss
of normal hormone secretion, causing
decrease in the release of PRL,
thyrotropin and gonadotropin.
There is also alteration in nitrogen,
carbohydrate and mineral metabolism
which result in increase body fat
138
And there is redistribution of fat
produces the typical truncal obesity
(buffalo hump) and moon face
Increase in the breakdown of tissue
protein and increase urine nitrogen
excretion causes decreased muscle
mass, atrophic(thin) skin and bone
density loss.
High level of glucocorticoid causes
abnormal sleep pattern

139
High level of corticoid kill lymphocytes
and shrink organ containing
lymphocytes like liver and spleen.
Increase androgen production causes
hirsutism, acne, it also interrupt the
normal hormone feedback
mechanism for the ovary decreasing
production of estrogen and
progesterone resulting in
OLIGOMENORRHEA(scant or
infrequent menstruation)
140
 Clinical Findings
Subjective: weakness, decreased
libido, mood swing or psychosis.
Objective:
Obese trunk thin arms and legs, moon
face, buffalo hump, acne, hirsutism
ecchymotic areas, purple striae on
breast and abdomen, amenorrhea,
increased susceptibility to infection

141
Cushing’s Syndrome
 Cont
Hypertension
Hyperglycemia, hypokalemia, elevated
plasma cortisol level.
Elevated 17-hydroxycorticosteroids and
17-ketosteroids in urine
Osteoporosis evident in X-ray

143
 Goal of treatment
◆ 1. Reduction of plasma cortisol level
◆ 2. Removal of tumor
◆ 3.Prevention of complication
◆ 4.Restoration of normal or acceptable
body appearance

144
 Management
Reduce dosage of externally administer
corticoids
Irradiation of the pituitary if caused by
hypersecretion of ACTH
Surgical intervention of adrenal tumor
Adrenal enzyme inhibitor (Trilostane)
Potassium supplements
High protein diet with sodium
restriction.
145
 Nursing Care
1. Monitor v/s, daily weight, intake and
output blood glucose and
electrolytes.
2. Protect from infection exposure.
3. Minimize stress
4. Instruct on diet and supplement
5. Encourage ventilation of feeling
regarding sexual life.
146
 Pre & post Operative Nsg Care
Adrenalectomy –removal of the gland
Pre-op care
1. Monitor electrolytes imbalance and
correct it
2. Control hyperglycemia

3. Prevent infection

4. Promote safety since patient is prone

to fracture
147
Administered glucocorticoid pre and
throughout the procedure to prevent
adrenal crisis.
Post op care
1. Monitor for signs of cardiovascular
collapse like shock, decrease urine
output.
2. Hemodynamic monitoring

3. Measure I &O

4. Monitor weigh, serum electrolyte level

148
 Primary Aldosteronismm
(Conn’s Syndrome)
Etiology
Aldosterone a mineralocorticoid secreted
in response to the renin-angiotensin
system and ACTH causes the kidney to
retain sodium and excrete potassium
and hydrogen.
Caused by an adenoma of the adrenal
cortex, may also be cause by
hyperplasia or carcinoma.
149
 Pathophysiology
Increased aldosterone affect the renal
tubules causing sodium retention with
potassium & hydrogen ion excretion
Hypernatremia, hypokalemia &
metabolic alkalosis result. Retention of
sodium causes the blood & intertistial
fluid volume to increase which
elevates BP & suppresses renin
production.
150
Elevated Bp may cause renal damage.
Peripheral edema may occur because
of renal escape mechanism in which
the proximal tubules decreases
sodium reabsorption.

151
 Intervention

Surgical removal of the tumor

Temporary management with
spironolactone.
Bilateral adrenalectomy
Life long corticosteroid.

152
 Nursing management
1. Regulate fluid intake
2. Encourage continous medical
supervision.
3. Care of client after bilateral
adrenalectomy:
Monitor v/s, hemodynamics, and blood
glucose level.
Administer steroid with milk or antacid.
153
 Protect client from infection and
stressful situation.
Explain drug and side effect to
client.
Instruct to carry medic alert ID or
bracelet.
4. Provide dietary instruction ;
encourage intake of food high in
potassium and avoidance of food that
contain sodium.

