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Thyroid and Parathyroid Disorders Overview

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0% found this document useful (0 votes)
71 views145 pages

Thyroid and Parathyroid Disorders Overview

Uploaded by

kanjazj
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd

ENDOCRINE DISORDERS-

THYROID AND PARATHYROID


GLAND DISORDERS

MED SURG 11
Nup 223
Sept 2018
Mildred Odhiambo
THYROID GLAND
Butterfly shaped organ
Largest single endocrine gland in
the body (15-20g)
Located anterior to the trachea and
inferior to larynx
Medial region called the isthmus-
with right and left lobes
Tissue composed of thyroid follicles
THYROID GLAND
Originates from Ratke’s pouch at
the base of the tongue at 4-8wks
(Intrauterine life)
Secretes hormones by 11wks-
critical to neurological
development
THYROID GLAND
Follicleshas a sticky fluid in the
central cavity called colloid

The colloid is center of thyroid


hormone production

Productionis dependent on the


hormones essential and unique
component iodine
THYROID GLAND
The thyroid gland
produces three
hormones:

1- Thyroxin (T4),
2- Calcitonine.
3- Triiodthyronine(T3),
THYROID GLAND
BLOOD SUPPLY

Superior thyroid artery is a branch of the


external carotid artery
It supplies the superior and anterior portions
The inferior thyroid artery arises from the
thyrocervical trunk
Supplies the postero-inferior aspect
10% of people have an additional artery- the
thyroid ima artery
Comes from the brachiocephalic trunk of the
arch of aorta
Supplies the anterior surface of the isthmus
BLOOD SUPPLY
Venous drainage- superior,
middle and inferior thyroid veins
form a venous plexus
Superior and middle veins drain
into the internal jugular veins
Inferior drains into
brachiocephalic vein
NERVE SUPPLY
Nerve supply is by branches
derived from sympathetic trunk
SYNTHESIS AND RELEASE OF THYROID
HORMONES
Thyroglobulin a glycoprotein is
secreted into the colloid by the
follicle cells

Atoms of the mineral iodine attach


to thyroglobulin and produce
hormones
SYNTHESIS AND RELEASE OF
THYROID HORMONES
Hormones T3 and T4 are bound
to specialized transport proteins
called thyroxine binding
globulins(TBGs), or albumin or to
other plasma proteins

Release of T3 and T4 from the


thyroid gland is regulated by
thyroid stimulating hormone
(TSH)
REGULATION OF THYROID
HORMONE LEVELS
FUNCTIONS OF THYROID
HORMONE
Influence basal metabolic rate
Raise body temperature
Protein synthesis
Fetal and childhood tissue
development & growth
Normal development of nervous
system in utero and early childhood
Support adult neurological function
FUNCTIONS OF THYROID
HORMONE
Deficiencies of thyroid hormones
can influence libido, fertility and
other aspects of reproductive
function
Increase body’s sensitivity to
catecholamines (epinephrine and
norepinephrine) from the adrenal
medulla
Excessive T3 and T4 accelerates the
heart rate, strengthens the heart
Thyroid Hormones

Hormone Function Stimulated by

T3/T4 h metabolic rate i metabolic rate


h protein synthesis i T3/T4
h energy production h TSH
Most important hormone in day
today regulation of metabolic rate

Calcitonin
i blood calcium concentration
i the reabsorption of Ca and Ph
h blood Ca levels
from bones to blood
Calcitonin “tones” down serum
Ca levels

29/11/2010 16
PATHOPHYSIOLOGY
 Thyroid hormone secretion leads
to hyperthyroidism
 hence thyrotoxicosis
EFFECT OF THYROID
HORMONES
Metabolism in all body organs
Stimulate the heart
 heart rate stroke volume
cardiac output blood flow
GOITRE
A condition that increases the
size of your thyroid
More common in women.
May affect thyroid functions.
A person with goiter can have
normal levels of thyroid hormone
(euthyroidism), excessive levels
(hyperthyroidism) or levels that
are too low (hypothyroidism).
Colloid Goiter (Endemic)
 A colloid goiter develops from the lack of
 People who get this type of goiter usually live in
areas where iodine is scarce.
 Nontoxic (Sporadic)
 The cause of a nontoxic goiter is usually
unknown
 May be caused by medications like lithium.
 Lithium is used to treat mood disorders such as a
bipolar disorder.
 Nontoxic goiters don’t affect the production of
thyroid hormone
 Thyroid function is healthy. They are also benign.
Endemic (Iodine-Deficient)
Goiter
CAUSES
Iodine deficieny
Grave’s disease
Hashimoto’s disease
thyroiditis
Thyroid nodules (cysts)
Thyroid cancer
Pregnancy
Clinical features
Neck swelling
difficulty swallowing or breathing
coughing
hoarseness in your voice
dizziness when you raise your
arm above your head
DIAGNOSIS
Physical examination
Blood tests
Thyroid scan
Thyroid ultrasound
Biopsy
Management
Many goiters of this type decreased after
correction of iodine insufficiency.
When surgery is recommended, post
operative complications can be minimized
by pre operative iodide administration to
reduce the size & vascularity of goiter.

Prevention
Providing children in iodine-poor region with
iodine compounds.
Use of iodized salt.
THYROTOXICOSIS
Hyper-metabolic clinical syndrome
resulting from serum elevation of
thyroid hormone levels (T3&T4)

CAUSES
 GRAVE’S disease
Multinodular goitre
Toxic adenoma

GRAVE’SDISEASE is the most


common form
GRAVE’S DISEASE
Autoimmune disease
Female : Male ratio- 5:1 or 10:1
Has a strong hereditary
component
Diagnosis is mainly made by the
symptoms
SIGNS AND SYMPTOMS
Skin is warm and moist, palms are
warm, moist and hyperemic and
Plummer’s nails (separation of nail
from nail bed )are seen
Peritibial myxedema
Alopecia and vitiligo
Severe cases of proptosis
(Exopthalmus)
Excessive sweating & heat
intolerance
Peritibial myxedema  Proptosis/exopthalmus

Vitiligo
SIGNS AND SYMPTOMS
Cardiovascular symptoms:-
palpitations, Congestive cardiac
failure (CCF), systolic
hypertension
Metabolic symptoms- weight loss
despite of increased in appetite
GIT (gastrointestinal): - hyper-
defecation
Exacercebate bronchial asthma
Cont.
CNS (central nervous system)-
nervousness, irritability, tremor,
insomnia, proximal muscle
weakness
In females: amenorrhea,
oligomenorrhea
Oligomenorrhea is a condition
that involves having light or
infrequent menstrual periods
Males: impotence and loss of libido
Eye signs
VON GRAFFE’S
SIGN- lid lag

JOFFROY’S SIGN-
absence of
winking of
forehead on
looking up
cont
STELLWAG’S SIGN- reduced
frequency of blinking
DALRIMPLE’S SIGN- Lid retraction
exposing upper sclera- widened
opening of eye lid
MOBIUS SIGN- absence of
convergence
COMPLICATIONS
Thyroid crisis (storm)
A sudden worsening of
hyperthyroidism symptoms that
may occur with infection or
stress.
Characterized by -Fever,
decreased mental alertness, and
abdominal pain
Immediate hospitalization is
needed.
Cont. COMPLICATIONS
Heart-related complications
including:
◦ Rapid heart rate
◦ Congestive heart failure
◦ Atrial fibrillation
Increased risk for osteoporosis, if
hyperthyroidism is present for a
long time
INVESTIGATIONS

Thyroid-stimulating hormone (TSH) assay


reveals a decrease in result (normal TSH:
0.5–1.5 mU/L).
Elevation of thyroid hormones decreased
TSH secretion by negative feedback.
Elevated Thyroxine (T4) radioimmunoassay
(normal values: 5.0–12.0 μg/dL).
Elevation reflects overproduction of thyroid
hormones; monitors response to therapy.
INVESTIGATIONS
Elevated Tri-iodothyronine (T3)
radioimmunoassay (normal values:
80–230 ng/dL).
Elevation reflects overproduction of
thyroid hormones.
Other Tests: 24-hr radioactive iodine
uptake;
thyroid autoantibodieS
antithyroglobulin
electrocardiogram (ECG)
MANAGEMENT
GOAL of treatment:
Reducing thyroid hyperactivity for
symptomatic relief
Removing the cause of complications.

Three forms of treatment are available:


Irradiation
Pharmacotherapy
Surgery with the removal of most of
the thyroid gland
Radio iodine treatment
Radio iodine ablation
postmenopausal women and
elderly men
pharmacotherapy
 Objectiveis to inhibit hormone synthesis or release
and reduce the amount of thyroid tissue.