154
 Addison’s disease
Etiology and patho
Hyposecretion of adrenocortical hormones.
Caused by autoimmune destruction of the
cortex or by idiopathic atrophy.
Addisonian crisis (acute adrenal
insufficiency) can be precipitated by
stress such as pregnancy, surgery,
infection, dehydration, emotional
turmoil.
155
 Clinical Findings
Subjective : weakness, fatigue,
anorexia and nausea
Objective: Increased bronze
pigmentation of the skin, vomiting
and diarrhea, hypotension, decreased
serum cortisol, increased plasma
ACTH, hyponatremia, hypoglycemia,
hyperkalemia

156
 Intervention
1.Replacement of hormones:
glucocorticoids to correct metabolic
imbalance and mineralocorticoids to
correct electrolytes imbalance and
hypotension.
2.Correction of fluid, electrolytes,and
glucose imbalances
3. High-carbohydrates, high-protein diet

157
 Nursing Management
1.Monitor v/s, be alert for elevation in
temp(dehydration & infection) pulse
rate and rhythm(hyperkalemia) and
alteration of BP.
2. Observe for signs of sodium and
potassium imbalance
3. Monitor weight daily and I & O
4. Administer steroids as ordered
158
 Cont.
5. Place client in a private room or isolation
room
6. Limit the number of visitor
7. Advise client to avoid emotional and
physical stress
8. Teach client about life long hormone
replacement.
9.Administer antiemetic to prevent fluid &
electrolytes imbalance
159
 DIABETES MELLITUS
A major health problem worldwide
A chronic disease that requires lifelong
behavioral and lifestyle changes.
Main feature is chronic
hyperglycemia(high blood glucose
level) resulting from problems with
insulin secretion, insulin action or
both.

160
 Classification of DM

Type 1 Diabetes (Insulin Dependent

Diabetes Mellitus)
Primary beta cell destruction leading
to absolute insulin deficiency
Autoimmune process
Idiopathic
Abrupt onset of symptoms, usually at
young age 161
◆ Type 2 Diabetes (Non-insulin-
dependent diabetes mellitus)

– Ranges from insulin resistance with an

insulin deficiency to secretory deficit
with insulin resistance.
Onset is usually after age 40 without
classic symptoms
Obesity and heredity have been
associated with susceptibility and onset

163
Gestational Diabetes mellitus
Carbohydrate intolerance with onset
or first recognized during pregnancy.
Children of mother with GDM are at
greater risk for neonatal mortality,
congenital malformation and
macrosomia (large body size.)
Children of mother with GDM have
increased risk of obesity and impaired
glucose tolerance during late
adolescence and young adulthood.
165
 Other specific Type
Genetic defects of beta cell function.
Genetic defects in insulin action.
Diseases of the exocrine pancreas,
pancreatitis, trauma, neoplasia, cystic
fibrosis
Endocrinopathies; acromegaly, Cushing
disease, hyperthyrodism.
Drug or chemical induced(like thyroid
hormone, beta-adrenegics
ago0nist,glucocorticoids.
166
 Physiology
Endocrine Pancreas has 1 million cell
islets of Langerhans, most of it has
digestive functions
Two types of islets cells that are
important to glucose control
1.Alpha cells produces glucagon
2. Beta cells produces insulin

167
◆ GLUCAGON-is a major counter
regulatory hormone. It release
glucose from cell storage sites
whenever blood glucose level are low.
◆ INSULIN- allows body cells to use
and store carbohydrate, fat and
protein.

168
◆ Insulin a protein peptide chains, this
protein is a precursor molecule.
◆ It is inactive and become active once
it become smaller.
◆ Proinsulin is a precursor that includes
the alpha and beta chains of insulin
molecule.
◆ Proinsulin is converted in the beta
cells into equal amounts of insulin
and C-peptide.