 Most commonly used medications are


 propylthiouracil (Propacil, PTU)
 methimazole (Tapazole)
 until patient is euthyroid.
 Maintenance dose is established
 followed by gradual withdrawal of the medication
over the next several months.
 Antithyroid drugs are contraindicated in late
pregnancy because of a risk for goiter and cretinism
in the fetus.
 Thyroid hormone may be administered to put the
thyroid to rest.
pharmacotherapy
Immediate control: propranolol
40mg/6hr orally
Long term control:
Antithyroid drugs- carbimazole
15mg tid initially and then
reducing it to 5mg tid for 12-18
months
pharmacotherapy
Adjunctive Therapy

Potassium iodide, Lugol’s solution, and


saturated solution of potassium iodide
(SSKI) may be added.
Beta- adrenergic agents may be used to
control the sympathetic nervous system,
effects that occur in hyperthyroidism;
for example, propranolol is used for
nervousness, tachycardia, tremor,
anxiety, and heat intolerance
Pharmacologic Highlights

1. Propylthiouracil (PTU) an antithyroid


agent is given to return the patient to the
euthyroid (normal) state.
PTU inhibits use of iodine by thyroid
gland
blocks oxidation of iodine
 inhibitis thyroid hormone synthesis

2. Methimazole (Tapazole) an antithyroid


agent is given to return the patient to the
euthyroid (normal) state by inhibiting use
of iodine by thyroid gland.
Pharmacologic Highlights
3. Other Drugs: Beta-adrenergic
blockers, corticosteroids,
radioactive iodine
Exopthalmos: corticosteroids,
tarsorrhaphy, orbital
decompression
Cardiac arrythmias- beta
blockers; cardioversion done in
euthyroid state
Nursing Interventions

Provide adequate rest.


Administer sedatives as prescribed.
Provide a cool and quiet
environment.
Obtain weight daily.
Provide a high-calorie diet.
Avoid the administration of
stimulants.
 Administer antithyroid medications
(propylthiouracil [PTU]) that block thyroid
synthesis, as prescribed.
 Administer iodine preparations that inhibit
the release of thyroid hormone as prescribed.
 Administer propranolol (Inderal) for
tachycardia as prescribed.
 Prepare the client for radioactive iodine
therapy, as prescribed, to destroy thyroid
cells.
 Prepare the client for thyroidectomy if
prescribed
SURGICAL MANAGEMENT
Why use surgery?
 Used to remove large goiter causing
tracheal or esophageal compression
 Used for patients who do not have
good response to antithyroid drugs
TWO TYPES OF SURGERIES:
1. Total thyroidectomy (must take
lifelong thyroid hormone
replacement)
2. Subtotal thyroidectomy
PREOPERATIVE CARE
Patient should become euthyroid
before surgery to prevent thyroid
crisis.

Assessment of vocal cord


condition

Low weight:
High protein, high carbohydrate
diet for days/weeks before
PRE-OPERATIVE CARE

1. Antithyroid drugs to suppress function


of the thyroid
2. Iodine prep (Lugols or potassium
iodide solution)
 To decrease size and vascularity of
gland
 To minimize risk of hemorrhage,
 Reduce risk of thyroid storm during
surgery
3. Tachycardia, BP, dysrhythmias must
be controlled preop
PREOPERATIVE TEACHING
Teach coughing and deep
breathing exercises
Teach support neck when coughing
& deep breathing
 Support neck when moving
reduces strain on suture line
Expect hoarseness for few days
(endotracheal tube)

29/11/2010
POST-OP THYROIDECTOMY
NURSING CARE
1. Vital signs
2. Intravenous fluids
3. Intake – output monitoring
4. Semifowlers
5. Support head
6. Avoid tension on sutures
5. Pain meds, analgesic lozengers
6. Humidified oxygen, suction
Cont. POST-OP THYROIDECTOMY
NURSING CARE
7. First fluids: cold/ice, tolerated
best, then soft diet
8. Limited talking , hoarseness
common
9. Assess for voice changes: injury
to the recurrent laryngeal nerve
POSTOP THYROIDECTOMY
NURSING CARE
 CHECK FOR  CHECK FOR
HEMORRHAGE 1st 24 RESPIRATORY DISTRESS
hrs:  Laryngeal stridor
 Look behind neck and (harsh high pitched
sides of neck respiratory sounds)
 Check for c/o pressure  Result of edema of
or fullness at incision glottis, hematoma or
site tetany
 Check drain  Tracheostomy
 Report if bleeding is set/airway/ O2, suction
high  Call doctor for extreme
hoarseness
Complication of operation
 Hemorrhage
 Recurrent laryngeal nerve damage.
 Superior laryngeal nerve damage
 Hypoparathyrodism
 Hypothyroidism
 Sepsis
 Postoperative infection
 Hypertrophic scaring (keloid)