169
◆ C-peptide levels are used to measure
the rate that beta cells secrete
insulin.

170
 Function of Insulin
1. Insulin allows glucose in the blood to
move into cells to make energy. It is
the key to open cell membrane to
glucose
2. It promotes production and storage of
glycogen in the liver. (Glycogenesis)
3. It inhibits glycogen breakdown into
glucose. (Glycogenolysis) conversion
of fats to acids (ketogenesis)
Conversion of protein to glucose.
(gluconeogenesis) 171
5. In muscle, insulin promotes protein
and glycogen synthesis
6.In fats cell, insulin promotes
triglyceride storage
GLUCOSE HOMEOSTASIS
Glucose is the main fuel for CNS cells.
Fatty acids can be used as fuel when
glucose is not available .
The fuels of glucose and fatty acids are
stored inside the cell, in the liver and
muscles as glycogen.
172
In fats cells it is stored as triglyceride.
Triglyceride is the most efficient
means of storing energy.
Protein can also be used as energy
only during starvation but in an
ordinary normal condition.
The combined actions of insulin and
counter regulatory hormone keep
blood glucose level within range of
6 8 - 1 0 5 m g / d L t o s u p p o r t b ra i n
function.
173
When glucose level falls, insulin
secretion stops and glucagon (counter
regulatory) hormone is released
causing glycogenolysis,
g l u c o n e o g e n e s i s a n d w h e n l i ve r
glucose is not available lipolysis and
proteolysis are process to provide fuel
or energy.
Other hormones that increases blood
glucose level are the epinephrine,
norepinephrine, growth hormone and
cortisol.
174
 Pathophysiology
The lack of insulin either due to lack of
production or problem with insulin
use at its cells receptors prevents
some cells from using glucose for
energy.
Without insulin the body enters into a
serious state of breakdown of body
fats and protein.

175
cont.
Counter regulatory hormone increases
to make glucose from other sources.
Without insulin, glucose are build up in
the blood, causing hyperglycemia
which causes fluid and electrolytes
imbalance

176
Increase blood osmolarity==ICF
dehydration
Glycosuria==glucose level exceeds
renal threshold (180mg/dl)
Polyuria==glucose exerts high osmotic
pressure within the renal
tubules==osmotic
diuresis==hypovolemia==ECF
dehydration==Polydipsia==increase
blood viscosity== sluggish circulation

177
◆ Prone to infection=poor wound
healing
◆ Polyphagia-cell are starved- liver will
react to convert glycogen, fats
stored into glucose to be use as
energy(lipolysis) causing
Hyperlipedemia.

178
 PRIMARY METABOLIC ABNORMALITY

Deficiency in function Abnormal ketogenesis blocked

of insulin

Associated illness Abnormal ketogenesis blocked

Counter-regulatory Glucose production

hormones Glucose utilization

Protein catabolism Hyperglycemia

Glycosuria
Blood Urea Nitrogen
Osmotic Fluid
diuresis intake Associated illness

ECF
Dehydration
Renal Severe Hyperosmolality Hypovolemia
insufficiency

Fluid Shifts Shock

Intracellular Tissue hypoxia

Coma Lactic 179
Acidosis
dehydration
180
 Clinical manifestation
3 P’s
1. Polyuria -frequent and excessive urination

2. Polydipsia -excessive thirst

3. Polyphagia- excessive eating

4. Dehydration

5. Glycosuria

181
6. Kussmaul respiration
7. Hemoconcentration
8. Hypovolemeia
9. Hypoperfusion
10. Hypoxia
11. Hypokalemia/hyperkalemia