56
Toxic Single Adenoma
(TSA)
 TSA is a single hyper functioning follicular
thyroid adenoma.
 Benign monoclonal tumor that usually is larger
than 2.5 cm
 Itis the cause in 5% of patients who are
thyrotoxic
 Nuclear Scintigraphy scan shows only a single
hot nodule
 TSH is suppressed by excess of thyroxines
 So the rest of the thyroid gland is suppressed
Toxic Single Adenoma
(TSA)
Nucleotide
Scintigraphy
Age and Sex
Age

◦ Graves disease 20 to 40
◦ Toxic multinodular goitre > 50 yrs
◦ Toxic Single Adenoma 35 to 50
◦ Sub Acute Thyroiditis Any age

Sex M : F ratio
◦ Graves Disease 1: 5 to 1:10
◦ Toxic MNG 1: 2 to 1: 4
Nucleotide Scintigraphy
Clinical Features

1. Those that occur with any type of


thyrotoxicosis

2. Those that are specific to Graves


disease

3. Non specific changes of hyper


metabolism
Thyroid hormone levels
Normal TSH levels range from 0.4 ‑ 4.0
mIU/L for the average adult
High TSH levels for the average adult are
4.2 mIU/L and over.
This reading typically indicates an
underactive thyroid.
Low TSH levels for the average adult are
less than 0.2 mIU/L.
This reading indicates an overactive
thyroid

Note: mIU/L- milli-international units per


liter
Thyroid hormone levels
Normal ranges for adults
generally fall between these
values
Total T4 5.0-12 μg/dL
(micrograms per decilitre)
Total T3 80-190 ng/dL
(nannogram per decilitre)
Free T4 1.0-3.0 ng/dL
Free T3 0.25-0.65 ng/dL
INVESTIGATIONS
LABORATORY TESTS
-serum T3, T4.
-serum TSH.
-serum LATS: (Long Acting Thyroid
Stimulator)
in grave’s disease
-thyroid antibodies:
in hashimoto’s disease.
-serum cholesterol
increase cholesterol level in hypothyroidism
INVESTIGATIONS
IN HYPERTHYROIDISM:
 T3
 T4
 TSH in Graves disease
 Radioactive Thyroid Scan
 Ultrasonography: used to determine goiter or
nodules
 ECG (electrocardiogram): note tachycardia

29/11/2010 65
Radiological Investigation

-chest and neck x-ray:


Show descend of thyroid gland
to thorax and mediastanal
shifting in retrosternal goitre.

-iodine isotopes
By i.v injection of I131. Then,
use gamma rays to show hot
and cold nodules.

-CT scan
Show thyroid size and if there is
compression to trachea
INVESTIGATIONS
Endoscopic investigation:
-bronchoscopy: show compression
and infiltration of trachea by
tumer
Biopsy:
-fine needle aspiration biopsy.
-true-cut biopsy.
MANAGEMENT
Depending on clinical features
Toxic Multinodular Goiter (TMG)

 TMG is the next most common hyperthyroidism -


20%
 More common in elderly individuals – long
standing goiter
 Lumpy bumpy thyroid gland
 Milder manifestations (apathetic hyperthyroidism)
 Mild elevation of FT4 and FT3
 Progresses slowly over time
 Clinically multiple firm nodules (called Plummer’s
disease)
 Scintigraphy shows - hot and normal areas
Toxic Multinodular Goiter (TMG)
Toxic Multinodular Goiter (TMG)
Toxic Multinodular goitre

Huge Toxic MNG Huge Toxic MNG


MULTINODULAR GOITRE
Excess production of thyroid
hormones from TSH
Occurs in individual over 60yrs
Females are mostly affected
SYMPTOMS
Large goitre with or without
tracheal compression
Goitre is nodular and palpable
Large goitre- Mediastinal
compression
With stridor, dysphagia, obstruction
of superior venacava
hoarseness
MANAGEMENT
Small goitre- no treatment-
Annual review
Large goitres: partial
thyroidectomy
 Radioactive
iodine
Recurrence is common in 10-20
yrs
THYROID STORM (CRISIS)
Rare but life threatening sudden
severe exarcerbation of
hyperthyroidism
CAUSES
Precipitated by stress or infection
Or Unrecognized thyrotoxicosis
Or inadequately treated
thyrotoxicosis
Following subtotal
thyroidectomy/radio active iodine
Trauma
Pregnancy
Emotional stress
SIGNS AND SYMPTOMS
Elevation of temperature
Increase in heart rate
Irritable
Delirius / comatose
Hypotension
Vomiting
Diarrhoea
MANAGEMENT
Treatment started immediately with
Propanolol 80mg/6hrs orally (dose
of 1-5mg/6hrs given IV)
Potassium iodide 60mg daily
orally/sodium iopodate 5oomg daily
orally
Carbimazole 60-120mg daily
Dexamethasone 2mg/6hrs IV
Fluid replacement
antibiotics
NURSING MANAGEMENT
ASSESSMENT
NURSING DIAGNOSIS
INTERVENTION
NURSING MANAGEMENT
Acute Care Patient
Management
Nursing Diagnosis:
 Decreased cardiac output
related to increased cardiac work
secondary to increased
adrenergic activity
Deficient fluid volume secondary
to increased metabolism and
diaphoresis.
NURSING MANAGEMENT
Outcome Criteria
Patient alert and oriented
Peripheral pulses palpable
Lung clear to auscultation
Urine output 30 ml/hr
Absence of life-threatening
dysrhythmias
NURSING MANAGEMENT
1. Patient Monitoring
Continuously monitor ECG for
dysrhythmias or HR ? 140
beats/min that can adversely
affect cardiac output and monitor
for ST segment changes
indicative of myocardial
ischemia.
Continuously monitor oxygen
saturation with pulse oximetry.
NURSING MANAGEMENT
CONT. MONITORING
Continuously monitor pulmonary
artery pressure.
Monitor fluid volume status;
measure urine output hourly and
determine fluid balance every 8
hours.
NURSING MANAGEMENT
2. Patient Assessment
Assess cardiovascular status; extra
heart sounds, complaints of
orthopnea or dyspnea on exertion.
Assess hydration status because
dehydration can further decrease
circulating volume and compromise
cardiac output.
Assess for pressure ulcer
development secondary to
hypoperfusion.
NURSING MANAGEMENT
3. Diagnostic Assessment
REVIEW THYROID STUDIES AS AVAILABLE.
Review serial serum electrolytes, serum
glucose, and serum calcium levels to
evaluate the patient’s response to therapy.
Review serial ABGs for hypoxemia and
acid-base imbalance, which can adversely
affect cardiac function.
Review serial chest radiographs for cardiac
enlargement and pulmonary congestion.
NURSING MANAGEMENT
4. Patient Management
Administer dextrose-containing
intravenous fluids as ordered to
correct fluid and glucose deficits.
Carefully assess the patient for heart
failure or pulmonary edema.
Dopamine may be used to support
blood pressure.
Provide supplemental oxygen to help
meet increased metabolic demands.
NURSING MANAGEMENT
 Once the patient is hemodynamically stable,
provide pulmonary hygiene to reduce pulmonary
complications.
 If the patient is in heart failure, typical
pharmacologic agents for treatment of heart
failure may also be indicated.
 Reduce oxygen demands by decreasing anxiety,
reduce fever, decrease pain, and limit visitors if
necessary.
 Anticipate aggressive treatment of precipitating
factor.
 Institute pressure ulcer strategies.
INFLAMMATORY GOITRE-(Thyroiditis)