182
 Laboratory assessment
Blood Test
a. Capillary blood testing using a blood
glucose meter
b. Fasting blood glucose level

c. Glycosylated hemoglobin assay

(HbA1c) this is a good indicator of
the average blood glucose level for 3
months.
183
d. Glycosylated serum protein and
albumin- this is indicate blood
glucose control over a shorter period
of time, useful when tight control of
blood glucose level is needed.
e. Oral glucose tolerance test (OGTT) is
the most sensitive test for diagnosing
DM
Urine Test
a. Urine test for ketone to determine
impending ketoacidosis
184
b. Urine test for renal function- test for
presence of micro
albumin
c. Urine for glucose- testing for
presence of glucose in the urine
Other test
a. Measuring level of islet cell antibodies
(ICA) for type 1 DM
b. Measurement of C-peptide level

185
 Medical management

Medication
a. Oral hypoglycemic

b. Insulin

Diet/ Meal Plan

Exercise
Monitoring/Control
Education
186
 Drug therapy
◆ Oral therapy prescribed after dietary
control is insufficient and client is
highly symptomatic.
◆ Drugs includes:

1. Sulfonylurea- this drug stimulates

insulin secretion which reduces liver
glucose output and increases cell
u p t a ke o f g l u c o s e a n d e n h a n c e
sensitivity of cell receptors sites.
187
2. Meglitinide Analogs- it lower blood
glucose by triggering insulin secretion
via interaction with the adenosine
triphosphate- sensitive potassium
channel on pancreatic beta cells.
3.Biguanides- lowers glucose by
decreasing liver glucose release and
decreasing cellular insulin resistance.
4. Alpha-Glucosidase inhibitors-reduce
hyperglycemia after meal by slowing
intestinal digestion and absorption of
carbohydrates
188
5. Thiazolidinedione Antidiabetic
agents- enhances insulin action, thus
promoting glucose utilization in
p e r i p h e ra l t i s s u e . T h e s e d r u g s
improves sensitivity to insulin in
muscle and fat tissue and inhibit
gluconeogenesis.
6. Combination Agents
-combining drug with different
mechanism of action
189
 Insulin Therapy
◆ Needed for type 1 DM but can be
used for type 2 DM.
◆ Type of Insulin

1. Source
a. Animal (beef or pork pancreas)
b. Combined animal source and
semisynthethetic human insulin
c. Synthetic human insulin

190
 2. Duration of Action
preparation Brand Onset (hr) Peak (hr) Duration
(hr)

Rapid acting Humalog 0.25 0.5-1.5 3-4

Short acting Humulin R 0.5 2-4 6-8

Intermediate NPH 1.5 4-12 24

acting

Long acting Lantus 2-4 none 24

192
 Pharmacokinetics of Insulin
D e p e n d s o n p hy s i c a l f a c t o r a n d
injection technique.
1. Injection site-site of injection affects
speed of insulin absorption
Fastest in the abdomen except for a 2-
inch radius around the navel. Rotation
within one anatomic site is preferred
to rotation from one site to another

193
◆ Deltoid, thigh and buttocks.
◆ Rotating injection sites prevents
lipohypertrophy or lipoatrophy
◆ 2. Absorption rate
◆ The longer the duration of action-
unpredictable absorption
◆ The larger the dose the more
prolonged the absorption
◆ 3. Injection depth – injection are
made in the subcutaneous tissue

194
◆ 4. Time of injection
◆ Regular insulin -30 min. before meal-
provides greater amount of plasma
free insulin
◆ Eating within few minutes after
injection reduces the ability of at
mealtime or before injecting reduces
the ability of insulin to prevent rapid
rises of blood glucose after meal and
increased the risk of delayed
hypoglycemia.
195
◆ 5. Mixing of Insulin-mixing different
types of insulin can change the timing
of the peak action.
◆ Mixture of short and intermediate acting
insulin- produces normal blood response
to other client than a single dose.
◆ Short acting or rapid acting insulin
mixed with long acting , withdraw the
short acting dose from the vial then the
long acting insulin t o p r e ve n t
contamination of the short acting
insulin.
196
197
 Complication of insulin injection
1. Lipoatrophy- a loss of tissue in areas
of repeated injection that result from
immune reaction to impurities in
beef or pork insulin
2. Lipohypertrophy- increased swelling
of fat that occurs at the site of
repeated insulin injections