Acute: rare and due to


suppurative infection of the
thyroid
Sub acute: also termed de
Quervains thyroiditis/
granulomatous thyroiditis –
mostly viral origin
Chronic thyroiditis: mostly
autoimmune (Hashimoto’s and
Acute Thyroiditis
Bacterial – Staph, Strep
Fungal – Aspergillus, Candida,
Histoplasma, Pneumocystis
Radiation thyroiditis
Amiodarone (acute/ sub acute)
Painful thyroid, ESR usually
elevated, thyroid function normal
Sub Acute Thyroiditis
Viral (granulomatous) – Mumps,
coxsackie, influenza, adeno and
echoviruses
Mostly affects middle aged
women, Three phases, painful
enlarged thyroid, usually complete
resolution
Rx: NSAIDS and glucocorticoids if
necessary
Sub Acute Thyroiditis (cont)
Silent thyroiditis
No tenderness of thyroid
Occur mostly 3 – 6 months after
pregnancy
3 phases: hyperhyporesolution,
last 12 to 20 weeks
ESR normal, TPO Abs present
Usually no treatment necessary
DEFINITION OF TERMS
ESR- Erythrocyte sedimentation
rate is a blood test that can
reveal inflammatory activity in
the body.
DEFINITION OF TERMS
Thyroperoxidase (TPO) is an enzyme
involved in thyroid hormone
synthesis, catalyzing the oxidation of
iodide on tyrosine residues in
thyroglobulin for the synthesis of
triiodothyronine and thyroxine
(tetraiodothyronine).
TPO is a membrane-associated
hemoglycoprotein expressed only in
thyrocytes and is one of the most
important thyroid gland antigens.
TPO VALUE <9.0 IU/mL
Reference values apply to all
ages.
Values above 9.0 IU/mL generally
are associated with autoimmune
thyroiditis, but elevations are also
seen in other autoimmune
diseases.
Clinical Course of Sub Acute
Thyroiditis
Chronic Thyroiditis
Hashimoto’s
◦ Autoimmune
◦ Initially goiter later very
little thyroid tissue
◦ Rarely associated with
pain
◦ Insidious onset and
progression
◦ Most common cause of
hypothyroidism
◦ TPO abs present (90 –
95%)
Chronic Thyroiditis
Reidel’s
◦ Rare
◦ Middle aged women
◦ Insidious painless
◦ Symptoms due to compression
◦ Dense fibrosis develop
◦ Usually no thyroid function
impairment
◦ Rule out thyroid cancer
Thyroiditis
The most common form of
thyroiditis is Hashimoto
thyroiditis, this is also the most
common cause of long term
hypothyroidism
The outcome of all other types of
thyroiditis is good with eventual
return to normal thyroid function
HYPOTHYROIDISM
Chronic deficiency of T4 and T3
Hypothyroidism results
from suboptimal levels of
thyroid hormone.
CLASSIFICATION
1. Central hypothyroidism.
 Failure of the pituitary gland,
the hypothalamus or
both to stimulate production of thyroid hormones.

2. Secondary or pituitary hypothyroidism.


 Due to pituitary disorder in secondary
hypothyroidism.
3. Tertiary or hypothalamic hypothyroidism.
 Due to a disorder of the hypothalamus resulting in
inadequate secretion of TSH due to decreased
stimulation of TRH.

4. The thyroid disorder is already present at


birth in cretinism
CAUSES

Autoimmune diseases-autoimmune
thyroiditis or Hashimoto’s disease (most
common cause of hypothyroidism in adults)
Atrophy of the thyroid gland. The thyroid
gland shrinks in size as a result of aging.
Therapy for hyperthyroidism- such
as radioactive iodine and surgery
(thyroidectomy)
Medications- lithium, iodine compounds,
and anti-thyroid medications- decrease
production of TSH.
Cont. CAUSES
Iodine deficiency or excess. Imbalance
in the iodine levels in the body also
affects the thyroid gland.

In adequate release of TRH or TSH from


hypothalamic –pituitary axis
(hypophysectomy or pituitary radiation)
PREVENTION
Increase in iodine intake.
Early detection. Undergoing
thyroid tests after a
thyroid surgery or therapy could
result in early detection and
prompt treatment of
hypothyroidism.
COMPLICATIONS
Hypothyroidism can be a life-
threatening disease if left
unchecked.

Myxedema coma-
decompensated state of severe
hypothyroidism
Patient is hypothermic and
unconscious.
ASSESSMENT AND DIAGNOSIS
Physical examination-inspect and
palpate routinely in all patients.
Serum thyroid-stimulating tests.
Serum T3 and T4. Measurement of
total T3 or T4 includes protein-bound
and free hormone levels that occur in
response to TSH secretion.
Thyroid antibodies- anti-thyroid
antibodies are positive in
Hashimoto’s thyroiditis (100%).
MEDICAL MANAGEMENT
Pharmacologic therapy.
Synthetic levothyroxine- the preferred
preparation for treating hypothyroidism
and suppressing nontoxic goiters.

Prevention of cardiac dysfunction- As


long as metabolism is subnormal and
the tissues require relatively little
oxygen, a reduction in the blood supply
is tolerated without overt symptoms
of coronary artery disease.
MEDICAL MANAGEMENT
Supportive therapy
Monitor oxygen saturation levels
Administer fluids cautiously
Avoid application of external
heat
Continue oral thyroid hormone
therapy
NURSING MANAGEMENT
Nursing Assessment
Assessment of the thyroid from an
interior or posterior position.
Auscultation of the lobes of the
thyroid gland using the diaphragm
of the stethoscope if there are
abnormalities palpated.
Assess thyroid gland for firmness
(Hashimoto’s) or tenderness
(thyroiditis).
NURSING MANAGEMENT
 Nursing diagnoses:
 Activity intolerance related to fatigue and
depressed cognitive process.
 Risk for imbalanced body
temperature related to cold intolerance.
 Constipation related to depressed
gastrointestinal function.
 Ineffective breathing pattern related to
depressed ventilation.
 Disturbed thought processes related to
depressed metabolism and altered
cardiovascular and respiratory status.
NURSING MANAGEMENT
Planning & Goals
To achieve a successful nursing care plan,
the following goals should be realized:
Increase in participation in activities.
Increase in independence.
Maintenance of normal body
temperature.
Return of normal bowel function.
Improve respiratory status.
Maintenance of normal breathing pattern
Improve thought processes
NURSING MANAGEMENT
 Nursing Interventions
 Promote rest. Space activities to promote rest and
exercise as tolerated.
 Protect against coldness. Provide extra layer of clothing
or extra blanket.
 Avoid external heat exposure. Discourage and avoid the
use of external heat source.
 Mind the temperature. Monitor patient’s body
temperature.
 Increase fluid intake. Encourage increased fluid intake
within the limits of fluid restriction.
 Provide foods high in fiber.
 Manage respiratory symptoms. Monitor respiratory
depth, rate, pattern, pulse oximetry, and ABG.
 Pulmonary exercises. Encourage deep breathing,
coughing, and use of incentive spirometry.
 Orient to present surroundings. Orient patient to time,
place, date, and events around him or her.
NURSING MANAGEMENT
Evaluation
A successful nursing care plan has
achieved the following goals:
Increased participation in activities.
Increased independence.
Maintained normal body temperature.
Return of normal bowel function.
Improved respiratory status.
Maintained normal breathing pattern.
Improved thought processes.
NURSING MANAGEMENT
 Discharge and Home Care Guidelines
 At the completion of the home care instruction, the
patient or caregiver will be able to:
 Medication compliance. State that compliance
to medical regimen is life-long.
 Cold intolerance. State the need to avoid
extreme cold temperature until condition is stable.
 Follow-up visits. State the importance of regular
follow-up visits with health care provider.
 Weight reduction. Identify strategies for weight
reduction and prevention of constipation such as
high-fiber, low-calorie intake and adequate fluid
intake.
PATHOPHYSIOLOGY
Hashimoto’s disease( autoimmune
thyroiditis)
A form of primary hypothyroidism.
The thyroid tissue is attacked by the
person’s own immune system.
Occurs through cell and antibody-
mediated destruction of the tissue
The thyroid tissue is invaded by
lymphocytes and thyroid
autoantibodies which destroy the
cells of the thyroid
PATHOPHYSIOLOGY
The damaged thyroid tissue is no longer
able to synthesize and secrete thyroid
hormones resulting in low T3 and T4
levels.
This stimulates the hypothalamus and
anterior pituitary to release TRH and TSH
in an attempt to elevate these levels
resulting in higher than normal levels.
Process occurs over months to years and
the resulting damage affects most of the
bodies systems
PREDISPOSING FACTORS
Genetic predisposition
Increased iodine intake
Decreased selenium
Smoking
Hepatitis C
CLINICAL FEATURES
fatigue, malaise, and weight gain
Non-pitting edema particularly in the face
Cold intolerance
Hoarse voice
Dry skin and hair
Constipation
Irregular menses
Sexual dysfunction
Impaired fertility
Difficulty with concentration and memory
CLINICAL FEATURES
 Myalgias and arthralgias
 Depression
 Outward signs:
 Goiter
 Non-pitting edema
 Coarse hair, dry skin and brittle nails
 Slowed relaxation of reflexes
 Psychosis
 Bruising/bleeding
 Pericardial or pleural effusion
 Ascites
MANAGEMENT
The treatment of choice for
Hashimoto thyroiditis is thyroid
hormone replacement.
The drug of choice is orally
administered levothyroxine
sodium
Given for life.
MANAGEMENT
Goal of therapy is to restore a
clinically and biochemically
euthyroid state.
The standard dose is 1.6-1.8
mcg/kg lean body weight per
day, but the dose is patient
dependent.
CRETINISM

Hypothyroidism during birth (deficiency


of thyroid hormone) leading to stunted
physical and mental growth.
CAUSES
Iodine deficiency
Impaired thyroid gland
Hereditary condition interrupting
thyroid synthesis
 Intake of antithyroid drugs
during pregnancy (uncommon)
SIGNS AND SYMPTOMS
SUBJECTIVE FINDINGS OBJECTIVE FINDINGS
Gradual development of a coarse, Foreshortened base of the skull
dry skin
Mild inflammation of face and Low hair line
tongue
Umbilical hernia Short and wide face
Drooling from an open mouth Pallor
Underdeveloped mandible/
Listlessness Overdeveloped maxill
a
Slow movement Large, thick and protruding tongue
(Macroglossia