198
3. Fasting Hyperglycemia
a. D a w n p h e n o m e n o n - r e s u l t f r o m
nighttimes' release of growth
hormone that causes the blood
glucose elevation at about 5-6am
b. Somagyi’s phenomenon-morning
hyperglycemia from the effective
counter regulatory response to
nightmare hypoglycemia

199
 Alternative method of insulin
administration
1. Continous subcutaneous infusion of
insulin-given by an externally worn
pump containing a syringe with rapid
or short acting insulin
2. Implanted insulin pumps-a pump is
planted on the peritoneal cavity,
where insulin are is absorbed by
local blood vessels

200
 Diet therapy
◆ Meal plan, education, counseling
program should be individualized
◆ Meal plan is based on the client’s usual
food intake. Consistency in the time
and amount of food eaten.
◆ Protein intake 15%-20% of total daily
calories those with normal kidney
function. If with micro-albuminuria
reduce to 10%
201
◆ Fat and Carbohydrate- based on
individual goals. From 80-90% of
calories, less than 10% should be from
saturated fat and up to 10% from
polyunsaturated fat.
◆ Food high in trans-fatty acids are
avoided or severely limited. For
carbohydrate emphasis is on total
amount of carbohydrate consumed
rather than the source of carbohydrate.

202
Fiber- high fiber diet improves
carbohydrate metabolism and lower
cholesterol levels.
This can also reduce abdominal
cramping, loose stools and flatulence.
Food rich in fiber are legumes, lentils ,
roots, all type of whole-grain.

203
 Education
1.Activity /Exercise
• Increase CHO uptake by the cells

• Decrease insulin requirements

2. Allow additional source of CHO-

snacks
3. Maintain IBW, monitoring of blood
glucose level regularly.
4. Follow diet prescribed by dietician
204
205
Long-Term Complications of Diabetes
◆ Macrovascular: result from changes in the
medium to large blood vessels.
– Blood vessel walls thicken, sclerose, and
become occluded by plaque that adheres to the
vessel walls.
– Eventually, blood flow is blocked.
◆ Accelerated atherosclerotic changes, coronary
artery disease, cerebrovascular disease, and
peripheral vascular disease
 Complication
◆ Macrovascular
1.CVD
2. MI
3. Hypertension
Cerebrovascular
1. Stroke

2. Peripheral vascular disease

207
◆ Microvascular: (or microangiopathy) is
characterized by capillary basement membrane
thickening.
◆ Diabetic retinopathy and Nephropathy
◆ Neuropathic: ulcers occur on pressure points in
areas with diminished sensation in diabetic
polyneuropathy.
◆ Because pain is absent, the ulcer may go unnoticed.
– Peripheral neuropathy, Autonomic neuropathies,
Hypoglycemic unawareness, Neuropathy, Sexual
dysfunction
Neuropathic Ulcers
◆ Microvascular
1. Diabetic Retinopathy
2. Diabetic Neuropathy
3. Diabetic Nephropathy
4. Male erectile dysfunction

210
 Disorder of the Posterior Pituitary
Gland
DIABETES INSIPIDUS- a disorder of the water
metabolism caused by a deficiency of ADH-
either decrease in ADH synthesis or inability
of the kidneys to responds appropriately to
ADH.
Classification:
1. Nephrogenic- is an inherited disorder. The
renal tubules do not respond to the actions
of ADH that result to inadequate water
reabsorption by the kidney.

211
2. Primary diabetes insipidus- is caused by a
defect in hypothalamus or pituitary gland,
resulting in a lack of ADH production or
release
3. Drug related diabetes insipidus-is caused
by administration of Lithium carbonate and
Demeclocycline, these drug can interfere
with kidney’s response to ADH

212
 Patho
ADH deficiency result in excretion of large volume of
diluted urine. If ADH is not present , the distal
tubules and collecting ducts of kidney remain
impermeable to water. So water is excreted as
urine rather than absorbed which leads to
polyuria. Dehydration results causing increase in
plasma osmolality that stimulates the
osmoreceptors to relay sensation of thirst to
cerebral cortex. Normally thirst promotes
increased fluid intake and aids in maintaining
water homeostasis.