Constipation Delayed eruption of primary and


permanent teeth

Feeding difficulties and choking Short and thickened long bones

Myxedema Late appearing of epiphyses


MANAGEMENT
Goal of treatment is to correct
hypothyroidism and ensure normal
growth and neuropsychological
development.
Early diagnosis and thyroid
hormone replacement essential
Optimal care includes diagnosis
before age 10-13 days and
normalization of thyroid hormone
blood levels by age 3 weeks
MANAGEMENT
Only levothyroxine is recommended for
treatment.
 It has been established as safe, effective,
inexpensive, easily administered, and easily
monitored.
 Initial dosages of 10-15 mcg/kg/day,
equivalent to a starting dose of 50 mcg in
many newborns, have been recommended.
 However, in up to 43% of infants and 10% of
older children with congenital
hypothyroidism, TSH elevation fails to
normalize despite appropriate LT4 treatment.
MYXEDEMA COMA
A state of extreme
hypothyroidism with a very high
mortality rate (approaching 60%).
Patients with this condition
usually present with an acute
precipitating condition
CAUSES
Acute deficiency of T4 and T3
Long-standing, undiagnosed
hypothyroidism
Discontinuation of T4
replacement therapy
Failure to institute T4
replacement after radioactive
iodine ablation of the thyroid in
Graves disease or after total
thyroidectomy
PRECIPITATING CAUSES

Infection
Cardiovascular accident
Pulmonary infection
Congestive cardiac failure
Drugs such as narcotics,
sedatives, anesthetic agents,
antidepressants, and tranquilizers
(all of which depress the
respiratory drive).
SIGNS AND SYMPTOMS
Subjective findings Objective findings
Diminished hearing Anasarca
Cold intolerance Hoarsness
Fatigue Pericardial & pleural effusions
Lethargy Diminished hearing
Complaints of constipation Paralytic ileus
Unresponsiveness
Decreased breathing
Hypotension
Hypoglycemia
hypothermia
Definition of terms
Anasarca affects the whole body
and is more extreme than regular
edema
MEDICAL MANAGEMENT
Levothyroxine is administered
intravenously in a loading dose of
4 mcg/kg of lean body weight; this
is about 300-600 mcg, which
should be administered by rapid IV
injection.
The daily maintenance dose is 50-
100 mcg/d, administered
intravenously until the patient can
take it orally.
MEDICAL MANAGEMENT
Steroids, preferably
hydrocortisone in stress doses
Treatment of infection or any
other precipitating causes
Lasix to promote water diuresis
SURGICAL MANAGEMENT
Indications for surgery include the
following:
A large goiter with obstructive
symptoms, such as dysphagia, voice
hoarseness, and stridor, caused by
extrinsic obstruction of airflow
 Evaluate patients with these
symptoms with a barium swallow study
and pulmonary function tests, including
flow volume loops and a neck
computed tomography (CT) scan
SURGICAL MANAGEMENT
Presence of a malignant nodule - As
found by cytologic examination via
fine-needle aspiration
Presence of a lymphoma diagnosed
on fine-needle aspiration - Thyroid
lymphoma responds very well to
radiotherapy and is the treatment
modality of choice in this situation
Cosmetic reasons - For large,
unsightly goiters
NURSING MANAGEMENT
IN ACU TE CARE UNIT (ICU)
Ventilatory support for
hypoventilation and carbon
dioxide retention
Monitor oxygenation
Electrocardiographic
monitoring and a Swan-Ganz
catheter for hemodynamic
monitoring of vital signs
NURSING MANAGEMENT
Judicious rewarming to avoid
excessive vasodilatation, which
would increase oxygen
consumption and could lead to
worsening of hypotension and
vascular collapse
NURSING MANAGEMENT
 Assess level of consciousness
Restrict IV fluids
Vasopressors to improve blood
pressure
Thyroid replacement hormone
SICK EUTHYROID SYNDROME
Underproduction of thyroid
stimulating hormone from
anterior pituitary(which
stimulates the production and
release of T4 and T3)

CAUSE
Acute illness
SIGNS AND SYMPTOMS
Subjective findings Objective findings
none Normal or low TSH
Abnormal T4 (low or high)
Low T3
Absence of thyroid symptoms
MANAGEMENT
Treatment of acute illness

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