213
 Clinical Manifestation
1. Polyuria
2. Excessive thirst
3. Poor skin turgor
4. Dry and cracked mucous membrane
5. Hypotension
6. Decreased pulse pressure
7. Tachycardia
8. Hemoconcentration, increased hgb, increased hematocrit
9. Increased urine output
10. Low specific gravity of urine
11. irritability

214
12. Decreased cognition
13. Hyperthermia
14. Lethargy to coma
15. Ataxia

215
 Medical Intervention
◆ Drug therapy
◆ for partial deficit oral Chlorpropamide
(Diabinese or clofibrate) these drug
increases action of existing ADH
◆ For severe deficiency- Desmopressin
acetate (DDAVP) administered intranasal
◆ Subcutaneous Vasopressin is used if
patient is with allergy or URTI.

216
 Nursing Intervention

1. Accuaretely measure I &O

2. Check urine specific gravity
3. Encourage to consume amount of oral
fluid equal to urine output.
4. Record client’s weight daily
5. Maintain patency of IV fluid.
6. Health instruction on vasopressin adverse
effect like polyuria & polydipsia
7. Wear an ID Medic alert bracelet
217
Syndrome of Inappropriate Antidiuretic
Hormone
◆ SIADH – also known as Schwartz-Barter syndrome
a condition when vasopressin (ADH) is secreted
even when plasma osmolarity is low or normal
◆ Conditions causing SIADH

1.Malignancies
Ca of the lungs
Hodgkin’s lymphoma
Non Hodgkin’s lymphoma

218
◆ 2. CNS Disorders
Trauma
Infection
Strokes
Systemic lupus ertheymatosus
3. Pulmonary Disorders
Viral & Bacterial Pneumonia
Active TB
Pneumothorax
Positive pressure ventilation

219
◆ 4. Drugs
Exogenous ADH
Chlorpropamide
Vincristine
Carbamazapine
Tricyclic antidepressant
General anesthetics

220
 Patho
◆ Decreased in plasma osmolality inhibits ADH
production and secretion. The feedback
mechanism that regulate ADH do not function
properly. ADH continue to released even when
plasma is hyposmolar. Water is retained which
result to dilutional hyponatremia and expansion of
ECF volume. This increase in plasma volume
causes an increase in the glomerular filtration rate
so it inhibit the release of Renin and aldosterone.
The combined effect is an increased sodium loss
in urine=further hyponatremia

221
 Clinical Manifestation
1. Loss of appetite
2. Nausea & vomiting
3. Weight gain
4. Urine volume decrease
4. Lethargy
5. Headache
6. Hostility & disorientation
7. Change in level of consciousness
8. Seizure & coma
9. Tachycardia(increase fluid volume)
10. Hypothermia(disturbance in CNS a drop of Na level to
115mEq/L

222
 Laboratory Exam
◆ Urine specific gravity- elevated
◆ Serum sodium level-decreased
◆ Radioimmunoassay of ADH- ADH
inappropriately elevated in relation to
plasma osmolarity
◆ Plasma volume increase & plasma
osmolarity decreased

223
 Interventions
◆ Fluid restriction

◆ Replacement of sodium

◆ Drug Therapy like Diuretics,

◆ Lithium Carbonate & Demeclocycline

◆ Preventing injury if client experience ICP or

seizure.

224
 Nursing Interventions
1.Measurement of I & O
2. Daily weight
3. Oral care-frequent rinsing to keep mucous
membrane moist.
4. Restrict fluid intake as low as 500-600 cc/24 hrs.
5. Used saline to mixed or dissolves medication
6. Iv fluid of Hypertonic Saline is used, saline
solution rather than water solution.
7. Observe for neurologic changes
8. Orientation to 3 spheres is done q2 hours
9.Environmental noise and lighting are reduce.
Safety measure like side rail securely in place
225
226